FMG The Handbook 1st Edition

Family Medicine Guide: The Handbook
Handbook Founders and Editors In-Chief

The Family Medicine Guide: The Handbook:
Dr. Hadi Alenazy
Dr. Abdulelah Bin Shihah
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Scientific Committee of The Family Medicine Guide: The

Handbook:
Dr. Areej Aldossary
Dr. Muna Almaghaslah
Dr. Aseel A.AlAssimi
Scientific Committee of The Family Medicine Guide The
Handbook:
Dr. Hossam Alawad Dr. Abdulelah Bin Shihah
Dr. Hanaa Almatrafi Dr. Rehab Aldubaisi
Dr. Samar Alsaigh Dr. Tahani Altamimi
Dr. Abdullah Almaqhawi Dr. Sultan Alharthi
Dr. Wael Basamad Dr. Rawan Alshreem
Dr. Khawlah Albatil Dr. Ahoud Alorayfij
Reviewers of The Family Medicine Guide:The Handbook:
Dr. Hossam Alawad Dr. Abdulelah Bin Shihah
Dr. Samar Alsaigh Dr. Ibrahim Algarni
Dr. Hussain Halawani Dr. Bayan Alajaji
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Authors of The Family Medicine Guide :The Handbook:

Dr. Abdulaziz Bagasi Dr. Zaenb Alsalman
Dr. Abdulaziz Suwaidi Dr. Waleed Alanazi
Dr. Abdulgader Mira Dr. Wael Basamad
Dr. Abdullah Alhelal Dr. Waad Almaramihi
Dr. Abdullah Almaqhawi Dr. Tariq Khushaym
Dr. Abdullah Alnughaymishi Dr. Tameem Alhomaid
Dr. Abdullah Khojah Dr. Tahani Asiri
Dr. Abdulmalik Aldeheem Dr. Tahani Altamimi
Dr. Abdulmhsen Alobidan Dr. Taghreed AL Shaban
Dr. Abdulrahman Al-mana Dr. Sultan Almuheza
Dr. Abdulrahman AlKthiry Dr. Sultan Alharthi
Dr. Abdulrahman Alrashed Dr. Suha Albahrani
Dr. Abdulrhman AlNaim Dr. Suaad fadhlalmawla
Dr. Abeer Theyab Dr. Shatha Alzahrani
Dr. Afnan Alotaibi Dr. Shahad Khawandanh
Dr. Ahmad Aldawalibi Dr. Sarah Alzaidi
Dr. Ahmed Allehyani Dr. Sara Aleraij
Dr. Ahmed I. Andijani Dr. Salwa Abbas
Dr. Ahmed Manaa Dr. Safa Alsaad
Dr. Akram Alandijani Dr. Reham Alanzi
Dr. Alanoud Alsubaie Dr. Reem Alqahtani
Dr. Alhanouf Altamimi Dr. Reem Alakeel
Dr. Amani Mahrous Dr. Razaz Wali
Dr. Anas Alonezan Dr. Razan Almuhyawi
Dr. Arwa Al-Mowaraie Dr. Rayana Ababtin
Dr. Atheer Alhumid Dr. Rawan Hemedy
Dr. Banan Almalki Dr. Rawan Al Shuraym
Dr. Bander Aldamkh Dr. Osama Alnafisah
Dr. Bashayer Alemam Dr. Omaymah Aljordi
Dr. Dakhel Almubarak Dr. Omar Alghamdi
Dr. Daniyah Alfitni Dr. Ohoud Aloraifej
Dr. Fahad Albahili Dr. Nourah Alageel
Dr. Fatimah Alhussain Dr. Nouf Albarnawi
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Dr. Ghadah Al-Ghamdi Dr. Norah Alenezi

Dr. Hanaa Almatrafi Dr. Naif Alshalhoub
Dr. Hanan AlAbdullah Dr. Naif Alotaibi
Dr. Hossam Alawad Dr. Murtada Alfayez
Dr. Husain Alraddadi Dr. Mohammed Ghazal
Dr. Khalid Alruwaili Dr. Mohammed Aldosari
Dr. Latifa Alanazi Dr. Malak Albalawi
Dr. Mai Alageel
Designing and Editing Committee for family medicine Guide :

Handbook:
Dr. Adel Yasky

Dr. Daniyah Alghaithi
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CONTENTS
SECTION 1: FAMILY MEDICINE ................................................................. 9

CHAPTER 1: HYPERTENSION ............................................................................... 9
CHAPTER 2: DYSLIPIDEMIA ............................................................................... 12
CHAPTER 3: DM................................................................................................ 17
CHAPTER 4: PERIODIC HEALTH MAINTENANCE ................................................. 38
CHAPTER 5: URTI .............................................................................................. 44
CHAPTER 6: COUGH ......................................................................................... 51
CHAPTER 7: HEADACHE .................................................................................... 58
CHAPTER 8: OBESITY ........................................................................................ 63
CHAPTER 9: ANEMIA ........................................................................................ 66
CHAPTER 10: SMOKING CESSATION .................................................................. 71
SECTION 2: INTERNAL MEDICINE .......................................................... 79
CHAPTER 1: EPILEPSY ....................................................................................... 79
CHAPTER 2: APPROACH TO DYSPNEA ............................................................... 84
CHAPTER 3: CNS INFECTIONS ........................................................................... 87
CHAPTER 4: BRUSING AND BLEEDING............................................................... 95
CHAPTER 5: ARTHARITIS ................................................................................ 102
CHAPTER 6: ASTHMA ..................................................................................... 115
CHAPTER 7: LOWER RESPIRATORY TRACT INFECTIONS ................................... 119
CHAPTER 8: COPD .......................................................................................... 122
CHAPTER 9: CHEST PAIN ................................................................................. 125
CHAPTER 10: HEART FAILURE ......................................................................... 128
CHAPTER 11: CARDIAC ARRHYTHMIA ............................................................. 132
CHAPTER 12: THYROID AND PARATHYROID DISORDERS ................................. 143
CHAPTER 13: PITUITARY AND ADRENAL DISORDERS ....................................... 151
CHAPTER 14: URINARY TRACT INFECTIONS..................................................... 155
CHAPTER 15: GASTRIC DISEASES .................................................................... 158
CHAPTER 16: STROKE AND TRANSIENT ISCHEMIC ATTACKS (TIA) .................... 163
CHAPTER 17: OSTEOPOROSIS ......................................................................... 167
CHAPTER 18: SEXUALLY TRANSMITTED INFECTIONS ....................................... 172
CHAPTER 19: HEPATIC DISORDER ................................................................... 184
CHAPTER 20: INFECTIOUS DISEASES ............................................................... 202
CHAPTER 21: FEVER OF UNKNOWN ORIGIN.................................................... 221
CHAPTER 22: NEUROLOGY ............................................................................. 226
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CHAPTER 23: NEPHROLOGY ........................................................................... 233

CHAPTER 24: PULMONARY............................................................................. 243
SECTION 3: PEDIATRIC ......................................................................... 250
CHAPTER 1: NEONATAL JAUNDICE .................................................................. 250
CHAPTER 2: DYSPEPSIA IN CHILDREN.............................................................. 251
CHAPTER 3: EMERGENCIES IN CHILDREN ........................................................ 252
CHAPTER 4: NEONATAL LEG AND FOOT ABNORMALITIES ................................ 259
CHAPTER 5: CONGENITAL HEART DEFECTS ...................................................... 263
CHAPTER 6: CHILDHOOD COMMON INFECTIOUS DISEASE .............................. 270
CHAPTER 7: INTELLECTUAL DISABILITIES ........................................................ 286
CHAPTER 8: GROWTH AND PUBERTY PROBLEMS............................................ 292
CHAPTER 9: APPROACH TO COUGH: ............................................................... 298
CHAPTER 10: ACUTE ABDOMINAL PAIN .......................................................... 303
CHAPTER 11: DIARRHEA IN CHILDREN ............................................................ 308
CHAPTER 12: INFANTILE COLIC ....................................................................... 309
CHAPTER 13: PEDIATRICS AND ADOLESCENTS MUSCULOSKELETAL PATHOLOGIES
.................................................................................................................... 311
CHAPTER 14: FAILURE TO THRIVE AND DEVELOPMENTAL DELAY ..................... 321
SECTION 4: OBSTETRIC AND GYN ...................................................... 327
CHAPTER 1: OBSTETRIC CARE ......................................................................... 327
CHAPTER 2: BREAST PAIN ............................................................................... 331
CHAPTER 3: LOWER ABDOMINAL PAIN IN FEMALES ....................................... 336
CHAPTER 4: COMMON PREGNANCY COMPLAINS ........................................... 347
CHAPTER 5: FAMILY PLANNING ...................................................................... 364
CHAPTER 6: COMMON GYNECOLOGICAL CONDITIONS ................................... 373
CHAPTER 7: INFERTILITY ................................................................................. 383
CHAPTER 8: MENOPAUSE & HORMONAL REPLACEMENT THERAPY ................ 388
SECTION 5: PSYCHIATRY ...................................................................... 396
CHAPTER 1: SLEEP DISORDERS ....................................................................... 396
CHAPTER 2: DEPRESSIVE DISORDERS .............................................................. 402
CHAPTER 3: ANXIETY DISORDERS ................................................................... 412
CHAPTER 4: ACUTE STRESS DISORDER ............................................................ 421
CHAPTER 5: OTHER PSYCHOLOGICAL DISORDERS ........................................... 427
SECTION 6: GERIATRICS AND PALLIATIVE CARE ............................. 445
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CHAPTER 1: PALLIATIVE CARE ......................................................................... 445

CHAPTER 2: COMMON GERIATRICS PROBLEM ................................................ 455
CHAPTER 3: DEMENTIA & ALZHEIMER’S DISEASE ........................................... 475
SECTION 7: DERMATOLOGY................................................................. 479
CHAPTER 1: PRIMARY VS SECONDARY SKIN LESIONS ...................................... 479
CHAPTER 2: SKIN CANCER .............................................................................. 480
CHAPTER 3: HAIR DISORDER .......................................................................... 484
CHAPTER 4: NAIL DISORDERS ......................................................................... 486
CHAPTER 5: HERPES SIMPLEX ......................................................................... 487
CHAPTER 6: TINEA INFECTION ........................................................................ 492
CHAPTER 7: COMMON DERMATOLOGICAL CONDITIONS ................................ 498
CHAPTER 8: ACUTE ALLERGIC REACTION ........................................................ 504
SECTION 8: SURGERY ........................................................................... 507
CHAPTER 1: PERIPHERAL ARTERY DISEASE...................................................... 507
CHAPTER 2: BREAST MASSES .......................................................................... 512
CHAPTER 3: HEAD INJURIES ............................................................................ 519
CHAPTER 4: ABDOMINAL PAIN ....................................................................... 525
CHAPTER 5: ANORECTAL AND COLORECTAL DISEASE ...................................... 534
CHAPTER 6: UROLOGY AND GENITAL DISORDERS ........................................... 542
SECTION 9: OPHTHALMOLOGY ........................................................... 565
CHAPTER 1: VISION LOSS ................................................................................ 565
CHAPTER 2: RED EYES IN CHILDREN ................................................................ 579
CHAPTER 3: EYE CONDITIONS IN CHILDREN .................................................... 583
CHAPTER 4: RED EYES IN ADULTS .................................................................... 587
CHAPTER 5: EYELID AND LACRIMAL DISORDERS ............................................. 593
CHAPTER 6: REFRACTIVE DISORDERS ............................................................. 596
SECTION 10: ENT ................................................................................... 599
CHAPTER 1: RHINITIS...................................................................................... 599
CHAPTER 2: DEAFNESS AND HEARING LOSS .................................................... 601
CHAPTER 3: PATIENT HEARING ASSESSMENT AND ANALYSIS .......................... 604
CHAPTER 4: BELL’S PALSY ............................................................................... 609
CHAPTER 5: DIZZINESS ................................................................................... 611
CHAPTER 6: EAR PAIN ..................................................................................... 615
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SECTION 11: ORTHOPEDICS ................................................................ 618

CHAPTER 1: SPORTS MEDICINE....................................................................... 618
CHAPTER 2: GENERAL APPROACH TO MUSCULOSKELETAL CASES ................... 619
CHAPTER 3: SHOULDER PATHOLOGIES ............................................................ 622
CHAPTER 4: ELBOW AND FOREARM PATHOLOGIES ......................................... 626
CHAPTER 5: HAND AND WRIST PATHOLOGIES................................................. 629
CHAPTER 6: SPINE PATHOLOGY ...................................................................... 638
CHAPTER 7: HIP AND THIGH PATHOLOGIES ..................................................... 643
CHAPTER 8: KNEE AND TIBIAL PATHOLOGIES .................................................. 645
CHAPTER 9: FOOT AND ANKLE PATHOLOGIES ................................................. 653
SECTION 12: URGENT CARE ................................................................ 656
CHAPTER 1: TRAUMA ..................................................................................... 656
CHAPTER 2: STATUS EPILEPTICUS.................................................................... 661
CHAPTER 3: HTN EMERGENCY ........................................................................ 663
CHAPTER 4: TOXICOLOGY ............................................................................... 667
CHAPTER 5: DKA ............................................................................................ 671
CHAPTER 6: OBSTETRIC EMERGENCY.............................................................. 676
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Section 1: Family Medicine

Chapter 1: HYPERTENSION
1.1. Definition:
 Hypertension is defined as increased systolic blood pressure or
diastolic blood pressure, or both above normal levels. Hypertension
Classified; primary hypertension, also known as essential
hypertension and secondary hypertension.
 According to the USPSTF (2021), ACC/AHA (2017), and ESC/ESH
(2018) recommendations, adults 18 years or older, without known
hypertension, should be screened for hypertension using office blood
pressure measurement.
1.2. Stages of hypertension according to ACC/AHA:
 Elevated blood pressure – SBP of 120 to 129 mmHg and DBP <80
mmHg
 Stage 1 – SBP 130–139 mmHg or DBP 80–89 mmHg
 Stage 2 – SBP >140 mmHg or DBP >90 mmHg
 Hypertensive crisis – SBP >180 mmHg or DBP >120mmHg (requires
immediate evaluation and treatment)
1.3. Symptoms & physical examination:
Symptoms that may suggest secondary causes of
hypertension
Table 1.1
Severe Nervous Eye visual Facial Heartbeat
headaches ness disturbance flushing not
regular
Dizziness Body Trouble Labored Hematuria
aches sleeping breathing
and
fatigued
body
Nosebleed Sweatin Angina Blood Pounding
g spots in in chest,
eyes neck, or
ears
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Physical exam
 Eye exam
o Conduct a fundoscopic eye examination to detect any symptoms
of early or late, chronic, or acute hypertensive retinopathy
 Pulse exam
o Evaluate all peripheral pulses.
o Weak or absent femoral artery pulse may be a sign of coarctation
of the aorta or severe peripheral vascular disease.
o The neck should be examined for distension of jugular veins;
carotid bruits, or enlarged thyroid gland.
o Bruit of the renal artery may be felt in the upper abdomen. If
present in both systole and diastole, it represents stenotic renal
arteries.
 Cardiac exam
o To evaluate for symptoms of LVH, a thorough heart exam should
be performed.
1.4. Diagnosis:
The best diagnostic procedure for hypertension (gold standard) is 24-
hour ambulatory blood pressure monitoring (ABPM).
Home BP or ABPM is important in diagnosing hypertension; routine
measures taken in the hospital environment should only be used for
screening purposes.
1.5. Investigations:
 Electrolytes and blood creatinine (for measuring the GFR)
 Fasting blood glucose
 Urinalysis
 CBC
 TSH
 Lipid profile
 ECG
 CVS risk calculations
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1.6. Management:
● All individuals with elevated blood pressure should consider changing
their lifestyle, not every patient requires pharmacological treatment.
● Lifestyle modification therapy:
o Nutritional salt limitation
o Potassium intake, particularly by dietary change, unless chronic
kidney disease or the use of medications that reduce potassium
output are contraindicated.
o Losing weight
o DASH diet
o Exercise
o Alcohol intake limitations
1.7. Pharmacologic therapy:
● Choice of initial antihypertensive agents
o Diuretics which are thiazide-like or thiazide-type
o Long-acting calcium channel blockers, mainly dihydropyridine
o Angiotensin-converting enzyme (ACE) inhibitors – inhibit the
action of an enzyme that converts angiotensin to its active form
o Angiotensin II receptor blockers (ARBs) – receptor blockers of
Angiotensin II
● In a patient with a systolic pressure of more than 20 mmHg systolic
and 10 mmHg diastolic, the recommended therapy is to use two
drugs in combination from two different classes. The combination
should be of first line medications.
1.8. Additional considerations in the choice of initial
therapy:
● In the black population or people living in North America and Africa,
the first therapy that should be given is drugs with actions much like
thiazide or other diuretics. It is also recommended to use calcium
channel blockers such as long-acting dihydropyridine.
● In patients with diabetic nephropathy or who are not diabetic but have
a severe kidney disorder, especially if proteinuria is present, the first
drug of choice is an ACE inhibitor or an ARB.
● Nowadays, beta-blockers are not used as the initial therapy;
however, they can be used in ischemic heart disease with decreased
ejection fraction in heart failure.
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1.9. Monitoring:
● Patients should be re-evaluated after starting antihypertensive
medication, and medications should be adjusted periodically
(monthly) until sufficient blood pressure control is attained.
● Once blood pressure control is attained, patients should be re-
evaluated every 3–6 months to maintain control.
Chapter 2: DYSLIPIDEMIA
2.1. Definition:
Dyslipidemia covers a range of abnormal lipid values and includes
genetic and multifactorial disorders of lipoprotein metabolism.
● Total Cholesterol ≥ 240 mg/dl
● Low-density lipoprotein (LDL) cholesterol > 160 mg/dl
● Triglyceride levels > 200 mg/dl
● Decreased high-density lipoprotein (HDL)cholesterol <40 mg/dl
Primary causes or genetic factors
(Familial hypercholesterolemia, Familial hypertriglyceridemia, Familial
combined hyperlipidemia)
Secondary causes
(Diabetes mellitus, Hypothyroidism, Cigarette smoking, Nephrotic
syndrome, Abdominal obesity and drug induced ...etc.)
2.2. Signs & Symptoms:
Dyslipidemia itself doesn’t cause any signs or symptoms but can lead to
atherosclerotic cardiovascular diseases e.g. (coronary artery disease,
myocardial infarction, etc.)
 Arcus cornea
 Tendon xanthomas at different locations.
 Xanthelasma.
 Acute pancreatitis, Lipemia retinalis (in severe hypertriglyceridemia).
2.3. Diagnosis:
Diagnosis always by laboratory tests as following:
 Total Cholesterol ≥ 240 mg/dl
 Low-density lipoprotein (LDL) cholesterol > 160 mg/dl
 Triglyceride levels > 200 mg/dl
 Decreased high-density lipoprotein (HDL) cholesterol <40 mg/dl
Abnormal lipid test results should always be confirmed with a repeat
specimen within 1–8 weeks of the initial test.
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Other tests for secondary causes of dyslipidemias and they

are:
 Fasting glucose
 Liver enzymes
 TSH
 Urinary protein
 Renal functions
Monitoring: to assess adherence, response to medications, and lifestyle
changes
Fasting lipid measurement should be repeated 4–12 weeks after starting
or changing statin therapy.
Afterwards, lipid measurement should be repeated every 3 to 12 months
as needed.
2.4. Management:
The guidelines for management involve:
 ASCVD risk assessment
 Lifestyle changes
 Pharmacologic treatment
Primary prevention: (to prevent or delay the onset of ASCVD)
 Risk of ASCVD is estimated using pooled cohort risk assessment
equations. Intended for patients with LDL-C < 190 mg/dl, no ASCVD,
and not on LDL-C lowering therapy. (ASCVD Risk Estimator +
(acc.org))
 Once the risk is calculated then patients need to be categorized
according to risk score.
 Statins are the treatment of choice for LDL cholesterol reduction
because they reduce cardiovascular morbidity and mortality.
2.5. Treatment:
Nondiabetic patients 40–75 years old with LDL between 70–
190 mg/dL
 High risk group: If 10-year ASCVD risk score is > 20%, start high
intensity statin.
 Intermediate risk group: if 10-year risk score is between 7.5–19.9%,
consider moderate intensity statins based on risk enhancers.
 Borderline risk group: if 10-year risk score is between 5–7.5%,
consider moderate intensity statin based on risk enhancers.
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 Low risk group: if 10-year risk score is <5%, focus on lifestyle

management.
Statin treatment is classified as high, moderate, and low intensity and is
based on the patient’s ASCVD risk group (Table 2.1). The choice
depends on the patient’s condition, their comorbidities, risk factors, cost,
and potential side effects of their medications.
Table 2.1 – Statin intensity
High intensity Moderate intensity Low intensity
LDL-C
more than or equal to 50% 30% to 49% less than 30%
lowering
Atorvastatin 10-20 mg
Atorvastatin 40-80 mg
Statins Rosuvastatin 5-10 mg Simvastatin 10 mg
Rosuvastatin 20-40 mg
Simvastatin 20-40 mg
Pravastatin 40-80 mg
Lovastatin 40-80mg Pravastatin 10-20 mg
Fluvastatin XL 80 mg Lovastatin 20 mg
Fluvastatin 40 mg BID Fluvastatin 20-40 mg
Pitavastatin 1-4 mg
2.6. Adverse effects of statins:

Muscle symptoms can occur without enzyme elevation. They occur in
10% of patients taking statins and may be dose dependent.
myositis and rhabdomyolysis seems to be most common when some of
the statins are used with drugs that inhibit cytochrome P3A4 (e.g.,
macrolide antibiotics, azole antifungals, cyclosporine and with fibrates,
especially gemfibrozil).
Liver enzyme elevations are uncommon, and serious liver toxicity is
extremely rare.
In some patients, changing from one statin to another or lowering the
dose (after temporarily discontinuing the drug) helps relieve or reduce
side effects. Giving them a statin holiday sometimes helps as well.
Statins are contraindicated during pregnancy and lactation.
2.7. Monitoring:
Prior to starting treatment, all patients should have their TSH, liver
functions and renal panel checked.
NICE guidance suggests checking liver function before and at 3 and 12
months after starting.
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If LFTs are elevated but less than three times the upper limit they should
not be stopped routinely. Statins can be started if the level is raised less
than 5 times the normal limit.
Renal impairment: eGFR is less than 30 avoid Rosuvastatin and reduce
Atorvastatin to half.
Pregnancy: mothers and discontinue 3 months before attempting to
conceive.
Breast feeding: avoid
Hepatic impairment: avoid
2.8. Secondary prevention:
Refers to efforts to treat known, clinically significant ASCVD and to
prevent or delay the onset of disease manifestations
Secondary prevention of ASCVD guidelines
In patients with clinical ASCVD (history of ACS, stable angina, coronary
revascularization, TIA, stroke, PVD) AND is very high-risk (2+ events or 1
event and 2 high risk conditions) prescribe: maximum tolerated statin to
a target LDL of 70 mg/dl. Add Ezetimibe and PCSK9 inhibitors to
accomplish this goal.
In patients with clinical ASCVD prescribe: high intensity statin and
Ezetimibe to patients less than 75 years old, moderate intensity statin for
patients older than 75 years old.
Table 2.2 – ADA recommendations for statin therapy in diabetics patients
ASCVD or 10-year
Age Statin Therapy
ASCVD risk > 20%
<40 years No No treatment
Yes High intensity
>40 years No Moderate intensity
Yes High intensity
2.9. Bile acid sequestrants:

 They are usually used with statins or with nicotinic acid to reduce LDL
cholesterol.
 They are proven to reduce cardiovascular mortality.
 Cholestyramine is the most commonly used and given as 4–8 grams
orally 1–3 times a day with meals.
 These are the drugs of choice in pregnancy.
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2.10. PCSK9 monoclonal antibodies:

PCSK9 monoclonal antibodies are newer agents and work by attaching
to LDL receptors leading to improved function of these receptors.
LDL is reduced by 40%-70%. They are available as subcutaneous
injections given once or twice per month.
Cardiovascular outcomes trials with evolocumab and alirocumab showed
a decrease in cardiovascular events in patients with prior atherosclerotic
cardiovascular disease.
2.11. Other lipid lowering agents:
Ezetimibe: can be used as an adjunct to dietary measures and statin
treatment in primary hypercholesterolemia, familial
hypercholesterolemia, and in adults in whom initial statin therapy is
contraindicated or cannot be tolerated.
Fenofibrate: can be used in severe hypertriglyceridemia (TG greater
than 500 mg/dL), if statin is contraindicated or not tolerated, adjunct to
statin if triglycerides are inadequately controlled in patients at high
cardiovascular risk.
Omega-3: In Isolated hypertriglyceridemia treat with omega-3 fatty acids
or fibrates to a target less than 500 mg/dl. If the patient is already on a
statin and triglycerides are persistently above 500 mg/dl then add
omega-3 fatty acids or refer to secondary care. If the patient has an
indication to start a statin and triglycerides are above 500 mg/dl then
they should be started on a statin first line.
2.12. Lifestyle management:
Diet:
Evidence based recommendations include:
 Mediterranean dietary pattern (highest evidence)
 Portfolio dietary pattern
 Dietary Approaches to Stop Hypertension (DASH) dietary pattern
 Low-glycaemic index (GI)/glycaemic load (GL) dietary pattern
 Plant-based dietary pattern
 Dietary patterns high in nuts, legumes, olive oil, fruits and vegetables,
total fiber, and whole grains.
Exercise:
Adults should accumulate at least 150 minutes of moderate to vigorous
aerobic activity per week. It may also be beneficial to add muscle and
bone strengthening activities at least two days per week
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When to refer:
 Suspected familial hypercholesterolemia
 Family history of premature heart disease
 Cholesterol > 290 mg/dl in the absence of family history
 Triglyceride level > 885mg/dl.
 Intolerance to statins.
Chapter 3: DM
3.1. Classifications of diabetes:
 Diabetes Mellitus type 1 (DM1):
o Autoimmune pancreatic beta cell destruction leading to absolute
insulin deficiency including latent autoimmune diabetes in adults
(LADA)
 Diabetes Mellitus type 2 (DM2):
o Progressive loss of adequate beta cell insulin secretion in the
background of insulin resistance
 Specific types:
o Monogenic diabetes: neonatal and maturity onset diabetes of the
youth (MODY)
o Disease of exocrine: cystic fibrosis, pancreatitis
o Drug induced: glucocorticoids, treatment of HIV, after transplant
 Gestational Diabetes Mellitus (GDM): diagnosed in second and
third trimester that was not previously diagnosed prior pregnancy
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Gestational diabetes (GDM)

Table 3.1 – Screening for and diagnosis of GDM
One step strategy
– 75- g OGTT
– The diagnosis of GDM is made when any of the following plasma
glucose values are met or exceeded: Fasting: 92 mg/dl (5.1 mmol/L),
1 h: 180 mg/dl (10.0 mmol/L), or 2 h: 153 mg/dl (8.5 mmol/L)
Two-step strategy
– Step 1: Perform a 50-g GLT (nonfasting), with plasma glucose
measurement at 1h at 24–28 weeks of gestation in women not
previously diagnosed with diabetes.
– If the plasma glucose level measured 1h after the load is >= 130, 135,
or 140 mg /dl (7.2,7.5, or 7.8 mmol/L), proceed to a 100-g OGTT.
– Step 2: The 100-g OGTT should be performed when the patient is
fasting.
– The diagnosis of GDM is made when at least two of the following four
plasma glucose levels (measured fasting and at 1,2, and 3 h during
OGTT) are met or exceeded: Fasting: 95 mg/dl (5.3 mmol/L), 1 h:
180 mg/dl (10.0 mmol/L), 2 h: 155 mg/dl (8.6 mmol/L), or 3 h: 140 mg
/dl (7.8 mmol/L
Screening for GDM: performed at 24–28 weeks of gestation in pregnant

women not previously found to have diabetes or high-risk abnormal
glucose metabolism detected earlier in the current pregnancy.
Obstetric and perinatal complications:
 Intrauterine fetal death (IUFD)
 Fetal macrosomia
 Neonatal hypoglycemia
 Jaundice
 Polycythemia
 Hypocalcemia
 Maternal hypertensive disorders
 Cesarean delivery
Long-term complication:
 Maternal risk for diabetes (50–60%)
 Offspring of women with GDM are at increased risk of:
o Obesity
o Glucose intolerance
o Diabetes in late adolescence and young adulthood
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3.2. Screening for diabetes:

Table 3.2 – Criteria for screening for diabetes or prediabetes in
asymptomatic adults
Testing should be considered in adults who are overweight or obese
(BMI > 25 kg/m2 or > 23 kg/m2 in Asian Americans) and have one or
more of the following risk factors:
– First degree relative with diabetes
– High risk race/ethnicity (e.g., African American, Latino, Native
American, Asia American, Pacific islander)
– History of CVD
– Hypertension (>140/90 or on therapy for hypertension)
– HDL cholesterol level < 35 mg/dl and/or a triglyceride level > 250
mg/dl
– Women with polycystic ovary syndrome
– Physical inactivity
– Other clinical conditions associated with insulin resistance (e.g.,
severe obesity, acanthosis nigricans)
Patients with prediabetes (A1C > 5.7% [39 mmol/mol], IGT, or IFG)
should be tested yearly.
Women who were diagnosed with GDM should have lifelong testing at
least every 3 years.
For all other patients, testing should begin at 35 years old.
If results are normal, testing should be repeated at a minimum of 3-year
intervals, with consideration of more frequent testing depending on initial
results and risk status.
People with HIV
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Table 3.3 – Risk based screening for DM2 or prediabetes in

asymptomatic children and adolescents
youth* who are overweight (>85th percentile) or obese (>95th percentile)
and who have one or more additional risk factors based on the strength
of their association with diabetes:
– Maternal history of diabetes or GDM during the child’s gestation
– Family history of DM2 in first or second degree relative.
– Race/ethnicity (e.g., African American, Latino, Native American,
Asia American, Pacific islander)
– Signs Of insulin resistance or conditions associated with insulin
resistance (acanthosis nigricans, hypertension, dyslipidemia,
polycystic ovary syndrome, or small-for-gestational-age birth
weight)
GDM: gestational diabetes, * After the onset of puberty or after 10 years
of age, whichever occurs earlier. If tests are normal, repeat testing at a
minimum of 3- year intervals (or more frequently if BMI is increasing or
risk factor profile deteriorating) is recommended.
3.3. Diagnosis of Diabetes:
Table 3.4 – Criteria for the diagnosis of diabetes
FBS >126 mg/dl (7.0 mmol/L)
OR
2-h PG >200 mg/dl (11.1 mmol/L) during OGTT. using 75 g glucose load
dissolved in water.
OR
A1C >6.5%.
OR
In a patient with classic symptoms of hypoglycemia or hyperglycemic
crises, a random plasma glucose >200 mg/dl (11.1 mmol/L
3.4. Prediabetes:
Table 1.1 Criteria defining prediabetes
FPG 100 mg/dl (5.6 mmol/L) to 125 mg/dl (6.9 mmol/L) (IFG)
OR
2-h PG during 75-g OGTT 140 mg/dl (7.8 mmol/L) to 199 mg/dl (11
mmol/L) (IGT)
OR
A1C 5.7-6.4%
Page | 20
3.5. Prevention of DM2:

3.5.1 Lifestyle modification:
Physical exercise:
 Exercise 150 minutes or more at moderate to vigorous intensity of
aerobic activity per week at least three days per week with no more
than two consecutive days without activity.
 2–3 sessions/week of resistance exercise on non-consecutive days
 Flexibility training and balance training are recommended 2–3
times/week for older adults with diabetes
Weight reduction:
 In prediabetes, the weight loss goal is 7–10% for preventing
progression to DM2
 A structured lifestyle plan that combines dietary modification and
exercise is vital for weight reduction
 Dietary modifications include reducing daily calories between 250–
500 calories, keeping in mind that the total daily calorie intake should
not be less than 1200 calories
Medical nutrition therapy:
Effective for diabetes is with an average reduction of A1C of 1–2%.
Examples of effective nutrition interventions include low calorie and fat
intake, carbohydrate counting, and individualized meal planning.
Macronutrient composition:
macronutrient distribution should be based on an individualized
assessment.
 Fat:
o fat quality is more important than quantity
o The total fat intake should be <35% of total calories
o Saturated fat should be <7% of total calories
o Monounsaturated and polyunsaturated fat should comprise the
rest of fat intake
● Protein:
o Protein intake should not be <1.2% g/kg, i.e., 20–30% of total
calorie intake
o Protein aids the sensation of fullness, reduce appetite, and
assists in maintaining weight reduction
 Carbohydrate:
o ideally 40–45% of total calorie intake
Page | 21
Micronutrient composition
 Sodium:
o Daily consumption should be <2300 mg
 Potassium:
o Daily consumption should be minimum of 4700 mg
3.6. Glycemic targets and assessment of glycemic
control:
Can be achieved by different methods:
 HbA1c measurement
 Self-monitoring blood glucose (SMBG)
o SMBG yields better glucose control, especially in patients using
insulin.
 Continuous glucose monitoring (CGM)
o Carries a vital role in prevention and treatment of hypoglycemia
in patients with DM1 and patients with DM2 who are taking
intensive insulin regimens
3.6.1 Glycemic goals:
 Assess glycemic control at least twice yearly for stable glycemic
control and quarterly for those who are not meeting glycemic goals or
recently changed therapy.
 HbA1c goal for many nonpregnant adults is < 7%
 achieving HbA1c levels less than 7% or less stringent <8% may be
appropriate based on several factors as shown (table 3.6)
 The preprandial capillary plasma glucose goal is 80–130 mg/dl (4.4-
7.2 mmol/L) for nonpregnant adults.
 Peak postprandial capillary plasma glucose is less than 180 mg/dl (10
mmol/L) for nonpregnant adults.
Page | 22
Table 3.6 – Approach to individualization of glycemic targets

according to patient/disease features
More stringent HbA1c Patient/disease Less stringent HbA1c >
< 7% Features 7%
Low Risks potentially High
associatedwith
hypoglycemia
andother drug
adverse effects
Newly diagnosed Disease duration Long-standing
Long Life expectancy Short
Absent Important Severe

comorbidities
Absent Established Severe
vascular
complications
High motivated, Patient preference Preference for less
excellent self-care burdensome therapy
capabilities
Readily available Resources and Limited
support system
3.7. Pharmacologic Therapy for DM2:
3.7.1 Initial therapy:
Metformin should be started when type 2 diabetes is diagnosed unless
there are contraindications.
A patient-centered approach should be used to guide the choice of
pharmacologic agents. Considerations include effects on the following:
cardiovascular and renal comorbidities, efficacy, hypoglycemia risk,
impact on weight, cost, the risk of side effects, and patient preferences.
It is common practice to initiate insulin therapy for patients who are
present with:
 Blood glucose levels ≥300 mg/dL (16.7 mmol/L)
 A1C >10% (86 mmol/mol)
 Patient has symptoms of hyperglycemia (i.e., polyuria or polydipsia)
 Evidence of catabolism (weight loss)
Page | 23
3.7.2 Combination therapy:

Initial combination therapy should be considered in patients presenting
with A1C levels 1.5– 2.0% above target.
If the A1C target is not achieved after approximately three months
metformin can be combined with any one of the preferred six treatment
options: sulfonylurea, a thiazolidinedione, DPP-4 inhibitor, SGLT2
inhibitor, GLP-1 RA, or basal insulin.
3.7.3 Combination injectable therapy:
If basal insulin has been titrated to an acceptable fasting blood glucose
level (or if the dose is >0.5 units/kg/day with indications of the need for
other therapy) and A1C remains above target, consider advancing to
combination injectable therapy. This approach can use a GLP-1 RA
added to basal insulin or multiple doses of insulin.
Intensification of insulin treatment can be done by adding doses of
prandial to basal insulin. Starting with a single prandial dose with the
largest meal of the day is simple and effective, and it can be advanced to
a regimen with multiple prandial doses if necessary.
3.7.4 Intensifying to injectable therapy:
 Initiation
o Start 10 IU a day OR 0.1-0.2 IU/kg a day
 Titration
o Set fasting glucose target
o Choose an evidenced-based titration algorithm, e.g., increase
two units every three days to reach fasting glucose target without
hypoglycemia.
o For hypoglycemia, determine the cause. If there is no clear
reason, lower the dose by 10–20%.
o Titrate up as per ADA standard
Page | 24
Continuous subcutaneous insulin infusion or ‘insulin pump’ therapy is

recommended for adults and children 12 years and over with type 1
diabetes mellitus if:
 Patients experience disabling hypoglycemia or DKA with multiple
daily injections, or
 HbA1c levels have remained high (8.5% or above) with multiple daily
injections despite trying to manage diabetes.
Page | 25
3.8. Immunizations:
Vaccines recommended for adults with diabetes demonstrated in table
Table 3.8 Recommended vaccinations for adults with diabetes
Vaccination Age group Frequency
Influenza All patients Annually
Hepatitis B All unvaccinated Three doses series
adults
Pneumococcal 19-64 years One dose
PPSV23 ≥65 years 2nd dose, at least 5
years apart
Pneumococcal 19-64 years None
PCV13 ≥65 years One dose
Td All adults Booster every 10
years
Zoster ≥50 years Two doses
Covid-19 All patients Two doses
3.9. Cardiovascular Disease and Risk Management:
Atherosclerotic cardiovascular disease (ASCVD):
Cardiovascular risk factors should be assessed at least annually (using
ASCVD risk calculator) in all patients with diabetes to prevent and
manage both ASCVD and heart failure.
Page | 26
3.9.1 Blood pressure management:

Treatment goals:
Table 3.9 Blood pressure target in special patients
Category Recommendation
Individuals with diabetes and BP target of <130/80 mmHg may
hypertension at higher be appropriate if it can be safely
cardiovascular risk (existing attained
atherosclerotic cardiovascular
disease [ASCVD] or 10-year
ASCVD risk ≥15%)
Individuals with diabetes and BP target of <140/90 mmHg
hypertensionat lower Risk for
cardiovascular disease (10-year
ASCVD Risk <15%)
Pregnant patients with diabetes BP target of 110–135/85 mmHg
and pre-existing hypertension is suggested to reduce the risk
for accelerated maternal
hypertension and minimize
impaired fetal growth
Treatment strategies include lifestyle interventions and pharmacologic
therapy (for details refer to hypertension section).
ACEI or ARB are first-line therapy for patients with Diabetes and
coronary artery disease
Avoid combining ACEI and ARB.
Avoid combining ACEI or ARB with direct renin inhibitors
In patients with Diabetes and microalbuminuria: Choose an ACEI or ARB
at the maximum tolerated dose for blood pressure treatment
If on ACEI, ARB, or diuretic, monitor the following annually: Serum
creatinine, estimated glomerular filtration rate serum potassium level.
Page | 27
3.9.2 Lipid management:

Primary Prevention (diabetic patient without ASCVD)
Table 3.10 Primary prevention (diabetic patient without
ASCVD)
Age Recommendation
20–39 years If there are other risk
factors
40–75 years Moderate intensity statin
50–70 years High-intensity statin
therapy, if there are
multiple risk factors
10 years ASCVD risk Add ezetimibe to lower
≥20% LDL by ≥ 50%
Secondary Prevention (diabetic with ASCVD)
 All ages: high-intensity statin
 If LDL ≥70 mg/dL on the maximum dose of statin, consider ezetimibe
or PCSK9 inhibitor
 >75 years on statin therapy, continue statin treatment
 >75 years, initiation of statin after discussion with the patient
3.9.3 Monitoring of lipids in diabetics:
Table 3.11 Monitoring of lipids in diabetics
Situation When
Not treatment for At the time of DM diagnosis
dyslipidemia Initial medical evaluation
Every 5 years if <40 years
If indicated
On treatment for At initiation 4–12 weeks after
dyslipidemia initiation or change of dose
Annually to monitor the
response and medication
adherence.
3.10. Microvascular complications:
3.10.1 Diabetic nephropathy – diabetic kidney disease
(DKD)
 Chronic kidney disease (CKD) is defined as estimated glomerular
filtration rate (eGFR) less than or equal to 60 for ≥3 months with or
without kidney damage or evidence of kidney damage for ≥3 months
with or without decreased GFR
Page | 28
Screening:
 Perform an early morning spot UACR and serum creatinine annually
after five years of DM1 diagnosis and at the time of diagnosis of DM2
 Two out of three spot urine samples have to be elevated within 3–6
months to confirm the diagnosis of albuminuria
 Patients with diabetes and an eGFR 30–60 mL/min/1.73 m2 and/or
UACR 300 mg/g creatinine should be monitored at least twice
annually to guide their management
Management:
 Optimize glycemic, blood pressure and lipid control
 Smoking cessation
 Sodium–glucose cotransporter 2 inhibitor (SGLT2) inhibitors is
recommended in patients with an eGFR ≥ 25mL/min/1.73 m2 and / or
UACR ≥ 300 mg/g creatinine.
 Either an ACE inhibitor or an angiotensin receptor blocker (ARB) is
recommended for patients with diabetes and hypertension with
elevated UACR ≥ 30 mg/g creatinine and/or eGFR < 60 mL/min/1.73
m2
 Serum creatinine and potassium levels should be monitored
periodically for any changes when ACE inhibitors, ARB, or diuretics
are used.
 Identification and correction of CKD complications like anemia,
hyperkalemia, hypoalbuminemia, malnutrition, metabolic disease,
bone disease, and fluid retention is an essential part of the follow up
plan of DKD patients.
 Refer to nephrology if:
o GFR <30
o Persistent albuminuria ACR >300 mg/g
o GFR declines > 30% within 4 months without explanation
o Resistance hypertension
o Mineral bone disorder
o Persistent hyperkalemia despite treatment
o Absence of diabetic retinopathy
o Uncertainty about the etiology of kidney disease.
Page | 29
3.10.2 Diabetic retinopathy:

Classification of diabetic retinopathy:
 Non-Proliferative Diabetic Retinopathy (NPDR)
 Proliferative Diabetic Retinopathy (PDR)
 Clinically Significant Macular Edema (CSME)
Screening
At the time of diagnosis of DM2 and within five years after the diagnosis
of DM1 in 10 years old patients or older.
Annually if the initial exam is normal while more frequent examination is
needed in case of advanced baseline retinopathy or diabetic macular
edema.
Management
 Optimize glycemic, blood pressure and lipid control to reduce the risk
or slow the progression of retinopathy
 Treatment options include:
● Intravitreal anti-vascular endothelial growth factor (anti-VEGF)
injections e.g., aflibercept or ranibizumab.
● Intravitreal corticosteroids injections.
● Focal and pan retinal laser photocoagulation (PRP)
Page | 30
Table 3.12 – Treatment options of diabetic retinopathy according to

the stage of retinopathy
Stages of diabetic retinopathy Treatment
Mild Non-Proliferative Diabetic Metabolic control and
Retinopathy (NPDR) Monitor progression
Moderate Non Metabolic control and
proliferative Diabetic Retinopathy (NPDR) Monitor progression
Severe Non Consider early pan retinal
proliferative Diabetic Retinopathy (NPDR) laser photocoagulation
(PRP)
Proliferative Diabetic Retinopathy (PDR) Pan-retinal laser
photocoagulation (PRP) or
Intravitreous injections of
ant vascular endothelial
growth factor (anti-VEGF)
Central Involved Diabetic Macular First line therapy:
Edema (CIDME) Intravitreous injections
of (anti-VEGF) which is
administered monthly for
the first year with fewer
injections needed in
subsequent years to
maintain remission +/-
macular laser Alternative:
Intravitreal corticosteroids
3.10.3 Diabetic neuropathy:
Types of diabetic neuropathy:
 Peripheral polyneuropathy, also known as distal symmetric
sensorimotor polyneuropathy (DSPN)
 Focal neuropathy
 Autonomic neuropathy
Page | 31
Screening
 All patients with diabetes should be screened annually for distal
symmetric polyneuropathy 5 years after diagnosis with DM1 and at
the time of diagnosis with DM2.
 Evaluation for DSPN include history and assessment of either
temperature or pinprick sensation (small fiber function) and vibration
sensation using a 128-Hz tuning fork (for large-fiber function).
 Assess for symptoms and signs of autonomic neuropathy in patients
with microvascular complications
Management
 Optimize glucose control as early as possible to prevent or delay the
development of DSPN and cardiovascular autonomic neuropathy
 Medication used for relief of symptomatic DSPN – Table
Table 3.13 Medication used for relief of symptomatic DSPN
Initial Effectiv Maximum
Drug class Agent dose e dose dose
Anticonvulsants Pregabalin 25-75 mg 150-300 600
Gabapentin 1-3 mg/day mg/day36
times/day1 Divided 00 mg/day
00-300 into BID
mg/day or TID
doses90
0- 3600
mg/day
Serotonin- Duloxetine 20-30 60 mg 120
norepinephrine Venlafaxine mg/day37. po od or mg/day22
reuptake inhibitors 5 mg/day 30 mg 5 mg/day
(SNRI) bid75-
225 mg
/day
Tricyclic Amitriptylin 10-25 25-100 100
antidepressants(TC e mg/day mg/day mg/day
As)
3.11. Diabetic foot:
3.11.1 Comprehensive foot examination:
Inspection:
 Skin changes
o Breaks in the integrity of the skin
o Dry fissured skin is common in neuropathic ulcers
o Distended veins indicate neuropathy
Page | 32
o Skin atrophy can indicate ischemia

o Webspace maceration is a sign of tinea pedis
 Color:
o Redness of the foot may indicate cellulites, critical ischemia,
Charcot foot
o Redness of the toes may indicate cellulites, osteomyelitis,
ischemia
o Blue discoloration of the toe may indicate severe infection or
ischemia
o A white foot, especially on elevation, may indicate ischemia
o Black areas may indicate ischemia, emboli, application of henna
or shoe dye
 Ulcers
o Venous ulcers moderate to no pain – larger/shallow – associated
with venous insufficiency/varicose veins
o Arterial ulcers are very painful – deep punched out appearance –
associated with diabetes mellitus/peripheral vascular disease.
 Calluses and corns
o Callus indicates areas of high pressure and friction
o Callus forms a plaque, while corns are smaller discrete areas
o You should refer all patients with callus and corns to a podiatrist
for removal to prevent later problems with ulceration
o You should discourage patients from removing their own corns or
calluses as doing so carries a high risk of injury
 Nails
o Look for the color of nails
o Observe if nails are thickened which could cause pressure on the
nail bed from a shoe
o Look for discharge from nails which may indicate an underlying
ulcer
o Fungal nail infections are common
 Swelling
o Swelling of a diabetic foot causes a high risk of ulceration due to
poorly fitting, too tight shoes
 Deformity
o Hammer toe and claw toes
o The Charcot foot is a specific deformity resulting in bone and
joint destruction. Charcot’s osteoarthropathy may have
symptoms of peripheral or autonomic neuropathy
Page | 33
Gait
o Observe the patient walking for:

 Symmetry/balance
 Turning – quick / slow / staggered
 Abnormalities – broad based gait / foot drop
 Palpation
o Temperature – cool (e.g., PVD) / hot (e.g., cellulitis)
o Capillary refill – normal = < 2 seconds. Prolongation suggests
Peripheral vascular disease (PVD)
o Pulses: Absent peripheral pulses are suggestive of peripheral
vascular disease
o Patients with clinical evidence of peripheral artery disease should
have ankle-brachial index (ABI) testing to guide further
management
Table 3.14 Ankle brachial index (ABI) interpretation
ABI Interpretation
> 1.3 False elevation: heavy vessel
calcification
1.0 – 1.29 Normal
0.91 – 0.99 Borderline
0.41 – 0.9 Mild to moderate PAD
< 0.4 Severe PAD
Neurologic assessment
 10 g monofilament + 1 of the following 4
 Vibration using 128 Hz tuning fork
 Pinprick sensation
 Ankle reflexes
 Vibration
3.11.2 Preventive foot care:
In conjunction with the comprehensive foot exam, advice for prophylactic
foot care should be given to all patients. This includes the following:
 Avoid smoking
 Avoid going barefoot, even at home, and especially on hot decks and
hot sand
 Test water temperature before stepping into a bath
 Trim toenails to the shape of the toe and remove sharp edges with a
nail file; do not cut cuticles
Page | 34
 Wash in lukewarm water, dry thoroughly (including between the toes),

and check feet daily
 Shoes should be snug, but not tight, and customized if feet are
misshapen or have ulcers
 Socks should fit and be changed daily
3.12. Hypoglycemia:
3.12.1 Classifications:
Table 3.15 Classification of hypoglycemia
Level Glycemic criteria/descriptions
1 Glucose <70 mg/dl (3.9 mmol/L) and 54 mg/dl (3.0 mmol/L)
2 Glucose < 54 mg/dl (3.0 mmol/L)
3 A severe event characterized by altered mental and/or physical
status requiring assistance for treatment of hypoglycemia
3.12.2 Risk factors:
 DM1
 older patients
 insulin use
 poor or moderate versus good glycemic control
 albuminuria
 poor cognitive functions.
Table 3.16 Symptoms of hypoglycemia
Autonomic symptoms Neuroglycopenic symptoms
palpitations behavioral changes
tremors fatigue
arousal/anxiety confusion
sweating seizures
hunger loss of consciousness
palpitations behavioral changes
irritability
hunger
3.12.3 Management of hypoglycemia:
If blood glucose less than 70 mg/dl (3.9 mmol/L):
Conscious patient and able to swallow:
 Give 15 g to 20 g of quick acting carbohydrate e.g., 4-5 glucose
tablets or 120-200 ml of pure fruit juice.
Page | 35
 Repeat their capillary blood glucose 10 to 15 minutes later. If it is still

less than 70 mg/dl (3.9 mmol/L) repeat step 1 but give no more than
three treatments in total
If the patient’s blood glucose is still less than 70 mg/dl (3.9 mmol/L) after 30
to 45 minutes, or three cycles, consider intramuscular glucagon, or
intravenous glucose
 Once their blood glucose is above 70 mg/dl (3.9 mmol/L) and the
patient has recovered, give them a long-acting carbohydrate, e.g., two
biscuits, or one slice of toast.
Conscious but confused, disoriented, unable to cooperate:
 Give intramuscular glucagon or intravenous glucose (if intravenous
access is available).
 check the patient’s blood glucose 10-15 minutes later.
 If it is still less than 70 mg/dl (3.9 mmol/L) give more intravenous
glucose
o Glucagon injection:
 Give glucagon 1 mg IV, intramuscularly, or subcutaneously
 0.5 mg in children < 25 kg
 Glucagon may take up to 15 minutes to work.
o Intravenous glucose:
 Give glucose 25 g IV bolus in adults
 0% dextrose 2-4 mL/kg IV bolus in children, followed by a
continuous infusion until the patient is able to eat
 Patients with known case of CKD with low potassium diet should not
use orange juice to treat hypoglycemia
 If the patient is taking acarbose, sugar dissolved in water will not be
an effective treatment for them, as acarbose prevents the breakdown
of sucrose to glucose
 Patients who are given glucagon need a larger amount of long-acting
carbohydrate to refresh their stores of glycogen, e.g., double the
amount stated above
 The patient should not omit their insulin injection if due, but you may
need to review their insulin regimen at a later time
 The patient should continue regular monitoring of their blood glucose
for another 24 to 48 hours after the hypoglycemic event
 If the hypoglycemia was due to treatment with a sulphonylurea or
long-acting insulin, the risk of hypoglycemia may remain for up to 24
to 36 hours following the last dose
Page | 36
3.12.4 Follow up:

 Prescribe glucagon to all individuals at risk for level 2 or level 3
hypoglycemia
 Instruct patients to carry carbohydrates at all times to treat
hypoglycemia
 Caution regarding driving motor vehicles
3.12.5 Prevention of recurrent hypoglycemia in diabetes:
Insulin-treated patients with hypoglycemia unawareness, one level 3
hypoglycemic event, or a pattern of unexplained level 2 hypoglycemia
should be advised to raise their glycemic targets to strictly avoid
hypoglycemia.
Help patients understand situations that increase their risk of
hypoglycemia, such as:
 fasting for medical tests or procedures
 delayed meals
 during or after intense exercise
 during sleep
Teach patients to balance medication use, carbohydrate intake, and
exercise, but these strategies may not always be sufficient for
prevention.
Meal planning
 Patients on long-acting insulin secretagogues and fixed insulin
regimens should follow a predictable meal plan
 Ensure that patients on more flexible insulin regimens understand
that prandial insulin injections should be coupled to mealtimes
Preventing or minimizing exercise-related hypoglycemia
 monitor blood glucose before and after exercise
 eat snack before exercise if blood glucose levels low or falling
 carry readily absorbable carbohydrates during any kind of exercise
 consider empirical adjustment of insulin doses on days of planned
exercise, especially in patients with well-controlled diabetes and
history of exercise- related hypoglycemia
Insulin choices for prevention of hypoglycemia
 For most patients with type 1 diabetes:
o multiple daily insulin injections of prandial and basal insulin or
continuous subcutaneous insulin infusion (CSII, insulin pump)
(ADA Grade A)
Page | 37
o use of rapid-acting insulin analogs to reduce risk of hypoglycemia

(ADA Grade A)
o matching prandial insulin dose to carbohydrate intake, premeal
blood glucose, and expected physical activity (ADA Grade C)
o continued access to continuous subcutaneous insulin infusion in
successfully treated patients with diabetes (ADA Grade E)
o long-acting basal and rapid-acting prandial insulin analogs may
reduce incidence of overall, symptomatic, and nocturnal
hypoglycemia
o continuous subcutaneous insulin infusion (CSII) may reduce
incidence of hypoglycemia compared to multiple daily injections
(MDI)
Chapter 4: PERIODIC HEALTH MAINTENANCE
4.1. Disease Prevention and Screening:
The Periodic Health Examinations (PHEs) of the Ministry of Health
(MOH) in Saudi Arabia incorporated the screenings recommended by the
United States Preventive Services Task Force (USPSTF):
 Colon cancer: for average-risk males and females:
o 45–75 years old: fecal immunochemical test (FIT) q 1 year,
sigmoidoscopy q 3 years, or colonoscopy q 10 years
 Breast cancer: for average-risk females
o 40–74 years old: consider mammography q 2 years
 Cervical cancer: for average-risk females
o 21–29 years old: Pap smear q 3 years
o 30–64 years old: Pap smear q 3 years or Pap smear + HPV
testing q 5 years
 Prostate cancer: Should be individualized in adult men 55–69 years
old (do not screen men >70 years old)
 Lung cancer: males and females
o 50–80 years old with a 20+ pack-year tobacco history and
smoked within past 15 years: low-dose CT (LDCT) chest,
annually
o Screening should be discontinued once a person has not
smoked for 15 years or develops a health problem that
substantially limits life expectancy or the ability or willingness to
have curative lung surgery.
Cardiovascular:
HTN: all adults
Page | 38
If last systolic blood pressure (SBP) 120–139 mmHg or last diastolic

blood pressure (DBP) 80–89 mmHg, q 1 year
If last SBP <120 or last DBP <80 mmHg, q 2 years
AAA: males, 65–75 years old, who have ever smoked abdominal
ultrasound once
Endocrine:
Diabetes: adults with BP>135/80 mmHg, HgbA1c, FBG, OGTT
ADA recommends screening:
● All adults >35 years old
● Overweight adults <35 years old with additional risk factors like
Physical inactivity, first degree relative with DM, women who
delivered macrosomic babies or were diagnosed with GDM
 or has blood pressure ≥ 140/90 or on therapy for hypertension,
 HDL cholesterol level < 35 mg/dl (0.9 mmol/l) or TG > 250 mg/dl (2.82
mmol/l), women with polycystic ovary syndrome
 or pre-DM or has history of CVD.
Hyperlipidemia: total cholesterol, HDL, and LDL q 5 years
 All adults at increased risk
 All males >35 years old
Osteoporosis: DEXA for hip and lumbar spine
 All-female >65 years old
 Females <65 years old at increased risk (based on FRAX score 10-
year fracture risk >9.3%)
Infectious diseases:
HCV: HCV antibody test once
 Adults 18–70 years old
 Hx of blood transfusion
 Hx of IVDU (more frequent testing if the risk is ongoing)
HIV: Adolescents and adults 15–65 years old once, more frequent if
ongoing risk (e.g., IVDU, MSM)
Chlamydia and Gonorrhea: All sexually active women <25 years old
and women >25 years old at increased risk (there is insufficient evidence
to screen men)
Syphilis: Adults at increased risk (USPSTF update in progress)
Social and substance use:
 Depression: All adults using a brief screening tool (e.g., PHQ-2)
 Alcohol use: All adults using a brief screening tool (e.g., AUDIT-C,
SASQ)
Page | 39
 Tobacco use: All adults

 Intimate partner violence: All females of childbearing age via brief
screening tool (e.g., HARK, HITS, PVS)
Well-adult Assessment:
4.1.1 Counseling:
 Pregnancy
Family physicians should be familiar with evidence-based
recommendations for contraception and preconception care
 Breastfeeding
 Intimate partner violence and abuse
 Behavioral counseling for STDs
 Smoking & Alcohol
 Sun exposure and vitamin D deficiency
 obesity counseling
 Fall assessment and prevention (>60 years old)
4.1.2 Risk assessment:
 History of falls
 Mobility problems
 Poor performance on the timed Get Up and Go Test
Counsel for interventions to minimize the risk of falls including:
Strengthening exercise, vitamin D supplementation, psychological
health, vision, and cognition
4.1.3 Screening:
Check BMI every 2 years in all adults (waist circumference may be and
acceptable alternative in certain populations)
Check Blood pressure annually for those who are at increased risk e.g.,
age>40 years old, SBP of 120 to 129 mmHg and DBP <80 mmHg and
overweight or obese
Adults 18–39 years old with normal blood pressure (<120/80 mm Hg)
who do not have other risk factors should be rescreened every 3 to 5
years
Pelvic exam
 AAFP recommends against screening pelvic examinations in
asymptomatic women
 USPSTF found insufficient evidence to make a recommendation for
or against pelvic screening
Page | 40
4.2. Premarital counselling and testing:

4.2.1 Labs and imaging:
 The USPSTF recommends screening for cervical cancer in women
21–65 years old with cytology (Pap smear) every 3 years or, for
women 30–65 years old who want to lengthen the screening interval,
screening with a combination of cytology and human papillomavirus
(HPV) testing every 5 years
 Biennial screening mammography for women between age 50–74
years old (Locally, The Saudi Expert Panel suggests screening with
mammography in women aged 40–49 years every 1 to 2 years).
(Conditional recommendation; low-quality evidence)
Sexually transmitted infections (STIs)
Based on age and risk factors follow National STI protocols to screen for:
Chlamydia, Gonorrhea, Syphilis, HIV, Hepatitis B and Hepatitis C virus
DEXA scan
 Women >65 years old
 Postmenopausal women younger than 65 years with risk factors like:
osteoporotic fractures, parental history of hip fracture, smoking,
excessive alcohol consumption, low body weight
Perform DEXA Scan for women at risk every 1.5 to 2 years.
No recommendation to screen asymptomatic men by USPSTF.
 Low-dose aspirin
The USPSTF recommends against initiating aspirin use for the primary
prevention of CVD in adults 60 years or older.
 Folic Acid
All women planning or capable of pregnancy should take a daily
supplement containing 0.4 to 0.8 mg (400 to 800 µg) of folic acid at least
1 month before conception and continue daily supplements through the
first 2 to 3 months of pregnancy. Women at high-risk for neural tube
defects (NTD) like epileptic, DM, or previous baby with NTD should take
4 mg per day.
 Vitamin D3
 Statins
Use a low- to moderate-dose statin for the primary prevention of CVD
events and mortality in adults without a history of cardiovascular disease
(CVD) (symptomatic coronary artery disease or ischemic stroke) when all
of the following criteria are met:
Age 40 to 75 years
Page | 41
Have 1 or more CVD risk factors (dyslipidemia, diabetes, hypertension,

or smoking)
Have a calculated 10-year risk of a cardiovascular event of 10% or
greater
Family history of a premature cardiovascular event
Obesity and overweight
4.2.2 Diseases included in the premarital screening:
 Hereditary hematological disorders
 Sickle cell disease
 Thalassemia
 Communicable diseases
 Hepatitis B
 Hepatitis C
 HIV
4.3. Well-child Assessment:
4.3.1 Under 6 Years of Age:
Counseling for:
 Breastfeeding
 Passive smoking
 Accident prevention
 Vitamin D and Sun exposure between 10 AM and 3 PM at least twice
a week to the face, arms, legs, or back without sunscreen.
Physical examination:
 Developmental milestones by Denver Developmental Chart up to 6
years old to assess child development.
 Growth parameters
Growth charts: use appropriate age- sex-specific growth charts to
monitor child growth. Use BMI charts from age 2 years. Use
Posterior fontanelle cannot usually be palpated after two months of age
but anterior fontanelle generally close
Vision
 Red Reflex: You should see an equal and bright red reflex from each
pupil as an absence of the red reflex, or an abnormal color may
indicate a serious illness.
 Corneal light reflex for ocular alignment (Hirschberg test)
 Cover/uncover test for amblyopia
 Visual acuity testing
Page | 42
Ears/hearing screening
 Evaluate gross hearing by observing an infant’s response to sound; a
startle response, eye blinking, and turning toward the sound is a
normal reaction.
 For older children, whisper testing can be used.
 Refer a child at 3 years of age for standardized audiometric testing to
ENT.
CVS
Abdomen
Hernia
Genitalia/ Circumcision
Lower Limbs
Skin
Labs
 ABO/RH (if not done)
 CBC
 Sickling Test and G6PD Test (Sickling test for newborns or can be
performed at 9 months).
 TFT for congenital hypothyroidism and PKU Test are (newborn
screening program)
Medications
 The AAP recommends that full-term, exclusively breastfed infants
start 1 mg per kg per day of elemental iron supplementation at 4
months of age until appropriate iron-containing foods are introduced.
 Formula-fed infants often receive adequate amounts of iron.
 Single-dose (1.0 mg) of intramuscular or oral vitamin K after birth is
effective in preventing hemolytic disease of the newborn and
improves biochemical indices of coagulation status at 1–7 days.
● Vitamin D3:
o 0–12 months 400 IU (10 mcg)
o 1–13 years 600 IU (15 mcg)
Infants who are exclusively breastfed should be supplemented with 400
IU of vitamin D daily, starting in the first few days of life and continuing
until they are 12 months of age.
Whole milk should not be used until after 12 months of age.
Page | 43
4.4. 6 to 17 years of age:

Counseling:
 Intimate partner violence and abuse
Clinical Examination (BMI).
Chapter 5: URTI
5.1. Common Cold:
5.1.1 Background:
It’s a type of a self-limiting acute URTI, known also as viral rhinitis,
rhinopharyngitis, and acute coryza
5.1.2 Symptoms:
Nasal congestion and rhinorrhea (the most reported symptoms), Dry
cough, Malaise, Headache, Low grade fever in children, Conjunctivitis,
dry throat scratchy.
Red flags in the pediatrics: Worsening sx such as a fever > 101°F
(38.3°C), SOB, Severe headache or facial pain, Poor feeding, Confusion,
Excessive crying.
Common cold DDx:
 Influenza: High fever, headache, and myalgias mostly
 Pharyngitis: Sore throat rather than rhinorrhea
 Acute bronchitis: Persistent dry or wet cough prominently
 Acute bacterial rhinosinusitis: Presence of facial pain associated with
purulent nasal discharge
 Allergic rhinitis: Chronic, with history of atopy
 Pertussis: Prolonged coughing, typically paroxysmal, with vomiting
and sometimes apnea
5.1.3 Physical Ex:
Conjunctival/Nasal congestion, Pharyngeal erythema, Adenopathy is
typically absent or minimal
5.1.4 Investigations:
It is Clinical diagnosis; Chest radiograph is only indicated if ais suspected
such as pneumonia.
5.1.5 Management:
Self-limiting, Last from 3 to 10 days in heathy people. Cough can last
even longer for up to 3 weeks after other symptoms resolve.
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5.1.6 Adult management:

 Analgesics: NSAIDs and paracetamol for headache and pain and
sneezing, give short term relief of rhinorrhea and nasal obstruction.
 Decongestants: Topical oxymetazoline or phenylephrine, reduces the
nasal congestion. Do not use it > 3 days due to risk of rhinitis
medicamentosa.
 Antihistamines combined with oral decongestant and/or analgesics
may provide some relief of cold symptoms.
 Ipratropium: improves cough within the first 10 days of treatment.
 Zinc and complementary treatments 75 mg showed significant ↓ in
duration of symptoms, Probiotics ↓ the duration by 1.5 days.
5.1.7 Paediatric management:
Supportive, hydration, warm fluid
 Fever: combining or alternating paracetamol and ibuprofen.
 Nasal congestion: Topical saline.
 A cool mist humidifier/vaporizer to loosen nasal secretions, although
this treatment is not well studied.
 Intranasal ipratropium: ↓ rhinorrhea but not congestion related to
URIs in children 5 years and older. It should not be used in children ≤
5 years.
 Cough: hydration, warm fluids, honey (in ≥ 1 year), cough lozenges
rather than prescription of antitussives, antihistamines or mucolytics.
 Complementary and alternative treatment: topical application over the
chest and neck with camphor ointment, and eucalyptus oils before
sleeping reduces night cough and easing the nasal obstruction.
Menthol is safely used in children >2 years and was perceived to
improve nasal patency.
 Vitamin C daily: may shorten the duration of illness.
5.1.8 Complications:
 Secondary acute bacterial rhinosinusitis
 May cause eustachian tube dysfunction which may lead to acute otitis
media
 bronchiolitis, pneumonia especially with RSV, parainfluenza virus.
Page | 45
5.1.9 Prevention:
 Good hand hygiene, whether using alcohol sanitizer or washing
hands with soap is the most effective and practical way to prevent
URIs in children and adults.
 Due to a variety of causative viruses that are continuously changing,
no vaccines are available.
5.2. Acute Pharyngitis:
5.2.1 Background:
Defined as infection covering the oropharyngeal area including the
tonsils. Commonly caused by viruses like adeno/rhino/coronaviruses or
bacteria like (GABHS).
5.2.2 Symptoms:
Viral or bacterial pharyngitis cannot be distinguished based
on presentation but some clues can aid
Table 5.1 Viral vs bacterial pharyngitis
Viral pharyngitis Bacterial pharyngitis
Rhinorrhea and cough followed by Acute onset sore throat, Fever,
sore throat after several days, Notable tender, Anterior cervical
Conjunctivitis, Diarrhea, Post. lymphadenopathy, Tonsillar
cervical lymphadenopathy are exudate or inflammation, Palate
common in infectious petechiae and scarlatiniform rash
mononucleosis (rare but highly specific)
Red flags (ER referral): muffled voice, drooling, stridor, Respiratory

distress or “tripod” position, Deep neck space infection, Severe unilateral
sore throat, pharyngeal wall/soft palate/oropharynx floor Bulging Neck
pain or swelling, torticollis (wry neck). Trismus, Stiff neck, rigors, Hx of
penetrating trauma
Page | 46
5.2.3 Diagnosis/Clinical tool:

Investigations: RDAT (rapid antigen detecting test) Throat culture
Table 5.2 Centor criteria strep pharyngitis

Absence of cough, swollen tender anterior cervical 1 point for each
LN, temperature > 38, tonsillar exudate, age 3-14
Age 15-44 0
Age 45+ -1
Cumulative Score
0–1 low risk and no 2–3 indicates testing >4 consider RADT
need for further with RADT and/or and/or culture, empiric
testing. culture. Abx.
Importance of distinguishing bacterial from viral pharyngitis

GABHS complications:
 OM, retropharyngeal abscess, mastoiditis, meningitis, endocarditis,
bacteraemia.
 Immune mediated or toxin complications: RF, PSGN, reactive
arthritis, scarlet fever
Table 5.3 Viral pharyngitis Treatment
Oral analgesics: acetaminophen/NSAIDs
Topical Therapies: lozenges/drops, gargles. Warm fluids and foods/avoid spicy
and rough food, if significant sore throat, hydration with frozen like ice which has
numbing-like effect or warmed liquids.
Environmental measures: humidifiers, avoiding exposure to tobacco smoke which
can cause irritation.
Bacterial pharyngitis Tx of choice for GABHS is the penicillin family for 10 days
Pediatric (Amoxicillin) Adult (Amoxicillin)
Mild to moderate: Severe:45 Mild to mod: 500 Severe: 875 mg
25 mg/kg/day BID mg/kg/day Max. mg BID or 250 mg BID or 500 mg
or TID. 1g /day (BID or Q8h 10D q8h 10D
TID)
-Use amoxicillin/clavulanic acid if treatment failed, recurrent infection within a
month, or OM, with a similar dose.
-If allergy to penicillin: 1st generation cephalosporins such as cephalexin, adults
dose is 500 mg BID and pediatric dose is 25-50 mg/kg/day BID.
-T1 hypersensitivity (angioedema/anaphylaxis): macrolides like azithro, or
clindamycin if resistance.
Page | 47
Azithromycin: Clarithromycin: Clindamycin:

Peds:12 mg/kg/day 5D Peds. 7.5 mg/kg BID for Peds. 7 mg/kg/day TID
(Max. 500) 10D Adult 250 BID OD for 10D Adult 300 mg q8h
Adult 500 mg 1st day then for 10D for 10 days
250 4D
Tonsillectomy: if recurrent pharyngitis with the following criteria:
● >7 episodes in 1 year or >5 episodes/year in two years or 3 episodes/year
in the last 3 years
● Each episode should be documented with one of the following: Fever >38o
or Tonsillar exudates or Cervical lymphadenopathy or +ve GABHS culture
Other indications: Airway obstruction, Sleep related difficulties.
5.3. Epiglottitis:
5.3.1 Background:
Uncommon, acute inflammation in the supraglottic region of the
oropharynx.
5.3.2 Symptoms:
Sore throat, odynophagia/dysphagia, muffled voice “hot potato voice,”,
stridor, URTI symptoms.
5.3.3 Physical examination:
A definitive diagnosis is made by the direct visualization of an
erythematous and swollen epiglottis under laryngoscopy with equipment
to secure the airway. If you examine the throat without securing the
airway you may provoke the risk of airway spasm or obstruction leading
to death.
May present with the following:
Hyper-extension of the neck, tripod posture.
Toxic appearance, Irritability
Stridor, muffled voice, horsiness
 Vital Signs: High temperature, Tachycardia, Hypoxia
 HEENT: Inflamed epiglottis, Pharyngeal redness
 Neck: Tenderness of anterior neck, Cervical lymphadenopathy
 Lungs: Respiratory distress, ↑ RR, ↓ air-entry depending on degree of
airway obstruction
 Extremities: Cyanosis
5.3.4 Investigation:
no specific test, some test may help:
 CBC for leukocytosis
 Blood cx and throat culture should be done under intubation for
organism specification
Page | 48
 ABG: respiratory acidosis

 Radiology: The thumbprint sign is a classic finding on the lateral neck
x-ray.
5.3.5 Management:
Call ER immediately, avoid agitating the patient and let to take a position
in which feels comfortable.
 1st line: high-flow O2, IV access, and calling the ENT specialist as
intubation may be required, cricothyroidotomy, or needle-jet should be
at the bedside.
 Antipyretic
 Adjuvant: corticosteroids and racemic epinephrine.
 Start empiric 7-10 days course of IV antibiotics to cover the most
common organisms: s. pneumoniae, beta-hemolytic strep, and S.
aureus.
Table5.4 Antibiotics and doses for epiglottis treatment
Pediatric Adult
Ceftriaxone: 2 g every 24
Ceftriaxone: 50–100 mg/kg/day OD or
hours
BID (Max 2g)
Cefotaxime: 2 g every 4–8
Cefotaxime: 150–200 mg/kg/day Q6h
hours
(Max 10 g)
Vancomycin: 2 g per day IV
Vancomycin: 40–60 mg/kg/day in Q6-8h
every 6–12 hours
(Max 2 g)
Clindamycin: 600–900 mg
Clindamycin: 30–40 mg/kg/day Q6-8h
every 8 hours
(Max 2.7 g)
Levofloxacin: 750 mg every
Levofloxacin: 8 mg/kg Q 12 hours
24 hours
5.4. Retropharyngeal abscess:
5.4.1 Background:
Abscess in the tissue in the retropharyngeal space. Abscesses in this
space were polymicrobial and caused by the following organisms:
Aerobic organisms, such as group A streptococci. and S.aureus,
including MRSA
Anaerobic organisms, such as species of Bacteroides. Gram-negative
organisms, such as Pseudomonas (in high-risk groups), Haemophilus
influenzae, H parainfluenza.
5.4.2 Symptoms:
Sore throat, croup-like cough, fever, drooling, dysphagia, odynophagia,
neck pain, dyspnea
Page | 49

 Posterior pharyngeal edema
 Stiff neck (limited neck mobility or torticollis)
 Nuchal rigidity
 Neck tenderness (in front of the neck or around the Adam’s apple)
 Cervical adenopathy
 Fever
 Drooling
 Stridor
 Trismus
 Lethargy
 Respiratory distress
 Dysphonia
 Tonsillar displacement
 Associated signs, including tonsillitis, peritonsillitis, pharyngitis, and
otitis media in children
no specific tests needed, but the following investigation may help:
 CBC with leukocytosis
 Blood culture before IV Antibiotics
 Culture of exudate, aspirated at the time of surgical drainage of the
abscess
 CRP/ESR may be high with inflammation
 COVID-19 testing – In adult or pediatric patients who present with a
sore throat
 Radiology: Lateral neck radiography (80% of the time) shows swelling
of the retropharyngeal space with more than 7 mm at level C2
vertebra. The definitive diagnostic imaging is a CT scan.
Page | 50
5.4.5 Management:
Apply supplemental oxygen + refer patient immediately to ER.
Secondary care management may include:
 Intubation
 IVF if the patient is dehydrated
 IV antibiotics.
 Surgical drainage
Empirical use of antibiotics (to eradicate infection, prevent complications)
such as:
 Ceftriaxone + metronidazole
 Levofloxacin + clindamycin
 Ampicillin-sulbactam
Chapter 6: COUGH
6.1. Definition:
Cough is one of the most common presenting symptoms in primary care
that may lead to a diagnosis, or it could be the only symptom in an
undifferentiated patient.
It can be categorized into three major groups based on symptom period:
 Acute (<3 weeks).
 Subacute (3-8 weeks).
 Chronic (>8 weeks).
Page | 51
Table 6.1 Causes of cough

Acute Subacute Chronic
< 3 weeks 3-8 weeks > 8 weeks
 Viral URTIs.  Post infectious  Angiotensin-
(commonest) cough. converting enzyme
 Bacterial URTI.  Pertussis. inhibitor use
 Inhaled foreign  Gastroesophageal
body. reflux disease
 Acute Pulmonary  Non asthmatic
embolism eosinophilic
 Pneumonia bronchitis
 Acute bronchitis  Tobacco use
 Acute exacerbation  Upper airway cough
of Asthma, COPD, syndrome
CHF  Asthma
 Environmental
triggers
 Bronchiectasis
 Chronic obstructive
pulmonary disease
 Obstructive sleep
apnea
 Post infectious
bronchospasm
 Bronchiolitis
 Bronchogenic
carcinoma
 Chronic aspiration
 Chronic interstitial
lung disease
 Psychogenic cough
 Sarcoidosis
 Tuberculosis
In the case of a coughing patient, to make a diagnosis a combination of a

carful history, physical examination, and diagnostic testing is
required.
Page | 52
6.2. History:
Provides the first key hints.
● Character/circumstance
o Productive, dry, or hemoptysis.
● Exacerbating/ relieving factors
o Look for triggers.
● Associated symptoms
o Systemic: Fever, chills, sweats, weight loss.
o Cardiac and pulmonary: Dyspnea, chest pain.
o HEENT: Sneezing, postnasal drip.
o Gastrointestinal: Heartburn.
● Severity
o Affecting work or sleep, causing syncope or incontinence.
● Timing
o Pattern: acute or chronic, constant or intermittent.
o Onset.
o Duration.
o Why is the patient coming now?
● Relevant past medical history
o Asthma, atopy, drug allergies, currently taking or recently took
any medications, exposure to TB or other infectious diseases
● Relevant social history
o Travel or immigration, occupation, hobbies (i.e., glue or chemical
exposures), alcohol or tobacco use, new pets, etc.
o What is the patient’s concern?
● Relevant family history
o Atopy, asthma, eczema, TB exposure.
6.3. Physical examination:
● Vital signs
● General appearance
o How sick does the patient look, distress, dyspneic, sweating,
cachectic, cyanosis, clubbing.
● HEENT
o Nasal passage (nasal polyps), sinuses, throat (cobblestoning),
adenopathy, neck veins if considering a cardiac problem.
● Chest/lungs
Page | 53
o respiratory rate, accessory muscle use, retractions, lung sounds.

Hyperinflation, dullness, crackles, wheeze, bronchial breathing,
pleural rub.
● Cardiovascular
o PMI size and location, heart sounds (gallops, murmurs, or rubs).
● Other parts of physical exam as indicated
Further investigation should be perused if the history and examination
did not indicate a diagnosis. Especially in patients whose cough is
continues > 3 weeks; consider obtaining:
 Plain chest X-rays. (To rule out most infectious, inflammatory and
malignant thoracic conditions)
 Pulmonary function tests /spirometry.
 Sputum cytology and culture. (Elevated with bacterial overgrowth,
bronchiectasis, TB, lung abscess, and bronchial carcinoma)
 CT scan.
Simple chest X-ray is required for any cough that lasts longer than three
weeks.
6.5. Management:
Acute cough (<3 weeks):
 Self-limiting, improving in 3 to 4 weeks without antibiotics and can be
manged by self-cure treatment including: honey, natural remedies,
and over-the-counter cough medicines.
 Peripheral cough suppressants can be considered for a short-term
relief in case of acute bronchitis such as levodropropizine.
Subacute cough (3-8 weeks):
Usually following the symptoms of acute respiratory infection; nasal sinus
congestion, non-purulent nasal discharge, sore throat.
● Antibiotics are not recommended. But may considered if clinically
indicated trial of:
o Inhaled ipratropium
o Inhaled corticosteroids
o Short trial of prednisone 30-40 mg/day
o Central acting antitussive medications such as codeine and
dextromethorphan
Page | 54
Chronic cough (>8 weeks):

By finding out what’s causing chronic cough, a medication can be aimed
at that particular etiology, which should be selected based on clues from
the initial evaluation.
Table 6.2 Differentials and management overview
Disease History/ physical exam Management
Present with heartburn,
Lifestyle Modifications in
dysphagia, acid
combination with acid
regurgitation, cough
suppression medication. (PPI
associated with a
GERD more effective than H2).
slouched posture,
If no improve within 2-3
phonation, rising from
months may require further
bed, or feeding, and it
workup
may even be silent.
Regular use of an inhaled
glucocorticoid and as-needed
use of an inhaled
bronchodilator or combined
When you suspect
inhaled glucocorticoid -
asthma, perform
Asthma formoterol. Combination
spirometry pre- and
therapy with a leukotriene
post-bronchodilator.
receptor antagonist and an
as-needed, short-acting
inhaled bronchodilator is a
reasonable alternative.
Frequent throat clearing,
First-generation
Upper Airway postnasal drip, nasal
antihistamine/decongestant, if
Cough Syndrome discharge, nasal
no improvement in 1-2 weeks
(Postnasal Drip) obstruction or sneezing
may add topical nasal steroid.
typical, halitosis.
Page | 55
Allergic UACS The: treated

with an intranasal steroid.
Combination therapy with an
intranasal steroid and an oral
antihistamine is an
Allergic UACS: personal
alternative, particularly in a
Upper airway cough or family history
patient with severe
syndrome (UACS) suggestive of atopy
symptoms.
Non-Allergic
Nonallergic UACS: trial of
therapy with intranasal
administration of one or more
of the following: azelastine,
steroid, or ipratropium.
prolonged cough
following an upper The treatment follows that for
Postinfectious cough respiratory infection and nonallergic UACS, as
clinical features described above
suggestive of UACS
Dry cough, begin within Stopping ACE inhibitor, cough

days or months of usually resolves in 1-12
ACE Inhibitor
initiating ACE inhibitor weeks. But it may last for 4
therapy. months
Inhaled bronchodilator,
History of smoking; inhaled anticholinergic,
Chronic productive cough; inhaled corticosteroid, and 1-
bronchitis/COPD associated with 2 weeks course of oral
exertional dyspnea corticosteroids (with or
without antibiotics).
Reversible airflow Regular use of inhaled

obstruction or a positive glucocorticoids and as-
Cough-variant Asthma
test for bronchial needed use of inhaled
hyperresponsiveness. bronchodilators.
Page | 56
Smoking history,
changes in recurrent
cough, hemoptysis,
hoarseness, chest pain, Referral to a
weight loss, superior pulmonologist. Perform
vena cava syndrome Chest-Xray if you suspect
(localized edema of the lung cancer. if suspicion
face and upper remains high, contrast-
Lung cancer
extremities, facial enhanced computed
plethora, distended neck tomography (CT) should be
and chest veins). May performed, followed by
result in unilateral positron emission
localized wheezing, tomography if necessary.
cachexia, and symptoms
of distant metastases
(e.g., bone pain).
Suggested initial treatment
with the nonopioid agent,
e.g., dextromethorphan.
The cause of chronic Benzonatate can be added if
cough cannot be the cough persists. For
Unexplained chronic
identified and empiric patient whose cough does
cough
therapy for suspected not respond, a trial of an
causes has failed opioid antitussive is
suggested. e.g., Codeine and
morphine. Gabapentin and
pregabalin are alternative.
6.6. Referral:
Referral to the pulmonologist is considered if the symptoms continue
after empiric treatment or if red flags present:
 Age >50 years
 Smoking history
 Asbestos exposure
 Persistent cough
 Overseas travel
 TB exposure
 Hemoptysis
 Unexplained weight loss
 Dyspnea
Page | 57
Chapter 7: HEADACHE
7.1. Definition:
 Headache is a pain in any region of the scalp, the pain may occur on
one or both sides of the head, be isolated to a particular location,
radiate across the head from one point, or have a viselike quality.
 Headache may appear as a sharp pain, a throbbing sensation, or a
dull ache.
 Headaches are divided into two main categories:
o primary headache (idiopathic, subtypes: tension type, migraine,
and cluster headaches)
o secondary headache (depends on the underlying etiology
example: Infection, head trauma, substance abuse, underlying
eye, ear, nose, sinuses, teeth, mouth, or facial disorders, etc.)
7.2. -Symptoms and physical examination signs:
7.2.1 History:
 Analysis of the headache: SOCRATE
 Triggers or precipitating events (Hormonal changes, stress, smoking,
caffeine, etc.)
 Head injury or trauma
 Past medical history and comorbidities
 Medication history to r/o Medication overuse headache e.g., opioids,
OCP, NSAID, Triptans, ergotamine
 Impact of the headaches on the quality of life
7.2.2 Risk factor:
 Hormonal changes, menstruation, pregnancy, and ovulation
 Stress, depression, anxiety
 Excessive or insufficient sleep
 Medications (e.g., vasodilators, oral contraceptives)
 Smoking
7.2.3 Red flags:
Systemic symptoms including fever, weight loss, Neoplasm history,
Neurologic deficit, Onset is sudden or abrupt, Older age (> 50-year-old),
Pattern change or recent onset of new headache, Positional headache,
Precipitated by sneezing, coughing, or exercise, Papilledema,
Progressive headache and atypical presentations, Pregnancy or
puerperium (eclampsia -preeclampsia), Painful eye with autonomic
features, Post-traumatic onset of headache, Pathology of the immune
Page | 58
system, Painkiller (analgesic) overuse (e.g., medication overuse

headache) or new drug at onset of headache
7.3.1 Vital signs:
Head and neck:
 Listen for bruit at neck, eyes, and head for clinical signs of
arteriovenous malformation
 Palpate the head, neck, and shoulder regions for any trauma
 Check temporal and neck arteries tenderness (to r/o temporal
arteritis)
 Examine the spine and neck muscles
 The neurologic examination should cover mental status testing,
cranial nerve examination, fundoscopy and otoscopy, HEENT, and
symmetry on motor, reflex, cerebellar (coordination), and sensory
tests. Gait examination should include getting up from a seated
position without support and walking on tiptoes and heels, tandem
gait, and Romberg test
 In primary headache types, all physical assessment is normal
However, some types of primary headache may be associated with
specific abnormalities:
 With TTH, there may be pericranial muscle tenderness
 With cluster headache, there may be evidence of autonomic
activation: conjunctival congestion, lacrimation, rhinorrhea, eyelid
edema miosis, and/or ptosis
7.4. Investigation and Monitoring:
 Lab investigation is not indicated for primary headaches
 CBC, CRP, ESR > if suspecting temporal arteritis
 Imaging is not recommended for tension type headaches, cluster
headaches, or medication overuse headaches to reassure patients
 Patients with red flags or other features suggesting a secondary
headache source > require imaging
o In emergency settings > CT scan has several advantages
compared with MRI
o Non-emergency settings > MRI is usually reserved as a non-
emergent elective study
 Lumbar puncture helps identify infection, CNS malignancies or
hemorrhage
Page | 59
 In adults with suspected subarachnoid hemorrhage, it is crucial to

perform a lumbar puncture to check for blood or xanthochromia if the
CT of the head was negative
7.5. Management:
Evidence-based guidelines from the United States, Canada, and Europe
provide consistent recommendations, including:
 Lifestyle modifications
 Avoidance of triggers
 Healthy coping mechanisms
A complete management plan includes:
 Patient headache diary
 Addressing risk factors
 Avoiding headache triggers
 Controlling common comorbid conditions such as depression, anxiety,
substance abuse, and chronic musculoskeletal pain syndromes that
can impair treatment effectiveness
 Regularly scheduled follow-up is essential to monitor progress
 Medication options for individualized management are based on the
patient’s symptoms severity, preferences, effectiveness, adverse
effects, and cost
Table 7.1.Medication options for treatment of primary type headache
Type of Migraine Tension-type headache
Cluster headache
management headache (TTH)
–Mild: – Mild: simple
(NSAIDs)/ analgesics such as
acetaminophen (NSAIDs)
– Recommend
/ – Reasonable
initial treatment
aspirin/caffeine choices include
with either
–Moderate to single dose of:
oxygen or
severe: – Ibuprofen (400
triptans
Acute Triptans mg),
management
– Alternatives
– 2nd line – Naproxen sodium
include: ipsilatera
treatment Opti (220 mg or 550 mg)
l
ons: – Aspirin (650 to
intranasal lidocai
antiemetics 1000 mg).
ne 1 ml with
e.g., metoclopr – Acetaminophen
moderate effect
amide and (1000 mg) is
prochlorperazi preferred in
ne pregnancy
Page | 60

Cluster headache
– The combination
of caffeine with the
simple
analgesics acetamin
ophen, aspirin or
ibuprofen is more
effective for the
treatment of TTH
than simple
analgesic
monotherapy
– Severe TTH:
parenteral chlorprom
azine,
metoclopramide, the
combination of
metoclopramide
plus diphenhydramin
e, or
intramuscular ketorol
ac
Indication for
prophylaxis
therapy: -≥ 4
headaches per
month or≥ 8
headache days – Preventive
– Prophylactic TTH
per month– therapy should
treatment is indicated
Prophylactic Debilitating be started
if headaches are
attacks despite without delay
management if frequent, long-
acute therapy- once cluster
criteria met lasting, or associated
Difficulty episode begins
with a significant
tolerating or to suppress
amount of disability
contraindicatio attacks over time
n to acute
therapy
– Overuse of
acute
medication -
Page | 61

Cluster headache
Patient
preference for
fewer attacks
– Presence of
migraine
subtypes
– Consider
first-line
therapy:
divalproex
(Depakote), – Verapamil is
topiramate the drug of
(Topamax), choice for
propranolol, prophylaxis with
metoprolol, an initial dose 80
timolol mg TID and
– If no first-line titrates 80 mg
agent is every 14 days
effective or if – Tricyclic – Most patients
intolerable antidepressants such respond to TDD
adverse effects as amitriptyline (first (Total Daily
Initiating
occur, consider line), SNRIas Dose) of 240 mg
pharmacolo
a combination (mirtazapine and divided into 2 or
gic
of two first-line venlafaxine) and 3 doses; other
prophylaxis
medications anticonvulsants patients require
– If no first-line (gabapentin and 960 mg TDD
agent or topiramate) –
combination is Oral prednisone
effective or if 60 to 100 mg
intolerable once a day for at
adverse effects least five days,
occur, consider followed by a
second-line taper with a dose
therapy: reduction of 10
amitriptyline, mg daily
venlafaxine,
atenolol,
nadolol
(Corgard)
Page | 62
Chapter 8: OBESITY
8.1. Definition:
The overall prevalence of obesity among Saudi adults is estimated to be
35.4%
8.2. Obesity risk factors, include:
 Age
 Race/ethnicity
 Sedentary lifestyle
 Unhealthy eating behaviors (e.g., too much saturated/trans fats; foods
high in added sugars)
 Lack of sleep
 High amounts of stress
 Genetics (e.g., Prader-Willi syndrome, Bardet-Biedl syndrome, Cohen
syndrome)
 Endocrine disorders (e.g., hypothyroidism, Cushing’s syndrome,
some tumors such as craniopharyngioma)
 Metabolic factors
 Gut bacteria
 Psychological and behavioral factors (18-30% increased risk with
PTSD)
8.3. Classification:
8.3.1 ADULT:
 Overweight BMI 25-29.9 KG/m2
 Obesity
 CLASS 1 30.0-34.9KG/m2
 CLASS 2 35.0-39.9 KG/m2
 CLASS 3 ≥40 KG/m2
8.3.2 PEDIATRICS:
 OVERWEIGHT: >85TH % for age and gender
 OBESITY: >95TH % for age and gender.
8.4. Implication of obesity:
8.4.1 Risks:
 high mortality 2x cardiovascular disease.
 DM 5x
 OA
Page | 63
 fatty liver disease

 BA
 infertiliy
 menstrual disease
 malignancy
 mental disturbance
8.4.2 Benefit of weight loss:
 Lower lipid profile, raise HDL.
 Lower bp.
 Decrease risk dm and use of medication if diseased.
 Improves sexual health status.
8.5. Obesity Comorbidities in Children:
 Hypertension
 Dyslipidemia
 Subclinical atherosclerosis
 Acanthosis nigricans
 type 2 diabetes mellitus (DM2)
 early-onset polycystic ovary syndrome (PCOS)
 non-alcoholic fatty liver disease (NAFLD)
 asymptomatic gallstones
 slipped capital femoral epiphysis (SCFE)
 low self-esteem, poor body image, anxiety, depression, and
disordered eating patterns.
 sleep apnea
 impaired kidney function
8.6. Assessments of Obesity:
Common anthropometric (physical examination methods) for assessing
obesity include:
 BMI (most common)
 Waist circumference
 Waist-to-hip ratio
 Hip circumference
 Skinfold thickness
Diagnosis of obesity is based on:
 Medical history
 Eating and physical activity habits
Page | 64
 Family history
 Evidence of other risk factors
 Physical examinations confirming high BMI
 Blood tests:
 Thyroid hormone levels to rule out hypothyroidism
 Cortisol and adrenocorticotropic hormone (ACTH) tests to rule out
Cushing’s syndrome
 Total testosterone, dehydroepiandrosterone sulfate (DHEAS) tests,
and pelvic ultrasound to rule out polycystic ovary syndrome (PCOS).
8.6.2 Management:
 Lifestyle changes around heart healthy diet, physical activity, healthy
sleep.
 Medication
 Surgery
 Devices
Weight loss of 5 to 7% of body weight carries numerous health benefits
and should be sought as an initial weight loss goal.
8.6.3 Medication therapy:
Table8.1 Medications approved for the long-term treatment of obesity
Medication and dosing Adverse effects
Semaglutide GI complaints, HA, fatigue, dizziness,
0.25-2.4mg SQ weekly hypoglycemia in DM2
Liraglutide GI complaints, dizziness, fatigue, increased
0.6-3 mg SQ daily lipase levels, hypoglycemia in DM2
Naltrexone/bupropion
GI complaints, dizziness, dry mouth, HA,
8/90 mg, two tablets twice
insomnia
daily
Orlistat Fecal incontinence, fecal urgency, flatus, oily
60 or 120 mg tid stool
Phentermine/topiramate Constipation, dizziness, dry mouth, insomnia,
7.5/46 or 15/92 mg per day dysgeusia, paresthesia
MTC = medullary thyroid cancer; MEN2 = multiple endocrine neoplasia type 2
Page | 65
8.6.4 Surgery:
If BMI ≥40 kg/m2, or a BMI of 35 to 39.9 kg/m2, one or more serious
comorbidity, and who have failed to meet weight loss goals with diet,
exercise, and drug therapy.
Bariatric surgery options:
 Roux-En-Y Gastric Bypass
 Laparoscopic Sleeve Gastrectomy
 Laparoscopic adjustable gastric banding (LAGB)
8.7. Devices:
● Electrical stimulation (vagal blockade) systems
● Intragastric balloon systems
● Gastric emptying (aspiration) systems
● Hydrogels
Chapter 9: ANEMIA
9.1. Background:
Reduction in ≥ 1 of the major RBC measurements obtained as a part of
the CBC: hgb, Hct, or RBC count.WHO and NCI defines normal
hemoglobin as 14 mg/dl for men and 12 mg/dl for women.
9.2. Kinetic approach:
Table 9.1
Decreased RBC production Increased RBC loss
Lack of substrate: Iron, folate, protein Hemolysis – inherited or
Marrow disorders: malignancies, acquired, G6PD,
aplasia(pancytopenia). autoimmune, transfusion, etc.
Decreased trophic hormones: TSH, ACTH Blood loss – occult or obvious
Chronic disease/inflammation: CRD, RA, SLE.
Page | 66
9.3. Morphologic approach:

More widely used. It depends on RBCs indices, specifically MCV to
classify the type of anemia
Table 9.2
Normocytic (MCV Microcytic (MCV below
Macrocytic (MCV > 100)
80-100) 80)
-Vitamin B12 deficiency in:
vegetarians, malnourished, -IDA
elderly). −↓ heme synthesis like
-Folic acid deficiency in: -Chronic diseases lead
alcohol abuse, cancer and (most common) poisoning/sideroblastic
chemotherapy) -Acute blood loss anemia.
-Pernicious anemia -Acute haemolysis −↓ globin synthesis like in
-chronic PPI, metformin use. (G6PD, autoimmune) thalassemia (beta or
-Acute haemolysis with high -Hypersplenism Alpha) Sickl cell disease.
reticulocyte count after birth. -Chronic /inflammatory
-Myelodysplasia. illness
-Liver disease
9.4. Symptoms:
Fatigue, palpitations, headaches, SOB, dizziness, blurred vision,
orthopnea, or pain.
9.4.1 Red flags:
rectal bleeding, weight loss, fever, or excessive sweating.
 Pallor, jaundice (hemolysis), tachypnea, and tachycardia.
 CHF in severe anemia, chest pain w/ exertion, nail/hair changes,
murmurs, hepatosplenomegaly.
 If thalassemia: dysmorphic features, slow growth, iron overload signs,
enlarged spleen.
 Sickle cell disease: acute manifestations:
o Pain: vaso-occlusive pain crisis, acute chest syndrome,
o Infection: sepsis, pneumonia
o Anemia: aplastic crisis, haemolysis, sequestration
o Stroke, seizure, acute renal failure, avscular bone necrosis,
cholecystitis, retinal artery thrombosis, priapism.
Page | 67
 CBC as initial
o Normal CBC in the past excludes inherited hemoglobinopathies.
o MCV is the most important one.
o Leukocytosis with infection/inflammation, severe leukocytosis
can be due leukaemia. Leukopenia may be a sign of bone
marrow suppression or hypersplenism.
o Plt/ RDW count can be ↑ in IDA or hemolysis and ↓ when bone
marrow is suppressed due to infection, aplasia, or malignancy.
 Blood smear
o Sickled RBCs in SCD
o Spherocytosis or elliptocytosis in hereditary elliptocytosis (HE)
and spherocytosis.
o Bite cells in G6PD deficiency
o High reticulocytes in case of hemolysis.
o Blast cells are seen in cases of leukemia.
o Parasites like malaria or leishmania that can be the cause of
anemia.
 ESR: Obtain if inflammatory processes like CTD or malignancy like
MM are suspected.
 Retic. Count: ↑ in acute hemolysis/neonatal anemia. Normal count
excludes hemolytic anemia.
 Iron panel and ferritin If IDA is suspected.
 RFT if CKD is suspected
 LFT: ↑ serum bilirubin can be indicative of hemolysis.
 Sickle cell screening If SCD is suspected.
 Hemoglobin electrophoresis If thalassemia or SCD or trait are
suspected.
 G6PD enzyme activity If deficiency is suspected in pt with acute
hemolysis.
 Vit B12 level, folate level: In macrocytic anemia if suspected
deficiencies in folate and vit B12.
 RBC antibodies, direct anti-globulin (immune mediated hemolysis) If
autoimmune hemolytic anemia is suspected.
 Bone Marrow aspiration/biopsy: May be needed if the reason for
anemia is challenging. Malignancy, myelodysplastic syndrome, or
aplasia can be detected.
Page | 68
9.7. Management:
9.7.1 Iron deficiency anemia:
(It is important to treat the causing factor of IDA)
Oral 60 mg of elemental oral iron OD for 4-6 m + Ascorbic acid to
enhance absorption.
Table 9.3 Types of oral iron
Tablet Dose Elixer Dose (Elemental
Generic name
(Elemental Iron), mg Iron), mg in 5 ml.
325 (65) 300 (60)
Ferrous sulfate
195 (39) 90 (18)
Extended release 525 (105)
325 (107)
Ferrous fumarate 100 (33)
195 (64)
Ferrous Gluconate 325 (39) 300 (35)
150 (150)
Polysaccharide Iron 100 (100)
50 (50)
Parenteral iron if oral treatment intolerance/SE, intestinal
malabsorption, or acute need for iron after erythropoietin or chronic blood
loss.
Formula to calculate the dose:
Deficit = [Body Wt (kg) x 2.4 x (Target hgb − Initial hgb [g/dl])] + 500 mg
9.7.2 Vit B12 deficiency and folic acid deficiency:
 Folate deficiency: 1 to 5 mg daily will replete deficiency in 4 to 6
weeks.
 B12 deficiency: Oral B12 1000 mcg/day or 1000 mcg IM monthly.
Oral Tx is as effective as IM
Page | 69
9.7.3 Sickle cell disease:

 Hydration and keeping a good room temperature is important.
 Pain crisis: NSAIDs, paracetamol, or opioids if needed. Treating SCD
pain with long-acting opioids ↓ hospital admissions and ER visits; oral
opioids are preferred to IV opioids.
 Sequestration crisis, aplastic crisis emergency with blood transfusion.
 Acute chest syndrome (ACS) (an emergency) giving the appropriate
analgesia for a pain crisis, Keeping O2 saturation above 92%,
bronchodilator and a short course
 of corticosteroid for those who wheeze or have asthma. Broad
spectrum antibiotic coverage is recommended
 Hydroxyurea for patients who have ≥3 painful episodes/year and who
have SCD complications.
 Long-term folic acid supplement is indicated.
 Blood transfusion in some cases.
 Immunizations: Strep. Pneumoniae, N. meningitidis, H influenza B,
Hep B, and viral influenza.
 Prophylaxis: age between 3m- 3 years require Penicillin V 125 mg
BID, ages 3–5 years; 250 mg BID, >5 years is controversial.
9.7.4 Thalassemia major:
 Treated with regular blood transfusion.
 In many cases splenectomy is required to reduce the frequency of
transfusion.
 Because of repeated transfusions, iron overload requires chelation
therapy with Desferrioxamine.
 All patients with thalassemia require folic acid supplement.
 All post-splenectomy patients should receive Haemophilus
Influenzae, Meningococcal, and the Pneumococcal 23 valent
polysaccharide (PPSV23) vaccines prior to surgery. PPSV23 vaccine
should be repeated 3 to 5 years later.
 Influenza vaccination annually.
Page | 70
Chapter 10: SMOKING CESSATION

10.1. Smoking cessation advice: 5 A’s model:
 5 As model is recommended for health care providers to ask
encountered patients about the status of smoking.
 It is composed of 5 components; Ask, Advise, Assess, Assist, and
Arrange. It takes on average 5 minutes to perform.
10.2. Nicotine addiction Diagnosis:

At least 2 of the below mentioned 11 criteria should be met in a 12
months period. Severity of addiction is determined by the number of
criteria met;
 Mild: 2–3 symptoms
 Moderate: 4–5 symptoms
 Severe: 6 or more symptoms
Table 10.1 Criteria for Nicotine Addiction, Substance Abuse-
Disorder
Symptoms Indication
1.Tobacco is mostly taken in larger Impaired Control
amounts or over a longer period
than was intended.
2.Persistent desire or unsuccessful
efforts to cut down or control
tobacco use.
3. Excessive time spent obtaining
and use.
4. Craving or strong desire to use
tobacco.
1. Its use is resulting in failure to Social Impairment
fulfill major role obligations at work,
school or home.
Page | 71
2. Continuous use in spite of

persistent or recurrent social or
interpersonal problems caused by
or exacerbated by tobacco use.
3. Important social, occupational,
or recreational activities are given
up for tobacco use.
1.Recurrent tobacco use in Risky Use
situations where it is physically
dangerous
2.Continued use despite
persistent, related psychological or
physical problems.
1.Tolerance. manifestations.Pharmacological
2.Withdrawal Indicators
10.3. Nicotine withdrawal:
 Upon abrupt cessation of tobacco use, nicotine levels drop causing a
number of symptoms.
 Most of these symptoms manifest in the first 1–2 days
o Peak within the first week and subside within 2–4 weeks).
o Irritability, frustration, anger
o Anxiety
o Difficulty in concentration
o Increased appetite/weight gain
o Restlessness/impatience
o Depressed mood/depression
o Insomnia
o Impaired performance
10.4. Smoking during pregnancy:
 Pregnancy is an optimal time for smoking cessation
 It is highly recommended for pregnant women using behavioral and
social therapy
 If behavioral and social therapy are not possible then short-acting
NRT
 the risk to the fetus of continued smoking by the mother far outweighs
any potential side effects of NRT.
Page | 72
10.5. Smoking and psychiatric disorder:

 Treating tobacco dependence in these patients is associated with
reduced depression, anxiety, and stress
 close monitoring of the psychiatric illness and its treatment is
important
 Stopping smoking may exacerbate a patient’s comorbid condition
(depression).
 It is recommended to offer tobacco dependence treatment when
psychiatric symptoms are not severe.
 NRT is safe and effective for smokers with a mental illness.
 Intensive counseling and close follow-up are important in such
patients.
 Varenicline and bupropion can be used but with cautions
Table 10.2 Pharmacological therapy for Nicotine addiction
Non-nicotine replacement therapy
Nicotine replacement therapy (NRT)
(Non NRT)
Transdermal nicotine patch (Long-acting)
Nicotine lozenge (Short-acting)
Varenicline
Nicotine gum (Short-acting)
Bupropion
Nicotine nasal spray (Short-acting)
Nicotine inhaler (short-acting)
Page | 73
Table 10.3 Nicotine replacement therapy (NRT)

Medication Types Dosing How to use Instruction Contraindication Precautions Side effect
24 hours less than 10 Start nicotine Can be – Pregnancy – Localized skin
Patches cigarettes/day patch in the prescribed for – Immediately reaction/irritation
– 21 mg – 14 mg / day quit day patients aged after MI – Sleep
– 14 mg for 6 weeks – Patches 12–17 years (within 2 disturbance
– 7 mg – 7 mg / day should be old weeks) – Headache
– 16 hours for 2 weeks placed over – No – Arrhythmia – Nausea
Patches (if – Discontinue relatively restriction of – Unstable – Dizziness
patient more than 10 hairless skin; daily activities Angina
develops sleep cigarettes/day typically, – Topical Pectoris
disturbance – 21 mg / day between the hydrocortison
Transdermal
nicotine with 24 h for 4-6 weeks neck and e cream (1%)
patch patch) – 14 mg / day waist, rotating or
– 15 mg for 2 weeks the site to triamcinolone
– 10 mg – 7 mg / day reduce local cream (0.5%)
– 5 mg for 2 weeks skin irritation can be used if
– Discontinue – Each patch mild redness
lasts for 24 or irritation
hours then occurs
should be
removed and
placed new
one
– 2 mg dose is – Week 1-6: 1 – Start – Do not – Mouth Irritation
recommended piece every 1-2 nicotine swallow, bite, or ulcers
Nicotine for those who hours / lozenge in the or chew – Hiccup
lozenge smoke after 30 whenever quit day – Do not eat – Nicotine dose-
minutes of there is an – Place or drink, other related
awakening urge to smoke lozenge in the than water, 15 symptoms;
Page | 74
– 4 mg dose is – Week 7-9: 1 mouth minutes abdominal pain,

recommended piece every 2-4 between before and nausea, vomiting,
for those who hours cheek and during using headache, and
smoke within – Week 10-12: gum lozenge palpitations
30 minutes of 1 piece every – Allow to
awakening 4-8 hours dissolve
– Maximum slowly in the
Dose: 20 mouth over
pieces per day 20–30
minutes
– 2 mg dose is – Week 1-6: 1 – Start – Avoid acidic Temporomand – Gastric Irritation
recommended piece every 1-2 nicotine gum beverages ibular joint (with fast
for those who hours / in the quit e.g., coffee disease chewing)
smoke after 30 whenever day – Do not chew – Poor – Jaw pain
minutes of there is an – Chew and more than one dentition – Hiccup
awakening urge to smoke Park piece of gum – Patients – Excess
– 4 mg dose is – Week 7-9: 1 Technique: at a time with dental salivation
recommended piece every 2-4 “Chew” slowly – Taste may appliances – Mouth irritation
for those who hours until peppery be unpleasant – Severe or ulcers
Nicotine smoke within 3 – Week 10-12: taste emerges at start cases with – Nicotine dose-
gum 0 minutes of 1 piece every then “park” CVD related
awakening 4-8 hours the gum symptoms;
– Maximum against the abdominal pain,
Dose: 15 buccal nausea, vomiting,
pieces per day mucosa until headache, and
the taste palpitations
disappears
– Duration: 30
minutes
Page | 75
Dosing How to use precautions Side effects

– Week 1-8: 0.5 to 1 mg (1-2 – Start nicotine nasal spray in - Dependence potential since – Throat irritation
spray) every hour or PRN the quit day the nicotine delivery is similar to – Rhinitis
– Week 9-12: 0.5 to 1 mg (1-2 – Using while the head is tilted the cigarettes – Sneezing
Nicotine
spray) every 2-3 hour slightly back for better – Severe reactive airway – Tearing
nasal spray
– Minimum: 8 spray/day absorption disease
– Maximum: 80 spray/day – Should not inhale, swallow or
sniff
-First 6-12 Weeks: 4 mg every 1- – Puff in short breaths – Mouth and
2 hours or PRN (6-16 cartridge – Cartridge remains effective throat irritation
Nicotine per day) for 24 hours after opening -Bronchospasm
inhaler – Next 6-12 Weeks: gradual
reduction
– Maximum: 16 cartridge per day
Page | 76
Table 10.4 Non-nicotine replacement therapy

Medication Dosing How to use Instructions Precautions Contraindication Side effect
Gradual increase – Gradual – Prescribed for – Creatinine – Sleep
of the dose decrease of patients aged 17 – Suicidal clearance less disturbance
– 0.5 mg once smoked years or older ideation has than 30 ml/min – Nightmare
daily on Day 1-3 cigarettes – Dose tapering been reported – Pregnancy – Headache
(morning) – Quit day should at the end of the after use: ask – – GI disturbance
– 0.5 mg twice be from day 8 – course is optional patient to report Neuropsychiatric – Nausea
daily on Day 4-7 35 of starting unusual mood Diseases;
Varenicline
– 1 mg twice medication changes depression,
daily on daily on – Take the – Patients with agitation, suicidal
Day 7and medication after renal impairment ideation, hostility,
thereafter the meal, then agitation
– Course: 12-24 take cup of water
week after to decrease
the GI upset
Gradual increase – Gradual – Prescribed for – Suicidal – Seizure – Insomnia
of the dose decrease of patients aged 14 ideation has disorders – Agitation
– 150 mg once smoked years or older been reported – Hepatic – Headache
daily on Day 1-3 cigarettes – Dose tapering but no causal cirrhosis – Dry mouth
– 150 mg twice – Quit day should at the end of the association – Pregnancy – Tremor
Bupropion
daily on daily on be from week 2 course is optional concluded (category C)
Day 4and of starting – Minimize/avoid – Patients with
thereafter medication alcohol use hepatic
– Course: 6-12 impairment
week
Page | 77
Table 10.5Factors of medication selection

Patient-related factors Medication-related factors Medical issues
 Nicotine dependence level  Availability  Pregnancy
 Enthusiasm and desire to take the step  Course treatment  History of psychiatry illnesses
(stage of change)  Drug-drug interaction  Existing comorbidities (COPD,
 Patient preferences/interest in medication  Side effects diabetes mellitus, coronary artery
 Patient age disease, seizure)
 Patient compliance  Organ impairment (renal or hepatic)
 Previous quit attempts and experience  Recent medical procedure
with the medication
Page | 78
Section 2: Internal Medicine

Chapter 1: EPILEPSY
1.1. Definition of Epilepsy:
Recurrent seizures, ≥ 2 unprovoked seizures occurring > 24 hours apart.
The probability of having further seizures ≥ 60% within ten years after
having one unprovoked seizure.
Major Etiologies:
 Genetic defects such as Down syndrome
 Congenital or acquired structural etiologies (e.g., tuberous
sclerosis), (e.g., stroke, traumatic)
 Metabolic: mitochondrial defects may be associated with epilepsy
 Immune: inflammatory central nervous system (CNS) disorders as
Rasmussen encephalitis
 Chronic CNS infections as in human immunodeficiency virus (HIV),
malaria, tuberculosis
 Idiopathic
Page | 79
Seizure Categories:
Figure 1.1 – International League Against Epilepsy (ILAE) classification
of seizure
Focal Generalized Unknown Unclassified

• Motor: • Motor: • Motor: Due to inadequate
information or
Aware Tonic-clonic Tonic-clonic
inability to place in
Impaired awareness Clonic Epileptic spasms other categories
Unknown awareness Tonic • Nonmotor:
Automatisms Myoclonic Behavior arrest
Atonic* Myoclonic-tonic-
clonic
Clonic
Myoclonic-atonic
Epileptic spasms*
Atonic
Hyperkinetic
Epileptic spasms
Myoclonic
Tonic • Nonmotor:
Focal to bilateral Typical
tonic-clonic Atypical
• Nonmotor: Myoclonic
Aware Eyelid myoclonia
Impaired awareness
Unknown awareness
Autonomic
Behavior arrest
Cognitive
Emotional
Sensory
Focal to bilateral
tonic-clonic
Page | 80
1.2. Symptoms & physical examination:

1.2.1 History:
1-obtain a detailed history from the patient and available eyewitnesses
2-Description of event
 Presence of aura, onset, progression, and duration
 Ictal Behavior; generalized/focal, +/- loss of consciousness (LOC),
bilateral/unilateral lateralization, tongue biting/urine incontinence.
 Timing in relation to sleep.
 Postictal phase: confusion and suppressed alertness/Todd
paralysis/aphasia, hemianopsia, or numbness, duration.
3-Aggravating factors
 strong emotions
 intense exercise
 loud music
 flashing lights
 fever
 lack of sleep, and stress
4-History of previous seizure
 Ask about focal seizures/auras that may go unrecognized until
patients experience a first-time (secondarily) generalized seizure:
 Olfactory or gustatory hallucinations
 Brief episodes of panic/anxiety
 Visual hallucinations
5-Drugs that mimic seizures or provoke seizures
 Opioids/Amphetamines/ Alcohol
 Anti-psychotics/ Antidepressants
 Anti-cancer medications
 Medications causing hypoglycaemia
 Decongestants
6-Past history:
● Head injury ● Alzheimer’s disease
● Abnormal early neurologic ● Stroke
development ● Alcohol/drug abuse
● Intracranial infection ● Immunosuppression
● History of cancer ● Rheumatologic
● Hematologic disorders disorders
7-Family history of epilepsy e.g.: absence seizures and myoclonic
seizures
Page | 81
8-In follow up→ Assess compliance, drugs side effects, control of

seizures
1.2.2 Physical Examination:
 Vital signs/general appearance/mental status (postictal, confusion)
 Neurological examination: e.g., weakness/hyperreflexia/positive
Babinski sign
 Tongue bite/laceration →generalized tonic-clonic seizures (not
specific)
1.3. Investigations and monitoring:
Initial work-up after a first-time seizure:
1-Labs:
 Complete blood count (CBC)
 Renal function tests (RFT)
 Liver function tests (LFT)
 Urinalysis
 Serum lactate
 Toxicology screen
 Electrolyte panel including Mg, Ca, Po
 Blood glucose
 Lumbar puncture after excluding space-occupying lesion by imaging
 Antiepileptic drug (AEDs) blood level
2-Radiology:
 MRI for first unprovoked seizure
3-ECG for all patients with POC to rule out arrhythmia
4-EEG if normal does not rule out epilepsy
1.4. Differential diagnosis:
● Psychogenic nonepileptic seizure (PNES) ● Syncope
● Narcolepsy with cataplexy ● TIA
● Paroxysmal movement disorders ● Migraine Aura
● Transient global amnesia ● Panic attack
Page | 82
1.5. Management plan:

1.5.1 General:
 Patient education/counselling
 Avoid seizure triggers: sleep deprivation, alcohol, some drugs,
illness.etc.
 Avoid supplements/herbal, or medications that may affect AED levels
 Avoid unsupervised danger activities
 No driving until seizure-free for ≥3–12 months
 Assure safety in the home environment and workplace
 Adherence to medications
 Screen for mood problems
 Educate caregiver/witness how to deal with active seizures
 Plan for special care for women during pregnancy or while lactating
1.5.2 Specific:
 In Epilepsy first seizure should always be evaluated by a neurologist
 Start anti-epileptic drugs mainly after the second unprovoked seizure
 Start anti-epliptic drugs for the first unprovoked if has risk factors
 Wait for at least 2 to 3 years of seizure freedom before stopping anti-
epileptic medications
Table 1.1: Therapeutic spectrum of antiseizure drugs
Category Drug First choice for
 Valproate  Generalized seizures
 Lamotrigine  Focal seizures
Broad spectrum
 Levetiracetam  Initiating during
 Topiramate pregnancy
 Carbamazepine
 Gabapentin
Narrow spectrum:
 Oxcarbazepine
Primary for focal Focal onset seizures
onset seizures  Phenobarbital
 Phenytoin
 Pregabalin
Narrow spectrum:
For absence  Ethosuximide Absence seizures
seizures only
Page | 83
Chapter 2: APPROACH TO DYSPNEA

2.1. Definitions:
 A subjective experience of breathing discomfort that is comprised of
qualitatively distinct sensations that vary in intensity.
 Dyspnea can be classified into Acute: Hours to Days, Or Chronic:
Lasting > 1 month.
2.2. Symptoms & Physical Exam Signs:
2.2.1 History:
 SOCRATES (Site, Onset, Character, Radiation, Associated
Symptoms, Timing, Elevating, and relieving factors, & Severity)
 Associated Symptoms: Cough, nasal congestion, chest pain,
peripheral edema, joint swelling, muscle weakness.
 Red Flags: Dyspnea at rest, Low LOC, confusion, chest pain, or
Constitutional symptoms.
 Past Medical & Surgical History (Malignancy, Radiation, ER visits,
Admissions, Surgeries, Pregnancy)
 Medications
 Occupational history
 Social History
 Family History
2.2.2 Physical Exam:
 Vitals
 General Appearance (Mental status, use of accessory muscles,
stridor, hyperventilation)
 Neck Exam (JVD, deviated trachea, Stridor)
 Cardiac Exam (Murmurs, Extra heart sounds, irregular heart rate)
 Pulmonary Exam (Wheezing, Rales, Hyper-resonance or Dullness,
subcutaneous emphysema)
 Abdominal Exam (Ascites, Hepatomegaly)
 Extremities (Edema, Cyanosis, Clubbing)
Page | 84
Indications of urgent evaluation and management (Or ER

Referral):
 HR > 120 bmp, RR > 30 breaths/min, O2 Saturation < 90%
 Use of accessory muscles
 Difficulty speaking in full sentences
 Stridor
 Asymmetric breath sounds or Diffuse crackles
 Diaphoresis
 Cyanosis
Assessment of patients with unstable dyspnea:
 Follow ABCs of urgent evaluation
 Monitor vital signs and pulse oximetry
 Obtain any history of cardiac or pulmonary disease or trauma
 Evaluate mental status
Acute Causes:
Table 2.1
System Possible Diagnosis
Cardiac CHF, CAD, Arrythmias, Pericarditis, Myocarditis
COPD, Asthma, Pneumonia, Pneumothorax, PE,
Pulmonary
Bronchiolitis
Psychogenic Panic Attack, Anxiety, Hyperventilation
Upper Airway
Epiglottitis, Foreign Body, EBV, Croup
Obstruction
Endocrine Metabolic Acidosis, Medication
Central Neuromuscular, Pain, Aspirin
Chronic Causes:
Table 2.2
System Possible Diagnosis
COPD, Asthma, Malignancy, Iatrogenic, Pleural
Pulmonary
Disease
CHF, CAD, Arrythmias, Pericarditis, Myocarditis,
Cardiac
Valvular
Gastrointestinal GERD, Malignancy
Neuromuscular Acidosis, ALS, Poliomyelitis
Other Anemia, Sedentary Lifestyle, Psychogenic
Page | 85
2.3. Investigations & Monitoring:

Investigations should be focused on patient’s history and physical exam
 Labs: (CBC, Glucose, Electrolytes, Creatinine, BUN, ABG, BNP,
D-Dimer, TSH)
 Chest X-ray
 ECG
 Pulmonary Function Test
 Chest HRCT
 Echocardiogram
2.4. Management Plan:
Management of Chronic Dyspnea:
Management should be targeted at the underlying cause
 Oxygen
 Inhalers (refer to Asthma/COPD chapter)
 Diuretics (HF)
 Opioids (Palliative care)
 Pulmonary Rehab  for COPD
 CBT  for Anxiety
 Dietitian counseling  for weight loss
 Smoking Cessation
Indications for Referral:
Referral depends on the overall assessment of the patient condition.
 E.g., COPD patients  Pulmonology / CHF patients  Cardiology
Page | 86
Chapter 3: CNS INFECTIONS

3.1. Encephalitis:
3.1.1 Symptoms & physical examination signs:
 Constitutional symptoms: flu-like
o Nausea and vomiting are common.
o typical findings (Altered mental status- Personality changes -
Focal findings (e.g., hemiparesis, focal seizures) -Ataxia-Cranial
nerve defects- Meningismus.
o Note: Presentation in infants and young children (Bulging
Fontanels-Irritability-Stiffness-Poor feeding)
 Neurologic examination
o mental status, ranging from lethargy to coma, some may
demonstrate irritability, confusion, disordered thinking, or delirium
o Cranial nerve deficits like oculomotor or facial nerve palsy.
o Brisk tendon reflexes, and elicited response of plantar extensor
o Eyes: Papilledema, retinitis presents and other manifestations:
3.1.2 Investigations & monitoring:
 Lumbar puncture the most important investigation, perform after head
imaging: Cerebrospinal fluid analysis (CSF) is essential, parameters
to be evaluated include the following:
o Pressure
o Cell counts and differential.
o Protein
o Gram stain and culture glucose
o Polymerase chain reaction for HSV-1 and HSV-2, varicella-zoster
virus, and enteroviruses; 90% of identifiable viral causes’’’ are
HSV, varicella-zoster virus, and enteroviruses
 Delay lumbar puncture if one of the following appear in the patient:
o Focal neurologic signs, papilledema, or significantly diminished
mental status requiring brain imaging (Glasgow coma score 10 or
less)
o Raised intracranial pressure results of the neuroimaging
o Patient experienced seizure or status epilepticus
o Coagulopathy or severe thrombocytopenia
 Brain radiography is recommended for all patients to
o MRI is sensitive and specific; it is superior to contrast- CT
o If MRI is not available or contraindicated then obtain CT
o Note: normal CT does not rule-out encephalitis
Page | 87
 Culture: Viral, bacterial, or fungal cultures.

 Heterophile antibody and cold agglutinin testing for EBV
 Serologic tests for Toxoplasma
 Work-up for non-infectious causes includes testing for autoantibodies
(NMDAR antibodies, ANA, double-stranded DNA, ANCA,
thyroperoxidase antibodies.
3.1.3 Management plan:
Supportive
 Management in the prehospital setting includes:
o Evaluation and treatment for shock or hypotension
o Airway protection in patients with altered mental status.
o Seizure precautions (use lorazepam as first line management)
o Oxygen and IV access should be obtained in all patients before
hospital referral.
 After supportive care, important initial measures in the ED include:
o Collection of laboratory samples and blood cultures before the
start of IV therapy
o Administration of the first dose of acyclovir, with or without
antibiotics or steroids, as quickly as possible. (Dose of acyclovir
is 10–15 mg/kg IV q8hr). If confirmed HSV or VZV, continue
acyclovir for 14 to 21 days and repeat lumbar puncture to
document a negative PCR before discontinuing therapy.
o Acute bacterial meningitis- should begin treatment within 30
minutes of arrival.
 Note: M. pneumoniae infections can be treated with doxycycline,
fluoroquinolones, or macrolides
 Note: If the patient has elevated intracranial pressure treat with
corticosteroids and mannitol
o Hypertonic saline is an alternative to mannitol if patient has
sodium levels within reference range.
o elevate head of bed to 30° to 45°, avoid compressing jugular
veins, hyperventilate to a PaCO₂ of around 30 mm Hg)
o Furosemide (Lasix), administer 20–40 mg, q 6–8 hours, until the
desired diuresis occurs. When treating infants, titrate with 1
mg/kg/dose.
 immune encephalitis, treat with immunotherapy as first line
(corticosteroids, immunoglobulin, or plasma exchange, alone or in
combination) Dexamethasone Dose for cortisone is 0.75–9 mg/day
IV/IM/PO divided q6–12hours.
Page | 88
3.2. Guillain -Barré Syndrome (GBS):

3.2.1 Definition:
 Progressive, symmetric muscle weakness and absent or depressed
deep tendon reflexes. Usually begins in the legs and advances
proximally.
 Can follow (GI illness, respiratory illness, immunization)
Table 3.1
Features casting Features that
Required Features supportive of
doubt on the rule out the
features diagnosis
diagnosis diagnosis
Progressiv Progression of symptoms Asymmetrical Hexacarbon
e over days to 4 weeks weakness abuse
weakness Relative symmetry Persistent bladder Abnormal
in both Mild sensory signs or and bowel porphyrin
arms and symptoms dysfunction metabolism
legs Cranial nerve Bladder or bowel Recent diphtheria
Areflexia involvement (bilateral dysfunction at onset infection
(or >50 mononuclear
facial weakness) Lead intoxication
hyporeflexi leukocytes/mm³ or
Recovery beginning 2 to Other similar
a) presence of
4 weeks after polymorphonuclear conditions:
progression ceases. leukocytes in CSF poliomyelitis,
Autonomic dysfunction Distinct sensory botulism,
Absence of fever at onset level hysterical
paralysis, toxic
neuropathy
 Once GBS is suspected, an emergency referral is necessary for LP
and neurophysiology testing.
 CSF usually shows high protein with a normal cell count
 Neurophysiology testing shows slowing of motor and sensory
conduction
 GBS is a medical emergency, all suspected cases should be
immediately admitted to the hospital.
 Treatment is usually supportive. Definite treatment for GBS includes
high dose steroids, plasmapheresis, and high dose intravenous
immunoglobulin. Most patients with GBS recover spontaneously.
 Disease is fatal in 3% of cases.
Page | 89
3.3. Meningitis:
Table 3.2
Bacterial Fungal Viral Tuberculous
The classic triad of - Often has a more - The presentation - Vague,
bacterial meningitis subacute course can range from nonspecific
consists of the than bacterial acute to protracted presentation of
following: Fever, meningitis with nonspecific fever, weight loss,
Headache, Neck -With almost the findings night sweats, and
stiffness. same history of - May have a malaise, with or
bacterial meningitis preceding systemic without headache
-Other classical
but a milder form symptom of (e.g.,
symptoms related
so that diagnosis of myalgia, fatigue, or
to bacterial meningitis is not anorexia)
meningitis include considered - Patients with
photophobia, meningitis caused
nuchal rigidity, by the mumps virus
lethargy, malaise, usually present
altered sensorium, with the triad of
seizures, vomiting, fever, vomiting. and
and chills. headache
Positive tests provide a strong suspicion for meningeal irritation:

 Kernig’s sign
 Brudzinski’s sign
 Jolt accentuation: Exacerbation of headache by moving head in
horizontal direction two to three times indicates positive test.
Findings on examination in Infants
 Neck stiffness
 Hypotonia
 Altered mental status
 Bulging fontanelle
 Convulsions
 Petechial rash (Skin rash could indicate Neisseria
meningitidis infection)
Note: III, IV, VI cranial nerve palsies are the most common
Note: sings of increase ICP: Decreased HR, Cranial nerve palsies
Page | 90

Cultures and bacterial antigen testing: These cultures include the
following:
 Blood: 50% positive in meningitis caused by H influenzae, S
pneumoniae, or N meningitidis
 PCR assay for enteroviruses has been demonstrated to be
substantially more sensitive than culture and is 94–100% specific.
Serum procalcitonin testing:
 Data suggest that serum procalcitonin (PCT) levels can be used as a
guide to distinguish between bacterial and aseptic meningitis in
children.
 Elevated serum PCT levels predict bacterial meningitis.
Neuroimaging:
 (CT) of the head and (MRI) of the brain generally do not offer help in
the diagnosis of meningitis.
 According to the Infectious Diseases Society of America guidelines,
the following are indications for urgent head CT before lumbar
puncture in adult patients:
o Immunocompromised state
o History of CNS disease (e.g., mass lesion, stroke)
o Seizure within one week of presentation
o Papilledema
o Abnormal level of consciousness
o Focal neurologic deficit
Page | 91
Lumbar puncture findings in different forms of meningitis:

Table 3.3
Aseptic
Normal Finding Bacterial Viral Fungal
Meningitis
Pressure Increased Normal or Normal or mildly 90-200
(mm H2 O) 200–300 mildly increased in
50-150 increased90 tuberculous
–200 meningitis; may be
increased in fungal
Cell count No cell count Cell count Hundreds of 10-300

(mononuclear result can usually < mononuclear cells lymphocytes
cells/µL) exclude 500, nearly
Preterm: 0– bacterial 100%
25Term: 0–22>6 meningitis. mononuclear
months: 0–5 Increase
PMN
Microscopy No Gram stain No organism AFB stain is 40% negative
organisms 80% sensitive for
sensitive tuberculosis
Glucose Decreased Normal lowest levels of CSF Normal
Euglycemia: glucose are seen in
>50% serum tuberculous
Hyperglycemia: meningitis, primary
>30% serum am’ebic
‘Wait 4 hr after meningoencephalitis,
glucose load and
neurocysticercosis
Protein (mg/dL) Usually Mildly Increased; >1000 Normal but

Preterm: 65– >150, maybe increased with relatively maybe
150Term: 20– >1000 benign clinical slightly
170>6 months: presentation elevated
15–45 suggestive of fungal
disease.
Page | 92

 Droplet isolation precautions.
 Stabilization of patients.
 Intravenous fluids may be beneficial within the first 48 hours.
 Initiating empiric antibiotics as soon as possible after blood cultures
are drawn and the LP is performed.
 dexamethasone should be given before or at the time of initial
antibiotics in all patients older than six weeks with suspected bacterial
meningitis.can be discontinued after four days or earlier if the
pathogen is not H. influenzae or S. pneumoniae or if CSF findings are
more consistent with aseptic meningitis
 Non-HSV management is focused on supportive care (bed rest and
fluids).
 Look to table 3.6 at chapter 3 CNS infections.
Antimicrobials:
 Acyclovir should be added if there is a concern for HSV meningitis or
encephalitis.
 A door-to-antibiotic time lapse of more than six hours has an
increased rate of mortality.
Page | 93
Table 3.4
Empiric
Age group Pathogen Duration (days)
therapy
Ampicillin plus
group B
cefotaxime
streptococcus, Listeria group B
Infant < 1 (Claforan)
monocytogenes, Escherichia streptococcus
months Alternative:
coli, other gram-negative (14 to 21)
ampicillin plus
bacilli
gentamicin
Streptococcus Vancomycin
plus ceftriaxone S.pneumoniae
pneumoniae, Neisseria
Children 1 to Alternative: (10 to 14)
meningitidis, S.
23 months meropenem H. influenzae
agalactiae, Haemophilus (Merrem IV) plus (7 to 10)
influenzae, E. coli vancomycin
Vancomycin plus
Children and ceftriaxone
N. meningitidis, N.meningitidis
adults 2 to 50 Alternative:
S. pneumoniae meropenem plus (5 to 7)
years
vancomycin
Vancomycin
Adults >
plus ceftriaxone
50years with S. pneumoniae,
plus ampicillin
altered N. meningitides, L.monocytogenes
Alternative:
cellular L. monocytogenes, aerobic (21)
meropenem
immunity or gram-negative bacilli
plus
alcoholism
vancomycin
Vancomycin
Patients with
plus ceftriaxone
basilar skull S. pneumoniae,
Alternative:
fracture or H. influenzae, group A beta-
meropenem
cochlear hemolytic streptococci
plus
implant
vancomycin
Staphylococcus aureus, Vancomycin
Patients with
coagulase-negative plus cefepime
penetrating
staphylococci, aerobic gram- Alternative:
trauma or
negative bacilli meropenem
post
(including Pseudomonas plus
neurosurgery
aeruginosa) vancomycin
Patients with Coagulase-negative
Vancomycin
cerebrospinal staphylococci, S. aureus,
plus cefepime
fluid shunt aerobic gram-negative bacilli
Page | 94
Chapter 4: BRUSING AND BLEEDING

4.1. Bleeding Disorders:
4.1.1 Definition:
condition that affects the way the blood normally clots. The cause of
abnormal bleeding can be related to the following (Platelet Disorder,
Clotting Factor Defect and Iatrogenic).
 Platelet defects: Mucocutaneous bleeding, Petechiae, Ecchymoses
and Excessive bleeding after minor cuts
 Clotting Factor Defect: Deep tissue bleeding, Hemarthroses/muscle
hematomas and Ecchymoses
Table 4.1 – Lab values in bleeding disorders
Differential
Platelet count PT aPTT
diagnosis
ITP, Wiskcott-
Low Normal normal Aldrich Syndrome,
or splenomegaly
Hemophilia, VWD,
Normal Normal prolonged
Heparin Tx, LA
Vit K deficiency, VII
deficiency, liver
Normal Prolonged Normal
disease, Warfarin
Tx
Vit K deficiency,
Normal Prolonged Prolonged DIC,
Afibrinogenemia
DIC, liver disease,
Low Prolonged prolonged heparin induced
thrombocytopenia
Vascular disorder,
HUS, XIII
Normal Normal Normal
deficiency, VWD,
Platelet dysfunction
Page | 95

ITP
80% chance of spontaneous recovery in children within 6 months vs 8 %
chance of remission in adults.
Treatment: is indicated when platelet count falls below 30,000 / μL or if
there is bleeding
 Prednisone 1 mg/kg daily, response within 4 – 7 days, usually by 2 –
3 weeks then taper, 50 – 75% response rate.
 Intravenous immunoglobulin (IVIg), 70 – 80% response rate
 Splenectomy if medical treatment fails.
Von Willebrand Disease (VWD)
 DDAVP (desmopressin ↑ VWF release from endothelial cells)
 Replacement therapy with VWF (more severe, factor VIII
concentrates)
Hemophilia A and B
 DDAVP (Desmopressin) releases factor VIII from tissue stores
 Specific factor replacement based on severity of bleeding.
iatrogenic bleeding complications
Heparin
 Stop heparin and give Protamine for urgent reversal, neutralizes
heparin – 1 mg per 100 units of heparin given over 4 hours: max dose
of 50 mg (slow IV push)
LMWH
 Protamine (partially effective in repeated smaller doses) 1 mg per mg
of Lovenox given if <8 – 12 hours; 0.5 mg per mg of Lovenox if 8 – 12
hours; none if > 12 hours.
Direct oral anticoagulants (DOACs)
Minor bleeding can usually be managed conservatively. Imminent risk of
death/major bleeding treatment options:
 Idarucizumab (Praxibind-monoclonal antibody) for Dabigatran
 Andexanet for Apixapan, Rivaroxban
 Prothrombin Complex Concentrate (PCC) for direct factor Xa
inhibitors
 Oral activated charcoal if last dose within prior two hours
 Hemodialysis
● RBC and platelets transfusions as needed.
Page | 96
Table 4.2 – Management of abnormal INR for warfarin therapy

INR Action
< 5.0 – Lower warfarin dose OR
– Omit a dose and resume at a lower dose (when INR is in therapeutic
range)
– Check INR / 24h
5.0 – 9.0 – Omit next 1 or 2 doses and resume at a lower dose (when INR is in
therapeutic range) OR
– Omit a dose and administer 1 – 2.5 mg Vit K1 po
– Check INR / 24h
> 9.0 – Hold warfarin AND
– Admin 2.5 – 5.0 mg Vit K1 po
– Resume warfarin at a lower dose when INR is in therapeutic range
– Frequent INR monitoring
– Administer more Vit K1 if needed
Serious – Hold warfarin AND
Bleeding – Admin 10 mg Vit K1 iv (slow infusion)
– Supplement with prothrombin complex concentrate (PCC), FFP,
recombinant human Vlla if needed
– Monitor and repeat if needed
Page | 97
4.2. Hematological Malignancies and

Myeloproliferative Disorders:
4.2.1 Leukemia:
Definition: is cancer of the blood forming tissue, including bone marrow
and lymphatic system. Leukemia is divided into 4 main types:
Table 4.3
Acute
mostly in children
Lymphoblastic Most common cancer in
(Peak incidence at Good prognosis
Leukemia kids
age 2–5 years)
(ALL)
Commonest leukemia
Chronic
Mature malignant B-cell
lymphocytic Leukemia of the
lymphocytes in peripheral Good survival
Leukemia elderly
blood, bone marrow, and
(CLL
lymph nodes
Acute Myeloid
It affects young increased number of
Leukemia Poor prognosis
adults myeloblasts (>20%)
(AML)
Philadelphia (Ph)
Chronic chromosome
Myeloid three phases, the chronic
It affects adults Good prognosis
Leukemia phase, the accelerated
(CML) phase, and the acute or
blast phase
Symptoms & physical examination signs:
pain, body aches, bruises or bleeding, fever, sweating, and weight loss.
pallor, gum hypertrophy, petechiae, lymphadenopathy, and
hepatosplenomegaly
Investigations & monitoring:
CBC (elevated WBCs, significant leukocytosis, lymphocytosis in CLL,
and neutrophilia and PMN in CML)
Peripheral blood smear (best initial): blast cells, increased number of
WBCs and immature structure
Bone marrow aspiration and biopsy (most accurate)
Management plan: chemotherapy, Hematopoietic stem cell transplant
(HSCT)
Page | 98
4.2.2 Lymphoma:
Definition:
Hodgkin’s lymphoma (HL):
presence of a type of cell called the Reed-Sternberg cell and is clinically
characterized by the spread of disease to lymph nodes, lymphoid
tissues, and extralymphatic organs such as the spleen, liver, bone
marrow, and lung. third most common cancer in the 15–29 year. Risk
factor: EBV
Non-Hodgkin’s lymphoma (NHL):
Malignant lymphocytes accumulate in L.N, peripheral blood smear and
other organs. second fastest growing cancer in terms of mortality.
Approximately 95% of cases occur in adults 40 to 70 years of age, and
men are more often affected than women.
 painless lymph node enlargement
 fever, fatigue, night sweating, and weight loss.
 with pallor, bruising, lymphadenopathy, hepatosplenomegaly.
Initial testing: open biopsy of enlarged lymph nodes.
Staging should include: labs (CBC, RFT, LDH, LFT, ESR Hepatitis B test.
Bone marrow biopsy and imaging (X-ray, MRI, and CT) of other organs.
Management plan:
Chemotherapy is the main treatment modality for both, HL the main type
of treatment is combination chemotherapy and radiotherapy.
4.2.3 Multiple myeloma (MM):
Definition:
malignancy of plasma cells in bone marrow. Median age at diagnosis 70
years old.
bone pain: especially if associated with back pain - spinal cord or nerve
root compression.
Bone marrow failure: anemia, recurrent bacterial infections, and
bleeding.
Page | 99

Table 4.4
Bone
CBC: Image:
marrow
increase Calcium: ESR: CT/MRI/XR
biopsy:
plasma increase increase LYIC BONE
infiltration by
cell. LESIONS
plasma cell
Management plan:
initiated immediately in patients with evidence of end-organ damage.
High dose chemotherapy (HDC) plus autologous stem cell transplant
(ASCT) is the preferred therapy.’
4.2.4 Myeloproliferative disorders:
Definition:
 Polycythemia vera (PV)/ erythrocytosis: The most common types.
 Essential thrombocytosis (ET)/ thrombocytosis: The most indolent
myeloproliferative disorder.
 Primary myelofibrosis: most aggressive myeloproliferative disorder. It
characteristically presents with bone marrow fibrosis, splenomegaly.
Polycythemia vera
 Major criteria (all 3 needed or the first two and presence of minor
criterion)
o Increased hemoglobin level: >16.5 g/dL in men or >16.0 g/dL in
women
o Bone marrow biopsy showing hypercellularity for age.
o JAK2 mutation
 Minor criterion:
o Serum erythropoietin level below the reference range for normal
Essential thrombocytosis
 Patient must meet all of the following criteria:
o Platelet count ≥450,000
o Bone marrow biopsy showing proliferation mainly of the
megakaryocyte lineage.
o Demonstration of a JAK2, CALR, or MPL mutation,
demonstration of another clonal marker, or no identifiable cause
of thrombocytosis (e.g., infection, inflammation, iron deficiency
anemia)
Page | 100

RBCs and hemoglobin may be elevated in polycythemia vera.
Platelets are significantly elevated in essential thrombocytosis.
There is hypercellular marrow in both conditions.
pancytopenia in myelofibrosis and the bone marrow biopsy shows
significant fibrosis.
Management plan:
Polycythemia vera
 Regular phlebotomy to maintain a hematocrit of 42 – 45%,
 hydroxyurea for patients at high risk for thrombosis (e.g., age > 60 or
prior thrombosis).
 Aspirin 100 mg daily reduces risk of vascular disease.
Essential thrombocytosis
 Low-risk (< 60 yrs., asymptomatic, no thrombosis, and platelets <
1,500,000 / μL): Observation or low-dose aspirin
 Non-low risk (hx of venous or arterial thrombosis, age ≥ 60)
o Hydroxyurea to reduce platelets < 400,000 / μL,
o Aspirin: thrombosis history and no bleeding risk
o Plateletpheresis for those with acute ischemic events and
platelets > 1,500,000 / μL
o Anagrelide: blocks megakaryocyte maturation, usually not
1st choice
Primary Myelofibrosis
 Supportive: transfusion, splenectomy
 Curative: bone marrow transplant if younger than 55 years old.
4.2.5 Myelodysplastic syndrome (MDS):
Definition:
bone marrow failure, which is the inability to produce normal numbers of
healthy blood cells and a risk of progression to acute myeloid leukemia.
 Consider MDS in elderly patients with low grade anemia and mild
macrocytosis.
 Diagnosis of MDS requires both of the following cytopenia(s):
o Hemoglobin <10 g/dL
o Absolute neutrophil count <1800
o Platelets <100,000
 Significant dysplasia (≥10% of erythroid precursors, granulocytes, or
megakaryocytes)
 Blast forms < 20% of nucleated cells (if > 20% then AML is present)
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 CBC with bone marrow aspirate and biopsy with cytogenetic testing is
the most essential diagnostic.
Management plan:
Immediate treatment is indicated for patients with symptomatic cytopenia
(anemia, thrombocytopenia, neutropenia with recurrent infections).
Selection of treatment for symptomatic MDS assisted by assessing
patient’s age, performance status, and MDS risk category include:
 Supportive care (e.g., transfusions)
 Low intensity therapies (e.g., hematopoietic growth factors)
 High intensity therapies (e.g., chemotherapy and HCT)
Chapter 5: ARTHARITIS
5.1. Osteoarthritis:
5.1.1 Definition:
Osteoarthritis (OA) is the most common type of arthritis, with various
presentations, which range from an asymptomatic incidental finding on
clinical or radiologic examination to a progressive disabling disorder. OA
affects hands, hips, knees, feet, and spine.
 Pain: worse with joint use and later in the day, usually relieved by
rest. The pain can progress in three stages-
o Stage 1: Predictable, sharp pain usually brought on by a
mechanical insult that eventually limits high-impact activities with
a relatively modest effect on function.
o Stage 2: Pain becomes more constant and starts to affect daily
activities. There may be unpredictable episodes of stiffness.
o Stage 3: Constant dull/aching pain punctuated by episodes of
often unpredictable, intense, exhausting pain that results in
severe limitations in function.
 Joint swelling and tenderness with or without crepitus
 Bony enlargement in prolonged or severe OA
 Limitation of motion for both active and passive movement may lead
to the formation of marginal osteophytes and capsular thickening.
 Joint deformity is a sign of advanced joint damage.
 Giving way or buckling is a common symptom in knee OA, which
causes instability.
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 No routine lab tests are indicated.
 Radiography is not required for diagnosis in the presence of risk
factors and typical presentation.
 Typical radiographic findings include joint space narrowing,
osteophytes, subchondral sclerosis, and cysts.
5.1.4 Management:
Non-pharmacological interventions
 Weight loss of 10% is associated with significant symptoms reduction.
 Exercise, e.g., swimming, bicycling, walking, and Tai Chi, a
combination of low impact aerobic and muscle strengthening
exercises are beneficial.
 Physical therapy
 Rest might be helpful for a short duration (12–24 hours) when
associated with pain.
 To raise the threshold of pain, heat and cold can be used.
 Assistive devices when required.
 Ineffective interventions: Vitamin D supplement, usage of
antioxidants, special shoes, ionized wrist bracelets, lateral wedge
insoles for medial knee OA, knee bracing, physical therapy for hip
OA.
Pharmacological therapy:
Should be used if non-pharmacological intervention is inadequate.
 Topical diclofenac gel or capsaicin
 Acetaminophen at a dose of 3 grams per day
 NSAIDs
o the most likely NSAID to be effective is diclofenac 150 mg per
day.
o naproxen is the next most effective.
o topical diclofenac and ketoprofen are of moderate efficacy.
 Topical capsaicin is associated with transient burning sensation but is
somewhat effective.
 Duloxetine (SNRI) is approved for the treatment of painful conditions
such as OA, but mild to moderate nausea is the most reported side
effect.
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 Opioids
o generally, should be avoided due to risks of nausea, dizziness,
and drowsiness in the elderly population.
o Tramadol and other opioids long term use is discouraged.
 Corticosteroid injections
o provide short-term relief of pain and function improvement but
don’t improve the overall quality of life.
o A large study suggested the presence of more cartilage damage
in patients receiving corticosteroid injections.
 Hyaluronic acid injections are not effective.
5.2. Rheumatoid Arthritis:
5.2.1 Definition:
Rheumatoid arthritis (RA) is the most common inflammatory arthritis. It is
a chronic inflammatory peripheral polyarthritis of multifactorial etiology
which affects up to 1 % of the population.
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 Pain and stiffness involved multiple joints, commonly the wrists,
proximal interphalangeal joints, and metacarpophalangeal joints.
 Morning stiffness of more than 1 hour.
 Arthralgias may present before the onset of joint swelling.
 During active disease, systemic manifestations may present as
fatigue, weight loss, and low-grade fever.
 A longer duration of symptoms is more suggestive of RA rather than
other causes such as acute viral polyarthritis.
 Palindromic rheumatism: Relapsing remitting symptoms in some
patients. May benefit from hydroxychloroquine monotherapy.
 Extraarticular manifestations may affect up to 40% of patients with
RA.
Synovitis in the form of boggy swelling or palpable fine synovial

thickening.
 Limited joint motion
 Extra-articular disease manifestations such as rheumatoid nodules
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 Rheumatoid factor: sensitivity 69% and specificity 85%.
 Anti-citrullinated protein antibody (anti-CCP): sensitivity 67% and
specificity 95%
 Antinuclear antibody: may be positive and have more prognostic
value in juvenile RA.
 Elevated C-reactive protein and erythrocyte sedimentation rate may
indicate active RA, can be helpful follow-up and monitoring response
to medication.
 CBC
 Renal and Liver function
 Uric acid level
 X-ray of hands and feet should be performed as a baseline and to
monitor the progression of the disease and to detect the erosive
changes of RA.
 MRI, CT, and US are more sensitive to detect erosions in patients
than plan X-rays, but it is not a part of routine evaluation.
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5.2.4 Management:
Patients with inflammatory joint pain should be referred to a
rheumatology clinic, especially if symptoms persist for more than six
weeks.
Goals of therapy
 Decrease joint pain and swelling.
 Prevent joint deformity and radiographic damage.
 Improve the quality of life.
 Control the extraarticular manifestations.
 Prevent premature atherosclerosis.
Factors affecting the choice of therapeutic options.
 Patient preference
 Women of childbearing age
Non-pharmacological therapy
 Patient education
 Exercise, physical, and occupational therapy, improves quality of life
and muscle strength.
Pharmacological therapy
 Disease-Modifying Anti-Rheumatic Drugs (DMARDs)
o The mainstay of RA therapy
o Include biologic and nonbiologic agents.
o Methotrexate is the first line nonbiologic treatment in active RA
unless there is contraindication or intolerance, TNF inhibitors are
the first-line biologic therapy.
o Hydroxychloroquine can be used alone with low disease activity.
o Combination therapy is more effective than monotherapy, but the
combination of two biological agents is not favorable due to the
high rate of adverse effects.
o No regimen of monotherapy is clearly superior to any other.
 NSAIDs and corticosteroids
o For short-term management only to control pain and
inflammation
o Does not affect the disease process.
o For those who do not respond to DMARDs, prednisone 5–10 mg
daily can be added, a higher dose may be helpful in the presence
of systemic manifestations.
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5.3. Connective Tissue Diseases:

5.3.1 Systemic Lupus Erythematosus (SLE):
Definition:
SLE is an autoimmune, multisystem disease, which has a recurrent
course with remission and flares. It is twice as common in black and
Asian populations and 10 times more common in females.
SLE is difficult to diagnose by primary care because most of the
symptoms are nonspecific, and in the early stage of the disease,
laboratory tests may give negative results. SLE should be suspected in a
patient with symptoms in at least two of the following organ systems:
reticuloendothelial, constitutional, gastrointestinal, musculoskeletal, skin,
hematological, renal, neuropsychiatric, cardiac, or pulmonary. Fatigue
and arthralgia are present in almost all cases of SLE.
 Antinuclear antibodies: Positive result is highly sensitive for SLE, but
it has low specificity.
 Anti-double-stranded DNA antibodies: Has a sensitivity of 70% and
specificity of 95%
 Anti-Smith antibodies have the greatest specificity and are considered
one of the diagnostic criteria for SLE.
 CBC
 ESR % C-reactive protein
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Management plan:
 Generally, all patients need education, counseling, and support.
 Hydroxychloroquine is the mainstay of treatment as it can control the
constitutional symptoms and decrease the risk of exacerbation.
 Most of the SLE manifestations can be managed by low-dose
glucocorticoids.
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 Family physicians can adequately monitor disease activity and

therapy by history, examination, and frequent measurement of anti-
dsDNA antibodies, complements, creatinine, complete blood count,
and urinalysis every three to six months.
 For patients using hydroxychloroquine, an annual eye checkup is
required.
 For patients using glucocorticoids, regular screening for dyslipidemia,
diabetes, and osteoporosis should be done.
5.3.2 Drug-induced lupus:
Some drugs can trigger an autoimmune response and lead to the
production of autoantibodies which may lead to certain clinical signs and
symptoms similar to those in idiopathic lupus erythematosus. Examples
of these drugs in order of higher to lower probability include
procainamide, hydralazine, penicillamine, minocycline, diltiazem,
isoniazid, quinidine, methyldopa, and practolol.
The most common clinical features include fever, arthralgia, arthritis,
myalgias, rash, and serositis. Severe or life-threatening manifestations
are uncommon.
 Antinuclear antibodies
 Antihistone antibodies: sensitivity is 95%, and specificity is more than
90%
Management plan:
 Discontinuation of offending drugs
 Medical therapy may be used temporarily until the symptoms are
resolved using the same approaches as those with idiopathic SLE.
5.3.3 Sjogren Syndrome:
Definition:
Sjogren syndrome (SS) is a chronic inflammatory disorder caused by
extensive focal lymphocytic infiltration, with glandular and ductal atrophy.
The hallmark signs in SS are persistent dry mouth (xerostomia) and dry
eye (sicca). Physical examination may show punctate conjunctiva,
corneal damage, chronic or episodic salivary gland enlargement, dental
caries, and oral candidiasis. SS may be primary or secondary to another
connective tissue disease.
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Diagnostic criteria
SS is diagnosed if the following two criteria are met, and other causes of
dry eye and mouth are excluded:
 Objective findings of ocular dryness (Schirmer test or abnormal ocular
surface staining), oral dryness (salivary hypofunction), or of glandular
parenchymal damage on MRI or US.
 Serologic or histopathologic evidence of autoimmunity: positive anti-
Ro/SSA antibodies with or without anti-La/SSB antibodies, patients
may have anticentromere antibodies, antinuclear antibodies, and
rheumatoid factor.
Management plan:
Management of primary SS requires a multidisciplinary approach.
Ophthalmology input is important for both diagnosis and ongoing care of
the eye related symptoms.
 Mild eye symptoms are controlled with avoidance of anticholinergic
medications, control of environmental factors, and artificial tears. In
severe disease patients may require punctal occlusion procedures or
topical/systemic immunosuppressive therapies.
 Xerostomia is managed by simple measures such as maintenance of
good hydration, avoidance of dehydrating agents, frequently sipping
water, and humidity control.
5.3.4 Mixed connective tissue disease:
Definition:
It is an overlap syndrome of systemic lupus erythematosus (SLE),
systemic sclerosis (scleroderma [SSc]), and polymyositis (PM).
Patients may have nonspecific symptoms such as fatigue, myalgias,
arthralgias, and low-grade fever. Nearly all patients have Raynaud’s
phenomenon, pulmonary hypertension, and erosive arthritis.
Antinuclear antibody is the initial screening test. Anti-U1
ribonucleoprotein (RNP) autoantibody has a sensitivity of 71–100% and
specificity of 84–100% and is the diagnostic test.
Management plan:
SLE-like symptoms are usually steroid responsive while scleroderma-like
symptoms are usually incurable. Some patients may require intermittent
steroids. Antimalarial and biologicals may be used.
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5.3.5 Scleroderma/Systemic Sclerosis SSc:

Definition: A rare, chronic multisystem disease characterized by tight
skin, interstitial lung disease, pulmonary hypertension, and diffuse organ
fibrosis.
 Skin thickening and hardening.
 Raynaud’s phenomenon
 Arthritis, tendinitis, joint contractures
 Dysphagia, choking, heartburn, hoarseness, bloating, alternating
constipation, diarrhea, fecal incontinence
 Interstitial lung disease, pulmonary vascular disease
 Albuminuria, mild elevation in the plasma concentration,
hypertension.
 Myopathy, central, peripheral, autonomic neuropathies
 Erectile dysfunction in male patients
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 Complete blood count with differential, which may show anemia
secondary to malabsorption or GI blood loss.
 Serum creatinine level
 Creatinine kinase may be elevated in patients with muscle
involvement.
 Urinalysis
 Serological tests:
o antinuclear antibody (ANA)
o Anti-topoisomerase I (anti-Scl-70) antibody
o Anti-centromere antibody (ACA)
o Anti-RNA polymerase III antibody
Management plan:
SSc patients are treated with organ based symptomatic therapy based
on organ involvement and extent of damage. However, skin
manifestations respond to immunosuppressive therapy.
5.3.6 Inflammatory myopathies: Dermatomyositis and
Polymyositis:
Definition:
Dermatomyositis (DM) and Polymyositis (PM) are multisystem
inflammatory disorders. They are characterized by proximal skeletal
muscle weakness, muscle inflammation, elevated muscle enzyme,
myopathic changes in electromyography, and muscle pathology.
 Muscle weakness
 Skin findings
o Gottron papules and heliotrope eruption are pathognomonic
features of DM.
o facial erythema
o photo distributed poikiloderma (skin with hyperpigmentation and
hypo-pigmentation, telangiectasias, and epidermal atrophy)
o nail fold abnormalities
 Interstitial lung disease
 Dysphagia, nasal regurgitation, and/or aspiration
 Cardiac involvement
 Around one-third of the patients have antisynthetase syndrome,
which includes non-erosive arthritis, fever, Raynaud’s phenomenon,
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interstitial lung disease, and fissuring on the distal fingertips

(mechanic’s hands)
 Increased rate of malignancies presents in patients with DM.
 Elevated muscle enzymes such as creatine kinase (CK), lactate
dehydrogenase (LDH), aldolase, AST, and ALT
 Autoantibodies including antinuclear antibodies, anti-Ro, anti-La, anti-
Sm, anti-RNP, should not be measured routinely in patients with
myalgias due to their low prevalence in affected patients.
 Erythrocyte sedimentation rate (ESR) is often normal or only mildly
elevated, even with active disease.
Management plan:
 Anti-inflammatories, prednisolone
 Initial therapy with steroids for prolonged periods, requires a
multidisciplinary approach once steroid-sparing therapies are started.
 Physical therapy to preserve function.
Chapter 6: ASTHMA
6.1. Definition:
Asthma is a chronic inflammatory disorder of the airways in which many
cells and cellular elements play a role. Chronic inflammation is
associated with airway hyper-responsiveness that leads to recurrent
episodes of wheezing, breathlessness, chest tightness, and coughing,
particularly at night or in the early morning.
6.2. Symptoms & physical examination signs:
 Difficulty breathing
 Chest tightness
 Cough that worsens a night
 Wheezing
Assess for symptom patterns suggestive of asthma.
 Recurrent/episodic
 Symptoms often occur/worse at night, or in the early morning.
 Symptoms occur/worsen with exposure to allergens (animal dander,
pollens, dust mites), irritants, viral infections, exercise, smoke or
strong fumes.
 Respond to appropriate asthma therapy.
 Examine the upper respiratory tract and skin for signs of other allergic
diseases.
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 Examine for wheezing on auscultation.

6.3. Investigations & monitoring:
6.3.1 Spirometry:
● Shows obstructive pattern and evidence of reversibility: ↓ FEV1, ↓
FEV1/FVC ratio (normally > 0.75–0.80 in adults, > 0.90 in children).
● More reliable than peak expiratory flow rate (PEF).
● Reversibility: FEV1 of ≥ 12% and 200-ml increase after
administration of a bronchodilator (200-400 mcg salbutamol).
● Asthmatics can have normal spirometry.
6.3.2 Peak flow meter:
Measures the maximum rate of air which a patient can forcibly exhale
after a full inspiration. It is more useful in the monitoring of patients with
established asthma than in making the initial diagnosis.
Ideally, a baseline PEF value should be obtained when the patient is
feeling well. The normal range for PEF: 80-100% of their personal best.
Readings below this normal range indicate airway narrowing.
Predicted/best PEF.
For each patient, determine predicted peak flow rate from peak flow
chart of predicted values depends on their sex, age, and height.
Compare the actual PEF with the predicted PEF from the chart.
Readings of up to 100 L /minute above or below predicted values can be
considered normal.
 Blood gasses are helpful in acute attacks.
 Chest X-ray
6.4.1 Non-pharmacological management:
Treat modifiable risk factors and control environmental
factors
A significant reduction in exposure to nonspecific airway irritants in all
patients or to inhaled allergens in atopic patients may reduce symptoms
and medication needs. Comorbid conditions that impair asthma
management, such as smoking, rhinosinusitis, gastroesophageal reflux,
obesity, and obstructive sleep apnea, should be identified and treated.
Non-pharmacologic interventions include increasing physical activity and
breathing exercises.
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Guided asthma self-management education and skills

training
Self-management includes self-monitoring of symptoms or peak flow, a
written action plan, and regular review of asthma control, treatment, and
skills with a healthcare professional.
6.4.2 Pharmacological management:
Personalized asthma management
A continuous cycle that involves assessment, treatment, and review with
the goals of symptom control and minimizing future risk. These goals
should be met while providing therapeutic agents with the fewest
adverse effects and while satisfying the patient’s expectations of asthma
care.
Management should include stepping up therapy if asthma remains
uncontrolled despite adherence and good inhaler technique and stepping
down to find the minimum effective therapeutic dose.
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Chapter 7: LOWER RESPIRATORY

TRACT INFECTIONS
7.1. Acute Bronchitis:
7.1.1 Definition:
Acute bronchitis is one of the most common conditions evaluated in
primary care. It results from inflammation of the lower respiratory tract.
Symptoms:
 Cough is the hallmark symptom of acute bronchitis.
 Other such as headache, nasal congestion, and sore throat.
physical examination:
 High fever
 Hypoxia.
 Moderate to severe ill-appearance.
 Signs of lung consolidation, (e.g., decreased breath sounds, crackles,
egophony, and increased tactile fremitus)
Laboratory testing is usually not indicated unless you suspect a patient
has developed pneumonia.
Radiology: chest x-ray usually not needed unless, in specific conditions,
it may help rule out pneumonia.
Indications:
 Dyspnea
 Bloody or rust colored sputum.
 Pulse >100 beats per minute
 Respiratory rate >24 breaths per minute
 temperature >100 F (37.8°C)
 Focal consolidation, egophony, or fremitus on chest examination
 Altered mental status in the elderly.
Symptoms are self-limited, resolving in about one to three weeks.
Reassurance and symptom control are the cornerstones of care.
Antibiotics are not recommended for routine use in all major guidelines
on bronchitis.
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Supportive management of cough:

 Non-pharmacologic therapy: Throat lozenges, Hot tea, Honey
Smoking cessation or avoidance of secondhand smoke.
 Pharmacologic therapy:
o Dextromethorphan or guaifenesin
(Benefits of these medications for symptom improvement in patients with
acute bronchitis are uncertain).
 Beta2 agonists
(Limited supportive evidence to use in the treatment of acute bronchitis
unless the patient has a known case of lung disease or evidence of
wheeze or airway obstruction).
Supportive management for cold symptoms:
Analgesics such as paracetamol or nonsteroidal anti-inflammatory
drugs.
7.2. Pneumonia:
7.2.1 Definition:
Community-acquired pneumonia (CAP) is the second most common
cause of hospitalization and the most common cause of infection-related
death.
Most common pathogens in adults: Streptococcus pneumoniae
Most common pathogens in pediatric: RSV (age 4 month to 4
years), Mycoplasma pneumonia (Age 5–18 years).
Symptoms:
 Cough (with or without sputum production)
 Dyspnea
 Pleuritic chest pain
 Fever/chills
 Malaise/weakness
physical examination:
Vital signs: fever, tachycardia, hypoxia, tachypnea
Chest: crepitations, bronchial breath sounds, signs of consolidation,
dullness to percussion.
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 CBC, blood cultures, sputum cultures, and urinary antigen testing are
not beneficial in patients with non-severe CAP.
 Procalcitonin: not routinely recommended.
 Chest x-ray: to confirms the clinical diagnosis (Lobar consolidation,
effusion, bilateral interstitial infiltrates).
 No need to routinely repeat CXR if symptoms resolved in 7 days or
less.
 CT chest: is not routinely requested but can be considered if you
suspect other conditions.
 Management differs based on if the patient is ambulatory vs.
hospitalized.
 Pneumonia Severity Index is a prognostic model, recommended to
determine the need for hospitalization.
Demographics Co-morbidities Physical exam/ Laboratory/

vital signs imaging
• Age • Neoplasia +30 • Mental confusion • Arterial pH +30
• Liver disease +20 +20 • BUN +20
(1 point per year) • CHF +10
Male Yr. • Respiratory rate +20 • Sodium +20
• Cerebrovascular
Female Yr. .10 disease +10 • SBP +20 • Glucose +10
• Nursing home • Renal disease +10 • Temperature +15 • Hematocrit +10
residency +10 • Pleural effusion +10
• Tachycardia +15 • Oxygenation +10
Table 7.1
Risk class (Points) Mortality (%) Recommended site of care
I (<50) 0.1 Outpatient
II (51-70) 0.6 Outpatient
III (71-90) 2.8 Outpatient or brief inpatient
IV (91-130) 8.2 Inpatient
V (>130) 29.2 Inpatient
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outpatient:
without comorbidities or risk factors for antibiotic-resistant pathogens:
(Duration for 7–10 days).
 Amoxicillin 1 g three times daily
 Doxycycline 100 mg twice daily
 Azithromycin 500 mg then 250 mg daily
 Clarithromycin 500 mg twice daily
 Clarithromycin extended release 1,000 mg daily.
Patients with comorbidities:
 Combination therapy:
o Amoxicillin/clavulanate or a cephalosporin (cefpodoxime 200 mg
twice daily or cefuroxime 500 mg twice daily) AND
o Macrolide (azithromycin, clarithromycin, or doxycycline 100 mg
twice daily
 Monotherapy:
o Respiratory fluoroquinolone (levofloxacin 750 mg daily,
moxifloxacin 400 mg daily, or Gemifloxacin 320 mg daily)
Chapter 8: COPD
8.1. Definition:
 progressive disorder characterized by airflow restriction.
 Tobacco smoking accounts for 90% of cases.
8.2. Symptoms, sign:
Consider copd If old >40 or smoker and have one of following:
 Chronic cough
 Wheeze
 Dyspnea
 Chronic sputum production
On examination:
 Hyperexpanded chest and poor expansion with inspiration
 Hyperresonant chest
 Wheeze or quiet breath sounds
 Increased respiratory rate.
 Pursed lip breathing
 Cyanosis
 Increased JVP
 Cachexia (weight loss/muscle wasting)
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8.3. Investigation:
 Post bronchodilator spirometry
 CXR: to exclude other diagnoses.
 CBC: to identify anemia/polycythaemia.
 Sputum culture, if persistent and purulent sputum
 α1 Antitrypsin: if young, minimal smoking or family history
Modified Medical Research Council (mMRC) dyspnea scale:
The degree of breathlessness can be graded using the Medical
Research Council’s Dyspnea score (mMRC) and/or CAT assessment
(Table 8.1). Chest pain and hemoptysis are uncommon in COPD
therefore alternative diagnoses need to be considered if present.
Table 8.1 – Subjective severity mMRC dyspnea score
Score Clinical presentation
0 Not troubled with breathlessness except with strenuous exercise
1 Short of breath when rushing or walking up a slight hill
2 Walks slower than peers on ground level due to breathlessness
Stops for breath after walking about 94 meters on ground level or after
3
few minutes
4 Too breathless to leave the house or when get dress
8.4. Management:
Treatment according to Modified Medical Research Council (mMRC)
dyspnea scale and /or COPD assessment tool (CAT)
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8.4.1 specific treatment:

Table 8.2 – COPD management
Group Symptoms Management
mMRC 0-1 SABA or SAMA or in
CAT <10 combination as needed.
A Mild infrequent symptoms
0-1 exacerbation a year (without
hospitalization
mMRC ≥ 2 Regular LABA or LAMA
CAT ≥ 10 SABA as needed
B Moderate to severe symptoms
0-1 exacerbation a year (without
hospitalization
mMRC 0-1 Regular LAMA
CAT <10 SABA as needed
C Mild or infrequent symptoms
≥2 exacerbations a year with one or more
leading to hospitalization
mMRC ≥ 2 Regular LAMA or
CAT ≥ 10 Regular LAMA + LABA or
D Moderate to severe symptoms ICS + LABA
≥2 exacerbations a year with one or more SABA as needed
leading to hospitalization
8.4.2 General management:
 Smoking Cessation (refer to smoking cessation chapter)
 Pulmonary rehabilitation if MRC dyspnea score >3 or high risk of
exacerbations, includes exercise training, nutrition counseling, and
education.
 Influenza, COVID19, and pneumococcal vaccination (PCV13 and
PPSV23) should be offered to all COPD patients.
 Tdap (tetanus, diphtheria, and acellular pertussis) vaccine is
recommended to protect against pertussis (whooping cough)
 Weight reduction in obese patients improves exercise tolerance.
 Regular physical activity
 Long term oxygen if indicated with chronic hypoxemia.
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Chapter 9: CHEST PAIN

9.1. Definition:
Chest pain accounts for 1% of all ambulatory visits in the primary care
setting, and 2– 4% of these patients will have unstable angina or
myocardial infarction. Chest wall pain (20–50%), reflux esophagitis (10–
20%), and costochondritis (13%) are the most common causes of chest
pain in the primary care population.
Acute Coronary Syndromes – ACS:
 STEMI: is diagnosed if there is > 1-2 mm of ST elevation in two
contiguous leads or new LBBB in patients with ischemic chest pain.
Classically the ST elevations are described as a tombstone and
concave or upwards in appearance.
 NSTEMI: represents typical clinical syndrome and elevated troponin
with ECG changes of ST-segment depression and T-wave inversion
but no ST-segment elevation. NSTEMI is differentiated from unstable
angina by elevated levels of cardiac enzymes.
 Unstable angina: presents with prolonged (>20 minutes) angina at
rest; new onset of severe angina; angina that is increasing in
frequency, longer in duration, or lower in threshold; or angina that
occurs after a recent episode of myocardial infarction in the absence
of biochemical evidence of myocardial damage.
Chronic Coronary Syndromes – CCS:
 Stable angina also is known as typical angina or angina pectoris, is a
symptom of myocardial ischemia. It is characterized by chest
discomfort or anginal equivalent provoked with exertion and alleviated
at rest or with Nitroglycerin. It results because of an imbalance
between the myocardial oxygen supply and the myocardial oxygen
demand.
9.2.1 Symptoms:
Classic symptoms:
 Deep, poorly localized chest or arm discomfort
 It is reproducibly associated with physical exertion or emotional
stress.
 Relieved promptly (specifically, in less than 5 minutes) with rest and
use of sublingual nitroglycerin.
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Atypical features of chest pain:

 Chest pain lasting for seconds.
 Constant pain lasting for hours or more without waxing and waning
intensity.
 Specific body movements or positions worsen the pain.
 Well localized, positional, or pleuritic chest pain
9.2.2 physical examination:
Vital signs:
 May be unremarkable.
 Signs of heart failure present: tachycardia (pulse > 90-100
beats/minute), systolic blood pressure < 90 mm Hg
 Fever may indicate pneumonia or acute pericarditis.
 Hypoxia, tachypnea, and tachycardia may indicate spontaneous
pneumothorax.
Skin: Look for any lesions near the site of pain Itching, dermatomal pain,
and paresthesia make a diagnosis of herpes zoster highly likely.
Cardiac: Pericardial friction rub suggests acute pericarditis, Pain
reproducible with palpation suggests musculoskeletal chest wall pain.
Lungs: auscultation to rule out pneumonia.
Extremities: Pulse deficits or differences in blood pressure in the right
and left arm suggest possible thoracic aortic dissection.
● ECG:
12-lead ECG should be performed on all patients in whom cardiac
ischemia is suspected.
ECG findings that increase the likelihood of ACS include:
 ST-segment elevation
 New onset left bundle branch block.
 Presence of Q waves
 New T-wave inversions
Imaging:
chest x-ray, the images are helpful to diagnose or exclude other
conditions such as pneumonia, pneumothorax.
Cardiac biomarkers:
Due to its high sensitivity and nearly complete cardiac specificity, cardiac
troponin is the biomarker of choice to detect myocardial injury. Other
markers are Creatine Kinase-MB and Myoglobin.
Page | 126

9.4.1 Acute Coronary Syndromes:
Initial therapy for ACS aims to stabilize the patient’s condition, relieve
ischemic pain, reduce myocardial damage, and prevent further ischemia.
 morphine for pain control: Initial dose 2–4 mg; Increments of 2–8 mg
q 5–15 minutes.
 oxygen
 nitroglycerin: Sublingual tablets 0.4 mg every 5 minutes up to 3 times.
Contraindications:
 SBP <90 or 30 mmHg below baseline
 HR <50 or >100
 RV infarction/severe aortic stenosis
 Recent use of phosphodiesterase-5 inhibitors (Sildenafil)
● soluble aspirin (162-325 mg).
● clopidogrel (300-600-mg).
9.4.2 Chronic Coronary Syndromes:
Therapeutic lifestyle modifications:
 Weight control, goal BMI less than 25 kg/m2
 Physical activity, recommend 150 minutes of moderate-intensity
exercise per week. or 75 minutes of high-intensity exercise per week.
 Diet high in fresh fruits, vegetables, and low‐fat dairy products
 Limited sodium intake
Pharmacological therapy:
 Aspirin 75–162 mg/daily
 Blood pressure control
 Cholesterol control: LDL <100 mg/dl or <70 mg/dl
 ACE/ARB for all patients with LVEF ≤40%
 Beta‐blockers for all patients with a history of MI, LVEF <40% unless
contraindicated.
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Chapter 10: HEART FAILURE

10.1. Definition:
Heart Failure (HF) is a complex condition that arises from an inability of
the heart to maintain adequate circulation. It is characterized by
ventricular dysfunction that results in low cardiac output. It affects around
26 million people worldwide and has a death rate of approximately 50%
within 5 years.
10.2. Etiology:
Table 10.1
Common causes
 Ischemic heart disease (50–60%)
 Hypertension (20–30%)
 Idiopathic cardiomyopathy
 Diabetes mellitus
 Renal disease
 Valvular heart disease
 Congenital heart disease
 Infiltrative diseases – hemochromatosis, amyloidosis
Specific causes of Systolic HF Specific causes of Systolic HF
 Cardiomyopathies – dilated  Cardiomyopathies – dilated
cardiomyopathy (30%) cardiomyopathy (30%)
 Cardiac arrhythmias  Restrictive cardiomyopathy
 Myocarditis  Constrictive pericarditis
 Infections – HIV, Lyme’s, viral  Pericardial tamponade
10.3. Risk Factors:
 Obesity
 Obstructive sleep apnea
 Endocrine disorders- thyroid disease
 Smoking
 Drugs recreational and prescription
 Alcohol abuse
 Chronic obstructive pulmonary disease (COPD)
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10.4. Clinical Presentation:

Table 10.2
Symptoms Signs
 Shortness of breath/dyspnea  Elevated jugular venous
 Orthopnea pressure -JVP.
 Paroxysmal nocturnal dyspnea  Displaced apex
 Fatigue/lethargy  Crackles/crepitations or wheeze
 Reduced exercise tolerance  Right ventricular heave
 Nocturnal cough/wheeze  Heart sounds S3/S4
 Ankle swelling  Tachycardia
 Anorexia  Pulsus alternans
 Weight loss  Edema
 Nocturia
 Hepatomegaly
 Ascites
 Cachexia and muscle wasting –
chronic severe HF
10.5. Staging:
Table 10.3 - The New York Heart Association (NYHA) classification system
Class I No limitation of physical activity
Class II Slight limitation of physical activity
Class III Marked limitation of physical activity
Class IV Symptoms occur even at rest; discomfort with any physical activity.
10.6. Workup:
 B-type natriuretic peptide levels/N-terminal pro-B-type natriuretic
peptide levels
Table 10.4 - natriuretic peptide levels
BNP Level >500: HF Likely <100: HF unlikely
>900 (aged 50-75), >1800 <300: HF unlikely
NT pro BNP
(Aged over 75): HF likely
 ECG: Helpful in ruling out left ventricular hypertrophy (LVH),
myocardial ischemia, infarction as causes of heart failure.
 Chest Radiography: help in differentiating HF from pulmonary
diseases
 Echocardiography: Gold standard.
Page | 129
Additional initial testing:

 Complete blood count (CBC)/Iron studies
 Urinalysis
 Electrolyte levels
 Renal and liver function studies
 Fasting blood glucose levels
 Lipid profile
 Thyroid-stimulating hormone (TSH)
10.7. Management:
10.7.1 General Principles:
 Control risk factors: DM, Hypertension, Obesity, Thyroid diseases,
Anemia
 Review medications that may worsen HF: NSAIDs
 Appropriate vaccinations: including pneumococcal and influenza
vaccine.
10.7.2 Non-pharmacological:
 Fluid restriction in patients with hyponatremia to 2L/day
 Sodium restriction to less than 2-3g/day
 Smoking and alcohol cessation
 Omega-3 polyunsaturated fatty acids (PUFAs): Reduced mortality
and morbidity and hospitalization for cardiovascular causes
 EPA- Plasma eicosapentaenoic acid: Can be considered for primary
prevention.
Page | 130
10.7.3 Pharmacological:
Table 10.5
Medication Indication Notes
Improve symptoms
ACEi/ARBs
and prognosis
NYHA Class I-IV Reduce
Initial Beta adrenergic
hospitalization and
optimized blockers
improve mortality
treatment
Mainstay of
In volume overloaded treatment, improves
Diuretics
patients symptoms and
reduce hospitalization
Aldosterone NYHA Class II-IV, EF Reduce symptoms,
Step 2 hospitalization and
antagonists < 35%
improve.
Step 3 SGLT-2 inhibitors NYHA Class II-IV mortality
In patients who
Hydralazine and
cannot tolerate Improve symptoms
nitrates
ACEi/ARBs
Supplementary
Reduce symptoms,
agents
hospitalization and
Digoxin Persistent symptoms
improve.
prognosis
10.7.4 Referral to cardiology:
 Once initial diagnosis of heart failure is made.
 Heart failure symptoms unable to be managed at home (ED)
 Severe heart failure
 Heart failure not controlled by first line medications.
 Angina, AF, symptomatic arrhythmia
 Heart failure due to valve disease or diastolic dysfunction
 Comorbidity that may impact heart failure (e.g., COPD, renal failure,
anemia, thyroid disease, PVD, urinary frequency, gout).
 Women with heart failure planning pregnancy
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Chapter 11: CARDIAC ARRHYTHMIA

11.1. Bradyarrhythmias:
Rhythms with a ventricular rate slower than 60 beats/min in adults, with
age-appropriate limits in children
Classifications:
 Bradycardias: sinus bradycardia (Most common), junctional rhythm,
idioventricular rhythm, and hyperkalemia-related sinoventricular
rhythm.
 Atrioventricular (AV) blocks: Second-degree (usually type II) and
third-degree AV block, as well as atrial fibrillation and atrial flutter with
a slow ventricular response.
11.1.1 Bradycardia:
Sinus Bradycardia:
Causes:
 Physiologic: In well-conditioned athletes, during sleep, with vagal
stimulation
 Pharmacological: B-blockers, digoxin, opioids, calcium channel
blockers
 Pathological: Hypoxia, acute inferior wall myocardial infarction or
ischemia, increased intracranial pressure, carotid sinus
hypersensitivity, hypothyroidism
Treatment:
 Generally, do not require treatment unless HR is less than 50 beats
per minute, signs of hypoperfusion.
 Address the underlying causes.
 Atropine in unstable patients, transcutaneous cardiac pacing and
dopamine/epinephrine infusion in patients not responding to atropine.
Rhythm strip:
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11.1.2 Atrioventricular blocks:

1st degree atrioventricular block:
Definition:
 In 1st degree atrioventricular block, each atrial impulse is conducted to
the ventricles but less rapidly than normal, as noted by a prolonged
PR interval greater than 200 milliseconds.
Causes:
 Normal finding
 Pathological: vagal tone of any cause, medication toxicity, inferior
myocardial infarction, and myocarditis
Treatment:
 No treatment is required.
 Close monitoring of the patients with acute MI
Rhythm Strip:
Second-degree Mobitz Type I (Wenckebach) block:

Definition:
 progressive prolongation of AV conduction (and the PR interval) until
an atrial impulse is completely blocked and no QRS is seen.
Causes:
 Often transient, can be caused by inferior myocardial ischemia,
medication toxicity, myocarditis, or after cardiac surgery.
Treatment:
 No treatment is required, unless patient develops signs of
hypoperfusion (Atropine
Rhythm Strip:
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Second-degree Mobitz type II AV block:

Definition:
● The PR interval remains constant across the rhythm strip, both
before and after the nonconducted atrial beats. Each P wave is
associated with a QRS complex until a non conducted atrial
depolarization (i.e., P wave) is noted without accompanying the QRS
complex.
Causes:
 Structural damage to infranodal conduction system, i.e., Acute
myocardial ischemia
Treatment:
 Most patients will require tranvenous cardiac pacing.
 Atropine can be tried but the effect is inconsistent.
Rhythm strip:
Third-degree atrioventricular block

Definition:
 It occurs if there is no AV conduction, manifesting as completely
unrelated P and QRS waves.
Causes:
● Nodal third-degree AV (Narrow QRS) block is caused by inferior
acute MI.
● Infranodal third degree AV block (Wide QRS) is caused by extensive
anterior acute MI.
Treatment:
● Asymptomatic patients require monitoring and admission.
● Symptomatic nodal blocks may respond to Atropine, if failed, use
transcutaneous or trans venous pacing
● Symptomatic infranodal blocks require transcutaneous or trans
venous pacing.
Page | 134
Rhythm strip:
11.2. Tachyarrhythmias:
Tachyarrhythmia describes rhythms with a ventricular rate greater than
100 beats/min in an adult, with ageappropriate limits in children.
Classifications:
 Narrow complex tachyarrhythmias: sinus tachycardia, atrial
fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia.
 Wide complex tachyarrhythmias: Ventricular tachycardia and
supraventricular tachycardia with aberrant conduction.
11.2.1 Narrow Complex Tachycardia:
Sinus Tachycardia:
Definition:
 Sinus rhythm with rates greater than 100 beats/min.
Causes:
 Generally, a reactive rhythm, occurring in response to a triggering
condition (Physiologic stress, fever, hypovolemia, anxiety, pain)
Treatment:
 Addressing the underlying causes
Rhythm strip:
Page | 135
Atrial fibrillation
Definition:
 Atrial fibrillation occurs when there are multiple, small areas of the
atrial myocardium continuously discharging and contracting. The ECG
hallmarks of atrial fibrillation include the absence of discernible P
waves and an irregularly irregular ventricular rhythm.
 Atrial fibrillation increases the risk of venous and atrial thrombosis,
with potential for pulmonary and systemic arterial embolism.
Causes:
 Ischemic or valvular heart disease; less common causes include
congestive cardiomyopathy, myocarditis, alcohol binge (holiday
heart), thyrotoxicosis, and blunt chest trauma.
Treatment:
 Varies according to patient stability, duration of symptoms, and
chronicity of atrial fibrillation (paroxysmal, persistent, or permanent).
 Either ventricular rate control (with calcium channel blocker
(diltiazem) or β-blockers (metoprolol and esmolol)) or rhythm control
(Electrical or pharmacological cardioversion)
 Anticoagulation: Based on CHA2DS2-VASc score on 2 or more, to be
started on warfarin
Clinical circumstance:
 Duration <48 h Low-risk for embolism
 Duration <48 h Low-risk for embolism
 Duration >48 h
 High-risk for embolic complications
Treatment:
 Chemical or electrical cardioversion to sinus rhythm
 Ventricular rate control <100 beats/min
Follow-up therapy
 If successful conversion, no antithrombotic therapy
 No antithrombotic therapy, close follow-up
 Therapeutic anticoagulation for 3–4 wk.
 Therapeutic anticoagulation for 3–4 wk.
Page | 136
Rhythm Strip:
Atrial flutter:
Definition:
 In atrial flutter, P waves are present and of a single morphology,
typically a downward deflection, called flutter waves resembling a saw
blade with a sawtooth pattern, best seen in the inferior ECG leads
and lead V1.
Treatment:
 Managed in the same fashion as atrial fibrillation: either rhythm
conversion or ventricular rate-control with βblockers or calcium
channel blockers.
Rhythm Strip:
Paroxysmal supraventricular tachycardia:

Definition:
 In paroxysmal supraventricular tachycardia, the QRS complex is of
normal width, rapid, and regular. P waves are buried within the QRS
complex in about 70% of cases. In the others, a P wave (so-called
retrograde P wave) is found immediately adjacent before, during, or
after the QRS complex without a measurable PR interval.
Causes:
● More frequently in females, with a peak in the late teenage and
young adult years. The majority of patients are without active
cardiovascular disease.
Page | 137
Treatment:
● Vagal maneuvers
● IV adenosine if no response to vagal maneuvers
● Electrical cardioversion If unstable
Rhythm strip:
Normal (left) vs Paroxysmal supraventricular tachycardia (Right)
Multifocal atrial tachycardia

Definition:
 An irregular rhythm resulting from at least three different ectopic atrial
foci competing to pace the heart. The electrocardiographic
characteristics require at least three distinct P-wave morphologies.
Causes:
 Most often in elderly patients with decompensated chronic lung
disease but may also complicate heart failure or sepsis.
Treatment:
 Addressing the underlying cause:
 In decompensated lung disease, oxygen, and bronchodilation
Rhythm strip:
Page | 138
11.2.2 Approach to narrow complex tachycardia:
11.2.3 Wide Complex Tachycardia:

Ventricular tachycardia:
Definition:
 The occurrence of three or more consecutive depolarizations from a
ventricular ectopic pacemaker at a rate faster than 100 beats/min.
 Can occur in a non sustained manner with short episodes, lasting
several beats, with spontaneous termination, or it can occur in a
sustained fashion, with longer episodes that typically require
treatment.
Page | 139
Causes:
 The most common causes of ventricular tachycardia are chronic
ischemic heart disease and acute myocardial infarction.
 Less common causes of ventricular tachycardia include dilated or
hypertrophic cardiomyopathy, valvular heart disease (including mitral
valve prolapse), inherited ion channel abnormalities, and drug toxicity.
Hypoxia, alkalosis, and electrolyte abnormalities, especially
hyperkalemia.
Treatment:
 Pulseless Ventricular tachycardia: Electrical defibrillation, chest
compressions, other advanced life support measures.
 Unstable patients with a pulse: Electrical cardioversion coupled with
sedation.
 Stable patients: Amiodarone (preferred), procainamide or lidocaine, if
unsuccessful, electrical cardioversion coupled with sedation.
Rhythm strip:
 A. Polymorphic ventricular tachycardia
 B. Torsades de pointes
Ventricular fibrillation:
Definition:
 Disorganized depolarization and chaotic contraction of small areas of
ventricular myocardium absent any effective mechanical cardiac
activity; there is no cardiac output. The ECG of ventricular fibrillation
shows a fine, irregular pattern without discernible P waves or
organized QRS complexes.
Page | 140
Causes:
 Most commonly seen in patients with severe ischemic heart diseases.
Less common causes include: direct stimulation of the myocardium
by catheters or other instruments, electrocution, and direct, blunt
chest trauma.
Treatment:
 Electrical defibrillation along with chest compressions and other
advanced life support measures.
 If unsuccessful, address triggers including: acute ischemia, metabolic
derangement, toxicologic insult.
Rhythm strip:
 A. Coarse amplitude
 B. Fine Amplitude
 C. Coarse amplitude
11.3. Arrhythmias Associated With Conduction

Abnormalities:
11.3.1 Wolf-Parkinson-White (WPW) syndrome:
Definition:
A form of ventricular preexcitation involving an accessory conduction
pathway that bypasses the AV node and creates a direct electrical
connection between the atria and ventricles.
ECG Findings:
 Sinus rhythm with a very short PR interval (< 120 ms)
 Broad QRS complexes with a slurred upstroke to the QRS complex
— the delta wave
 Dominant R wave in V1 — this pattern is known as “Type A” WPW
and is associated with a left-sided accessory pathway.
Page | 141
Rhythm strip:
11.3.2 Brugada Syndrome:

Definition:
An inherited disorder of myocardial depolarization that predisposes
young individuals to malignant ventricular arrhythmias and sudden death.
ECG Findings:
 Type 1:
o Coved-shaped ST-segment elevation >2 mm followed by an
inverted T wave.
 Type 2:
o ST-segment elevation >2 mm with a trough in the ST segment at
least 1 mm deep followed by a positive or biphasic T wave
Producing a saddleback pattern.
Symptoms:
 The majority of patients with Brugada syndrome are asymptomatic
and are only found via an incidental ECG. Symptomatic patients
present with palpitations, near to complete syncope, or seizures due
to ventricular tachyarrhythmias.
Treatment:
 Risk stratification is done to identify patients with Brugada syndrome
at significant risk for malignant ventricular tachyarrhythmias.
 An important role for primary care providers is to recognize this ECG
pattern and to refer for appropriate follow-up.
Rhythm strip:
 A- Type 1
 B-Type 2
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Chapter 12: THYROID AND

PARATHYROID DISORDERS
12.1. Hypothyroidism:
12.1.1 Definition:
Hypothyroidism
 High TSH level and low T4 level > overt hypothyroidism
 High TSH level and normal T4 level > subclinical hypothyroidism

Table 12.1 – Signs and symptoms of hypothyroidism
General Cold intoleranceWeight gain with poor appetite
Head & neck Hair lossCoarse hairLoss of the outer third of the
eyebrowPeriorbital edema Hoarseness Goiter
Lungs Shortness of breath Pleural effusion
Heart BradycardiaFlattened T wavesPericardial effusion
Muscular Delayed reflex relaxation
Skin Paresthesia Myxedema
Intestine Constipation Ascites
Extremities Coldness Delayed DTR Carpal tunnel syndrome
Reproductive systems Menstrual irregularities Infertility
Psychiatric Poor memory and concentrationFatigue Depression
Endocrine Dyslipidemia

 Start with history and physical examination.
 Lab investigation, which includes: TSH, T4, thyroid antibodies.
 In primary hypothyroidism > TSH is elevated, and free T4 is low >
consider checking TPO.
 Secondary (pituitary) or tertiary (hypothalamic) hypothyroidism > both
TSH and T4 are low.
 Re-measure TSH level after 6 weeks, In pregnancy every 4 weeks.
 TSH or free T4 levels are monitored annually in most patients with
hypothyroidism once a stable maintenance dosage of levothyroxine is
achieved.
Page | 143
12.1.4 Management plan & Monitoring:

 Starting dose is 1.6 mcg/kg.
o This is the starting dose for young healthy adults.
o Older patients with coronary artery disease: Lower starting dose
of 25–30 mcg daily
o Pregnant patients: immediately increase to 9 doses weekly.
 For Subclinical hypothyroidism, treatment may be beneficial in case
of:
o TSH > 10 μU/ml
o Positive anti‐thyroid peroxidase (TPO) antibodies
o Treatment-resistant depression
o In case of untreated subclinical hypothyroidism, retest at 6–12-
month intervals. The treatment dose in (adult) is 25‐50
mcg/daily.
12.1.5 Reasons to refer to endocrinology for
hypothyroidism:
 Age 18 years or younger
 Elusive euthyroid state
 Myxedema coma
 suspected pregnancy
 Simultaneous presence of another endocrinopathy
 Structural change in thyroid gland (e.g., goiter, nodule)
 Symptoms do not improve or worsen after treatment with
levothyroxine
 Unstable ischemic heart disease
12.2. Hyperthyroidism:
12.2.1 Definition:
 Hyperthyroidism: Low TSH level and High T4 Level
 Female to male ratio is 8:1.
Page | 144

 Weight loss with increase appetite
 Heat intolerance
 Sweating
 Anxiety
 Tremor
 Palpitation
 Oligomenorrhea
 Goiter
 Fatigue
 Insomnia
 Headache
● Dyspnea on exertion
Management plan:
Graves’ disease:
 Antithyroid medication > methimazole is first line except in first
trimester use PTU.
 Radioactive iodine (I-131) ablation (contraindicated in pregnancy and
relatively contraindicated in moderate to severe orbitopathy)
 Surgical thyroidectomy (if compressive symptoms)
Pharmacological management of hyperthyroidism:
Beta-blockers (symptom control)
 Atenolol 25-100 mg od.
 Propranolol 10-40 mg TID immediate release
 Antithyroid medication
 Imidazoles
 PTU: 2nd line, except in first trimester and lactation
 Radioactive iodine
 Ancillary agents
 NSAID
 Glucocorticoids
 Cholestyramine
 Supersaturated potassium iodide
Page | 145
12.3. Thyroid Disorders in Pregnancy:

 TSH goal in pregnancy is different depending on trimester.
 Levothyroxine is indicated for subclinical hypothyroid with positive
thyroid peroxidase antibodies.
 Women who are already on levothyroxine should increase the dose
by 25–50% during pregnancy
 For Graves’, use PTU in the 1st trimester, then Methimazole
Table 12.2
Clinical RAI uptake
Disorder Lab findings Treatment
findings and scan
Antithyroid
TSH receptor
medications
antibody 80%
Diffusely (MMI, PTU);
to 90% diffusely
enlarged beta blockers;
Graves’ disease sensitive; TPO increased
thyroid; radioactive
50% to 85% uptake
possible bruit Iodine;
sensitive; low
ablation (RAI);
specificity
thyroidectomy
Single Single focus
Solitary toxic Medications or
palpable of increased
nodule RAI
nodule uptake
Lumpy bumpy Multiple hot
Multinodular Medications or
enlarged and/or cold
goiters RAI
thyroid nodules
Tender, Diffusely NSAID +
Subacute Post viral,
enlarged decreased possible
thyroiditis elevated ESR
thyroid uptake steroids
Discontinue or
Diffusely
Exogenous Thyroglobulin decrease
Normal decreased
hyperthyroidism levels are low thyroid
uptake
hormone
12.4. Thyroid Nodules:
12.4.1 Definition:
 Very common, particularly women > 40 years
 Commonly noted as an incidental finding on neck CT or ultrasound
 Mostly benign, but 5% malignancy rate
 Hot nodule > hyperfunctioning, low likelihood of malignancy
 Cold nodule > hypofunctioning, approximately 20% malignancy
Page | 146

 Typically presents with a single, firm, palpable nodule. Otherwise,
often asymptomatic unless associated with thyroid hormone
abnormalities or advanced carcinoma.
12.4.3 Red flags:
 Female gender
 Age < 30 or > 60 years
 Positive history of head/neck irradiation
 Family history of thyroid cancer or cancer syndromes
 A hard, fixed nodule > 4 cm
 Rapid growth of the nodule
 Symptoms related to local invasion (dysphagia, hoarseness, LAD)
 Start with TSH and thyroid US in all patients with a thyroid nodule.
 If TSH is low > do RAI scan:
 If hot nodule (high iodine uptake), low likelihood of malignancy > don’t
perform FNA.
 If cold nodule (low iodine uptake) > FNA is indicated to rule out
malignancy
 If TSH is normal or high and suspicious findings on US > FNA
 Cytopathology result will give you Bethesda category 1 to 6.
Benign nodules:
 Observe if asymptomatic and confirmed to be benign.
 T4 suppression therapy is only 50% effective.
 Surgical excision can be considered.
Malignant nodules:
 Total thyroidectomy followed by RAI ablation.
 Markers such as thyroglobulin and calcitonin (medullary carcinoma
only) can be used to monitor for recurrence.
 For low-risk cases with very small nodules (< 1 cm), lobectomy can
be considered.
Page | 147
12.5. Thyroid Cancer:

 Gender: female to male 3:1 ratio
 Age
 Low iodine intake
 Radiation
 Genetic predisposition
12.5.2 Screening and worrisome findings:
 Lump found in the neck.
 Swelling in the neck
 Pain in the front of the neck
 Persistent hoarseness or voice changes
 Swallowing difficulties
 Persistent cough not due to a cold
12.5.3 Thyroid cancer types:
Table 12.3
Main type of
Subtypes Features
cancer
– 80% of all thyroid cancer
Papillary
– Grow slow
thyroid
– Rarely fatal
carcinoma
– Often spreads to the lymph node in the neck
Differentiated Follicular – 10% of all thyroid cancer
thyroid cancer thyroid – Spreads to lungs and bones through the
carcinoma bloodstream
– 3% of all thyroid cancer
Hurthle cell
– Harder to locate through radioactive iodine
carcinoma
results in a worse prognosis
Medullary – 4% of all thyroid cancer
Poorly thyroid – Develops from the thyroid gland’s parafollicular
differentiated carcinoma cells (C cells), which produce calcitonin to help
and (MTC) control blood calcium levels
undifferentiate Anaplastic – 2% of all thyroid cancer
d thyroid – Tends to spread quickly into the neck and other
carcinoma parts of the body, making it very difficult to treat.
Page | 148
12.6. Hyperparathyroidism:
12.6.1 Etiology:
 Primary hyperparathyroidism is mostly (80–90%) from single benign
adenoma; May be associated with multiple endocrine neoplasias
(MEN), rarely parathyroid cancer.
 Secondary hyperparathyroidism is typically due to vitamin D
deficiency, chronic kidney disease, or other causes of low blood
calcium.
 Tertiary hyperparathyroidism is seen in renal failure.
 Mostly asymptomatic, found incidentally.
 Associated symptoms
o Hypercalcemia
o Renal: polyuria, polydipsia, renal stones
o Skeletal: arthralgia, bone pain, fracture
o Neuromuscular: anxiety, confusion, depression, fatigue, insomnia
o GI: anorexia, constipation, epigastric pain, nausea, vomiting
o Cardiovascular: Angina, dyspnea, palpitation, syncope
Table 12.4
Calcium PTH Phosphate
Primary hyperparathyroidism High High Low
Secondary hyperparathyroidism Low/ normal High High/normal
Tertiary hyperparathyroidism High Very high High
 Primary hyperparathyroidism > Surgical parathyroidectomy only cure
o Indications for surgery:
 < age 50; serum calcium > 11 mg/dl, reduced bone density
(‐2.5 T score or lower), decreased GFR, or kidney stones.
 Secondary hyperparathyroidism > treat the underlying cause.
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12.7. Hypoparathyroidism:
Hypoparathyroidism > restore calcium & mineral balance thru Ca++ & Vit
D supplements.
12.7.1 Etiology:
Head and neck surgery account for the majority of cases—
thyroidectomy, parathyroidectomy, radical surgery for head and neck
malignancies. Non-Surgical hypoparathyroidism is rare.
Clinical Features (hypocalcemia)
 Cardiac arrhythmias
 Rickets and osteomalacia
 Increased neuromuscular irritability due to hypocalcemia.
o Numbness/tingling circumorally, fingers, toes
o Tetany
o Grand mal seizures
 Prolonged QT interval on ECG
 Cataracts
 Start with: serum magnesium, albumin, ionized calcium, corrected
calcium levels.
 Verified hypocalcemia > Serum phosphorus, creatinine, PTH, 25-
hydroxyvitamin D levels.
 PTH level normal or low: Calcium/creatinine ratio with 24-hour urine
collection.
 IV calcium gluconate in severe cases, oral calcium in mild to
moderate cases
 Vitamin D supplementation (calcitriol)
 Note that both vitamin D and calcium replacement can increase
urinary calcium excretion, precipitating kidney stones. Therefore,
administer with caution to avoid hypercalciuria.
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Chapter 13: PITUITARY AND ADRENAL

DISORDERS
13.1. Hyperprolactinemia:
13.1.1 Etiology:
 Physiological: Stress, pregnancy, etc.
 Pharmacological: SSRIs, Methyldopa, Metoclopramid, etc.
 Pathological: Prolactinoma, other hypothalamic or pituitary disorders,
chronic renal failure on dialysis
 History should focus on the following important points.
 Women: galactorrhea, menstrual irregularity, amenorrhea, infertility
 Men: hypogonadotropic hypogonadism, erectile dysfunction,
decreased libido, gynecomastia.
 Symptoms of mass effect such as visual field abnormalities and
headaches
 Elevated serum prolactin level
o Normal level is 5 to 20ng/mL.
o If initial serum concentration is slightly elevated (21 to 40ng/mL)
test should be repeated in a fasting sample
 CT scan or MRI to identify any mass lesions.
o Microadenoma: 10mm or less (90%)
o Macroadenoma: More than 10mm (10%)
 Order pregnancy test and TSH level, both pregnancy and primary
hypothyroidism are on the differential diagnosis.
Medical Treatment:
Dopamine agonist
 Cabergoline is the drug of choice, it is the best tolerated and longest-
acting, 0.25–5 mg twice a week.
 Bromocriptine is preferred if pregnancy is planned.
Other treatment options:
 Trans-sphenoidal surgery in people with microadenoma
 Radiotherapy usually controls adenoma growth and is slowly effective
in lowering prolactin, 3rd line of treatment.
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13.2. Cushing's Disease:

13.2.1 Definition:
 Cushing’s disease vs syndrome:
o Cushing’s syndrome results from excessive levels of
glucocorticoids due to any cause.
o Cushing’s disease results from pituitary Cushing’s syndrome
(pituitary adenoma)
 ACTH-secreting adenoma of the pituitary (Cushing’s disease) is the
most common cause and leads to bilateral adrenal hyperplasia.
Table 13.1
Central obesity, Proximal muscle weakness, Hypertension,
General
Headaches, Psychiatric disorders.
Wide (>1 cm), purple striae, Spontaneous ecchymoses, Facial
Skin plethora, Hyperpigmentation, Acne, Hirsutism, Fungal skin
infections.
Endocrine and Hypokalemic alkalosis, Osteopenia, Delayed bone age in
metabolic children, Menstrual disorders, decreased libido, impotence,
derangements Glucose intolerance, diabetes mellitus, Kidney stones, Polyuria.
Hematologic Elevated white blood cell count
 Initial screening test: overnight (low-dose) dexamethasone
suppression test
o If the serum cortisol is < 5, Cushing’s syndrome can be excluded
(sensitive)
o If the serum cortisol is > 5 (and often > 10), the patient has
Cushing’s syndrome.
 Measure ACTH level
o If Low: adrenal tumor or hyperplasia
o If high: order a high-dose dexamethasone suppression test to
determine the cause (Cushing’s disease vs. ectopic ACTH tumor)
 In Cushing’s disease, the result is a decrease in cortisol
levels (>50% suppression)
 If cortisol suppression does not occur and plasma ACTH
levels are high, an ectopic ACTH-producing tumor is likely
the diagnosis.
 24-hour urinary free cortisol level (values >4 times normal)
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Imaging studies
 Following confirmation of Cushing’s syndrome, imaging studies
should be performed to look for adenomas (MRI scan) or adrenal
tumors (CT scan). If both of these studies are negative, chest
radiography or CT scanning should be performed to look for ectopic
sources of ACTH production.
Treatment of Cushing’s disease (pituitary-dependent hyperadrenalism)
 Trans-sphenoidal removal of the tumor
 External pituitary irradiation (± Stereotactic radiotherapy) is mainly
used after failed pituitary surgery.
 Bilateral adrenalectomy
 Children respond much better to radiotherapy.
13.3. Primary Hyperaldosteronism (Conn's Syndrome):
 Hypertension
 Hypokalemia (unprovoked hypokalemia in the face of HTN associated
with Conn’s 50% of the time)
 Plasma aldosterone/plasma renin ratio > 20
 Plasma aldosterone > 15 mg/dl is abnormal.
 Confirm by urine 24‐hr aldosterone (>20 mg/day)
 CT‐ABD useful: Solitary adenoma 70%., bilateral hyperplasia 30%
 Solitary adenoma:
o Surgery – 70% normotensive; 95% normal potassium
o Aldosterone antagonist as medical therapy
● Bilateral hyperplasia:
o Aldosterone antagonist therapy
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13.4. Pheochromocytoma:
13.4.1 Definition:
 90% sporadic, 10% genetic
 Pheochromocytoma rule of 10s
o 10% extra-abdominal
o 10% malignant
o 10% bilateral
o 10% in children
 30% genetic/syndromic
Suspect if:
 Resistant hypertension (> 3 drugs needed)
 Episodic exacerbations including headache, sweating, palpitations,
especially with position change, exercise, or any ↑ in intra‐abdominal
pressure.
Diagnostic testing: depends on demonstrating excessive catecholamine
production.
 24‐hr urinary catecholamines or metanephrines
 Plasma free for metanephrines or catecholamines
 VMA (vanillylmandelic acid) in the urine
 Localization of lesion by MRI
o Usually, unilateral
o 10% bilateral
o 10% extra‐adrenal
 Surgical removal
 Alpha‐blockade to control HTN (phenoxybenzamine)
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Chapter 14: URINARY TRACT

INFECTIONS
14.1. Acute simple cystitis:
14.1.1 :Definition
 No symptoms of upper UTI
 Excludes pregnant women and renal transplant recipients.
14.1.2 :symptoms and Physical examination
 dysuria
 Frequent voiding of sm all volumes
 Urinary urgency
 Hematuria
 Urine that appears cloudy
 Supra-pubic discomfort
 Strong-smelling urine
14.1.3 :Investigation & monitoring
● low risk patient diagnosed based on symptoms.
● high risk patient diagnosis is by urinalysis and urine culture.
● Diagnostic Testing
o Best initial test: urinalysis (either dipstick or microscopic)
 dipstick: positive for Nitrites and leukocyte esterase
 microscopic: Leukocyturia > 3‐5 WBC/hpf in men and
women
o Most accurate test: urine culture
 In patients with underlying urologic abnormalities, comorbidities,
immunocompromised, or poorly controlled diabetes mellitus, need to
be followed more closely.
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14.1.4 :Management plan

Table 14.1
Medication Dose pregnancy Category
first line
fosfomycin 3g single dose B
Nitrofurantoin 100 mg twice per day for five days B
trimethoprim/ 160/800 mg twice per day for three
C
sulfamethoxazole days
second line
Ciprofloxacin 250 mg twice per day for three days C
ciprofloxacin,
500 mg per day for three days C
extended- release
200 mg per day for three days or
Levofloxacin C
400 mg single dose
Third line
500/125 mg twice per day for seven
amoxicillin/clavulanate B
days
Cefdinir 300 mg twice per day for 10 days B
100 mg twice per day for seven
Cefpodoxime B
days
14.2. :Acute Complicated UTI / Pyelonephritis
14.2.1 :Definition
 Infection of the kidney/upper urinary tract.
14.2.2 Symptoms And physical exam:
 Usual presentation: urinary frequency, urgency, burning, and dysuria
as in cystitis with flank pain and tenderness in addition.
 More severe disease therefore, higher fever, patients are much more
ill, with chills, rigors, significant fatigue or malaise beyond the
baseline, or other features of systemic illness, vomiting, and
costovertebral angle tenderness.
14.2.3 :Investigation & monitoring
 Urinalysis and urine culture are preferred as in cystitis.
 sonography and CT scan are used to determine the etiology of a
urinary tract infection.
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14.2.4 :Management plan

 Oral outpatient treatm ent
o Quinolones (Ciprofloxacin 500 mg bid, Levofloxacin 750 mg qd)
o Cefixime (400 mg qd)
o Trimethoprim/sulfamethoxazole
o Augmentin
 Parenteral Inpatient therapy, quinolones, or ampicillin combined with
gentamicin.
o Ceftriaxone: 1 gm IV qd
o Quinolones: Ciprofloxacin 500 mg BID, Levofloxacin 750 mg QD
in IV doses
o Gentamicin +/‐ampicillin (or Unasyn if enterococcus suspected)
o Ertapenem
 Duration: 7–14 days total
 Switch from IV to PO when possible pending clinical improvement
 Patients with acute pyelonephritis and any of the following should be
admitted to the hospital for intravenous antibiotic treatment, and
possible urology consult:
o Concurrent urinary tract obstruction
o Failure of outpatient therapy or intolerance of oral antibiotics
o Pregnancy
o Sepsis
o Unstable coexisting medical conditions
14.3. :Asymptomatic bacteriuria
14.3.1 Definitions:
isolation of a specified quantitative count of bacteria (of ≥10^5cfu/ml) in
an appropriately collected urine specimen from an individual without
symptoms or signs of urinary tract infection.
 women: two consecutive clean-catch voided urine specimens with
isolation of the same organism in quantitative counts of ≥10^5 cfu/ml.
 men: single clean-catch voided urine specimen with isolation of a
single organism in quantitative counts of ≥10^5 cfu/ml in the absence
of symptoms.
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14.3.3 Management:
Indications for treatment of asymptomatic bacteriuria are:
 Pregnancy
 Patients undergoing urologic procedures in which mucosal bleeding is
anticipated.
Chapter 15: GASTRIC DISEASES

15.1. Dyspepsia:
15.1.1 Definition:
 defined by Rome IV criteria is predominant epigastric pain lasting for
at least one month.
15.1.2 Symptoms and physical examination:
 common: epigastric pain, heartburn, and/or regurgitation with mild
epigastric tenderness.
 risk factors: female, smoking, NSAIDS use.
15.1.3 :investigations
 patients with red flags must undergo endoscopy.
 initially test for helicobacter pylori (H. pylori) and treat if positive.
15.1.4 :Management
 initially test for helicobacter pylori (H. pylori) and treat if positive.
 If H. pylori test is negative or patient continues to have symptoms
after eradication, they may undergo a trial of proton pump inhibitors.
 Nonresponding patients may be offered prokinetic therapy or tricyclic
antidepressant therapy.
 Patients with Functional dyspepsia may benefit from psychotherapy if
no resolution.
15.2. Chronic gastritis and peptic ulcer disease:
15.2.1 Definition:
 inflammation of the gastric layer, if left untreated it may lead to
damage of the gastric layer progressing to peptic ulcer disease
(PUD).
 epigastric pain with possibility of having epigastric fullness, nausea,
vomiting, and heartburn. In addition, finding such as hematemesis,
melena, and/or hematochezia may strongly suggest PUD.
 risk factors include: previous history of PUD, H. pylori infection,
NSAID use, Steroid use, Smoking , Family history of ulcers
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15.2.3 :investigations
 Test for H.pylori with stool antigen, or urea breath
 CBC to rule out anemia
 Serum gastrin if recurrent ulcers
 Endoscopy is the gold standard
15.2.4 :Management
 Treat H. pylori if presen
 stop offending medication
 Proton pump inhibitors (PPI) 4–6 weeks for DU and 12 weeks for GU
 H2 blockers may be used instead but for a longer duration and higher
dosage.
 Surgical treatment may be necessary if complications present, or
malignancy arise.
15.3. NSAIDs induced ulcers:
15.3.1 risk factors:
 Age < 65
 High dose of NSAID
 Concomitant use of glucocorticoids, anti-coagulant, aspirin
 Prior history of uncomplicated ulcer
15.3.2 :assessment
 Low risk if patient has no risk factors.
 Moderate risk if patient has 1–2 risk factors.
 High risk if patient has >2 risk factors or history of previously
complicated ulcer
15.3.3 :prevention
Table 15.1
Cv Risk GI risk ACG Recommendations
Low Low NSAID
Moderate NSAID + PPI or misoprostol
High Alternative therapy, or COX-2 in. PPI/misoprostol +
High Low Naproxen + PPI/misoprostol
Moderate Naproxen + PPI/misoprostol
Avoid NSAID and COX-2 inhibitor; alternative
High
therapy
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15.4. Gastroparesis:
15.4.1 Definition:
 Gastric motility is decreased might be caused by Mechanical/outlet
obstruction or Functional obstruction (drugs, diseases, pregnancy )
 postprandial pain and early satiety.
15.4.3 investigations:
 clinical diagnosis, but scintigraphy may be done if needed.
15.4.4 :Management
 Stop offending medications and control causative disease.
 Small, low-fat meals
 Medications such as metoclopramide, erythromycin, and prokinetics
can help.
 Surgery may be needed if conservative and medical therapy fail.
15.5. Dumping syndrome:
 Nausea, vomiting, abdominal pain, sweating, and flushing in addition
to dyspepsia 15–30 minutes after eating.
 Usually clinical, but scintigraphy may be done if needed.
15.5.3 :Management
 Small, low carbohydrate meals
 Avoid excessive liquids
 Medications such as opiates, anticholinergics, and fiber are helpful
 Surgery if needed
15.6. Gastroesophageal Reflux Disease (GERD):
15.6.1 Definition:
 passage of stomach contents into the esophagus with or without
accompanied regurgitation and vomiting.
Typical:
 Heartburn
 acid regurgitation
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Atypical
 Wheezing, hoarseness
 Chronic cough
 Atypical chest pain
15.6.3 :Investigations
 Diagnosis is made usually through clinical suspicion, but 24-hour
monitoring may be performed if the patient is refractory to treatment.
Endoscopy is done for patients with alarming signs and symptoms.
15.6.4 :Management
 Conservative treatment is the first line therapy for GERD with
empirical PPI use once daily for 8 weeks.
 H2 blockers can be used alone in higher doses or in combination with
PPI if needed.
 Surgery may be needed in long-term GERD patients, not
recommended in patients not responding to PPI.
15.7. :Barrett’s esophagus
15.7.1 :Risk factors
 Male sex
 Ager >50
 Central obesity
 Hiatal hernia
 Caucasian
 Smoking
 Family history of BE or esophageal carcinoma
screening Should be performed in patients with chronic and/or frequent
gastroesophageal symptoms.
 Men with ≥ 2 risk factors
 Women with multiple factors
Diagnosed by endoscopy
15.8. :Upper GI malignancies
15.8.1 :Gastric cancer
 Most common of GI tumors
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symptoms
 Older age >55
 Smokers
 Early satiety
 Anemia
 Hematemesis, melena or hematochezia
 Weight loss
 Personal or family history of GI cancer
Diagnosis
 By endoscopy
Management :
 surgical resection
15.8.2 :Esophageal Tumor
:Red flags
 Age >55
 Dysphagia
 Choking
 Odynophagia
 Hoarseness
 Chronic cough
 Early satiety
 Hematemesis
 Hematochezia
 Melena
 Anemia
 Weight loss
 Personal or family history of peptic ulcer disease or GI cancer
Diagnosis:
 by Endoscopy
Management:
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15.9. Pancreatic cancer:

 Abdominal pain
 Weight loss
 Jaundice
 Abdominal mass
 Ascites
15.9.2 :Investigations
 Ultrasound
 Endoscopic ultrasound
 CT
 MRI
 ERCP
 FNA
 CA 19-9
15.9.3 :Management
Chapter 16: STROKE AND TRANSIENT
ISCHEMIC ATTACKS (TIA)
16.1. Stroke:
16.1.1 Types of stroke:
 Ischemic Stroke: 85% of cases, Thrombotic stroke (most common)
Embolic stroke, Lacunar stroke (least common).
 Hemorrhagic stroke: 15% of cases Intracerebral Hemorrhage and
Subarachnoid Hemorrhage.
 Non-modifiable risk factors: Age > 65, Ethnicity (African American
or Hispanic race), Family history of stroke or hyperlipidemia.
 Modifiable risk factors: Hypertension (most common), DM, AF,
hyperlipidemia, hypothyroidism, obesity, sedentary lifestyle, coronary
artery disease, increased apolipoprotein-a, OSA, migraine with aura,
cigarette smoking.
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16.1.3 Acute stroke:

 Ischemic Stroke: awakening with acute onset of symptoms including
unilateral body weakness and speech disturbance.
 Hemorrhagic stroke: Causes: Hypertension, Neoplasm,
Anticoagulant use, Trauma, Alcohol abuse, Infection
Brain aneurysm rupture, Amyloid angiopathy
 Subarachnoid Hemorrhage (SAH): Caused by a ruptured
aneurysm, manifested by a severe headache that starts suddenly
(worst headache in his/her life).
16.1.4 Assessment:
History:
Mnemonic (LOST MIND) for history: Last well, Onset, Seizure, Trauma,
Migraine, Illness Neck injury, Diabetes mellitus.
Findings Suggestive of Ischemic Stroke
Symptoms: Acute onset of focal neurologic deficit, Subjective arm, or leg
weakness
Subjective speech disturbance, Subjective facial weakness.
Signs: Arm or leg paresis, Dysphagia or dysarthria, Hemiparesis or
ataxia, Facial paresis Eye movements or visual fields abnormalities.
16.1.5 Investigation and imaging:
 Neuroimaging is necessary to differentiate between ischemic and
hemorrhagic stroke (non-contrast brain CT or brain MRI)
 If subarachnoid hemorrhage is suspected, non-contrast head CT
scan should be done before performing lumbar puncture (LP)
 Blood tests including CBC, BG, RFT and electrolytes, PT, aPTT, and
INR. ECG
Page | 164
16.1.6 Acute stroke management:
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16.1.7 Post stroke management:

Prevention of medical complications:
Venous thromboembolism (VTE), Pressure sores, Infection such as
aspiration pneumonia, Delirium, Depression.
16.2. Transient Ischemic Attack (TIA):
TIA is defined as a transient episode of neurologic dysfunction caused by
focal brain, spinal cord, or retinal ischemia, without acute infarction.
16.2.1 Differential diagnosis:
Structural brain lesion (tumor, hemorrhage, AVM, aneurysm), Infection
(focal abscess, septic emboli), Seizure/Todd’s paralysis, Complicated
migraine, Hypoglycemia, Syncope from any cause (especially
arrhythmia), Labyrinthine disorders, Temporal arteritis, Multiple sclerosis
(flare), Neck pain and TIA symptoms consider: Carotid dissection, Atrial
fibrillation Severe carotid stenosis.
16.2.2 Assessment:
History:
Obtain history from witnesses who observed the episode, The timing,
and resolution of symptoms, Common symptoms are sudden
transient, including unilateral paralysis, speech disturbance, and
monocular blindness, Evaluate TIA risk factors (hypertension, diabetes,
smoking, obesity), TIA mimics.
Physical Examination:
Vital signs, Assess for carotid bruit, atrial fibrillation, and heart murmur.
Funduscopic examination and neurologic examination.
Cranial nerve examination: Diplopia, unilateral blindness, facial drooping,
hemianopia, deconjugate gaze, lateral tongue movement
Cerebellar examination: Ataxia, nystagmus
Investigations and Imaging:
Neuroimaging should be done immediately (MRI is more sensitive than
CT).
Routine tests for all patients with suspected stroke: CBC, BG, fasting
lipid electrolytes, RFT, ESR, and/or C-reactive protein, and ECG.
Selected patients may require additional tests: catheter angiography,
chest radiography, syphilis serology, vasculitis screening, and
prothrombotic screen.
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16.2.3 Management:
For most patients with TIA Start Aspirin (162 to 325 mg/daily) alone for
low-risk TIA, defined by an ABCD2 score <4 ,For high-risk TIA, defined
as an ABCD2 score of ≥4, start dual antiplatelet therapy Aspirin (162 to
325 mg loading dose, followed by 50 to 100 mg daily) plus Clopidogrel
(300 to 600 mg loading dose, followed by 75 mg daily) for the first 21
days.
ABCD2 score to calculate a patient’s short-term risk of developing
stroke:
 1 point age > 65, 1 point BP SPB > 140 or DBP > 90, 2 points for
unilateral weakness
 1 point speech impairment without weakness, 2-point duration of
symptoms > 60 minutes
 1 point 10- 59 minutes, 1 point for diabetes.
16.3. Primary Prevention of stroke/ TIA:
 Hypertension: annual screening in pre-hypertensive patients, treat if
blood pressure >140/90 mmHg to keep readings below this target
 Atrial fibrillation: start oral anticoagulant therapy if CHA 2DS2-VASc
score ≥ 2.
 Diabetes: screen for diabetes.
 Lipids: If 10-year-ASCVD risk >20%, start high-intensity statin
therapy.
 smoking cessation, weight reduction and Physical activity.
 Aspirin: start aspirin if the calculated 10-year-ASCVD risk > 10%
depending on the patient age
 Alcohol: ≤ 2 drinks/day for men and ≤ 1 drink/day for women might be
reasonable.
Chapter 17: OSTEOPOROSIS
Osteoporosis is a disease characterized by low bone mass, resulting in
decreased bone strength and increased risk of fracture.
Fragility fractures are defined as fractures that occur with low or minimal
trauma. The most common sites are the spine (vertebral compression
fractures), hip, and wrist, humerus, rib, and pelvis.
17.1. Risk factors:
Age (post-menopausal for female, >70 in males), Female sex, (BMI)<20
kg/m2, Smoking, Alcohol use ≥3 drinks per day, White or Asian race, Low
dietary calcium, Prior fragile fracture as adult, Parental history of hip
fracture, Physical inactivity, 10% decrease in weight.
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17.2. Evaluation:
All postmenopausal women age ≥50 years of age should undergo clinical
assessment for osteoporosis and detailed history, physical exam, and
clinical fracture risk assessment with the Fracture Risk Assessment tool
(FRAX®).
17.3. History:
 Ask about the risk factors above.
 Falls in the past 12 months.
 High-risk medical conditions: Rheumatoid arthritis, primary
hyperparathyroidism, type 1 diabetes, osteogenesis imperfecta,
uncontrolled hyperthyroidism, Cushing’s disease, chronic malnutrition
or malabsorption, chronic inflammatory conditions (e.g., inflammatory
bowel disease)
 Medications such as glucocorticoids (use >3 month), Tamoxifen,
antidiabetic agents; thiazolidinedione (Actos) SGLT-2 inhibitors
(Empagliflozin), Methotrexate, PPI, SSRI, antiepileptic, heparin.
17.4. Examination:
 Height loss, Kyphosis (increased risk of vertebral fracture).
 weight
 Balance and gait (Get up and Go Test).
 CBC, calcium, phosphate, LFTs, creatinine, and electrolytes, 25-
hydroxyvitamin D, TSH.
 X-ray lateral thoracolumbar
 Evaluation for causes of secondary osteoporosis: PTH, SPE.
Testosterone, Antibodies associated with gluten enteropathy,
prolactin, 24-H urine calcium.
Bone mass density measurement method:
Dual-energy x-ray absorptiometry (DXA) Mostly used method.
 Osteoporosis based on DXA:
 Normal: T-score > -1.0 SD, Osteopenia: T-score < -1 and > -2.5 SD
 Osteoporosis: T-score < -2.5 SD, Severe osteoporosis: more than
2.5 SD in the presence of one or more fragility fractures.
Page | 168
17.6. Screening:
 By age All Saudi women above 60 years, and men above 65 years.
 Menopausal women and men aged 50-64 years with clinical risk
factors for fracture.
 All women ≥40 years who have sustained a low-trauma fragility
fracture. Hypogonadism or premature menopause, prolonged
secondary amenorrhea (>1 year).
 X-ray findings suggestive of osteoporosis.
17.7. Prevention:
 sun exposure.
 Advice on dietary vitamin D and calcium intake All patients should
have normal serum ca and vit D levels prior to starting therapy.
 If diet fails, 1000 mg/d of ca for women 19 to 59 of age, men 19 to 70
of age.
 1200 mg/d of ca for women > 50 and men > 70.
 Smoking cessation.
 weight-bearing physical activity.
Page | 169
17.8. Treatment:
17.8.1 Pharmacological treatment:

 Alendronate 70 MG/week, should be taken at morning before food,
take with 8 oz of water and remain upright for 30 mins.
 Side effects:
o Hypocalcemia
o atypical fracture of the femur
o osteonecrosis of the jaw.
Page | 170
 Contraindicated:
o active esophageal abnormalities or peptic ulcer disease. And the
inability to remain upright.
o pregnancy
o creatinine clearance below 30 mL/min.
 Zoledronate 5 mg iv once yearly
 Side effects:
o Hypersensitivity,
o flu-like reaction,
o risk of atypical fracture,
o ONJ,
o atrial fibrillation.
o in pregnancy,
o women who plan to be pregnant,
o creatinine clearance below 30 mL/min.
 Denosumab 60 mg SC every six months.
 Side effects:
o Eczema,
o cellulitis,
o low calcium.
o In pregnancy,
o women who plan to be pregnant,
o risk of atypical fracture,
o ONJ.
 Raloxifene 60 mg/d oral (stop in periods of prolonged
immobilization).
 Side effects:
o Premenopausal women worsening of hot flashes,
o leg cramps,
o increase risk of DVT.
 Teriparatide 20mcg/d SC
 Abaloparatide 80 mcg/d SC
 Potential for osteosarcoma (animal studies), hypocalcemia, nausea,
vomiting, injection site reaction.
 Calcitonin 200 IU intranasally once daily, 100 IU SC every other day.
Drug holiday after five years of oral bisphosphonate and three years after
IV bisphosphonate.
Page | 171
17.9. Follow up:

Annually reassess Risk factors for falls and fractures, Treatment
compliance, Calcium and vitamin D intake, Medications, Height,
Secondary causes of osteoporosis.
Chapter 18: SEXUALLY TRANSMITTED
INFECTIONS
18.1. Background:
 STIs are caused by different microorganisms, bacteria, viruses and
others.
 If left undiagnosed and untreated, STIs may lead to severe
complications such as PID, infertility, ectopic pregnancy, congenital
infections and cancer.
 All STDs have subclinical or latent periods and patients may be
asymptomatic.
 All patients who seek STD testing should be screened for syphilis and
HIV.
 Partner notification and treatment are important to prevent further
transmission and reinfection.
 Respect, compassion, and a non-judgmental attitude toward
everyone, are essential for obtaining a sexual hx, below is the 5P’s
approach to obtain sexual hx.
Table 18.1
1/ Are you currently having sex of any kind?
Partners
2/ What is the gender(s) of your partner(s)?
1/ To understand your risks for STIs, I need to ask more about the
kind of sex you have had recently.
Practices
2/ What kind of sexual contact do you have, or have you had?
3/ Do you have vaginal sex? Or anal sex?
1/ Do you and your partner(s) discuss prevention of STIs and HIV?
Protection
Or discuss getting tested?
from STIs
2/ What protection methods do you use? Do you use condoms?
1/ Have you ever been tested for STIs and HIV? Or diagnosed with
Past history
an STI?
of STIs
3/ Have any of your partners had an STI?
1/ Are you using contraception or practicing any form of birth
Pregnancy
control?
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USPSTF recommendations for behavioral counseling STI

screening
Table 18.2
Provide  All sexually active adolescents
counseling for:  Adults who are at increased risk of STIs
Screen for  Sexually active adolescents and adults 24 years and
chlamydia and younger
gonorrhea In:  All pregnant women 24 years and younger
 Older women who are at increased risk of infection
Screen for HBV  Patients at increased risk of infection
infection in:  pregnant women at their first prenatal visit
Screen for HIV  Adolescents and adults 15 to 65 years of age
infection in:  all pregnant women: including those who present in labor
and whose HIV status is unknown
Screen for  patients at increased risk of infection
syphilis in:  all pregnant women
18.1.1 Prevention of STIs in Women:
 vaccines for: HPV, HepB and HepA.
 Screening for: chlamydia, gonorrhea, HIV, HepB, HepC and Syphilis.
 Other: Male condom.
18.2. Chlamydia Infection:
18.2.1 Chlamydia infection in females:
 majority of infected females are asymptomatic.
 Cervicitis: if symptomatic, Sx mimic vaginitis with abnormal vaginal
discharge, intermenstrual vaginal bleeding, and post-coital bleeding.
 Urethritis: may complain Sx of UTI such as, frequency and dysuria,
and may be misdiagnosed as cystitis unless C. trachomatis is
detected.
 PID: abdominal and pelvic pain, in presence of chlamydial infection
Signs of PID: include cervical motion and uterine or adnexal
tenderness.
PID due to C. trachomatis is ass. with ↑ rates of tubal infertility,
ectopic pregnancy and chronic pelvic pain when compared with PID
caused by gonorrhea.
 Proctitis: Females can have rectal infection with chlamydia (Anal sex).
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18.2.2 Chlamydia infection in males:

 The major rationale for chlamydia and gonorrhea screening among
men is to reduce infection or reinfection of existing partners and
transmission to new partners.
 Urethritis Sx: mucoid or watery urethral discharge and dysuria.
 Epididymitis Sx: unilateral testicular pain and tenderness, hydrocele,
and palpable swelling of the epididymis.
 Prostatitis Sx: dysuria, urinary dysfunction, pain with ejaculation, and
pelvic pain.
 Proctitis: Occurs in men who have sex with men (MSM) as a
receptive anal intercourse.
18.2.3 Diagnosis of chlamydia infections:
 Nucleic Acid Amplification Testing (NAAT) is the test of choice.
 Preferred specimens for testing:
o Females: vaginal swab, first-catch urine is also acceptable
o Males: first-catch urine is the specimen of choice
o Rectal infection: rectal swab
18.2.4 Treatment approach:
 Active antimicrobial therapy
o Primary:
 Doxycycline 100 mg PO BID x 7 days. (Contraindicated in
pregnancy)
 Or Azithromycin 1 g PO single dose. (Preferred in
pregnancy)
o Alternatives:
 Erythromycin base 500mg PO QID x 7 days.
 Or Erythromycin ethylsuccinate 800 mg PO QID x 7 days.
 Or Levofloxacin 500 mg PO OD x 7 days.
 Or Ofloxacin 300 mg PO BID x 7 days.
 Empiric Tx for concomitant gonococcal infection with Ceftiraxone
dose based on weight. in case of hypersensitivity to cephalosporin:
high dose azithromycin with gentamicin.
 Testing for other STIs, Discussing the need for HIV testing.
 Counseling on abstinence for 1 week following Tx, And Treatment of
sexual partners.
 Counseling to return for persistent or recurrent Sx.
 Case report to health authority.
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18.3. Gonorrhea Infection:

18.3.1 Urogenital gonococcal infections in females:
 Cervicitis: MC site of infection, mostly asymptomatic. If symptomatic:
vaginal pruritus and/or a mucopurulent discharge, postcoital bleeding,
abdominal pain, dyspareunia. O/E: inguinal lymphadenopathy.
Cervical exam: cervix may be friable and easy to bleed by swab, it
may appear normal, or show signs of frank discharge.
 Urethritis: asymptomatic, or dysuria, frequency and urgency,
mimicking acute cystitis. Urethral exam may show mucopurulent
discharge.
 Pelvic Inflammatory disease (PID): is a serious complication include
salpingitis, pelvic peritonitis, and pelvic abscesses. Half of PID cases
are caused by untreated N. Gonorrhea. Sx include: pelvic/abdominal
pain, abnormal vaginal bleeding, and dyspareunia. O/E: T ≥ 38.3,
cervical motion tenderness, uterine or adnexal tenderness, cervical or
vaginal mucopurulent discharge may be seen.Women with PID may
develop infertility due to significant tubal scarring. Gonococcal
infection that leads to PID may be associated with Fitz-Hugh-Curtis
Syndrome.Sx include sharp RUQ pain, nausea, vomiting, fever, and
mild or slightly LFTs.
 Bartholinitis: S&S include perilabial pain and discharge, labia
swelling, and tenderness.
18.3.2 Urogenital gonococcal infections in pregnancy:
 chorioamnionitis, premature rupture of membranes, preterm birth
(PROM), preterm birth, , low birth weight or small for gestational age
infants, spontaneous abortions.
 Infants born to untreated mothers may have neonatal conjunctivitis,
pharyngitis, arthritis, and gonococcemia.
18.3.3 Urogenital gonococcal infections in males:
 Urethritis: mostly symptomatic, discharge and dysurea. The discharge
is present at the urethral meatus, purulent or mucopurulent in color,
and copious in amount. Genital exam: purulent, yellow-green urethral
discharge, and an inflamed meatus.
 Epididymitis: Its more commonlydue to C. trachomatis but, can be of
gonococcal infection.
 Sx: gradual onset unilateral scrotal pain and swelling, dysuria,
frequency, urgency, fever.
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18.3.4 Extragenital gonorrhea infections:

 Proctitis: Occurs in men who have sex with men as a receptive anal
intercourse.Most are asymptomatic, if symptomatic: anorectal pain or
itching, cloudy rectal discharge, constipation, and anal bleeding. O/E:
proctoscope may show erythema or purulent exudate on the rectal
wall.
 Pharyngitis: transmitted via oral sex, majority are asymptomatic,
some may present with sore throat, pharyngeal exudates, or cervical
lymphadenitis.
 Disseminated gonococcal infection: occur in 0.5–3% of infected
patients. mainly as arthritis-dermatitis syndrome: fever, migratory pain
or joint swelling, and pustular skin lesions. Rare: may lead to
endocarditis, meningitis, and osteomyelitis.
 Conjunctivitis: mainly affects infants born to untreated mothers from
exposure to infected cervical secretions during delivery. In adults and
adolescents, due to autoinoculation. Sx range from mild to
aggressive: conjunctival redness, purulent discharge and periorbital
edema, if untreated can progress to corneal ulceration, perforation,
and blindness.
18.3.5 Diagnosis in symptomatic patients:
 Typically diagnosed clinically by history and PE. Treatment of N.
gonorrhea urogenital infection is empiric before results of diagnostic
tests are available.
 Nucleic Acid Amplification Testing (NAAT) is the test of choice for
initial diagnosis.
o Urogenital gonorrhea: (first-catch urine for men and vaginal swab
for women).
o Extragenital infections: pharyngeal and rectal swabs.
 In men, urethral swab for microscopic evaluation of urethritis shows
polymorphonuclear leukocytes with intracellular gram-ve diplococci on
gram stain.Is enough to establish the diagnosis of N. gonorrhea.
 Testing for co-infections, specifically C. trachomatis.
 Diagnostic testing for urogenital gonorrhea in asymptomatic patients
is the same (i.e., NAAT of first-catch urine for men and vaginal swab
for women).
 Routine screening for oropharyngeal and rectal gonorrhea is
warranted in MSM.
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18.3.6 Treatment:
 Gonorrhea should be reported to public health authorities after
confirmation.
 patients should receive empirical treatment.
 Recommended regimen if chlamydia infection has been excluded.
o Weight <150 kg: Ceftriaxone 500 mg IM once
o Weight ≥150 kg: Ceftriaxone 1 g IM once
 Recommended regimen if chlamydia Infection has not been excluded.
o Ceftiraxone dose based on weight + Doxycycline 100 mg PO BID
x 7 days.
o Pregnancy: Ceftiraxone dose based on weight + azithromycin 1 g
as a single dose.
 Alternative regimen if ceftriaxone is not available.
o Gentamicin 240 mg IM as a single dose + azithromycin 2 g PO
as a single dose
o or Cefixime 800 mg PO as a single dose
 Abstain from sexual activity for 7 days after treatment and until all sex
partners have completed 7 days of treatment and resolution of
symptoms if present.
 All pts diagnosed with gonorrhea should be tested for other STIs such
as chlamydia, syphilis, and HIV.
 Screening for viral hepatitis may also be warranted.
18.4. Syphilis Infection:
18.4.1 Background:
 Can be transmitted sexually or congenitally from mothers to fetus
through placenta.
 With diverse clinical manifestations depending on the stage of
infection.
18.4.2 Screening:
 Should be performed using rapid plasma reagin (RPR) test or VDRL
test.
 USPSTF 2016 recommends against screening patients not at
increased risk.
 All pregnants at 1st prenatal visit; in patients at high risk, repeat
testing in 3rd trimester and at delivery.
 Patients visiting STD clinics.
 Men who have sex with men (MSM) and engage in high-risk
behaviors.
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 Patients with HIV infection.

 Any patient with aortic insufficiency or thoracic aortic aneurysm.
18.4.3 Clinical Presentation:
● History: Obtain a thorough sexual hx, time course of symptoms for
proper staging. In children and infants: maternal hx, hx of exposure
to syphilis and sexual abuse or Blood products.
Table 18.3 - Historical findings of syphilis according to classification

Painless ulcer at the inoculation site (chancre), MC in the
Primary syphilis anogenital region that presents at 21 days after exposure and
persists for 1-3 wks.
Secondary – Patient may or may not recall a chancre.
syphilis – May remain completely asymptomatic.
– Generalized skin rash of trunk and extremities, including
symptoms 2-8 palms and soles (occurring simultaneously).
wks. after – Systemic Sx may occur fever, fatigue, malaise, anorexia, and
chancre weight loss.
resolution – May presents with nausea, vomiting, and abdominal pain.
– Myalgia and arthralgia.
– Headache may be a symptom of neurosyphilis.
Latent syphilis Asymptomatic.
not transmissible sexually but can transmit in utero
Tertiary syphilis Neurosyphilis
● Syphilitic meningitis.
significant organ ● Meningovascular syphilis Sx: vision changes (loss of
damage: peripheral vision) and hearing loss.
● Late neurosyphilis (parenchymatous disease) Sx: decline in
1-20 yrs. after
cognitive function, personality change, painful paresthesias,
infection
and gait disturbance.
Not sexually Cardiovascular syphilis: chest pain or dyspnea.
transmissible. Gummatous syphilis: unusual scarring on the skin, abdominal
pain, or changes in the nasal septum and palate.
Painless ulcer at the inoculation site (chancre), MC in the
Primary syphilis anogenital region that presents at 21 days after exposure and
persists for 1-3 wks.
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Table 18.4 - Physical examination of syphilis according to classification
Primary chancre is usually a single lesion, Papule is indurated.
syphilis Gradually becomes ulcerated and clean based with firm borders. Mostly
seen in the perineum, cervix, anogenital area, lips, oropharynx, and
hands. Easy to miss if in vagina.
Secondary Skin and mucous membranes
syphilis  Maculopapular erythematous rash that involves the trunk and
extremities, including palms and soles.
Lymphadenopathy is generalized.
Hepatosplenomegaly may be present
Tertiary Cardiovascular syphilis
syphilis  Diastolic murmur d.t. aortic regurgitation
 Displaced cardiac apex d.t. cardiomegaly.
 Rales d.t. CHF with pulmonary edema
Gummatous disease
 Atrophic scarring of skin
 Flattened or perforated nasal septum.
 Perforation of palate
Neurosyphilis
 Altered mental status, Meningismus, Aphasia or slurred speech,
Ocular syphilis.
 Signs of iridocyclitis with Argyll Robertson pupils
(pupils that constrict upon accommodation but fail to constrict to
bright light)
 Episcleritis, Retinitis, Retinal detachment.
Hemiparesis or hemiplegia
Peripheral neuropathy
Tabes dorsalis (wide-based ataxic gait with foot slap)
 Initial is Nontreponemal serologic tests: (VDRL test, or RPR test).
 If +ve confirm with Trponemal serologic tests: (TPPA test, or FTA-
ABS).
 Definitive diagnosis is by observing T. pallidum on dark field
microscopy, Or by PCR but often are not readily available.
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18.4.6 Management:
 The treatment of choice for all stages of syphilis is parenteral
penicillin G.
 Treatment of choice for primary, secondary, and early latent syphilis
is. single-dose IM benzathine penicillin G
 Treat late latent syphilis and tertiary syphilis with
IM benzathine penicillin G once/week for 3 weeks
 In pregnancy, it is recommend a 2-dose regimen for patients with
primary, secondary, or early latent infection.
o Benzathine penicillin G, 2.4 million units weekly for 2 doses
o Penicillin-allergic patients: desensitize and give penicillin.
 Jarisch-Herxheimer reaction: Acute febrile reaction that occurs in the
first 24 hrs. after treatment, anticipate it and provide guidance on Sx
management to patients prior Tx.
o Symptoms include fever and chills, myalgia, headache.
18.4.7 Prevention:
 There is no vaccine for syphilis.
 Safe sex practices reduce the risk of sexually transmitted syphilis.
 Screening of all pregnant patients, offering treatment, and confirming
treatment effect reduces the risk of congenital syphilis.
18.5. HIV and AIDS:
18.5.1 Background:
 HIV is a retrovirus infection to human lymphocytes and macrophages,
eroding the integrity of human immune system over years. Which
leads to susceptibility to a series of opportunistic infections as well as
the development of certain malignancies.
18.5.2 HIV Transmission:
 Sexual transmission, including via heterosexual and homosexual
contact.
 Parenteral transmission, predominantly among injection drug users
(IDU)
 Perinatal transmission
18.5.3 HIV Stages:
If people with HIV don’t get treatment, they typically progress through
three stages:
 Stage 1: acute HIV infection
 Stage 2: chronic HIV infection
 Stage 3: acquired immunodeficiency syndrome (AIDS)
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18.5.4 Acute HIV infection:

 Early HIV infection is a period of rapid viral replication with very high
viral RNA levels.Sx of acute HIV infection: Fever, lymphadenopathy,
sore throat, oral thrush, rash, headache, myalgia, arthralgia, or
asymptomatic.
18.5.5 Chronic HIV infection:
 It’s called asymptomatic HIV infection or clinical latency. HIV is still
active but reproduces at very low levels. The infected individual
remains well with no evidence of the disease and may only have
generalized lymphadenopathy on the exam.
 HIV is transmissible in this phase. In ten years, if left untreated 50%
will have AIDS.
 CD4 count below 500 but more than 200 cells/microL.
18.5.6 Acquired immunodeficiency syndrome (AIDS):
 AIDS is the outcome of chronic HIV infection and consequent
depletion of CD4 cells.
 It is defined as a CD4 cell count <200 cells/microL or the presence of
any AIDS-defining condition regardless of the CD4 cell count.
 Advanced HIV infection occurs when the CD4 cell count is <50
cells/microL.
 AIDS-defining conditions: P. jirovecii pneumonia (most common),
Wasting, Esophageal candidiasis, , Kaposi’s Sarcoma, Tuberculosis,
Mycobacterium avium, CMV, HIV associated dementia, Recurrent
pneumonia.
18.5.7 Assessment:
HIV screening and testing in primary care
 All patients 15-65 yrs. old at least once.
 Reasonable to re-screen at-risk patients at a 1-yr interval:
o Engage in high-risk behaviors.
o Live in or receive medical care in high prevalence settings, (e.g.,
correctional facilities, homeless shelters, TB clinics, STI clinics,
and clinics that serve men who have sex with men MSM).
 All pregnant patients, including in labor whose HIV status is unknown.
 All patients for pre-and post-exposure prophylaxis.
 People with recent exposure hx and Sx of recent viral infection.
(acute HIV infection).
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 People with risk or exposure hx and Sx of chronic untreated HIV

including weight loss, and undiagnosed opportunistic infections and.
(chronic HIV infection).
Screening
 For routine screening of HIV:
o 4th gen. ELISA that detects IgM and IgG antibodies and p24
antigen.
o If ELISA +ve, confirmatory tests using HIV-1/HIV-2 differentiation
immunoassay.
o If HIV-1 and HIV-2 both are -ve or indeterminate, RNA viral load
should be done.
 For Discrete Exposure to HIV:
o The most diagnostic tests: HIV viral load test (RT-PCR-based
viral load test).
o Followed by antigen/antibody immunoassay test (4 th gen.
ELISA).
Baseline investigations
CD4, HIV RNA, and resistance test, Pregnancy test, CBC with diff.,
LFTs, Elect., S-Cr. And eGFR, UA for proteinuria, Lipid profile, Blood
sugar, HepA,B,C serology, Varicella Ab, STDs (gonorrhea, chlamydia,
syphilis), Toxoplasma serology (IgG), Pap smear at diagnosis and at 6
mths then yearly, TB skin test and CXR.
Subsequent investigations
 CD4, HIV RNA every 3-4 months
 Yearly PPD, lipid profile, fasting glucose, UA, and STD screening if at
risk.
Other important tests
 Serum HIV DNA PCR
o For diagnosis of HIV, especially during the window period
 CD4 count
o Indicates immune status and assists in the staging process.
o CD4 >500 cells/ mL: patients are usually asymptomatic.
o CD4 <350 cells/mL implies substantial immune suppression
o CD4 <200 cells/ml defines AIDS, high risk of most opportunistic
infections.
o CD4 <50 cells/ml: advanced HIV infection
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18.5.9 Management:
Giving results: HIV positive
 Must give results confidentially in person with Brief HIV education.
 Partner notification (screen for domestic violence)
 Linkage to care: confirm contact information and insurance status.
 All new diagnoses must be reported to local/state health authorities.
Goals of treatment
 Reduce HIV-associated morbidity and prolong duration and quality of
survival.
 Restoration of immune function (CD4 count)
 Prevention HIV transmission: ART → 96% reduction in sexual and
vertical transmission
 To keep the viral load to an undetectable level, usually takes 6 mths.
 Start with a combination of 3 antiviral drugs from 2 or more drug
classes.
Prophylactic antimicrobial agents
 P. jiroveci prophylaxis: (TMP-SMX) if CD4 <200 cells/mm3.
 M. tuberculosis: Treat for latent TB if +ve PPD with -ve CXR, or recent
TB contact.
 Toxoplasma gondii prophylaxis: TMP-SMX 1 DS tab daily.
 M. avium complex prophylaxis: Azithromycin 1,200 mg PO.
Patient monitoring
 HIV RNA (viral load) 2- 8 wks. after starting therapy and repeat every
3-6 mths until suppressed.
 HIV RNA, CD4, and CBC every 3-4 mths for first 2 years of ART or if
CD4<300 cells/mm3
 Space CD4 monitoring to 12 mths if suppressed viral load and CD4
>300 cells/mm3.
 Annual HIV RNA and CD4 count once viral load undetectable and
stable.
 Once viral load has been suppressed consistently for >2 yrs. and
CD4 cell counts are consistently >500/μL, monitoring CD4 cell counts
is optional unless virologic failure.
 Confirm HIV-1 RNA level is >50 copies/mL within 4 wks. of medication
management.
 Annual fasting lipids and fasting glucose; basic metabolic panel, LFTs
every 6 to 12 mths.
 Hepatitis C as clinically indicated
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 Annual cervical cytology (regardless of age) until 3 -ve screens and

then every 3 yrs.
 Pregnancy test in women of childbearing age.
 UA every 6 - 12 months or as clinically indicated .
Immunizations for adults with HIV
Note: Adults with a CD4 count < 200 cells per μL should not receive live
vaccines
 HepA, HepB, Herpes Zoster, HPV, Influenza (inactivated only), MCV,
PCV, Tdap.
Chapter 19: HEPATIC DISORDER
19.1. Elevated Liver Enzymes:
19.1.1 Liver Enzymes:
ALT, AST, ALP, and bilirubin are biochemical markers of liver injury.
Albumin, bilirubin, and PT are hepatocellular function markers.
Reference ranges: vary based on lab and reference population selected.
Risk Factors: Alcohol abuse, IV drug abuse, Blood product transfusions,
Polypharmacy, Illicit drug use, Herbal supplement use, Obesity,
Diabetes, Hyperlipidemia
19.1.2 Etiology:
 Common: Non-alcoholic fatty liver disease (NAFLD), Alcoholic liver
disease.
 Uncommon: Medications, HBV, HCV, Hereditary hemochromatosis.
 Rare: Alpha1- antitrypsin deficiency, Autoimmune hepatitis, Wilson’s
disease.
 Extrahepatic cholestasis: Choledocholithiasis, Biliary strictures,
Malignant obstruction, Infections such as AIDS.
 Intrahepatic cholestasis: Drug associated with cholestasis, Primary
biliary cholangitis, Primary sclerosing cholangitis, Intrahepatic
cholestasis of pregnancy,TPN, Infiltrative diseases: (amyloidosis,
lymphoma, sarcoidosis, TB), Hepatitis: viral, alcoholic, cirrhosis
 Non-hepatic/physiologic causes: Physiologic (children and
adolescents), 3rd trimester of pregnancy, Influx of intestinal ALP after
eating a fatty meal.
19.1.3 Assessment:
 Most patients with abnormal LFTs are asymptomatic, abnormalities
found incidentally.
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19.1.4 History:
 Focused on chronic or autoimmune disease that can cause liver
disease and risk factors as well as, medication history.
 Medication ↑ liver enzymes:
o Antihypertensives: Lisinopril, Losartan
o Pain relievers and anti-inflammatories: Acetaminophen,
Allopurinol, Aspirin, NSAIDs.
o Antimicrobials: CiprofloxacinIsoniazid, Ketoconazole,
Pyrazinamide, Rifampin, Tetracycline.
o Psychiatric: Bupropion, Risperidone, SSRI, Trazodone, Valproic
acid.
o Chemotherapy: Imatinib, Methotrexate
o Others: Acarbose, Amiodarone, Baclofen, Herbal and dietary
supplements, Omeprazole, Statins.
 Focused on signs of chronic liver disease or hepatic decompensation:
hepatomegaly, ascites, edema, palmar erythema, telangiectasias,
jaundice, and scleral icterus.
 Pattern of LFTs may suggest whether the underlying cause of liver
disease is primarily:
o Hepatocellular pattern (↑ ALT,AST)
o Cholestatic pattern (↑ALP)
o Isolated hyperbilirubinemia (↑ bilirubin) .
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19.1.7 Management:
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Page | 187
When to refer to a specialist?

 patients with unexplained, persistent liver biochemical test elevations
(≥2x ULN for ALT and AST or 1.5x ULN for ALP)
 patients who are considered for liver biopsy.
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19.2. Viral Hepatitis: Hepatitis A:

19.2.1 Background:
HAV is an RNA virus. Transmitted by fecal-oral route or contaminated
food or water.
Incubation period is 28 days. cause acute, self-limited disease of the liver
that does not result in chronic infection or chronic liver disease.
Fulminant hepatic failure occurs in less than 1% of cases. Infection
confers lifelong immunity and is preventable by vaccination.
19.2.2 Assessment:
 Clinical features:
o < 6 yrs. old 70% asymptomatic.
o In adults and children > 6 yrs old flu-like Sx (fatigue, fever,
anorexia, nausea, vomiting, RUQ abdominal pain, and
headache) progressing to more specific Sx (jaundice, dark urine,
and pale stools).
o physical exam findings are jaundice (40-80%) and hepatomegaly
(80%).
 Investigations:
o Anti-HAV IgM antibody is required for diagnosis.
o It is detectible 5 days before onset of Sx and remains +ve for
more than 6 mths.
o IgG anti-HAV provides lifelong immunity.
o markedly ↑ AST and ALT (>1000 U/L, usually ALT>AST), ↑ ALP,
and ↑ direct and total bilirubin (5-40 mg/dL)
o Check hepatitis B and C serology is needed to R/O acute
infection.
o Patients who present with severe illness need to have additional
tests like CBC, PT, PTT, albumin, electrolytes, and glucose.
19.2.3 Management:
 Self-limited; rest and rehydration; hospitalization is required in 20% to
30% of patients with severe Sx such as vomiting, dehydration, and
signs of hepatic decompensation.
 In the case of fulminant liver failure, liver transplant may be required.
 Follow ALT/AST every 1–2 weeks until levels normalize (4–12
weeks).
Page | 189
19.2.4 Prevention:
 Routine vaccine (1st dose and 2nd dose: 6-12 mths after 1st dose)
is recommended for:
o Children aged 12–23 mths.
o High risk patients (illegal drug users, travellers to endemic areas,
homosexual men, homeless, incarcerated people, patients with
chronic liver disease or HIV).
o Pregnant patient with an indication for vaccination.
o Any patient who requests immunization.
 Immunoglobulin provides passive immunization for up to 3 mths only
and can be given as preexposure prophylaxis to:
o Travelers to endemic areas
o Healthy children younger than 6 mths
o Persons with an allergy to the hepA vaccine
o Persons > 40 yrs. and those > 6 mths who are
immunocompromised or have chronic liver disease should
receive both the vaccine and immune globulin.
19.3. Viral Hepatitis: Hepatitis B:
19.3.1 Background:
HBV is a DNA virus, Transmission by percutaneous (bite or needle-stick)
or mucosal exposure to the blood or body fluids of an infected person or
perinatal transmission from mother to infant. Incubation period from
exposure to clinical hepatitis or serologic evidence is 1-4 mths.
19.3.2 Assessment:
Screening: according to USPSTF and CDC recommendations to screen
these population groups:
 Household contacts with hepatitis B
 Sexual partner with hepatitis B Injection drug users
 Homosexual men
 Infants born in Africa, Asia, Eastern Europe
 Infants born to mothers +ve for HBsAg
 Persons with elevated ALT and AST of unknown etiology
 Persons on hemodialysis, cytotoxic therapy, or immunosuppressive
therapy
 Persons who are +ve for HIV
 Pregnant women
 Donors of blood, plasma, organs, tissue, or semen
Page | 190
Screening tests
Screening for hepB includes HBsAg and, if +ve, testing anti-HBs and
anti-HBc to distinguish between infection and immunity
HBcAb HBcAb
HBsAg HBsAb Interpretation
IgM IgG
- - - - Susceptible to HBV infection
- - - + Immune 2ry to vaccination
- - + + Immune due to natural HBV

infection
+ - - - Early acute infection; transient (up

to 18 days) after vaccination
+ + + - Acute infection
- + + +/- Acute resolving infection
+ - + - Chronic infection
19.3.3 Clinical features:

 Acute hepatitis B: Sx appear in 30% to 50 % of children > 5 yrs and
adults.
o Common: are fatigue, upper abdominal pain, anorexia, nausea,
vomiting, fever.
o Uncommon S&S include extrahepatic Sx such as rash, arthritis,
and polyarteritis nodosa. Arthralgias occur in 10% to 20% of
patients with acute hepatitis B.
o Jaundice appears later in the course of the disease and can
occur in as many as three-fourths of patients.
 Chronic hepatitis B
o 3-5% of adult patients with HBV infection will develop chronic
infection and 90% of children will develop chronic infection (if not
given HBIG and vaccine series).
o Chronically infected patients typically have no Sx unless they
develop chronic liver disease. defined as the persistence of
HBsAg for > 6 mths.
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o The presence of HbeAg may indicate high infectivity correlated

with HBV DNA.
o Take careful Hx and PE including S&S of liver cirrhosis, alcohol
intake, metabolic risk factors, family hx of HCC, and vaccination
status especially hep A.
 HBsAg, HBsAb, and anti-HBc to distinguish between infection and
immunity.
 HbsAg, HBeAg, anti-HBe, HBV DNA levels or viral load are markers
of (active virus replication and infectivity), should be assessed in
patients with chronic HBV, to help guide treatment in combination with
ALT levels.
o Levels of HBV-DNA < 2000 IU/ml suggest inactive infection.
o and levels > 20,000 IU/ml suggest active disease.
 In acute HBV infection, (AST/ALT) are typically 500 to 10,000 IU/L.
 In chronic HBV infection, (AST/ALT ) levels are normal or minimally
elevated (<100 IU/L).
 Only in severe late-stage disease are (AST/ALT) levels elevated.
 Other tests include CBC with PLT, total bilirubin, ALP, albumin, and
international normalized ratio help in patients with advanced liver
disease.
 Test for HIV and HCV in all HBV carriers d.t. high rate of co-infection.
 Test for HAV to determine the need for vaccination.
 AFP and abdominal ultrasound testing for HCC screening.
 Liver biopsy is recommended for assessing inflammatory activity and
fibrosis. Other noninvasive tests: (transient elastography or a serum
fibrosis panel), are also useful.
19.3.5 Management:
Occupational post exposure management
If a healthcare worker is exposed to blood or body fluid
 Vaccination status for the healthcare worker: anti-HBs level ≥ 10
mIU per mL.
 Obtain HBsAg from the source person after taking informed consent.
 If it is not possible to test the source person’s blood, manage as it is
+ve.
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Exposed patient Source patient Action

status status
Anti-HBs ≥ 10 - No action needed

mIU per mL
Anti-HBs < 10 -ve HBsAg No action needed
+ve HBsAg or 2 doses of HBIG separated by 1 month.

unknown
Full vaccination or booster vaccination
may be needed (refer to 2ry prevention)
Perinatal exposure management

All infants born to HBsAg +ve mothers should receive HBIG promptly
and the HBV vaccine by 24 hours of life. Vaccination series should be
completed, and postvaccination serologic testing should be performed at
9-12 mths of age to assess response to vaccination. Additional vaccine
doses if the infant is non-responder.
Infected person management
 The primary treatment for acute HBV infection is supportive.
 The management of chronic HBV infection is complex and depends
upon multiple factors, including clinical variables (e.g., presence of
liver inflammation and/or cirrhosis), the patient’s immunologic
response to infection, virologic factors, and risk factors for disease
progression (e.g., age >40, family hx of HCC)
 The goals of antiviral therapy are suppression of HBV DNA, loss of
HBeAg (in patients who were initially HBeAg +ve), and loss of HBsAg.
 Antiviral agents for chronic HBV fall into 2 classes:
o Peginterferon alfa-2a agents:
 entecavir and tenofovir are first -line treatment options.
o Nucleoside/ nucleotide analogues
Pregnancy
Treating pregnant women who are HBsAg +ve reduces perinatal
transmission rates. Tenofovir is the preferred antiviral agent because it
has a better resistance profile.
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19.4. Viral Hepatitis: Hepatitis C:

19.4.1 Background:
HCV is an RNA virus, t may present clinically as acute hepatitis, chronic
hepatitis, chronic liver disease, cirrhosis, or any of its complications,
including HCC and extrahepatic manifestations.
HCV is mostly transmitted through blood or body fluids. Sexual and
perinatal transmission are other modes of transmission but are less
common. Incubation period is 3 to 20 weeks.
19.4.2 Assessment:
 Screening
o The USPSTF recommends one-time screening for adults aged
18 to 79 years. Repeat testing may be warranted in persons who:
ever used injectable drugs, received clotting factor concentrates
produced before 1987, are on long-term hemodialysis, have
evidence of chronic liver disease, had a transfusion of blood or
blood components or organ transplantation before July 1992, all
persons with HIV infection.
 Screening test and diagnosis
o An anti-HCV antibody test is recommended for screening of HCV
infection (Sen of 95%, Spe of 99%. Depending on the anti-HCV
antibody test and the infection circumstances will determine the
need for HCV RNA.
19.4.3 Clinical features:
 Acute Hepatitis C infection
o Most patients are asymptomatic. The most common Sx if any
are: Jaundice (65–75%), Flu-like symptoms (28%), Abdominal
pain/anorexia (17%).
 Chronic hepatitis C infection
o Tends to be asymptomatic until the development of cirrhosis.
Extrahepatic manifestations may arise in: Cryoglobulinemia,
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Non-Hodgkin’s lymphoma, Porphyria cutanea tarda, Lichen

planus, Sjogren’s syndrome, Arthralgia/arthritis.
 In patients with confirmed HCV infection, the degree of liver fibrosis
and cirrhosis must be assessed to determine the urgency of
treatment. The degree of liver fibrosis predicts disease progression
and clinical outcomes. The Metavir scoring system grades fibrosis
from 0 to 4, treatment should be considered in patients with
substantial fibrosis (score ≥ 2 ).
 Anti-HCV Enzyme Immunoassay (EIA) is the first-line test.
 HCV RNA used for confirmation.
o Used for diagnosis in seronegative immunosuppressed patients
with acute or chronic hepatitis and babies of HCV-infected
mothers.
 Quantitative HCV RNA testing is recommended before initiating
therapy to determine the baseline viral load.
 HCV genotype is recommended to help guide treatment decisions.
 Testing for HIV and HBV due to the high rate of co-infection, shared
risk factors, and that they might accelerate liver fibrosis.
 Testing for HAV to determine the need for vaccination.
19.4.5 Management:
 The goal of therapy is to reduce all-cause mortality and liver-
associated complications.
 Treatment is dependent on genotype, the extent of fibrosis or
cirrhosis, prior treatments, comorbidities, and potential adverse
effects.
 Treatment is generally recommended for adults with abnormal ALT
values, fibrosis, compensated liver disease, those treated previously
for HCV, patients with well-controlled depression, and with acceptable
hematologic and biochemical parameters.
 Treatment is generally contraindicated for patients with uncontrolled
depression, transplant recipients, those w/ autoimmune disease,
untreated hyperthyroidism, pregnant, or who have severe
comorbidities.
 The decision should be individualized for all other patients.
 Therapy is complex and rapidly changing and should be supervised
by a physician experienced in treating HCV infection. Although
interferon-based regimens have been the mainstay of treatment for
HCV infection.
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 Referral for possible liver transplantation should be considered for

patients with HCV-related cirrhosis.
19.4.6 Monitoring:
 At every visit, for pts w/ HCV assess for adherence to therapy and
advers effect, new or worsening psychiatric illness, and screen for
alcohol and substance abuse.
 Baseline tests include TSH level if pegylated interferon will be used;
CBC; Cr with GFR ;AST, ALT; ALP; and pregnancy testing in women
of childbearing age.
 CBC, Cr, AST, ALT should be measured at week 4 of treatment and
as clinically indicated.
 Quantitative HCV viral load is recommended at week 4 of treatment
and at 12 and 24 weeks after completion of therapy.
19.5. Cirrhosis:
19.5.1 Background:
Cirrhosis represents a late stage of progressive hepatic fibrosis
characterized by distortion of the hepatic architecture and the formation
of regenerative nodules. It is generally irreversible in its advanced
stages, at which point the only treatment option may be liver
transplantation.
19.5.2 Etiology:
The most common causes of cirrhosis are:
 Viral hepatitis C is the leading cause.
 Viral hepatitis B
 Alcoholic liver disease
 Non-alcoholic steatohepatitis (NASH) and non-alcoholic liver disease
(NAFLD)
o It is estimated that non-alcoholic liver disease (NAFLD) will
become the leading cause of cirrhosis over the coming 10 years
because of its increasing prevalence.
Other causes include:
 Biliary tract disease (such as biliary cirrhosis, biliary atresia),
Hemochromatosis, Auto-immune chronic hepatitis, Drugs and toxins,
Genetic metabolic disease (e.g., alpha-1-antitrypsin deficiency,
Wilson’s disease), Granulomatous liver disease.
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19.5.3 Assessment:
 Clinical Presentation
o Most patients with compensated cirrhosis may remain
asymptomatic for years.
o Patients with compensated cirrhosis caused by HBV, HCV, and
alcoholic liver disease develop clinical signs of decompensation,
including ascites, hepatic encephalopathy, jaundice, or bleeding.
o When Sx occur, they include fatigue, weakness, loss of appetite,
RUQ discomfort, and unexplained weight loss. With the onset of
decompensation, patients may report Sx of impaired liver
function such as jaundice, pruritus, coagulopathy, portal
hypertension (including ascites and peripheral edema),
esophageal varices (gastrointestinal bleeding) and hepatic
encephalopathy (such as confusion and disordered sleep).
 Evaluation
o When chronic liver disease is suspected, a thorough hx and PE
should be conducted looking for the cause including reviewing
any potentially hepatotoxic medications, alcohol consumption,
ruling-out hepatitis, and family hx of liver disease.
o After the diagnosis of cirrhosis is established, Child-Pugh or
Model for End-Stage Liver Disease scores should be used to
identify the stage of cirrhosis and mortality risk.
In early compensated disease, laboratory findings may be normal.
Incidentally, elevated liver enzymes or evidence of hepatic disease on
imaging may prompt the initial suspicion of chronic liver injury.
CBC, PT/INR, viral hepatitis serology, ferritin, Transferrin saturation,
HbA1C (if NAFLD suspected), ANA and smooth muscle antibodies (if
autoimmune hepatitis suspected) Other tests may be done depending on
the suspected cause.
Findings suggestive of cirrhosis include
 Low albumin
 Thrombocytopenia
 Elevated bilirubin
 AST: ALT ratio greater than
 1 Prolonged PT/elevated INR
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19.5.5 Imaging:
 Standard Ultrasonography
o Useful for diagnosing cirrhosis, cirrhosis complications.
o Pts w/ cirrhosis need RUQ ultrasonography every 6 mths to
screen for HCC.
 Ultrasound transient elastography (FibroScan) for liver stiffness
measurement (LSM) can be used to exclude bridging fibrosis and
cirrhosis.
 Diagnostic abdominal paracentesis should be performed, and ascitic
fluid obtained from pts w/ clinically evident ascites.
 Liver biopsy is used in pts w/ suspected cirrhosis in whom non-
invasive testing is inconclusive.
19.5.6 Management:
 The primary goals of liver disease management are to prevent
cirrhosis complications, liver decompensation, and death.
 These goals are accomplished with prevention counseling,
monitoring, and management by primary care physicians, in
consultation with subspecialists as needed.
19.6. Non-alcoholic fatty liver disease (NAFLD):
19.6.1 Background:
NAFLD is a fatty infiltration of the liver when the patient has evidence of
hepatic steatosis in either imaging or histologically and the absence of
secondary causes to his/her steatosis.
Histologically divided into:
 Non-alcoholic fatty liver (NAFL): ≥ 5% of hepatic steatosis w/o
hepatocellular injury
 Non-alcoholic steatohepatitis (NASH) ≥ 5% of hepatic steatosis w/
inflammation of hepatocellular injury with or without fibrosis
 Hepatic steatosis is diagnosed by either imaging or histology.
 Common risk factors: Obesity (most common risk factor), T2DM,
Dyslipidemia, male, Age (> 45), Ethnicity (Hispanic), Metabolic
syndrome, PCOs.
 Others: Hypothyroidism, Obstructive sleep apnea, Hypopituitarism,
Hypogonadism, Pancreaticoduodenal resection, Psoriasis.
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19.6.3 Assessment:
 Patients w/NAFLD usually asymptomatic, may include RUQ pain,
jaundice, and pruritus.
History should include:
 Common causes of liver injury, such as hepatitis risk factors, alcohol
and drug use.
 Drugs that can cause hepatic steatosis (Amiodarone, Aspirin,
Glucocorticoids, NSAIDS, Tetracycline, Valproic acid, Methotrexate,
Chemotherapy, Cocaine)
 Diet, physical activity, and increase in weight.
 Assessment of associated conditions (DM, HTN, hyperlipidemia,
obesity, sleep apnea).
 Risk factors for NASH (> 45 years, AST > ALT, DM, insulin resistance,
low albumin, low plt, metabolic syndrome, obesity, and portal HTN on
imaging).
 Family hx for cardiovascular and metabolic disorders, and chronic
liver disease.
19.6.4 Examination:
 May be ↑ BP , central obesity, insulin resistance signs,
hepatosplenomegaly.
 Pts w/ unsuspected hepatic steatosis detected on imaging who have
Sx or signs of liver disease or abnormal liver lab. should be evaluated
as if they have suspected NAFLD.
 Pts w/ incidental hepatic steatosis detected on imaging who lack any
liver disease Sx or signs and have normal liver lab. should be
assessed for metabolic risk factors (e.g., obesity, DM, or dyslipidemia)
and alternate causes for hepatic steatosis such as significant alcohol
consumption or medications.
19.6.5 Screening:
 Routine Screening for NAFLD is not advised, there should be a high
index of suspicion for NAFLD in patients with obesity and T2DM.
 Clinical decision aids such as NAFLD fibrosis score, fibrosis-4 index
(FIB-4), or vibration controlled transient elastography (VCTE) can be
used to identify those at low or high risk for advanced fibrosis.
 Patients with NASH cirrhosis should be screened for
gastroesophageal varices.
 Patients with cirrhosis suspected of NAFLD should be considered for
HCC screening.
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19.6.6 Diagnosis and investigations:

Patients with NAFLD are found to have:
 ↑ AST and ALT
 Mild serum ferritin ↑
 ↓ titers of serum anti-smooth muscle and antinuclear antibodies
Non-invasive tools for the assessment of the presence of advanced
fibrosis in NAFLD:
 Clinical:
o NAFLD fibrosis score (NFS)
 Score<–1.455 had 90% Sen and 60% Spe to exclude
advanced fibrosis.
 Score>0.676 had 67% Sen and 97% Spe to identify
presence of advanced fibrosis.
o Fibrosis-4 index (FIB-4 index)
 Score <1.45, advanced fibrosis is unlikely.
 Score >3.25 are likely to have advanced fibrosis.
 Laboratory:
o AST to platelet ratio index (APRI)
o Serum biomarkers (Enhanced Liver Fibrosis [ELF] panel)
 (Hyaluronic acid, tissue inhibitor of metalloproteinase 1,
and N-terminal procollagen III peptide), 80% Sen and 90%
Spe for detecting advanced fibrosis.
 Imaging:
o To measures liver stiffness
 Vibration controlled transient elastography (VCTE)/
Fibroscan
 Magnetic resonance elastography (MRE)
o Important note: Serum ALT/AST levels and imaging tests do not
reliably reflect the spectrum of liver histology in patients with
NAFLD.
Liver biopsy (gold standard)
Should be considered in:
 Pts w/ NAFLD who are at increased risk of having steatohepatitis
and/or advanced fibrosis: (The presence of metabolic syndrome, High
NFS, High FIB-4, Liver stiffness measured by VCTE or MRE)
 Suspected NAFLD in whom competing etiologies for hepatic steatosis
and the presence and/or severity of coexisting chronic liver diseases
cannot be excluded w/o liver biopsy.
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Histopathological diagnosis
 Not NAFLD (<5% steatosis, by definition)
 NAFL, not NASH (≥ 5% steatosis, with or without lobular and portal
inflammation)
 Borderline steatohepatitis, zone 3 or borderline steatohepatitis, zone
1
 Definite steatohepatitis (all criteria present)
Any of these diagnostic categories, including not NAFLD, may have no
fibrosis or any amount of fibrosis up to cirrhosis.
19.6.7 Management:
 The goals of therapy: prevention or reversal of hepatic injury and
fibrosis.
 Management includes treating liver disease and the associated
metabolic comorbidities such as obesity, hyperlipidemia, Insulin
resistance, and T2DM.
 Aggressive modification of CVD risk factors should be considered in
patients w/ NAFLD.
Lifestyle modification
 Diet, exercise, and weight loss and avoid consumption of heavy
amounts of alcohol.
Pharmacotherapy (improve liver enzymes)
 Pioglitazone, Vitamin E daily dose of 800 IU/day, GLP1 analogues.
Surgical treatment
 Bariatric surgery (for obese pts w/ NAFLD), Liver transplant (in
selected pts).
19.6.8 Monitoring:
After initiating intensive lifestyle changes, repeat liver enzyme
measurements and ultrasonography in 6-12 mths. If abnormalities persist
and the patient is at:
 Low risk of fibrosis, monitor every 12-24 mths with a CBC; liver
enzyme, lipid, and fasting glucose or A1C levels; and calculation of
fibrosis risk scores.
 High-risk patients (AST:ALT ratio > 1.0, who have an NAFLD Fibrosis
Score or Fibrosis-4 Score showing high risk, w/abnormal results on
non-invasive testing or who have imaging or clinical evidence of
cirrhosis. should be referred to a specialist.
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Chapter 20: INFECTIOUS DISEASES

20.1. Seasonal influenza:
20.1.1 Symptoms, sign , physical examination:
 beginning with the abrupt onset of systemic symptoms: fever,
headache, myalgia, and malaise.
 Associated symptoms: nonproductive cough, sore throat, and nasal
discharge.
 children may come with atypical presentation such as vomiting and
diarrhea
On examination :
General look: may appear hot and flushed
ENT: congested throat.
Lymph nodes: mild cervical lymphadenopathy. Chest exam: generally
unremarkable
 Diagnosis of influenza is based on the clinical presentation.
 in hospitilazion patient may consider CXR And Rapid influenza
diagnostic tests and CBC
20.1.3 Management :
 supportive treatment for seasonal influenza. Acetaminophen or non-
steroidal anti-inflammatory drugs (NSAIDs) for systemic symptoms
associated with influenza.
 anti-influenza drug is an option in specific group Prevention :
influenza vaccine.
20.2. Tuberculosis:
is a multi-systemic disease caused by mycobacterium tuberculosis.
TB is spread by aerosolized droplets from patients with active
pulmonary TB.
20.2.1 Symptoms, sign, physical examination:
Depend on TB location.
Latent TB:
Patient asymptomatic and accidentally diagnosis
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Pulmonary tuberculosis:
SOB
Fever and night sweats: general onset with low or high grade and could
reach 39°C (102.2°F) and last for an average of 14 to 21 days.
Pleuritic chest pain Weight loss
Productive cough containing purulent or bloody sputum can last longer
than 3 weeks.
Extrapulmonary tuberculosis:
Meningitis TB
Headache that has been either intermittent or persistent for 2-3 weeks
Subtle mental status changes that may progress to a coma over a period
of days to weeks Low-grade or absent fever.
Skeletal TB:
Synovitis or osteomyelitis can occur insidious onset.
Vertebral osteomyelitis of lower thoracic and lumbar regions causes back
pain.
Genitourinary tuberculosis and renal tuberculosis:
Flank pain Dysuria
Frequent urination
In men, a painful scrotal mass, prostatitis, orchitis, or epididymitis In
women, symptoms mimicking pelvic inflammatory disease Hematuria
Gastrointestinal TB (according to the site):
Non-healing ulcers of the mouth or anus Difficulty swallowing (with
esophageal disease)
Abdominal pain mimicking peptic ulcer disease (with gastric or duodenal
infection) Malabsorption (with infection of the small intestine)
Pain, diarrhea, or hematochezia (with infection of the colon)
Tuberculous peritonitis:
Immunocompromised patients and those using peritoneal dialysis can
increase the risk Present with acute onset of abdominal pain and fever.
Tuberculous pericarditis
Can present with subacute onset of fever, night sweats, dyspnea, and
pedal edema.
on examination :
for pulmonary tuberculosis:
 If there is pleural thickening or effusion will find a dullness to
percussion or decreased tactile fremitus
 Crackles
 Egophony can be found with consolidation.
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For extrapulmonary tuberculosis:

 Cachexia and malnourishment indicate long-standing infection.
 lymphadenopathy
 Unilateral nontender supraclavicular and posterior cervical can be
found with tuberculous lymphadenitis.
 Pericardial tuberculosis appeared as muffled heart sounds.
 Tenderness to palpation or palpable swelling over affected areas (eg,
abdomen, flank, bladder, scrotum, prostate, vertebrae, joints)
 In meningitis caused by TB could be appeared like altered mental
status, nuchal rigidity, and weakness with tuberculous meningitis.
 Ascites and abdominal tenderness could be seen in tuberculous
peritonitis.
20.2.2 investigation:
 TB skin test for latent TB
 Interferon-γ release assay for latent TB
If history and physical examination suspected pulmonary
tuberculosis obtain
 three samples for sputum culture
 Chest x-ray
If extrapulmonary tuberculosis is suspected based on history
and physical examination perform the following:
Tuberculin skin test or interferon-γ release assay
Laboratory testing on the aspirate sample from the site affected with TB:
Acid-fast bacilli.
Nucleic acid amplification test Culture with antimicrobial sensitivity Fluid
aspiration analysis
Biopsy with histopathology
 On all patients starting antituberculosis therapy obtain baseline liver
functions, creatinine level, and platelet count.
 HIV testing should be done in all patients diagnosed with
tuberculosis.
20.2.3 Management:
for hospitalized patients with active tuberculosis recommend
the following:
Patients should be placed in negative pressure respiratory isolation.
Continue isolation until sputum smears are negative three consecutive
times, usually after approximately 2-4 weeks of treatment.
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Pharmacological treatment for active TB

For initial empiric treatment of TB, start patients on a 4-drug regimen:
isoniazid (INH), rifampin, pyrazinamide, and ethambutol.
 Pyrazinamide and ethambutol can be discontinued after 2 months or
until confirmed drug susceptibility.
 Isoniazid and rifampin are continued daily or 3 times weekly for at
least 4 months and for a total of 6 months.
 Vitamin B6 (pyridoxine) 25–50 mg orally daily with INH to prevent
neuropathy.
Treatment should be extended to 9 months in patients who:
have cavitary disease on radiology.
remain culture-positive after two months of treatment weigh less than
10% of ideal body weight.
actively smoke have DM.
are immunocompromised (HIV)
CDC guidelines recommend for latent TB treatment in the
following patients:
have positive interferon-γ release assay result.
 have positive tuberculin skin test reaction of 5 mm or more who:
o are HIV positive
o have contact with someone who has active tuberculosis.
o have chest radiograph that shows fibrotic changes consistent
with old tuberculous infection have received organ transplant.
o are immunosuppressed for other reasons (equivalent of 15 mg
prednisone or more daily for a month or longer; tumor necrosis
factor-α antagonists)
 have positive tuberculin skin test reaction of 10 mm or more who:
o emigrated within 5 years from a country with a high prevalence of
tuberculosis.
o use IV drugs.
o are- residents or employees in high-risk settings (eg, hospitals,
nursing homes, homeless shelters, correctional institutions)
o work in mycobacteriology laboratory
o are younger than 4 years old.
o are children or adolescents exposed to adults in high-risk
categories
Pharmacological treatment for latent TB:
Isoniazid 300 mg – Daily for 9 months
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20.3. Malaria:
caused by Plasmodium species transmitted by Anopheles mosquitoes.
20.3.1 Sign, symptoms, physical examination:
Usually, patients presented 1–2 weeks after exposure with a history of
returning or residing in malaria-endemic areas.
Symptoms: Fever(cycle can occur every 2nd or 3rd day),
Character of tertian malaria is periodic fever which spikes every 42
hours. Character of quart an malaria is periodic fever which spikes every
72 hours. Character of falciparum malaria is irregular, spikes without
noticeable rhythm.Also, may come with headache, sweats, myalgia’s,
and malaises.
In severe disease, patients may present with: Altered mental status,
jaundice, renal failure, acute respiratory distress syndrome, seizure,
coma and if untreated- may progress to death.
On examination:
tachycardia, tachypnea, fever, pallor, jaundice, systolic murmur, and
confusion.
 Thick blood smear is best initial test (highly sensitive, detects
presence of parasite).
 Thin blood smear is used as confirmatory test (low sensitivity but
highly specific).
 If initial test is negative, blood test should be repeated 3 times every
12–24 hours.
 Intraerythrocytic ring forms or schizonts on microscopy confirm the
diagnosis and can identify the plasmodial species.
 CBC: hemolytic anemia
 Liver and renal function.
20.3.3 Management:
 For Uncomplicated malaria: Plasmodium falciparum or unknown
species : Chloroquine resistant or unknown resistance :
Artemether-lumefantrine:
o Adults: 4 tabs/dose
o Child : 5-<15kg: 1 tab/dose 15-<25kg: 2 tabs/dose
o 25-<35kg: 3 tabs/dose
o >35kg: 4 tabs/dose—
o 3-day course:
 Day 1 – initial dose and second dose 8 hours later
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 Day 2 and 3 – 1 dose BID

 For Uncomplicated malaria: P. vivax or P. ovale Chloroquine
sensitive:
o Chloroquine phosphate Or Hydroxychloroquine
o Doses 2-4 at 6, 24, 48 hrs.: 300 mg base (500mg salt) PO/dose
And Anti-relapse treatment:
o Primaquine phosphate
o 30mg base PO QID x b14 days OR
o Tafenoquine 300mg PO x 1 dose
 Prophylaxis:
o Chemoprophylaxis for malaria depends on the traveler’s location
and the presence of chloroquine resistance.
 Mefloquine
o Start 1 tablet 250 mg 2-3 weeks before the trip; take weekly
during and 4 weeks after return.
 Doxycycline
o Start 100 mg daily 1-2 days prior to the trip, taken during and for
4 weeks after return.
 Chloroquine
o Start 500 mg 1-2 weeks before travel, take weekly during and for
4 weeks after return.
 Primaquine
o Start 30 mg(base) daily 1 day prior to the trip, during, and 1 week
after return. Tafenoquine
 Prophylaxis for malaria:
o 200 mg daily for 3 days before travel, then
o 200 mg weekly during travel starting 1 week after the last pre-
travel dose 200 mg once 1 week after travel.
20.4. Leishmaniasis:
Leishmaniasis is a vector-borne disease caused by protozoa parasites,
are transmitted by infected female phlebotomine sandflies.
20.4.1 Sign ,symptoms , physical examination:
there are many different forms: cutaneous leishmaniasis (CL),
mucocutaneous leishmaniasis (MCL), and visceral leishmaniasis (VL)
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Table 20.1
Visceral leishmaniasis Cutaneous leishmaniasis Mucocutaneous
(VL) (CL) leishmaniasis (MCL)
– Also known as kala- – The most common form of – It is a less common form.
azar. leishmaniasis. – Can affect the mucosal
– Life threatening and – Appears typically on membranes of the nose
fatal in untreated patients uncovered body parts. (most common location),
in more than 95% of – Can leave a life-long throat or mouth.
cases. depressed scars or serious – The initial presentation of
– Characterized by weight disability. mucosal leishmaniasis is
loss, irregular fever, – Typically, the lesion can unusual nasal stuffiness or
hepatomegaly, be found in different shapes bleeding. However, oral or
splenomegaly, anemia, as papules, nodular pharyngeal symptoms may
leukopenia, plaques, or ulcerative be noticed first.
thrombocytopenia, high lesions. The border is raised – Untreated disease can
total protein level and a with central depression and lead to perforation of the
low albumin level, with sometimes covered by scab nasal septum.
hypergammaglobulinemia or crust (Figure 20.7).
20.4.2 Investigation :
 The cutaneous Leishmaniasis requires sampling via scrapping, fine
needle aspiration, and punch biopsy for the laboratory criteria to be
positive parasitology in Giemsa-Stained smear, culture, or by
Polymerase Chain Reaction-PCR.
 For visceral Leishmaniasis, the diagnosis can be made through the
combination of clinical signs with parasitological or serological tests.
20.4.3 Management:
 For Cutaneous leishmaniasis
o The treatment depends on several factors ,which can be divided
into mild and complex diseases.
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Table 20.2 Management of Leishmania

Severity Mild disease Complex disease
-Infection with species not ->4 skin lesions
likely to be associated with -One skin lesion
mucosal leishmaniasis more than 4 cm in
-No mucosal involvement diameter
-Single lesion or a few -Skin lesion on top
lesions of joints or in
-Small lesion size (eg, <1
cm) cosmetically
-Immunocompetent host sensitive area
-Failure of
previous
management
-Associated with
lymphatic nodules
or large regional
lymphadenopathy
Managemt -Only observation in most of -Fluconazole 200

the cases is preferred for mg po daily x 6
spontaneous healing. weeks. Data
-Follow-up care must be available for L.
done on day 14, 30, 45, and major only.
180. -Ketoconazole 600
-If not healing or the L. mg po daily for 30
tropica species is suspected, days.
local therapy should be -Data available for
started. L. major only.
-Debride any necrotic tissue -Referral to the
before local treatment starts. hospital for:
-Local therapy includes: -Sodium
Paromomycin ointment bid x Stibogluconate or
20 days. Meglumine
Intralesional antimony; antimoniate 20
Sodium Stibogluconate 100- mg/kg/day IV/IM x
500 mg (1-5 mL) per session 20 days.
every week for 1-5 -Liposomal
sessions. Amphotericin B 3
Cryotherapy, Heat or Laser mg/kg IV once daily
therapy. for 7 days.
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-Amphotericin B 0.5-
1 mg/kg IV daily or
qod to total dose of
15-30 mg/kg.
 For mild :
o Only observation in most of the cases
o Follow-up care must be done on day 14, 30, 45, and 180.
o If not healing local therapy should started:
 Paromomycin ointment bid x 20 days.
 Intralesional antimony.
 Sodium Stibogluconate 100-500 mg (1-5 mL) per session
every week for 1-5 sessions.
 Cryotherapy, Heat or Laser therapy.
 for complex :
o Fluconazole 200 mg po daily x 6 weeks. Data available for L.
major only.
o Ketoconazole 600 mg po daily for 30 days.
o Refer to hospital.
20.5. -Foodborne Infections and Gastroenteritis:
The main route of transmission is swallowing contaminated food with
germs or toxic substances.
20.5.1 Sign , symptoms , physical examination:
-Usually, foodborne illnesses are associated with vomiting and/or
diarrhea (generally more than 3 loose stools in 24 hours).
-Other symptoms include: fever, bloody diarrhea, abdominal cramping,
headache, dehydration.
 Red flags:
o High fever (temperature over 102°F, measured by mouth)
o Continuous vomiting which prevents keeping liquids in the
stomach (which can lead to dehydration)
o Signs of dehydration include: little or no urination, very dry
mouth, and throat, or feeling dizzy when standing up.
o Bloody stools
o Diarrhea lasts more than 3 days.
 On examination :
o The Clinical Dehydration Scale evaluates 4 clinical features to
estimate the degree of dehydration.
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Table 20.2 - Clinical Dehydration Scale

Characteristic 0 Point 1 Point 2 Points
Normal Thirsty, restless, or lethargic Drowsy, limp, cold,
Appearance
and irritable upon touched sweaty, comatose
Eyes Normal Slightly sunken Very sunken
Mucous Moist Sticky Dry

membranes
Tears Tears Decreased tears Absent tears
Scoring: 0 points = less than 3% dehydration; 1 to 4 points = mild (3% to 6%)
dehydration; 5 to 8 points = moderate / severe (more than 6%) dehydration
o Mental status:Drowsiness (due to dehydration)
 lab testing is usually not necessary.
 Definitive diagnosis is based on stool culture.
 Other labs that can be done to assess severity and pattern of
symptoms include: serum chemistry (including albumin levels), c-
reactive protein levels, complete blood count, blood cultures,
urinalysis, abdominal radiography, and endoscopy. The only
laboratory finding by which we can determine the likelihood of 5% or
less dehydration is: a serum bicarbonate concentration (more than 15
mEq per L or 15 mmol per L).
20.5.3 Management:
 Management focus on:
o Symptom management , antiemetic ondansetron (Zofran)
o Rehydration if dehydrated.
o Antibiotic therapy , if clinical( fever ,symptoms more than one-
week ,severe diarrhoea) or laboratory evidence suggests
bacterial infection as most cases of acute diarrhea are due to
viral infection. fluoroquinolone is generally recommended for
empiric antibiotic therapy.
 Red flag:
o Referral for hospital admission indicated for:
o Severe dehydration.
o Social concerns (i.e., ability to follow directions for rehydration
therapy) Failed rehydration.
o Suspected serious alternative diagnoses.
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20.6. Giardiasis:
It is a protozoan parasite infection; it is most prevalent in areas with poor
water treatment or unsanitary conditions.
 diarrhea without blood or mucus, most common symptom of acute
Giardia infection, occurring in 90% of symptomatic subjects.
 foul-smelling stool
 flatulence (70– 75%)
 abdominal pain
 malabsorption
 failure to thrive.
 weight loss, as extensive as 10–15 pounds in an adult, occurs in
approximately 66% of symptomatic patients.
 lack of weight gain
 anorexia
 nausea
 post infection lactase deficiency is a common finding, occurring in 2–
40% of cases.
 on examination:
o Weight loss may be evident,
o On abdominal examination, patients may have nonspecific
tenderness without evidence of peritoneal irritation.
o Rectal examination should reveal heme-negative stools.
o In severe cases, evidence of dehydration or wasting may be
present.
 Stool examination easily provides the diagnosis.
 The diagnosis is confirmed by presence of cysts or, less frequently,
trophozoites in stool specimens.
20.6.3 Management:
 The illness may resolve spontaneously, but symptoms may persist for
weeks and sometimes for months.
 All symptomatic or likely symptomatic patients should be treated.
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Table 20.3 Medications and dosages

Medication Dosage
Metronidazole 250 mg three times per day for five days (15 mg
per kg per day)
Quinacrine 100 mg three times per day for five days (6 mg
per kg per day)
Furazolidone 100 mg four times per day for seven to 10 days
(6 to 8 mg per kg per day)
Paromomycin 25 to 30 mg per kg per day in three doses for
seven days
Albendazole 400 mg per day for five days
Tinidazole 2 g (in a single dose)
20.7. Amoebiasis:
damage to the skin and underlying soft tissues by trophozoites of
Entamoeba histolytica.
20.7.1 Sign ,symptoms, physical examination:
 however most infected people are asymptomatic.
 Symptoms may develop within 2 to 4 weeks of infection, and they
include:
o fever- the presenting symptom in 10-15% of patients
o liquid stools containing blood and mucus.
o abdominal cramps
o chills
o prostration (extremely weak)
o nausea
o headache
o tenesmus
 for Extraintestinal amebic diseases:
o Present with or absence of intestinal symptoms
o Amebic liver abscesses develop acutely or gradually, right lobe of
the liver is usually affected and might cause referred pain to the
right shoulder.
 on examination :
o Patients with acute amebic colitis present with
 lower quadrant abdominal tenderness (12-85% of cases)
 rebound tenderness.
o Patient with amebic liver abscess present with :
o hepatomegaly with or without tenderness
o Right lower intercostal tenderness
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o Breath sounds diminished at the right lung base.

 Rales may be heard.
o Jaundice is unusual (6-10%)
20.7.2 investigation :
 Stool Antigen detection
 Serum Antibody detection
 Culture: Performed either with fecal or rectal biopsy or with liver
abscess aspirates.
 CBC : leukocytosis , mild anemia
20.7.3 Management:
Most individuals with amebiasis may be treated as outpatients.
Table 20.4 Medications
Luminal disease
Iodoquinol (Yodoxin) 650 mg used orally three times daily for 20
days
Paromomycin 500 mg orally three times daily for seven
days
Diloxanide furoate 500 mg take orally three times daily for10
(Furamide) days
Tissue
Metronidazole 750 mg orally three times daily * 10 days
Liver Abscess
Metronidazole 750 mg orally three times daily * five
days, then
Paromomycin 500 mg three times daily * seven daysor
600 mg orally per day for two days, then
Chloroquine (Aralen) orally per day for two to three weeks
20.8. Brucellosis:
It mostly infects cattle, sheep, goats, camels, pigs and is transmitted to
humans by those infected animals.
-The most common modes of transmission of brucellosis to humans
are:
 Consumption of infected, unpasteurized animal products
 Contact of skin or mucous membranes with infected animal tissue or
infected animal fluids likes placenta, miscarriage products, blood,
urine, or milk.
 Inhalation of infected aerosolized particles
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20.8.1 sign, symptoms, physical examination:

-Flu-like symptoms are the most presenting symptoms.
-Fever ranges from intermittent in acute and chronic brucellosis and
undulant fever in subacute brucellosis .
-Associated with constitutional symptoms: chills, night sweats, weight
loss, fatigue, malaise.
-Other common symptoms include arthralgia, low back pain, muscular
pain, headache, dizziness, anorexia, cough, depression, non-specific
gastrointestinal disorders (dyspepsia, abdominal pain), hepato and/or
splenomegaly, adenopathy (particularly in children), and orchitis.
-on examination:
 Generally, physical examination findings are normal or only minimally
abnormal.
Table 20.5 Physical findings in patient with brucellosis
General Usually, well-appearing
Appearance
Vital Signs Pulse rate: Normal or Tachycardia with regular
rhythm Temperature: Normal or elevated
Blood pressure: Normal
Respiratory rate: Normal or tachypnea (lung
involvement)
Skin Normal or reveal the following:
Maculopapular rash
Erythema nodosum like eruptions and ulceration
Abscesses
Neck Cervical lymphadenopathies present in few
patients
Lungs Depending on the part involvement (pneumonia,
pleural effusion, or empyema):
Increased tactile fremitus
Dullness on percussion
Decreased breath sounds
Bronchial breath sounds
Rhonchi
Crackles, Rales
increased vocal fremitus
Heart Murmurs on auscultation (endocarditis)
Abdomen Tenderness
Hepatomegaly
Splenomegaly
Lymphadenopathy
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Genitourinary Inguinal lymphadenopathy

Swollen testicle or testicles (orchitis)
Extremities Fluid around a joint
Warm, red, tender joints
Difficulty moving joints
Neuromusculr Meningeal signs of irritation Nuchal rigidity,
Kernig’s sign, and Brudzinski’s sign In case of
(meningitis or meningoencephalitis).
-Gold standard test for diagnosis of brucellosis is the isolation of the
organism from blood or tissues (e.g., bone marrow biopsy)
-Culture: diagnosis is definitive when organisms are recovered from
blood, bone marrow, or other tissue. Any fluid (e.g., synovial fluid or
cerebrospinal fluid [CSF]) can be cultured, but the sensitivity is usually
low.
-CSF analysis patients with neurobrucellosis: analysis of CSF shows
Protein levels are elevated with normal glucose levels.
-Serology Is one of the most commonly used methods of diagnosing
brucellosis. Repeated testing is sometimes recommended if the initial
titer is low.
-CBC: neutropenia. anemia with chronic infection, thrombocytopenia
-Liver enzymes: may elevated
20.8.3 Management:
Treatment of uncomplicated brucellosis in adults and children eight years
of age and older:
-Tetracycline (500 mg every six hours orally) administered for at least
six weeks.
Or Doxycycline is given in a dose of 100 mg every 12 hours orally
and is administered for a period of six weeks.
-Plus Streptomycin (1 g/day intramuscularly) administered, 2-3
weeks.
Treatment in children less than eight years of age:
-TMP/SMZ (8/40 mg/ kg/day twice daily orally) administered for 6 weeks
PLUS Streptomycin (30 mg/ kg/day once daily intramuscularly)
administered for 3weeks
OR Gentamicin (5 mg/kg/day once daily I.V. or I.M.) administered for 7 –
10 days.
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during pregnancy:
-The most common recommendation is for rifampin, alone or in
combination with TMP-SMZ.
20.9. Viral hemorrhagic fever:
VHF is a group of infectious diseases that are caused by many viruses
viral hemorrhagic fevers are:
Dengue Ebola Lassa Marburg Yellow fever
Hantavirus diseases
Crimean–Congo hemorrhagic fever (CCHF) Rift Valley fever (RVF)
presenting with fever, vomiting, mucosal or gastrointestinal (GI) bleeding,
edema, and hypotension.
 CBC will show leukopenia with lymphopenia and thrombocytopenia
 Liver function test (mild to moderate elevation in liver enzymes (AST
and ALT)
 Renal function
 prolonged prothrombin (PT) and partial thromboplastin times (PTT)
 Malaria test (thick blood films)
 Specific antibodies (IgM antibodies and IgG antibodies)
 Viral nucleic acid and virus isolation
 Viral antigens (ELISA)
20.9.3 Management:
 No known treatment for these diseases
 Treatment is mostly supportive with fluid, pain relief and assisted
breathing
20.10. Dengue Fever:
Dengue viruses (DENV) are of the family Flaviviridae (genus Flavivirus).
The DENV complex comprises four serotypes, which are transmitted by
mosquitoes. Aedes aegypti is a vector of all four dengue serotypes.
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20.10.1 Sign, symptoms ,physical examination:

Table 20.3 Phases of dengue fever
1- Febrile Phase
History Physical exam Laboratory
-Sudden high-grade -A positive -Leukopenia and
fever (≥ 38.5°C) and tourniquet test after thrombocytopenia (≤
lasts for 2 – 7 days, blood pressure 100,000 cells/mm3).
5% have biphasic measure, 10 or -elevated serum
fever more new petechiae aspartate
-Accompanied with appear in the skin transaminase (AST)
headache, eye pain, below the cuff one levels (2 to 5 upper
arthralgia, muscle to two minutes after limit)
ache, and some of deflating the cuff. -elevated PTT
them could have -Also, patients could partial-
mild gastrointestinal have conjunctivitis, thromboplastin time
symptoms (vomiting, pharyngeal -leukopenia
abdominal pain, and erythema,
diarrhea) and cold lymphadenopathy,
like symptoms hepatomegaly, facial
-Macular or puffiness, petechiae
maculopapular rash, (on the skin, mouth),
occurs 2 to 5 days and bruising.
from the onset of
fever, associated
with pruritus (Picture
3 – 4)
-minor hemorrhagic
manifestations
(petechia,
ecchymosis,
epistaxis, bleeding
gums, purpura,
haematuria).
2- Critical Phase
History Physical exam Laboratory
-Typically, days 3 to -signs of vascular -Moderate-to-severe
7 of infection. leakage, plasma thrombocytopenia (≤
-Mostly with patients leakage, bleeding, 20,000 cells/mm3)
have medical shock, and organ followed by rapid
comorbidities, or impairment improvement
result from second -elevated PTT
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infections more than -Blood pressure -decrease in

18 months after the either low, normal or fibrinogen levels.
first infection and in high -elevated
children less than 1 -Narrowing Bp hematocrit level (≥
year of age (systolic pressure 20 percent from
-Hemorrhagic minus diastolic baseline)
manifestations pressure ≤ 20
-Rapid recovery mmHg)
within 24 to 48 -Sign of pleural
hours effusion and
peritoneal fluid
-other
manifestations
could occur with
critical phase likes
include liver
failure, central
nervous system
involvement,
myocardial
dysfunction, acute
kidney injury, and
others
3- Convalescent Phase
-The recovery phase lasts from two to four days and could
continue for weeks with symptoms of fatigue.
-Plasma leakage and hemorrhage resolve
-Vital signs improve
-A new rash could appear during this phase and last from
one to five days
 Dengue virus can be seen in serum, plasma, circulating blood cells,
and tissues during the first weeks of disease (early phase).
 The most useful tests during this phase are virus isolation, nucleic
acid detection, and antigen. After the acute phase, the serology is the
most useful test.
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-Approach to diagnostic testing for dengue:

 If the specimen was collected within the first week (≤7 days), the test
to be done is NAAT. If the result of NAAT turns positive, that
confirmed acute dengue virus infection.
 If the first test NAAT is negative or the specimen was collected after
the first week of infection (> 7 days), the test to be done is IgM
serology:
 If it is negative so no evidence of dengue
 If it is positive, do virus PRNTs:
Recent dengue infection if the PRNT ≥ 10
No evidence of dengue infection of the PRNT <10
-The IgM serology can be detectable for 3 months or more after dengue
infection
-The following laboratory is characteristics finding in dengue:
 Thrombocytopenia (platelet count < 100 x 109/L)
 Leukopenia
 Mild to moderate elevation of aspartate aminotransferase and alanine
aminotransferase values
-The following may be present with severe dengue:
 Increased hematocrit level secondary to plasma extravasation and/or
third-space fluid loss
 Hypoproteinemia
 Prolonged prothrombin time
 Prolonged activated partial thromboplastin time
 Decreased fibrinogen.
 Increased amount of fibrin split products
20.10.3 Management:
 There are no specific treatments or antiviral agents for dengue fever.
 It is a self-limited illness and mostly supportive management is
needed.
 Inpatient management is indicated for patients with warning signs of
severe infection, severe dengue infection, or with coexisting
conditions.
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Chapter 21: FEVER OF UNKNOWN

ORIGIN
21.1. Definition
It is defined as temperature ≥ 38.3°C, lasts for > 3 weeks or occurs
frequently, without obvious cause despite an evaluation of at least 3 days
in the hospital or 3 outpatient visits or 1 week of intensive outpatient
testing.
21.2. Types:
 Classic:
Temperature >38.3°C (100.9°F), Duration of >3 weeks, Evaluation of at
least 3 outpatient visits or 3 days in hospital
Most common causes: Infection, Malignancy, and collagen vascular
disease
 Nosocomial
Temperature >38.3°C, in hospitalized patient for ≥24 hours but had no
fever or incubating on admission, without obvious cause despite
evaluation of at least 3 days.
Most common causes: Clostridium difficile enterocolitis, drug-induced,
pulmonary embolism, septic thrombophlebitis, sinusitis.
 Immune deficient (neutropenic)
Temperature >38.3°C, neutrophil count ≤ 500 per mm3, without obvious
cause evaluation of at least 3 days.
Most common causes: Opportunistic bacterial infections, aspergillosis,
candidiasis, herpes virus.
 HIV-associated
Temperature >38.3°C, duration of >4 weeks for outpatients, or >3 days
for inpatients, patient with confirmed HIV infection.
Most common causes: Cytomegalovirus, Mycobacterium avium-
intracellulare complex, Pneumocystis carinii pneumonia, drug-induced,
Kaposi's sarcoma, lymphoma
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21.3. Differential diagnosis:

 Infections
(25-50%): Tuberculosis and abdominal or pelvic abscesses are the most
common, Intra abdominal abscesses are associated with perforated
hollow viscera (appendicitis), diverticulitis, malignancy, and trauma,
Other common infections: subacute bacterial endocarditis, sinusitis,
osteomyelitis, and dental abscess.
As the duration of fever increases, the likelihood of an infectious etiology
decreases.
 Malignancy
(5-35%): malignancy is a common etiology to consider in elderly patients.
Malignancies that sometimes are difficult to diagnose, such as chronic
leukemias, lymphomas, renal cell carcinomas, and metastatic cancers,
often are found in patients with FUO.
 Autoimmune Conditions
(10-20%): adult Still’s disease and temporal arteritis are the most
common autoimmune sources of FUO as they are difficult to diagnose.
Rheumatoid arthritis and rheumatic fever are inflammatory diseases that
used to be commonly associated with FUO, but with advances in
serologic testing, these conditions usually are diagnosed more promptly.
Multisystem inflammatory diseases such as temporal arteritis and
polymyalgia rheumatica have emerged as the autoimmune conditions
most frequently associated with FUO in patients older than 65 years.
 Miscellaneous
(15-25%): drug-induced fever is the most common, As a part of a
hypersensitivity reaction to specific drugs such as diuretics, pain
medications, antiarrhythmic agents, antiseizure drugs, sedatives, certain
antibiotics, antihistamines, barbiturates, cephalosporins, salicylates, and
sulfonamides.
21.4. Risk factors:
Recent travel, work environment, recent contact with persons with similar
symptoms, returning from areas where tuberculosis and malaria are
common, contact with pets or other animals.
21.5. Geriatric Essentials:
 Causes of FUO in older patients are usually like general population,
but connective tissue disorders are more common.
 The most common causes are: Giant cell arteritis, lymphomas,
abscesses, tuberculosis.
Page | 222
21.6. Assessment:
History
 Temperature more than 38°C for babies or 37.5°C for children and
adults, Sweating, Chills, Headaches.
 body or joint aches, weakness, sore throat, fatigue, cough, rash,
sinus congestion.
 Fever with rigors or chills infection
 Fever that occurs every other day (tertian) or every 3rd day (quartan)
malaria
 Evening fevers and sweats which resolve by morning brucellosis
 Week-long fevers with week-long remissions tick-borne fever in
borreliosis, Pel-Ebstein in Hodgkin disease
 Periodic fevers cyclic neutropenia
 Double quotidian fever (two fever spikes a day) adult Still’s disease,
malaria, typhoid, and others.
 Morning fevers polyarteritis nodosa, tuberculosis, and typhoid
 Review of systems: nonspecific symptoms, such as: Weight loss,
anorexia, fatigue, night sweats, headaches, myalgias, arthralgias,
rashes (connective tissue disorders), diarrhea, steatorrhea,
abdominal discomfort (gastrointestinal disorders)
 Past medical history: history of Cancer, tuberculosis, connective
tissue disorders, alcoholic cirrhosis, inflammatory bowel disease,
rheumatic fever, hyperthyroidism
 Medication history: drug-induced fever or Injection drug use
Social history:
 Unprotected sex, multiple partners, etc..
 Contact with infected person (e.g., tuberculosis).
 Travel and possible exposure to animal or insect and tick vectors
 Smoking, alcohol use, and occupational exposure to chemicals.
 Exposure to birds (new pets, sick birds) Chlamydia psittaci infection
 Exposure to cats or cat litter toxoplasmosis
 Family history:familial Mediterranean fever
 Immunization status and dental history
Page | 223

full assessment should be performed and repeated
 General appearance: Sick or well
 Vitals: Unequal pulse in upper extremities Takayasu arteritis
 Skin, eyes, lymph nodes, throat, teeth
 Eyes Roth spots, retinal artery occlusion
 Oral ulcers
 Tender tooth on percussion, caries/gingivitis
 Abdominal palpation: Looking for organomegaly
 PR exam: prostatitis, perirectal abscesses
 Cardiovascular assessment:
 Cardiac murmur
 Tenderness to palpation of sternum hematologic malignancy
 Osler nodes, petechial, and splinter hemorrhages
 Pelvic exam
 Mental state changes meningitis and encephalitis
 Nails, joints, temporal arteries
 Inspect the perineum and feet, particularly in diabetics patients
 The entire body: palpated for areas of tenderness, swelling, or
organomegaly
 Thyroid exam
Complete blood count with differential:
 Eosinophilia 🡪polyarteritis nodosa, drug fever, or visceral
leishmaniasis
 Acute drop in hemoglobin may suggest hemorrhage or hematoma
(often retroperitoneal)
Liver function tests
 Alkaline phosphatase elevation suggests lymphoma or
granulomatous hepatitis
Erythrocyte sedimentation rate
 ESR > 100 in the absence of anemia may indicate giant cell arteritis,
multiple myeloma, or osteomyelitis
Page | 224
Urinalysis
 Hematuria may indicate renal cell carcinoma, tuberculosis,
endocarditis, brucellosis, lymphoma, or periarteritis nodosa
 Normal urinalysis or urine culture results do not eliminate perinephric
abscess. Almost 30% of patients with perinephric abscess have a
normal urinalysis, up to 40% present with sterile urine cultures
Basic cultures
Electrolytes:
Elevated total protein or calcium may suggest multiple myeloma.
HIV antibody test
Tuberculin skin test or interferon-gamma release assay
Peripheral blood smear
Biopsy:
Required if abnormality is suspected that can be biopsied (eg, liver, bone
marrow) must be evaluated by histopathology and cultured or sent for
PCR testing
Endoscopy:
to diagnose of inflammatory bowel disease and sarcoidosis.
Imaging tests:
 Chest radiograph
 CT of abdomen or pelvis with contrast agent
 MRI of brain
 PET scan
 Transthoracic or transesophageal echocardiography
 Venous Doppler study
21.8. Management:
 Treatment of FUO focuses on the causative disorder.
 Antipyretics should be used, considering the duration of fever.
 Close follow-up and reevaluation studies to prevent clinical
worsening.
Referral for:
 Any patient with progressive weight loss and other constitutional
signs
 immunocompromised patient (e.g., transplant recipients and HIV-
infected patients)
Admission for:
 Patient who is rapidly declining with weight loss
 If hospital admission may provide more work-up assessment options
Page | 225
Chapter 22: NEUROLOGY

22.1. Multiple sclerosis (MS)
22.1.1 Definition:
Is a chronic immune-mediated inflammatory illness involving the central
nervous system (CNS), brain, and spinal cord affecting sensation,
movement, vision, and other body functions with variable remissions and
progressions.
22.1.2 Etiology of MS:
It is unclear but could be related to: genetic factors and environmental
factors; low vitamin D, obesity, smoking, Epstein-Barr virus (EBV).
22.1.3 Deferential diagnosis:
 Degenerative Disease: Amyotrophic Lateral Sclerosis (ALS),
huntington Disease.
 CNS Infections: Tertiary Lyme, tertiary syphilis, human
immunodeficiency virus (HIV).
 Genetic Disorders: Mitochondrial disease.
 Nutritional & metabolic disorders: Folate deficiency, vitamin
B12 deficiency, hyponatremia, hypoglycemia, hypothyroidism,
diabetes mellitus.
 CNS Vascular Disease: Migraine with aura-Vasculitis -
Cerebrovascular accident (Stroke).
 Demyelinating Disease: Chronic inflammatory demyelinating
polyneuropathy.
 CNS Inflammations: Sarcoidosis, systemic Lupus Erythematosus
(SLE), sjogren Syndrome.
 Medications/ Recreational Drugs: alcohol abuse, cocaine abuse,
isoniazid.
 Psychiatric Disease: anxiety, conversion disorder, somatization.
 CNS Structural Disease: CNS neoplasm, arteriovenous malformation
22.1.4 Assessment:
History:
Presentation is varies among patients. Typical MS symptoms are as
follows:
 Insidious or sudden onset
 Fatigue
 Optic neuritis
 Sensory loss (as paresthesia)
Page | 226
 Spinal cord symptoms (motor)

 Spinal cord symptoms (autonomic)
 Cerebellar symptoms
 Heat intolerance
 Mental status examination: depressed mood
 Neurological and cranial nerves examination
 Special tests: Lhermitte’s sign –> electrical sensation down the spine
on neck flexion
 Investigations to exclude other causes: CBC, ESR, CRP, LFT, RFT,
electrolytes, calcium, TFT, FBG, HBA1c, vitamin B12 level and HIV
serology.
 Brain MRI: show white matter plaques.
 Spine MRI: if needed
 Evoked potentials: abnormal visual response
 Cerebrospinal fluid (CSF) analysis: if no clear radiological signs;
showed high protein content and oligoclonal bands of
immunoglobulin.
22.1.7 Diagnosis
 involvement of ≥ 2 areas of central nervous system (dissemination in
space) at different time (at least 3 months apart)
 exclusion of other conditions
 Refer suspected cases of MS to a neurologist
 There is no single diagnostic test for MS
22.1.8 Management:
 Multidisciplinary care is important to improve patients’ quality of life
 Treatment Goals: Treating acute exacerbations, Shortening the
duration of acute relapse, reducing frequency of relapses, preventing
disease progression and disability.
 Corticosteroids: use for acute exacerbations
 Disease-modifying therapies (DMTs)
 Monoclonal antibodies include natalizumab, ocrelizumab, rituximab,
ofatumumab, and alemtuzumab.
 Oral therapies include the fumarates, sphingosine 1-phosphate (S1P)
receptor modulators, teriflunomide, and cladribine.
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 Platform injection therapies: older injectable (intramuscular and

subcutaneous) forms of DMT include recombinant human interferon
beta-1b, recombinant human interferon beta-1a, and glatiramer
acetate.
22.2. Neuralgia:
The most common form of neuralgia is trigeminal neuralgia (TN) and
Postherpetic neuralgia (PHN).
22.2.1 Trigeminal neuralgia (TN):
Characterized by recurrent brief episodes of severe, sharp, unilateral
pain in the distribution of one or more branches of the trigeminal nerve.
22.2.2 Causes:
 Classic TN: NO apparent cause other than neurovascular
compression
 Secondary TN: caused by an underlying disease (e.g., multiple
sclerosis (MS), cerebellopontine angle tumor, and arteriovenous
malformation)
 Idiopathic: defined as TN with neither electrophysiological tests nor
MRI is showing significant abnormalities
22.2.3 Assessment:
History:
 Triggers: touching face, eating, talking, cold wind, shaving, applying
make-up
 Pain lasting from a fraction of a second to two minutes, severe
intensity, and electric shock-like, shooting, stabbing or sharp in quality
 Pain precipitated by triggers within the affected trigeminal distribution
22.2.4 physical examination:
 Generally normal examination
 General examination, comprehensive neurological exam and cranial
nerve examination.
 ENT and TMJ should be examined to rule out other differential
diagnosis.
 MRI to rule out structural lesion, MS, or vascular lesion.
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22.2.6 Diagnosis:
It is a clinical diagnosis by Diagnostic criteria by the ICHD-3 as below:
A) Recurrent paroxysms of facial pain unilaterally in the distribution of
trigeminal nerve and fulfilling criteria B and C.
B) Pain has the following characteristics:
 Pain lasting a fraction of a second to about 2 minutes
 Pain with severe intensity
 Electric-shock like or shooting pain with sharp quality
C) Innocuous stimuli precipitate the pain in the affected distribution
D) No alternative ICHD-3 diagnosis better explains the symptoms
22.2.7 Management:
 First line: carbamazepine or oxcarbazepine
 If the patient doesn’t respond, then consider using baclofen or
lamotrigine or Gabapentin
 Narcotics are not generally recommended
 If medical treatment fails, surgical decompression can be considered
 For acute pain may consider IV lidocaine or IV fosphenytoin
22.3. Myasthenia Gravis (MG)
22.3.1 Definition:
It is an autoimmune disease caused by antibodies against postsynaptic
membrane acetylcholine receptor > impaired neuromuscular
transmission > skeletal muscle weakness and muscle fatigue.
22.3.2 Clinical forms:
Generalized MG ( all skeletal muscles may be involve)
 Generalized Fatigue:
o Lack of energy or tiredness usually develops by the end of the
day (Fatigability is never a sole symptom).
 Amyotrophic Lateral Sclerosis [ALS]:
o Progressive neurodegenerative disorder
o It can involve the bulbar muscles  facial weakness, dysarthria,
or dysphagia.
o Ocular muscles are spared
o Positive upper motor neuron signs (hyperreflexia and Babinski
signs) and lower motor neuron signs (atrophy and fasciculations)
 Myasthenic Syndrome (Lambert Eaton Syndrome)
o Proximal limb weakness that improves with activity and
extraocular muscles are usually spared ,Associated with small-
Cell Lung Carcinoma.
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Ocular MG ( Weakness is limited to the extraocular and/or

eyelid muscles )
 Thyroid Ophthalmopathy:
o proptosis, lid retraction, lid lag, and periorbital edema without
ptosis.
 Brainstem & Cranial Nerve Pathology
o Third, fourth, and sixth cranial nerves
 Oculo-pharyngeal Muscular Dystrophy:
o Variable ptosis and weakness of the face, jaw, and neck & limb
weakness.
 Kearns-Sayre Syndrome
o Mitochondrial disorders, progressive symmetric ophthalmo-
paresis, and ptosis, no diplopia
22.3.3 Assessment:
History:
 The clinical hallmark of MG is that symptoms worsen with increase
muscle use throughout the day and improve by rest.
 Specific muscle weakness and not generalized muscle fatigue
 Early in the disease, symptoms may be absent upon awakening
 50% will present with ocular symptoms e.g. Diplopia, ptosis, blurry
vision.
 Asymmetric, alternating from one side to the other
 50% will present with bulbar symptoms: Dysarthria (nasal quality or
low-intensity voice, hypophonia with prolonged speech), Dysphagia,
Fatigable chewing
 Facial muscle weakness presents noticed by family members .
 Produced ptosis by sustained up-gaze for 1-2 minutes
 Diplopia > resolves by covering one eye
 Cogan’s Lid Twitch
 Eyelid curtaining
 Rest test: ptosis improvement by eye closure for 2-5 minutes.
 Facial muscles weakness ( expressionless face) especially loss of
smile or sneer appearance, dropped head if neck muscle weakness.
 Power: weakness in arms more than legs, proximal more than
distal(asymmetrical)
 Reflexes and sensory: normal
 Specific tests:
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o Ice Pack Test

o Tensilon Test
MG diagnosis can be established clinically, if MG suspected patient
should be referred to neurologist for for further investigations and
management.
 Acetylcholine receptor antibodies (AChR-Ab)
 Antibodies to muscle-specific receptor tyrosine kinase (MuSK-Ab)
 Electrophysiologic tests
 Screen for other autoimmune diseases; Thyroid, Sjogren syndrome,
rheumatoid arthritis, and SLE
 Brain MRI for a patient with bulbar or ocular symptoms
 Chest CT or MRI for all patients to exclude the presence of underlying
thymoma .
22.3.6 Management:
There are Four Principles in Treating MG:
 Symptomatic treatment by Acetylcholinesterase inhibitors, such as
pyridostigmine > it’s the First-line treatment
 Chronic immunosuppressive therapies; oral glucocorticoids are First-
line, then immunosuppressive agents as azathioprine.
 Rapid but short-acting immunomodulating treatments (therapeutic
plasma exchange and intravenous immune globulin [IVIG])
 Surgical treatment (thymectomy): for a patient with thymoma, or
generalized MG and positive AChR antibodies in patients <60 years
of age.
22.3.7 Precaution and prevention:
 Avoid drugs that may exacerbate myasthenia as some antibiotics,
Beta-blockers/Botulinum toxin,Chloroquine/Hydroxychloroquine…etc
 Avoid live-attenuated vaccines in patients with MG that taking
immunosuppressive
 Annual seasonal influenza vaccination and pneumococcal vaccines
are recommended.
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22.4. Paresthesia and neuropathy:

Peripheral neuropathies can be divided into three clinical syndromes:
 Mononeuropathies: Isolated disorders affecting single peripheral
nerve, mostly caused by nerve compression or entrapment
 Mononeuropathy multiplex: Involve multiple noncontiguous
peripheral nerves, either simultaneous or sequentially.
 Polyneuropathy (most common): Diffuse, generalized and usually
symmetric peripheral neuropathy (e.g., DM, Vitamin b12 deficiency,
exposure to alcohol or some medications).
22.4.1 Assessment:
History:
Neuropathic pain is shock-like or stabbing, more at night and ssociated
with hyperesthesia.
Important points:
 Is it progressive or not?
 Painful or not
 Associated symptoms of fever, night sweat, weight loss
 Exposure to neurotoxins like alcohol
 Previous chemotherapies, lead, mercury, arsenic, and thallium
 Medical history of diabetes
 Medication use, such as: Metronidazole, nitrofurantoin, phenytoin,
colchicine, amitriptyline, cimetidine, lithium, amiodarone, hydralazine,
isoniazid.
 Detailed Neurological examination and whether it is sensory, pure
motor,and autonomic
 Distribution of symptoms like distal, symmetric, proximal, and
asymmetrical or multifocal
Should be guided by history
 FBC, ESR, TSH
 Fasting glucose level and cholesterol panel
 Vitamin B12 level
 Hepatitis B and C, HIV, Lyme, and syphilis serologies
 Antinuclear antibodies (ANA)
 Nerve conduction studies and needle electromyography (EMG)
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22.4.4 Management:
 treatment of the underlying disease
 alleviation of symptoms related to the illness: FDA approved
medications for painful neuropathy are: pregabalin, gabapentin
(Starting dose:100 to 300 mg once to three times daily– Maximum
dose: 900 to 3600 mg daily in three divided doses), amitriptyline
(Starting dose: 10 to 25 mg daily – Maximum dose:150 mg daily),
duloxetine (Starting dose: 20 to 30 mg daily– Maximum dose), and
tapenade (extended release).
Chapter 23: NEPHROLOGY
23.1. Hematuria:
23.1.1 Etiology:
 False‐positive (contaminants)
 UTI
 Tubulointerstitial disease
 Nephrolithiasis (irritation)
23.1.2 Gross Hematuria:
Figure 23.1 – Approach to gross hematuria
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23.1.3 Microscopic Hematuria:

It is the presence of three or more red blood cells on a single, correctly
collected, non-contaminated urinalysis without evidence of infection is
considered clinically important microscopic hematuria. The causes of
Microscopic hematuria include:
 Unknown,
 UTI
 BPH
 Calculi, Bladder Cancer
 Polycystic kidney disease
 Renal disease
 Kidney Cancer
 Prostate Cancer
 Urethral stricture disease
23.1.4 Renal medical disease:
You should suspect renal disease if the patient has microscopic
hematuria, dysmorphic red blood cells, proteinuria, cellular casts, raised
serum creatinine level, or hypertension. Causes are:
 Glomerulonephritis (GN)
 Renal causes such as Arteriovenous malformation, hypercalciuria,
hyperuricosuria, medullary sponge kidney, polycystic kidney, renal
artery embolism, renal vein thrombus, and sickle cell disease
 Urologic such as Benign prostatic hyperplasia, cancer (kidney,
ureteral, bladder, prostate), cystitis, nephrolithiasis, trauma (foley,
exercise‐induced), and coagulopathies
23.1.5 Benign causes of hematuria:
Isolated, not persistent hematuria is typically benign. Many causes of
microscopic hematuria do not need a full diagnostic workup such as:
 Vigorous exercise
 Infection or viral illness
 Menstruation
 Exposure to trauma or recent urologic procedures (e.g.,
catheterization)
 BPH
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23.1.6 History
Historical red flags: The most common risk factors for urinary tract
malignancy in patients with microscopic hematuria:
 >35 years old
 Male sex
 Analgesic abuse NSAID
 Past or current smoking
 Exposure to chemicals or dyes at work (benzenes or aromatic
amines)
Risk factor for cancer of the urinary tract history of any of the following
 Gross hematuria
 Chronic indwelling foreign body
 Chronic urinary tract infection
 Pelvic irradiation
 History of exposure to recognized carcinogenic agents or alkylating
chemotherapeutic agents
 Irritating voiding symptoms
 Urologic disorder or disease
23.1.7 Examination:
 Women should have a pelvic examination to identify urethral masses,
diverticula, atrophic vaginitis, or a uterine source of bleeding.
 Men should have a rectal examination to assess the prostate.
 A serum creatinine level should be checked for medical renal disease
and to evaluate renal function before doing a contrast-enhanced
radiology test.
 Patients who are taking anticoagulants and found to have
asymptomatic microscopic hematuria, require a full urologic and
nephrological evaluation, including cystoscopy.
 The urinalysis (U/A): Color abnormalities
o Cloudy – often the result of precipitated phosphate crystals;
pyuria
o Orange – bile pigments, Pyridium
o Red – hematuria, hemoglobinuria, beets, blackberries, rifampin
o Yellow – concentrated urine, carrots
 Computed Tomography (CT) urography and cystoscopy for all
patients over 35 years of age with microscopic hematuria to rule out
malignant causes.
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 Multiphasic computed tomography (CT) urography is the image of

choice in the assessment of microscopic hematuria.
 The upper urinary tract is best assessed with multiphasic computed
tomography urography.
 The lower urinary tract is best assessed with cystoscopy for urethral
stricture disease, BPH, and bladder masses.
 cystoscopy (Assessment of lower urinary tract): it should be
performed on all patients with asymptomatic microscopic hematuria
who present with risk factors for malignancy, regardless of age.
 Renal ultrasound is less sensitive in detecting urinary calculi, small
renal masses, and urothelial lesions.
 Magnetic resonance urography: Sensitivity is greater than 90% for
detecting renal lesions.
 Retrograde pyelography
Figure 23.3 – Approach to asymptomatic microscopic hematuria
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23.2. Acute Kidney Injury (AKI)

23.2.1 Definition:
Increase in serum creatinine by ≥0.3 mg/dL (≥26.5 micromol/L) within 48
hours or increase in serum creatinine to ≥1.5 times baseline, occurred
within the prior 7 days or urine volume <0.5 mL/kg/hour for 6 hours.
23.2.2 Most common causes:
 Acute tubular necrosis (ATN) – 45%
 Prerenal disease – 21%
 Acute on chronic kidney disease – 13%
 ATN with prerenal disease
 Urinary tract obstruction – 10%
 Benign prostatic hyperplasia (BPH)
 Glomerulonephritis or vasculitis – 4%
 Acute interstitial nephritis – 2%
 Thromboembolic disease – 1%
23.2.3 Classification of AKI:
 Prerenal causes
o Actual intravascular volume depletion
o Gastrointestinal volume loss secondary to acute diarrhea or
malabsorption
o Urinary volume loss or cutaneous losses
o Diseases that lead to decreases in the effective arterial blood
volume
o Medications that reduce renal perfusion, ACE inhibitors
 Intrarenal causes
o Acute Tubular Necrosis (ATN)
o Acute Interstitial Nephritis (AIN)
 Postrenal causes
o Renal/ureteral calculi bilateral
o BPH
o Prostate cancer
o Retroperitoneal or pelvic neoplasms
o Anatomic abnormalities, urethral valves
o Urethral stricture, stenosis
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23.2.4 Clinical Presentation of AKI:

 Mild to moderate acute kidney injury are asymptomatic and
diagnosed by laboratory testing.
 Patients with severe AKI present with restlessness, confusion,
fatigue, anorexia, nausea, vomiting, edema, anemia, or bleeding,
Uremic encephalopathy (altered mental status, asterixis), anuria
(urine output less than 100 mL per day), oliguria.
 Serum creatinine: An increased serum creatinine level in a patient
with a previously normal documented level suggests a disease,
whereas a rise over weeks to months represents a subacute or
chronic disease.
 Urinalysis: It is the most important noninvasive test in the initial
workup.
 Complete Blood Count: The presence of acute hemolytic anemia with
the peripheral smear showing schistocytes in the setting of acute
kidney injury should raise the possibility of hemolytic uremic
syndrome or thrombotic thrombocytopenic purpura.
 Renal ultrasonography to rule out obstruction (i.e., a postrenal cause)
 Computed tomography or magnetic resonance imaging may be
required to diagnose extrarenal causes of obstruction (e.g., pelvic
tumors).
 Renal Biopsy: For diagnosis of intrarenal causes
 Fractional Excretion of sodium Na (FENa): Urine electrolytes can
help to differentiate between prerenal and renal AKI.
23.2.6 Important medications in renal disease:
 Metformin: Caution if GFR < 60 mL/min and reduce dose. Do not start
if GFR < 45 mL/min and do not use if GFR < 30 mL/min.
 Enoxaparin: cautious use if creatinine > 2 mg/dL, reduce dose by
50% if GFR < 30 mL/min.
 Nitrofurantoin needs GFR > 60 mL/min for clinical effectiveness and
to avoid toxicity.
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23.2.7 Contrast-Induced Nephropathy CIN:

Due to iodinated contrast agents, it is the 3rd leading cause of AKI in
hospitalized patients. It increases morbidity and length of hospitalization.
Diagnosis:
 Decline in renal function following the procedure.
 Increase in serum Cr ≥ 0.5 mg/dL and increase > 25% above
baseline in 2-3 days.
 Follows a predictable time course and begins to improve in 3-7 days.
 Usually reversible – resolves by 2 weeks.
 Most importantly, it is preventable.
 Risk of developing ESRD is ~ 4%.
 Incidence is 1 – 2% in patients with normal renal function (even if DM)
and up to 25% in patients with CKD
 Prevention general guidelines include avoid volume depletion, avoid
nephrotoxins (NSAIDs), and hold metformin for 48 hours.
CIN Management of At-Risk Patients
 Before a Dye Study: Stop all diuretics, ACE-I/ARB, metformin, NSAID
 Prevention – high risk (Cr >1.5 mg/dl, GFR <60 ml/mm)
 IV Normal saline
23.2.8 Management:
 Patients with AKI generally should be hospitalized. Unless mild and
resulting from an easily reversible cause.
 Management is primarily supportive, treat the underlying cause if
identified
 AKI with volume overload treated with:
o Furosemide IV q 6 hrs is the initial Rx • 20-100 mg initially
o If inadequate response after 1 hr, double the dose, Repeat the
process until adequate urine output
o Ultrafiltration via dialysis (last resort)
 Hyperkalaemia treated with Sodium polystyrene sulfonate Orally 25-
50 g mixed with 100 mL of 20% sorbitol and Rectally 50 g in 50 mL of
70% sorbitol and 150 mL of tap water. Other ways of treating
hyperkalemia are as follows:
o Cardio protective/membrane stabilizer temporarily reverses the
neuromuscular effects of hyperkalemia Calcium gluconate 10%
solution – 10 mL IV
o Temporarily shift K+ intracellularly: Insulin – 10 units IV and
glucose 25 gm, Inhaled beta-agonists and Sodium bicarbonate, 3
ampules in 1 L of 5% dextrose are used.
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o Dialysis if refractory.
 AKI – Acidosis: If serum level <15 mEq/L or pH <7.2 give Sodium
bicarbonate IV or PO
23.3. Chronic Kidney Disease (CKD):
23.3.1 Definition of CKD could be any of the following:
 Kidney damage for > 3 months, structural or functional abnormalities,
with or without decreased kidney function (GFR); changes could be
pathological abnormalities, markers of kidney damage, including
abnormal blood, urine, imaging tests, or persistent Albuminuria. Or a
GFR < 60 mL/min/1.73 M2 for > 3 months With or without kidney
damage.
 > 3 months Duration is necessary to distinguish chronic from acute
kidney diseases. Clinical evaluation can often suggest duration,
recheck GFR and albumin after 3 months to differentiate between
Acute Kidney Injury (AKI) and CKD.
Pathologic abnormalities: The cause is based on underlying illness
and pathology.
 Glomerular diseases (autoimmune diseases, drugs)
 Vascular diseases (atherosclerosis, hypertension, vasculitis)
 Tubulointerstitial diseases (stones, obstruction, urinary tract
infections, drug)
 Cystic disease (polycystic kidney disease)
23.3.2 Etiology:
 Diabetic kidney disease (39%)
 Nondiabetic kidney disease (61%)
o Vascular diseases 25%: Hypertension, ischemic renal disease
o Glomerular diseases 18%: lupus nephritis, vasculitis,
membranous nephropathy, minimal change disease, focal
segmental glomerulosclerosis, immunoglobulin A nephropathy
o Polycystic kidney disease 7%
o Tubulointerstitial disease 4% Urinary tract infections,
nephrolithiasis, obstruction, sarcoidosis, multiple myeloma, drug
toxicity (e.g., proton pump inhibitors, NSAIDs)
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23.3.3 Clinical presentation:

Patients with kidney disease may have a variety of different clinical
presentations.
 Systemic symptoms include hypertension, edema, pruritus, hiccups,
and uremia.
 Symptoms due to the kidney include gross hematuria, and flank pain
 Asymptomatic and noted on routine examination to have a raised
serum creatinine concentration or an abnormal urinalysis proteinuria
or hematuria
 UA with microscopic exam
 24-hour urine creatinine clearance or estimated GFR
 24-hour urine or random protein excretion or ACR: Albumin/Creatinine
Ratio and PCR: Protein/Creatinine Ratio
 CBC
 Comprehensive Metabolic Panel (CMP)–Includes BUN, CR.,
GLUCOSE, ALB., Total Protein, Hepatic panel.
 Calcium & phosphorus levels
 Uric acid level
 Serum protein electrophoresis (SPEP)
 Hepatitis BsAg, Hepatitis C antibody, HIV
 ANA
 C3, C4, & CH50
 ANCA
 Anti-GBM antibody
 Renal ultrasound
 CT scan of the kidneys and liver
 MRI of the kidneys
 Renal angiogram
 Voiding cystourethrogram
 Renal biopsy
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23.3.5 Management:
Table 23.1 Management of CKD based on stages
Stage I Management of comorbidities, slowing progression,
CV risk reduction
Stage II Management of comorbidities, slowing progression,
CV risk reduction
Stage III Evaluation and treatment of complications
Stage IV Nephrology referral
Stage V Replacement/dialysis
23.3.6 Monitoring CKD:

 eGFR should be obtained at least yearly (eGFR Cockcroft-Gault
equation)- More often in patients with:
o GFR < 60 mL/min/1.73 m2 stage G3
o Risk factors for faster progression
 Chronic Kidney Disease medication review
o Review medications at all visits. Paying attention to over-the-
counter medication, NSIAD, and herbal supplements.
o Each visit medications dosage adjustment based on eGFR level.
 Detection of potentially adverse effects on renal function or
complications of CKD such as diuretics, Ace inhibitors.
23.3.7 Indications for Nephrology Referral:
 Acute, complex, or severe cardiovascular disease
 Anemia of CKD
 Bone and mineral disorder of CKD
 Difficult to manage adverse effects of medications
 Hyperkalemia K+ > 5.5 mEq/L (despite treatment)
 Refractory proteinuria Urinary albumin/creatinine ratio > 300 mg/g
 Resistant hypertension. Target blood pressure not achieved with the
use of at least three BP drugs
 Stage 4 CKD GFR < 30 mL/minute
 Unexplained decrease in GFR > 30% over 4 months
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23.3.8 Renal Replacement: dialysis and kidney

transplant
 Absolute indications
o Refractory hyperkalemia
o CHF
o Refractory metabolic acidosis
o Pericarditis
 Relative indications
o GFR <10 ml/min or <15 ml/min in diabetes
o Creatinine > 8 mg/dl or >6 mg/dl in diabetics
o Uremic symptoms
 Relative contraindications
o Quality of life limits meaningful survival
o Debilitating chronic diseases
o Terminal illness
Chapter 24: PULMONARY
24.1. Hemoptysis:
24.1.1 Definition:
Hemoptysis is the term for the expectoration of blood from the lower
respiratory tract
24.1.2 Etiology:
 Infectious: Tuberculosis, Viral bronchitis, Streptococcus pneumonia,
etc
 Vascular: Pulmonary embolism with parenchymal infarction, etc
 Mechanical and other causes
 Malignancy: Bronchogenic carcinoma or Pulmonary metastases
24.1.3 Assessment:
Key features of the history and examination include the following points:
Table 24.1
History and examination Suggested etiology
Cough Bronchiectasis, COPD, foreign body,
pneumonia, TB
Fever Bronchitis, lung disease, neoplasm,
pneumonia, pulmonary embolism, TB
Sputum production Bronchiectasis, COPD, pneumonia, TB
Weight loss COPD, lung cancer, TB
Smoking Bronchitis, COPD, lung cancer
Page | 243
Trauma Airway trauma, pulmonary embolism

Anticoagulant use Coagulopathy
Recent surgery or Pulmonary embolism
immobilization
Immunosuppression Bronchitis, lung abscess, pneumonia and
TB
Heart disease Congestive heart disease, valvular heart
disease
Is there blood in the To differentiate between hemoptysis and
anterior nose? pseudohemoptysis
Any abnormalities on COPD, pneumonia, bronchitis
chest examination (eg,
focal wheeze,
adventitial sounds or a
bruit)?
Audible chest bruit or large pulmonary arteriovenous
murmur that increases malformation
with inspiration
pulmonic heart sound pulmonary hypertension.
(P2) augmented, or
murmurs of tricuspid
regurgitation or
pulmonic insufficiency
telangiectasias on the hereditary hemorrhagic telangiectasia
lips, tongue, or buccal
mucosa
Clubbing Lung cancer
Skin rash vasculitis, systemic lupus erythematosus
(SLE), fat embolism, or infective
endocarditis
Bruising coagulopathy or thrombocytopenia
Conjunctival endocarditis or vasculitis
hemorrhage or splinter
hemorrhage
Needle-tracks right-sided endocarditis
 Hemoglobin and hematocrit (to assess the chronicity and magnitude
of bleeding) and white blood cell count and differential (evidence for
infection)
 Urinalysis and renal function (to screen for pulmonary-renal
syndromes).
Page | 244
 Liver function tests, and a coagulation profile (to exclude

thrombocytopenia).
 Chest Radiography is the initial analysis for all patients with
hemoptysis
 Chest CT: If diagnosis remains unclear
 Bronchoscopy when a CT scan is unrevealing
24.1.5 Management:
Massive hemoptysis: stabilize the patient, ABCs and transfer to EMS.
Non-massive Hemoptysis: Treat the underlying cause.
Red flags
 Massive bleeding
 Shortness of breath
 Reduced/absent breath sounds
 Malaise
 Weight loss
 Fatigue
 Back pain
24.2. Fibrosing Alveolitis (Idiopathic Pulmonary
Fibrosis)
24.2.1 Definition:
Idiopathic chronic fibrosing (IPF) is an interstitial pneumonia with a
histopathologic or radiographic pattern of interstitial pneumonia (UIP).
 ≥60 years old
 Men > women
 history of cigarette smoking
24.2.3 Clinical manifestations:
 Gradual onset (over several months) of dyspnea on exertion
 Nonproductive cough
 Fatigue
 Fever
 Myalgias
 Arthralgias
 Bibasilar crackles in auscultation (unilateral in early finding)
 Clubbing (advance disease)
Page | 245
 Laboratory testing with selected serologic tests can help identify
underlying rheumatic disease and hypersensitivity pneumonitis or DD.
 Chest Xray
 High resolution computed tomography (HRCT).
 Bronchoalveolar lavage (BAL)
 Lung biopsy
 Rheumatic diseases (e.g., rheumatoid arthritis, systemic sclerosis)
 Chronic hypersensitivity pneumonitis
 Asbestosis
 Certain drug-induced lung diseases
24.2.7 Management:
 Supportive care
 supplemental oxygen
 Pulmonary rehabilitation
 Vaccines: COVID-19, pneumococcal, and seasonal influenza
 Antifibrotic therapy
 Lung transplantation
24.3. Extrinsic Allergic Alveolitis (Hypersensitivity
Pneumonitis) (HP)
24.3.1 Definition:
It is a pulmonary disease that occurs due to inhalational exposure to a
variety of antigens leading to an inflammatory response of the alveoli and
small airways.
Classified as acute, subacute, or chronic based on its clinical
manifestations or classified as non-fibrotic and fibrotic subtypes.
24.3.2 Clinical manifestations:
 Dyspnea
 Cough
 Fever
 Chills
 Weight loss
 Malaise
 Chest tightness
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 Auscultation: crackles, mid inspiratory squeaks, and occasional
wheezes
 Clubbing
 Laboratory panels for measuring specific blood immunoglobulin (Ig) G
antibodies (eg, precipitins)
 Chest x-ray
 High-resolution computed tomography (HRCT)
 Bronchoalveolar lavage (BAL)
 Transbronchial lung biopsy (TBLB)
24.3.5 Diagnosis:
A clinical diagnosis via initial evaluation of:
 Exposure to an offending antigen (with or without positive serum
specific immunoglobulin G [IgG])
 Clinical symptoms ( as mentioned above)
 HRCT finding compatible with HP
 Improvement with antigen avoidance
 Hot tub lung
 Inhalation “metal fume” fever
 Organic dust toxic syndrome
 Chronic bronchitis
 Asthma
 Airway-centered interstitial fibrosis
 Other causes of centrilobular nodules on HRCT
24.3.7 Management:
 Avoidance of suspected or causative antigen
 Corticosteroids can be used severe or progressive disease
 Lung transplant.
24.4. Solitary Pulmonary Nodule (SPN)
24.4.1 Definition:
It is defined as a single, well-circumscribed, radiologic opacity that
measures up to 3 cm in diameter and is surrounded completely by
aerated lung.
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24.4.2 Etiology of SPN:

 Benign Causes such as Infectious granuloma by TB or Atypical
mycobacteria, Hamartoma, Sarcoidosis
 Malignant Causes such as Adenocarcinoma, Squamous cell
carcinoma, Solitary metastasis, etc
24.4.3 Assessment:
 Most solitary pulmonary nodules are incidental findings on imaging
studies of the chest, abdomen, and upper extremities.
 It is important then to have full history and physical examination for
the patient to evaluate the risk factors for pulmonary malignancy.
 Ask about recent symptoms, history of smoking, history of lung
diseases, and any malignancies for the last 5 years. Consider patient
age, traveling and family history and occupational exposure for
assessing cancer risk.
 Physical examination: SPNs usually have no specific physical
findings in asymptomatic patients.
24.4.4 Risk assessment
 The probability of malignancy can be assessed clinically or by
quantitative predictive models as one of three risk categories:
o Very Low Probability (less than 5%)
o Low/Moderate Probability (5% to 65%)
o High Probability (greater than 65%)
Table 24.2 (Mayo Clinic Prediction Model) Calculating the
Malignancy Probability of a Pulmonary Nodule
Age Patient’s age in years
Cancer history 1 if patient has a history of extra thoracic
cancer diagnosed more than five years before
nodule detection (otherwise = 0)
Diameter Diameter of the solitary pulmonary nodule in
mm
Location 1 if nodule is located in the upper lobe
(otherwise = 0)
Smoking 1 if patient is a current or former smoker
history (otherwise = 0)
Spiculation 1 if spiculation is present (otherwise = 0)
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24.4.5 Diagnostic evaluation:

 Chest x-ray
 Chest CT thin slice (1mm) section is the recommended modality for
assessment of SPN.
 Positron emission tomography (PET) scan:
 Non-surgical biopsy
 Surgical resection:
24.4.6 Indications for Referral:
 When the patient has lesions that require biopsy by bronchoscopy,
interventional FNA or thoracoscopic surgery.
 When the best management approach is unclear.
24.4.7 Red flags- SPN risk of malignancy:
 Old age
 History of smoking
 History of exposure to asbestos or radiation.
 History of malignancy.
 Family history of lung cancer
 History of emphysema and fibrotic lung disease
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Section 3: Pediatric
Chapter 1: NEONATAL JAUNDICE
Definition:
 Yellowish discoloration of skin and sclera that resulted from
hyperbilirubinemia.
 The American Academy of Pediatrics (AAP) recommends universal
screening with bilirubin levels (either with TSB or TcB) or targeted
screening based on risk factors.
 Classified to:
Table 1.1 – Classification of newborn jaundice
Benign hyperbilirubinemia Pathological hyperbilirubinemia
(physiological jaundice)
– Appears after 24 hours of life – Appears within 24 hours of age
– Maximum intensity by 4th-5th day – Increase of bilirubin > 5 mg

in term & 7th day in preterm /dl/day or at a rate of 0.2 mg/dl/hr
– TSB levels within normal – Serum bilirubin >95 percentile

percentiles for age in hours based for age in hours based on
on nomogram nomogram
– Clinically not detectable after 14 – Jaundice persisting after 14

days days in full-term babies
– Disappears without treatment – Stool clay/white color and urine

staining clothes yellow
– Direct bilirubin >2 mg/dl or 20%

of TSB

 Skin and sclera yellowish discoloration
 Growth and development
 Signs of CV dysfunction
 Organomegaly
 Abdominal masses
 Ascites
 Neurological involvement
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 Bilirubin (total, direct)
 CBC
 Coombs test
 Blood type and Rh status
Prevention:
 The goal is to prevent the occurrence of encephalopathy and
kernicterus.
 Ensure adequate feeding.
 All hospitalized newborns should be routinely monitored for the
development of jaundice every eight to 12 hours.
 Promote and support breastfeeding.
 Measure bilirubin levels in all infants with jaundice in the first 24 hours
after delivery
Chapter 2: DYSPEPSIA IN CHILDREN

Definition:
 The passage of stomach content into the esophagus with or without
regurgitation (spitting up) and vomiting.
 Infants reflux or regurgitate a portion of their feeding, refuse or
prolonged feeding.
 Failure to thrive or poor weight gain.
 Chest pain, asthma symptoms such as cough or wheezing may be
worsened.
 Generalized stomach aches, nausea, vomiting.
 Sandifer syndrome (neck tilting), lethargy, or seizure
 Diagnosis based on symptoms and physical exam finding.
o Common differential diagnosis includes (Acute gastroenteritis,
Cow’s milk allergy, Hiatal hernia, Infectious etiologies outside the
GI tract, Rumination syndrome)
 Monitor for vitals and growth parameters.
 Monitor for bilious or forceful vomiting, GI bleeding, or persistent
diarrhea.
 Monitor for apnea or cyanosis.
 Upper intestinal endoscopy with biopsies & pH probe are helpful in
making diagnosis.
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Management plan:
 Nonpharmacological by:
o Providing small, frequent feeds thickened with cereal
o Upright positioning after feeding
o In older age: lower fat diet, avoid spicy, citrus products, coffee,
tea, cola, or chocolate.
 Pharmacological: Long-term acid suppression therapy, empirical 4
weeks trial using acid suppressing therapy with H2 receptor
antagonist or proton pump inhibitors.
 Surgical intervention by Fundoplication may be required for severe
cases.
Chapter 3: EMERGENCIES IN
CHILDREN
3.1. Meningitis:
3.1.1 Definitions:
 Meningitis: inflammation of the leptomeninges tissue covering the
brain and spinal cord.
 Encephalitis: is an inflammation of brain parenchyma.
 Meningoencephalitis: is an inflammation of the brain and meninges
(less common but devastating).
3.1.2 Signs and symptoms:
 Fever
 Vomiting
 Poor feeding
 Seizures.
 Neck stiffness
 Headache
 Confusion.
 Nuchal rigidity
 Focal neurologic findings
 Cutaneous findings – petechiae and purpura
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3.1.3 Investigations
 Examination of the cerebrospinal fluid (CSF) is the cornerstone of the
diagnosis.
o CSF exam includes:
 Opening pressure
 Cell count (and differential count)
 Chemistry (i.e., CSF glucose and protein)
 Microbiology (i.e., gram stain and cultures) which confirm
the diagnosis.
o Spinal fluid should be sent for cell count, protein, glucose, gram
stain, and culture.
 PCR is helpful in diagnosing viral meningitis.
 Blood culture – positive in approximately 60 to 85% of patients
 Lactate level if there is concern for septic shock.
 Other investigations: ESR, CRP, Procalcitonin, latex agglutination
test, counter immunoelectrophoretic.
3.1.4 Management
 Unstable children suspected to have bacterial meningitis should
receive antibiotics as soon as possible.
 Head CT if focal neurological signs are present (Treat! don’t wait for
results of LP or scan)
 Antibiotics:
o Due to difficulty in penetrating the blood brain barrier, antibiotic
doses used to treat meningitis are higher than what is used in
other infections.
 For viral meningitis and meningoencephalitis:
o Supportive treatment
o Acyclovir should be used when HSV infection is suspected.
 Steroids
o Inflammatory response of bacterial meningitis can cause CNS
damage mostly as labyrinthitis, producing a sensorineural
hearing loss.
o Dexamethasone therapy may reduce CNS inflammation and can
be used adjunct to antibiotic therapy.
 Disposition and follow up.
o After discharge, children need long-term monitoring for
neurodevelopmental problems and hearing loss.
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Table 3.1
Length of
Etiology Suggested therapy
treatment
Empirical Vancomycin 10-15 mg/kg IV q8hrs
+ ceftriaxone 2 g IV q 12 hrs
+/- Dexamethasone 0.15 mg/kg q6 hrs
for 4 days or
0.4 mg/kg ql2 hrs for 4 days
If > 50 years, add ampicillin 2 g IV
q4hrs
S. pneumoniae If PCN MIC Al ug/ml: ceftriaxone 2 g IV 14 days
ql2hrs
If PCN MIC 2 ug/ml or ceftriaxone MIC
1ug/ml: vancomycin 10-15 mg/kg IV
q8hrs
N. meningitidis If PCN MIC <0.1 ug/ml: ampicillin 2 g 7 days
IV q4hrs
If PCN MIC 0.1ug/ml: ceftriaxone
2 g IV ql 2hrs
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L.monocytogenes Ampicillin 2 g IV q4hrs 21 days
If PCN allergy use TMP/SMX 5 mg/kg
q8hrs
Viral meningitis Supportive measures acyclovir for
HSV or HZV
Antiretroviral drugs for HIV
3.2. Epiglottitis:
3.2.1 Definition:
 Acute inflammatory condition of the epiglottis that may progress
rapidly to life-threatening airway obstruction.
 Haemophilus influenzae type B vaccine has significantly reduced the
number of cases of childhood epiglottitis.
 In the post vaccine era, most cases of infectious epiglottitis are
caused by:
o Streptococcal and staphylococcal species
o Candida species in immunocompromised patients
 Non-infectious causes:
 Thermal injury
o Caustic bums
o Direct trauma
3.2.2 Signs and symptoms:
 Sudden onset of high fever
 Stridor
 Drooling
 Tripod posture
 Change in voice (muffled, “hot potato” voice)
 Severe sore throat and dysphagia.
 Toxic appearance and distress (agitation, restlessness, irritability).
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 Classic presentation of epiglottitis is diagnostic, no need for
investigations or radiography.
 In case of Uncertain diagnosis: ordering neck radiographs may show
“thumb sign” an enlarged epiglottis protruding from the anterior wall of
the hypopharynx and thickened aryepiglottic folds.
3.2.4 Management
 Keep the child calm and transfer to the ED!
 Provide oxygen.
 The most skilled individual available should perform intubation as
soon as the diagnosis is made, if failed surgical airway is required.
 Medication:
o Nebulized racemic or l-epinephrine ( +/- steroids)
o Second or third generation cephalosporins: typically continued
for 7 to 10 days
 Cefuroxime (50 milligrams/kg IV) or Ceftriaxone (50
milligrams/kg IV)
 Vancomycin (10 milligrams/kg IV): may be added due to
increasing incidence of Staphylococcus aureus and highly
resistant Streptococcus pneumonia as a cause of
epiglottitis.
3.3. Airway Foreign Body
 Most foreign body ingestions occur in children between ages of six
months and three years.
 Most ingested foreign bodies pass spontaneously:
o Only 10 to 20% require endoscopic removal.
o Less than 1% require surgical intervention.
 Common foreign bodies:
o Coins, button batteries, sharp objects, food impaction, magnets,
multicomponent objects, superabsorbent polymers, and objects
containing lead.
3.3.1 Signs and Symptoms:
 Most of the cases are asymptomatic, but when symptoms do occur,
they are often related to the location of the foreign body:
 Esophagus:
o Refusal to eat.
o Dysphagia
o Drooling
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o Respiratory symptoms including wheezing, stridor, or choking.

o Ulceration.
o Sharp objects may perforate the oesophagus, resulting in neck
swelling, crepitus, or pneumomediastinum.
 Stomach:
o Vomiting
o feeding refusal
o Non- bilious vomiting
o Gastric distension
 Intestines: Objects that pass beyond the pylorus and into the
intestines are usually asymptomatic and pass spontaneously.
 Plain x ray
 Us
 CT or MRI
3.3.3 Management:
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3.4. Poisoning:
3.4.1 Definition:
 Defined as any substance that causes cell injury or destruction either
by inhalation, ingestion, injection, or absorption of that substance.
 Drugs and corrosive agents are the most frequent agents.
 The index of suspicion should be raised if:
o At-risk age group: one to four years of age (peak at 2 years)
o Previous history of ingestion.
 Medication poisoning should be considered in the differential
diagnosis of children who present with:
 Acute onset of multi-organ system dysfunction.
 Altered mental status.
 Respiratory or cardiac compromise
 Pupillary findings: Mydriasis/miosis/nystagmus
 Unexplained metabolic acidosis
 Seizures
 Puzzling clinical picture
 State of physiologic excitation:
o Central nervous system stimulation
o Elevated: temperature, pulse, blood pressure, and respiratory
rate
 State of depression:
o Depressed mental status
o Depressed: temperature, pulse, blood pressure and respiratory.
 acid-base status, electrolytes, Renal function.
 Blood glucose
 Serum osmolality, AST, ALT, urine dipstick test.
 Quantitative acetaminophen serum concentration: If acetaminophen
ingestion suspected
 Quantitative salicylate serum concentration: if respiratory alkalosis
and/or metabolic acidosis
 ECG
 CXR
 Toxicology screen.
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3.4.4 Management:
 Supportive care:
o Airway protection
o Blood pressure stabilization
o Agitation treatment
o Controlling the cardiac rhythm and seizure.
 Decontamination: (e.g. Activated charcoal)
 Antidote
 Enhanced elimination:(e.g. Ion Trapping, Multi- dose Charcoal,
Hemodialysis, Chelation, Hemoperfusion)
Chapter 4: NEONATAL LEG AND FOOT

ABNORMALITIES
Background:
 It is normal for a parent to be concerned about the health and future
of their children as they are growing up.
 Although many of these conditions can be easily corrected without
any help as the child grows, it is still essential to observe them
throughout this period.
Common paediatrics foot conditions
4.1. In-Toeing
4.1.1 Definition:
 is a condition where the toes point inward when a child walks (instead
of pointing forward). It is commonly called “Pigeon-Toed”, and it is one
of the most common reasons for parents to bring their child to a
doctor.
 It is important to emphasize that most cases are part of normal child
development and will resolve on their own.
4.1.2 Diagnosis:
 The in-toeing (internal rotation of the leg) is typically seen by parents
once the child begins walking (most commonly noticed between the
ages of 1-3 years old). It’s usually seen in both legs.
 falling or tripping more frequently.
 The first step in diagnosis is for the doctor to simply watch the child
walking and to look at the angle of the foot.
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 Femoral anteversion
 The most common cause of in-toeing in school-aged children and is
most severe between four and seven years of age.
 Increased internal rotation (60 to 90 degrees) with reduced external
rotation (10 to 15 degrees) is diagnostic of femoral anteversion.
 Spontaneous resolution occurs in more than 80% of children by eight
years of age.
 Special shoes, braces, connective bars, and other orthotics are not
effective. Surgical intervention is indicated for children older than
eight years with severe functional or cosmetic abnormality.
 Internal tibial torsion
 A common normal rotational variant, usually present in toddlers. The
child walks with patellae facing forward and feet pointing inward,
producing an internally rotated thigh-foot angle and negative foot
progression angle on the torsional profile.
 Internal tibial torsion usually resolves spontaneously by five years of
age.
 Braces, night splints, shoe modification/wedges, other orthotics, and
serial casting are not recommended for this condition.
4.2. Out-toeing
4.2.1 Definition:
 an outward-pointing foot, is less common than in-toeing.
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4.2.2 Types and Management:

4.2.3 External tibial torsion:
 Usually presents between four and seven years of
 Physical examination reveals a positive foot
progression angle and a thigh-foot angle greater
than 30 degrees.
 Surgery to correct external tibial torsion is rarely
recommended before 10 years of age.
4.2.4 Femoral retroversion:

 Common in newborns because of contracture of the hip from
intrauterine positioning and is diagnosed when the feet of a pre-
walking child are rotated outward by nearly 90 degrees (i.e., Charlie
Chaplin appearance).
 It typically improves during the first year of walking.
 Persistence after three years of age warrants radiography of the
pelvis, hips, and lower extremities and referral to an orthopaedist.
 If femoral retroversion is diagnosed after eight years of age, it may
be associated with a slipped capital femoral epiphysis (SCFE).
4.3. Toe Walking
 a pattern of walking in which a child walks on the balls of his or her
feet, with no contact between the heels and ground.
 Toe walking is common in children who are learning to walk. After the
age of 2, however, most children outgrow toe walking and begin to
walk with a normal heel-to-toe pattern.
 In the vast majority of children, toe walking is idiopathic, however,
persistent toe walking can be a sign of an underlying medical
condition, such as:
o cerebral palsy
o muscular dystrophy
o spinal cord abnormality
4.3.1 Nonsurgical treatment
 For children who are 2 to 5 years old and able to walk flat-footed
 This includes observation, serial casting, bracing, and botox therapy.
4.3.2 Surgical treatment
In children over the age of 5 years.
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4.4. Angular Variations Problems

4.4.1 Genu varum deformities
 Typically bilateral, symmetric, and self-limited.
 Bracing, connective bars, and other orthotics are not necessary for
most patients.
 Persistence after two years of age is unusual.
 Adolescents who participate in high-impact sports may develop genu
varum.
 Pathologic genu varum may be due to rickets, skeletal dysplasia, or
Blount disease (abnormal growth of medial proximal tibial physis that
is associated with obesity).
4.4.2 Genu valgum

 Also known as knocked knees.
 Child’s knees meet when they stand and have a gap between the two
ankles.
 This condition almost always corrects itself by the age of seven, so
there is no need for any treatment. However, when one side is a lot
more pronounced and is painful, they may need surgery.
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4.5. Tips to Ensure Healthy Feet

 While toddlers are still learning to walk, let them go barefoot or wear
only socks. Shoes will inhibit their feet and toes’ growth.
 If your child is into sports, make sure they warm up before physical
activity and cool down afterward. Encourage them to stretch and do
exercises to strengthen their calf muscles.
 Shoes: Finding the Right Fit.
 Avoid heels.
 Children’s shoes should be replaced:
o Children under 3: replace 3-4 times a year.
o Children 4- 8: 2-3 times a year.
o Children above 8 to 12: 2 times a year.
o Teenagers: 1 a year
Chapter 5: CONGENITAL HEART

DEFECTS
5.1. Acyanotic Congenital Heart Diseases
5.1.1 Ventricular septal defect (VSD):
Background
 Ventricular septal defect (VSD) is one of the most common congenital
heart defects (second only to bicuspid aortic valve) at birth, but
accounts for only 10% of congenital heart defects in adults because
many close spontaneously.
 Small defects: asymptomatic closes spontaneously over time.
Assessment
Presentation
 Small VSD: typically present with an asymptomatic cardiac murmur.
 Moderate to large VSD: typically present by 3 to 4 weeks of life with
symptoms and physical findings of heart failure, which may include:
o Tachypnea & Tachycardia
o Poor feeding, Poor weight gain
o Hepatomegaly
o Pulmonary rales, grunting, and retractions.
o Pallor (from peripheral vasoconstriction)
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Physical exam
 Small defects: loud holosystolic murmur at LLSB (may not last
throughout systole if defect is very small)
 Medium or large defects:
o symptoms such as CHF, symptoms of bronchial obstruction,
frequent respiratory infections, failure to thrive.
o Split or loud single S2; holosystolic murmur at LLSB without
radiation; grade 2 to 5; may also hear a grade 1 or 2 mid-diastolic
rumble.
Investigations
 ECG
 Chest x-ray
 Echocardiogram
Management
 Surgical repair
 Transcatheter repair
5.1.2 Atrial septal defect (ASD):

Background
 Atrial septal defects (ASDs) are common, accounting for
approximately 10 to 15 % of congenital heart disease.
 Usually asymptomatic and found incidentally.
 Infants with large ASDs present with symptoms of heart failure,
recurrent respiratory infections, or failure to thrive. Failure to thrive in
infants with ASDs may be associated with extracardiac pathology.
Physical examination
Physical examination findings are dependent on the size of the defect,
the degree of shunting, and the pulmonary arterial pressure.
Characteristic findings include:
 Mid-systolic pulmonary flow or ejection murmur accompanied by a
fixed split second heart sound (S2) .
 Ejection systolic murmur and/or fixed split of S2 was present in >90
percent of patients with ASD.
Investigations
 ECHO
 MRI in selected cases
Page | 264
Management
Important considerations in the management of a child with an isolated
ASD include:
 Size, degree of shunting, and persistence of the ASD.
 Likelihood of spontaneous closure.
 When closure is indicated, deciding between surgical and
percutaneous transcatheter closure.
5.1.3 Patent ductus arteriosus (PDA):
Background
 The ductus arteriosus (DA) is a fetal vascular connection between the
main pulmonary artery and the aorta that diverts blood away from the
pulmonary bed. After birth, the DA undergoes active constriction and
eventual obliteration. A patent ductus arteriosus (PDA) occurs when
the DA fails to completely close postnatally.
Assessment
 Small patent ductus arteriosus — no identifiable symptoms and
commonly identified incidentally by the detection of the characteristic
continuous flow murmur.
 Moderate patent ductus arteriosus — may present with exercise
intolerance. In these patients, the moderate left-to-right shunt
increases the volume load on the left atrium and ventricle, which
results in left ventricular dilation and dysfunction.
 Large patent ductus arteriosus — initially causes left ventricular
volume overload. Over time, there may be a progressive rise in
pulmonary artery pressures, which, in the uncorrected patient, may
lead to irreversible pulmonary vascular changes. With sufficiently
increased pulmonary vascular resistance, flow reverses to a right-to-
left shunt, and over time, these patients develop cyanotic heart
disease (ie, Eisenmenger syndrome). The characteristic continuous
murmur decreases as the pulmonary pressure rises and ultimately
disappears. The pulmonary component of S2 increases.
Investigations
 Echocardiography
 2-dimensional ECHO
 MRI
Management
Indications for closure:
 Moderate and large PDAs
 Prior episode of endocarditis
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 Patients with severe pulmonary arterial hypertension

Interventions for PDA closure include:
 Pharmacologic therapy, used exclusively in premature infants,
inhibitors of prostaglandin synthesis (indomethacin and ibuprofen)
 Surgical ligation.
 Percutaneous catheter occlusion.
5.1.4 Pulmonary stenosis (PS):
Background
Right ventricular outflow tract (RVOT) obstructive lesions are
characterized by obstruction to flow from the RV to the pulmonary
arteries (PAs). Obstruction can occur at different levels, including valvular
pulmonic stenosis (PS), sub valvular PS, supravalvular PS, and
peripheral PS (PPS). These lesions can occur in isolation or may be
associated with other cardiac defects (eg, tetralogy of Fallot [TOF],
tricuspid atresia).
Assessment
 Severe and critical pulmonic stenosis: after delivery present with
cyanosis due to right-to-left shunting through a patent foramen ovale.
In some cases, the severity of the RVOT obstruction is life-threatening
(ie, critical PS). For neonates with critical PS, survival is dependent
on maintaining patency of the ductus arteriosus by the administration
of prostaglandin E1.
 Mild or moderate pulmonic stenosis: typically, asymptomatic and
usually present later in childhood; however, PS may be identified
during the routine newborn physical examination based on the
characteristic cardiac findings.
Cardiac findings
 The S1 is normal. In patients with mild or moderate PS, it is typically
followed by an audible click.
 The split between the S2s is dependent on the severity of the
obstruction.
 The characteristic murmur of valvular PS is a systolic ejection murmur
heard at the second left intercostal space.
 In more severe cases, a thrill is palpable at the second and third
intercostal space.
Investigations
 ECHO
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Management
 Surgical procedures
 Transcatheter procedures
5.1.5 Coarctation of the aorta (CoA):
Background
 Coarctation of the aorta (CoA) is a narrowing of the descending aorta,
which is typically located at the insertion of the ductus arteriosus just
distal to the left subclavian artery.
 This defect generally results in left ventricular pressure overload.
Assessment
Manifestations according to age:
 Neonates: The newborn infant may remain asymptomatic if there is a
persistent patent ductus arteriosus (PDA) or if the CoA is not severe.
o A clinical diagnosis is made if:
 There is an absent or delayed femoral pulse (when
compared with the brachial pulse).
 A murmur may be associated with other cardiac defects,
such as PDA, aortic stenosis, or ventricular septal defect
(VSD).
 A systolic click may be heard due to a bicuspid aortic valve.
 Older infants and children: most patients are asymptomatic.
 Physical examination:
o Measurement of blood pressure and palpation of pulses in all
four extremities suggest the clinical diagnosis with lower systolic
blood pressure in the lower extremities compared with upper
extremities and brachial or radial artery to femoral artery pulse
delay.
o Cardiac examination: Cardiac auscultation may be normal if
there are no associated cardiac abnormalities.
Investigations
 Echocardiogram
 ECG
 Cardiac CT
Management
 Balloon angioplasty
 Stent placement
 Surgery
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Complications
In unoperated patients or those operated on during later childhood or
adulthood may have complications such as:
 systemic hypertension
 accelerated coronary artery disease.
 stroke
 heart failure
 aortic dissection
5.2. Cyanotic Congenital Heart Disease:
5.2.1 Tetralogy of Fallot (TOF)
Background
Is one of the most common congenital heart lesions requiring
intervention in the first year of life. Tetralogy of Fallot (TOF) includes the
following major features:
 Right ventricular outflow tract (RVOT) obstruction
 Malalignment ventricular septal defect (VSD)
 Overriding aorta
 Concentric RV hypertrophy
Assessment
 Undiagnosed infants with severe RVOT obstruction and inadequate
pulmonary flow typically present in the immediate newborn period
with profound cyanosis and require intervention.
 Infants with minimal obstruction are also asymptomatic initially. They
may develop symptoms of pulmonary over circulation and heart
failure in the first four to six weeks after birth as the initially elevated
perinatal pulmonary vascular resistance falls to normal.
 Tet spells: Patients with unrepaired TOF are at risk for episodic
hypercyanotic (tet) spells with profound cyanosis.
 Cardiac auscultation: S1 is normal and the S2 is most commonly
single because the pulmonic component is rarely audible. S3 and S4
heart sounds are uncommon. An early systolic click along the left
sternal border may be heard, which is thought to be due to flow into
the dilated ascending aorta.
 Murmur: The murmur in TOF is due primarily to the RV outflow
obstruction, not the ventricular septal defect (VSD). The murmur is
typically a systolic, crescendo-decrescendo murmur with a harsh
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ejection quality; it is appreciated best along the left mid- to upper

sternal border with radiation posteriorly.
Investigations
 Prenatal diagnosis: Improvements in prenatal screening and fetal
echocardiography have led to an increase in rates of prenatal
diagnosis of TOF.
 Echocardiography: Two-dimensional echocardiography and Doppler
examination
 ECG
 CXR
 Cardiac catheterization
 CT
 Cardiac MRI
Management
 Surgical repair
5.2.2 Transposition of the great arteries (TGA):

Background
Transposition of the great arteries (TGA) is a ventriculoarterial discordant
lesion in which the aorta arises from the right ventricle and the
pulmonary artery from the left ventricle.
Assessment
Presentation
 Cyanosis
 Tachypnea
 Murmurs
 Diminished pulses
Investigations
 ECG
 CXR
 Echocardiography
Management
 Prostaglandin infusion
 Balloon arterial septostomy
 Surgery
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5.3. Still’s Murmurs

still’s murmurs may occur in as many as a third of all children. This type
of murmur occurs most often in children two to seven years of age but
can occur in younger or older children.
Key features:
 Louder in supine position, with exercise, fever, or anemia
 Grade II or less, always soft, vibratory systolic. – Normal S 1 and S2
and no extra sounds
 Patient is asymptomatic.
 Stable vital signs, no clubbing, or cyanosis on exam
When to refer to cardiology:
 Presence of symptoms such as exertional chest pain, SOB, fatigue,
dizziness, and syncope
 Exercise intolerance, failure to thrive, presence of positive family
history of congenital heart disease in first degree relative.
 Family history of Marfan syndrome or sudden unexplained death in
younger persons
 Suspected pathological causes or uncertain of the murmur.
Chapter 6: CHILDHOOD COMMON

INFECTIOUS DISEASE
6.1. Measles (Rubeola):
 Caused by a virus called Measles which belong to the genus
morbillivirus in the Paramyxoviridae family.
 Quickly spread from person to person by droplets or
through airborne during coughing, sneezing or talk.
 Infected droplets spray into the air where the person can inhale them,
also the infected.
 droplets may land on the surface and remain active and contagious
for several hours.
6.1.1 Clinical assessment
Measles signs and symptoms appear around 10 to 14 days after
exposure to the virus
The measles infection can be subdivided into the following stages:
 Incubation period
o 6-21 days
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o The period of contagiousness is from 4 days before

appearance of the rash to 4 days after.
o Patients are asymptomatic
 Prodrome:
o Usually lasts for 2 to 4 days but may persist to 8 days.
o Symptoms include fever, malaise, and anorexia, followed by
conjunctivitis, coryza, and cough(3Cs).
 Exanthem:
o Approximately 2 to 4 days after onset of fever.
 Symptoms consist of erythematous, maculopapular,
blanching rash, classically begins on the face, and spreads
cephalocaudally to involve the neck, upper trunk, lower
trunk, and extremities (picture 6.1).
 Approximately 48 hours before the onset of the exanthem,
patients may develop an enanthem characterized
by Koplik spots (picture 6.2) which are 1 to 3 mm whitish,
grayish, or bluish elevations with an erythematous base,
seen on the buccal mucosa, can spread to cover the
buccal and labial mucosa as well as the hard and soft
palate.
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6.1.2 Investigation
 Measles is clinically diagnosed; lab tests are indicated in case of
suspension of other differential diagnosis.
 Elevated serum aminotransferases
 Leukopenia
 T cell cytopenia
 Chest radiography may demonstrate interstitial pneumonitis.
6.1.3 Complications
 Bacterial ear infection
 Bronchitis and Laryngitis
 Encephalitis
 Pneumonia
 Diarrhea
 Gingivostomatitis
 Gastroenteritis
 Hepatitis
 Mesenteric lymphadenitis and appendicitis
6.1.4 Management
 Supportive measures
 There is no specific antiviral therapy approved.
 WHO recommends that vitamin A be administered to all children with
acute measles:
 administered orally once daily for two days.
 nonimmune contact: measles vaccine within 72 hrs of exposure or
IgG within 6 days of exposure
6.2. Rubella (German Measles/Three-day Measles)

6.2.1 Background
 It is a viral infection caused by rubivirus
 Transmitted by droplets.
 Incubation period: 2-3weeks.
 Symptoms include a low-grade fever, sore throat, and a rash that
starts on the face and spreads to the rest of the body.
 Contagious period is 7 days before and 7 days after the rash eruption
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6.2.2 Clinical Assessment

 Mild symptoms may occur 1 to 5 days before the rash appears.
 Symptoms include low-grade fever, headache, mild pink eye, general
discomfort, swollen and enlarged lymph nodes, cough, and runny
nose.
 Pink macules on the face, spreads to neck, trunk, arms, and becomes
generalized within 24 hours (Picture 6.3).
 Forchheimer spots: petechia on hard/soft palate (picture 6.4).
 Clinically diagnosed, lab tests are indicated in case of suspension
of other differential diagnosis.
 IgG and IgM serology
 Rubella virus can be isolated from throat swabs, blood, urine, and
spinal fluid by polymerase chain reaction (PCR) testing and molecular
typing.
 CBC to detect thrombocytopenia and leucopenia.
6.2.4 Complications
 Arthralgia and arthritis
 Encephalitis
 Otitis media
 Fetus: congenital rubella syndrome (CHD, cataract, blindness,
deafness, mental retardation)
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6.2.5 Management
 No specific treatment.
 The disease is usually mild and self-limiting.
 Bed rest and antipyretic are most useful.
 The best protection against rubella is MMR (measles-mumps-rubella)
vaccine.
6.3. Scarlet Fever:
6.3.1 Background
 Bacterial illness caused by certain strains of group A beta-hemolytic
streptococci that release a streptococcal pyrogenic exotoxin
(erythrogenic toxin).
 People who are infected spread the bacteria by coughing or
sneezing, which creates small respiratory droplets that contain the
bacteria.
 Scarlet fever generally has a 1–4 days incubation period.
 It usually takes 2 to 5 days for someone exposed to group A strep to
become sick.
 Seen in children older than 3 years at overcrowded environment such
as boarding schools, daycare and military camp.
6.3.2 Clinical Assessment (Picture 6.5)
 Usually starts with a prodrome of fever, sore throat, vomiting,
abdominal pain followed by rash 1- 2 days later.
 After 1 to 2 days, rash starts on the neck, axillae, groin, spreads to
trunk and extremities, sparing the palms and soles, with characteristic
circumoral pallor.
 On examination, Pastia lines which is erythematous, non-blanching
linear eruption may develop on skin folds such as the axilla,
antecubital fossa, and buttock creases.
 Petechiae on the palate may occur, as well as erythematous, swollen
papillae with a white coating on the tongue (white strawberry tongue).
 After several weeks, the rash fades and is followed by desquamation
of the skin, especially on the face, in skin-folds, and on the hands and
feet, lasting four to six weeks.
 Sore throat
 Circumoral pallor
 Antecubital fossa petechiae- pastia
 Rash (Sandpaper)
 Lymphadenopathy
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 Tongue (Strawberry)
 Throat swab culture or rapid streptococcal antigen test can support
the diagnosis.
 Anti-deoxyribonuclease B and antistreptolysin-O titers
6.3.4 Complications
 Rheumatic fever
 Otitis media
 Pneumonia
 Septicemia
 Glomerulonephritis
 Osteomyelitis
6.3.5 Management:
 Antibiotics is prescribed, usually penicillin, for up to 10 days.
 Patients allergic to penicillin may be treated with an alternative
antibiotic, such as erythromycin.
 Additional treatments include:
o Drink plenty of fluid and paracetamol.
o Oral antihistamines and emollients help to relieve the itchy rash.
 The fever usually improves within 12-24 hours after starting
antibiotics.
 People with scarlet fever should stay home until they are afebrile + 24
hours after starting the antibiotic therapy.
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6.4. Erythema Infectiosum (5th disease):

6.4.1 Background
 Caused by Parvovirus B19.
 It is a single-stranded DNA virus that targets red cells in the bone
marrow.
 It spreads via respiratory droplets. but can also occur by contact with
contaminated hands and, rarely, with infected blood products.
 After the onset of the exanthem the patient is no longer contagious
 The majority of parvovirus B19 infections are clinically silent or
manifest as a “flu-like” illness.
 The typical exanthem is observed in only 15–20% of patients infected
with parvovirus B19.
 After an incubation period of 1–2 weeks, there is a homogenous,
marked redness of the cheeks (“slapped cheek “) and a lacy pattern
or reticulate maculo-urticarial exanthem,
6.4.3 Investigation
Erythema infectiosum is a clinical diagnosis in a child with
characteristic slapped cheek and lacy rash.
The diagnosis can be confirmed by blood tests.
6.4.4 Complications
 Arthralgia
 Hydrops fetalis
6.4.5 Treatment:
Supportive therapy.
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6.5. Roseola Infantum (Exanthema Subitum/6th

disease):
6.5.1 Background
 Roseola is most commonly caused by human herpes virus 6 (HHV-6)
and affects infants and children younger than three years.
 Incubation period approximately 9-10 days after exposure.
 Roseola spreads from person to person via the saliva of
asymptomatic family members.
 Classic roseola infantum is a clinically based diagnosis.
 It begins with a high fever that may exceed 40 C (104 F) for 3-5 days
and is associated with respiratory flu symptoms such as a sore throat,
cough, runny nose or congestion, irritability and tiredness.
 As the fever subsides, the rash appears around day 3-5, typically
small rose-pink or red raised spots (2–5 mm in diameter) that blanch
when touched.
 Some spots may be surrounded by a lighter halo of pale skin, mainly
affects the trunk, and rarely spreads to involve the neck, face, arms,
and legs.
 Similar spots occur on the soft palate and uvula (Nagayama spots),
non-itchy, painless, does not blister, and may fade within a few hours
or persist for as long as two days.
 Laboratory tests are unlikely to be necessary for the evaluation of
roseola infantum but are sometimes drawn during the febrile phase of
the illness to rule out other diagnosis.
 Children infected with HHV-6 can have an elevated WBC count that
will gradually return to normal over 7 to 10 days following the illness.
 Febrile seizure/ convulsions (most common complication, occur in 5-
15% of children)
 Myocarditis
 Rhabdomyositis
 Guillain-Barre syndrome and hepatitis
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6.5.5 Management
 There is no specific treatment for roseola Infantum.
 The majority of cases of roseola infantum are mild and self-limited.
 Treatment is supportive with rest, maintaining fluid intake, and
antipyretics such as acetaminophen or ibuprofen to control the fever.
6.6. Chickenpox (Varicella)
6.6.1 Background
 Highly contagious disease caused by the initial infection
with varicella-zoster virus (VZV) of the Herpesviridae family.
 This virus is sometimes called herpesvirus type 3.
 However, most cases occurring in children before they are 10 years
of age, characterized by acute onset of fever and blister rash.
 Reinfection is rare because of lifelong immunity.
 Transmits via contact with aerosolized droplets from
nasopharyngeal secretions of an infected patient or by direct
cutaneous contact with vesicle fluid from the skin lesion.
 Easily transmits and spread between immunocompromised people.
 An itchy rash is the most common symptom of chickenpox, usually
begins as itchy red papules.
 Progressing to vesicles on the abdomen, back, and face, and then
spreading to other parts of the body (picture 7.7).
 Blisters can also arise inside the mouth.
 Some children may experience high fever, headache, cold-like
symptoms, vomiting, and diarrhea.
 A clue to the diagnosis is in knowing that the patient has been
exposed to an infected contact within the 10–21 days incubation
period
 Patients infected with chickenpox can transmit the disease 1-2 days
before appearance of the rash until the lesions have crusted
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6.6.3 Investigation
PCR detects the varicella virus in skin lesions and is the most accurate
method for diagnosis.
6.6.4 Complications
 Encephalitis
 Otitis media
 Pneumonia
 Hepatitis
 Strept/ staph superinfection of ruptured vesicles
6.6.5 Management
 Symptomatic therapy.
o Cut children’s fingernails to minimize scratching, apply
moisturizing cream.
o Paracetamol can reduce fever and pain (do not use aspirin in
children as this is associated with Reye syndrome).
o Calamine lotion and oral antihistamines may relieve itching.
6.6.6 Antiviral indications:
 Healthy people 12 years of age and older
 People with chronic skin or lung disease
 People taking long term salicylate or steroid therapy
 Pregnant
 People with weak immune system
6.7. Hand-foot-and-mouth disease:

6.7.1 Background
 Common mild and short-lasting viral infection most often affecting
young children but can occur in all age groups.
 Also called enteroviral vesicular stomatitis.
 Caused by the coxsackie virus, most common during the late
summer or autumn months.
 Spreads by direct contact with the skin, nasal and oral secretions of
infected individuals, or by fecal contamination.
 Incubation period: 3-6 days
 Patients transmit the disease mainly in the first week of illness and
active virus can be seen in stool up to 4-8 weeks
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The vesicles have an erythematous base, and the oral enanthems are
painful, and found on buccal mucosa, tongue, and soft palate which
resolve after 7-10 days.
Brief prodromal symptoms such as a low-grade fever, anorexia, sore
throat, and maculopapular or papulovesicular on the hands and soles of
the feel (picture 8 and 9) oral ulcerations.
 The diagnosis is typically made clinically due to the characteristic
appearance of blisters in typical sites, i.e., hands, feet, and mouth.
 In ill children, blood tests may show:
 Raised WBC, atypical lymphocytes.
 Raised serum C-reactive protein (CRP)
 Positive serology for the causative virus, which may be isolated from
swabs of vesicles, mucosal surfaces, or stool specimens, confirms
the infection but is rarely necessary.
6.7.4 Management
 No specific therapy for most; self-limited, paracetamol and cool
liquids for pain, encourage good hand hygiene to prevent spread.
 Some recommend magic mouthwash/oral lidocaine if not tolerating
PO intake, although evidence suggests no better than placebo.
 In infants, do not use oral lidocaine due to risk of lidocaine toxicity
and FDA black box warning.
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6.8. Kawasaki Disease:

6.8.1 Background
 Acute febrile illness with inflammation of small- and medium-sized
blood vessels throughout the body, in particular, the coronary
arteries.
 Without treatment, Kawasaki disease is usually a self-limiting illness
and resolves spontaneously within 4-8 weeks. However, about 20% of
untreated cases develop coronary artery damage, and approximately
2% of patients will die, most commonly from a heart attack.
 Peaks age at 18-24 months, rare in 5yr.
 Overall, it occurs more commonly in boys than girl.
 The cause of Kawasaki disease is unknown.
 Kawasaki disease cannot be passed on to other family members.
 There is a 2% risk of recurrence of Kawasaki disease within several
years.
6.8.2 Clinical Assessment (picture 6.10)
 High swinging fever (beyond 39 C), associated with several other
features.
 The 5 cardinal signs of Kawasaki disease are:
 Rash – the rash of Kawasaki disease may be morbilliform (measles-
like), maculopapular, erythematous, or target-like and may be
persistent over days or evanescent. Skin peeling may occur in the
convalescent stage of the illness.
 Oral signs – the typical changes include redness within the mouth or
on the pharynx, strawberry tongue, and red or cracked lips.
 Eye signs – redness of the bulbar conjunctivae without exudate or
stickiness
 Peripheral limb signs – including firm swelling of the hands and feet,
sometimes including the fingers and toes, with redness of the palms
and soles. Periungual desquamation (peeling of skin around the
fingernails) may occur during the convalescent stage of the illness.
 Lymphadenopathy – swollen lymph glands can occur, often on one
side of the neck. One lymph gland of at least 1.5cm in length is
considered diagnostically enlarged.
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6.8.3 Kawasaki Mnemonic:

 Conjunctival injection Rash
 Edema of hands and feet
 Adenopathy
 Mucosal changes
6.8.4 Diagnosis
 The diagnosis is considered established when the
following diagnostic criteria are met:
 Fever for at least 5 days AND
 At least 4 of the 5 cardinal signs listed above AND
 The absence of any other illness to account for the signs and
symptoms.
 There is no specific lab test that establishes the diagnosis of
Kawasaki disease.
 Some helpful laboratory and diagnostic workups:
 CBC (leukocytosis, elevated platelets)
 LFTs- elevated
 ESR, CRP- elevated
 Blood culture, urinalysis
 ECG
 TTE (Coronaries, LV, valves) Consider if f ESR≥ 40, CRP≥ 3, or if
desquamation occurs
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6.8.6 Management
 Antipyretic and analgesic medications.
 Once the diagnosis of Kawasaki disease is made, a single large dose
of intravenous Immunoglobulin (IVIG), IVIG 2gm/kg over 12hr given.
IVIG is most effective when given between the 5th and 10th days of
illness.
 Low dose oral aspirin 20mg/kg/dose q6h also usually commenced
at this time.
 Once children are treated, they generally improve rapidly; most of the
acute symptoms and signs resolve within 24 to 48 hours.
 Follow-up cardiac evaluation for coronary aneurysm screening.
6.9. Mumps
6.9.1 Background
 Is an acute infection of the parotid glands.
 Most often caused by paramyxoviruses (e.g., mumps), but should
consider influenza; less commonly by parainfluenza, coxsackie, echo,
HIV.
 Most common in children.
 Some children who get mumps may have mild symptoms like
headache and arthralgia, myalgia, fever, loss of appetite, typically
precede the parotid swelling by 12-24 hours
 Then unilateral or bilateral parotid swelling may occur (picture 6.11).
 On examination, the swollen parotid gland most finding which may
cause trismus.
 Other salivary glands such as submandibular and sublingual may
also be involved.
 Fever usually resolves within 3 to 5 days, and parotid swelling
subsides within 7-10 days.
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 Nonspecific usually leukopenia with relative lymphocytosis, elevation
in serum amylase return to normal within two weeks.
 The microbiologic diagnosis by serology or virus culture.
 Enzyme immunoassay (IgG).
6.9.4 Complications
 Pancreatitis
 Aseptic meningitis
 Hearing loss
 Myocarditis
 Polyarthritis
 Hemolytic anemia
6.9.5 Management
 Supportive
6.10. Pertussis:
6.10.1 Background
 Also known as whooping cough, is a highly contagious respiratory
disease.
 It is caused by the bacterium Bordetella pertussis.
 After the adoption of vaccination in the 1940s, pertussis incidence
and outbreaks declined significantly.
 The incubation period is seven to 10 days.
 Transmitted by aerosolized droplets.
Clinical manifestations include three stages:
Catarrhal stage:
 Lasts 1 to 2 weeks.
 Symptoms include malaise, rhinorrhea, sneezing, lacrimation, and
mild cough, low-grade fever but body temperature is often normal.
 The cough gradually becomes more frequent.
 During this stage, the disease is highly contagious.
Paroxysmal stage:
 Lasts 2-4 weeks.
 Fever improves, cough worsens, Staccato cough + whoop (present in
1/3 kids), post tussive emesis.
 Infants can present as apnea.
 Patients often appear well between coughing episodes.
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 Petechiae, epistaxis, pneumothorax, and/or subconjunctival

hemorrhage may occur due to high intra thoracic pressures during
coughing.
 On examination: subconjunctival hemorrhage, ulcer of the lingual
frenulum, and periorbital edema.
Convalescent stage:
 Cough subsides over few weeks to months.
 Episodic coughing may occur.
 The CDC recommends the use of both culture and polymerase chain
reaction (PCR) testing to confirm the diagnosis.
 Serologic testing or direct fluorescent antibody tests are not
recommended for routine use in establishing a diagnosis of pertussis.
 WBC elevated in infants (20-100) with a large amount of lymph
(85%), adults and infants may be within normal.
 CXR with peribronchial thickening, atelectasis, and/or consolidation.
 The nasopharyngeal swab can identify it in 3-7 days; often negative in
adults.
6.10.4 Complications
 Include anorexia, dehydration, difficulty sleeping, epistaxis, hernias,
otitis media, and urinary incontinence.
 Adolescents and adults can also develop complications from
pertussis. However, complications are usually less severe in this older
age group, especially in those who received pertussis vaccines.
 Most serious complications include syncope and pneumothorax,
seizure, and subdural hematoma.
6.10.5 Management
 Antibiotics do not help with severity or duration but may decrease
infectivity.
 Azithromycin for 5 days.
6.10.6 Prevention
 The best way to prevent pertussis is to get vaccinated.
 Tdap is only for children 7 years and older, adolescents, and adults.
 Adolescents should receive a single dose of Tdap, preferably at age
11 or 12 years.
 Pregnant women should get a dose of Tdap during every pregnancy
to protect the newborn from pertussis.
 Adults who have never received Tdap should get a dose of Tdap.
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 Pertussis can also be more severe for infants younger than 2 months
of age whose mothers did not get Tdap while pregnant.
Chapter 7: INTELLECTUAL
DISABILITIES
7.1. Cerebral Palsy (CP)
7.1.1 Definition:
a group of motor deficits due to injury to the developing brain which leads
to irreversible encephalopathies.
 Hypertonia
 Hyperreflexia
 Clonus
 Asymmetric reflexes.
Clinical features vary, as predominantly abnormal

movements.

 Non-curable disease
 Lifelong condition
 Multidisciplinary management.
1-Medical intervention
 Antispasmodic as
o Central (baclofen, diazepam)
o Peripheral: OnabotulinumtoxinA (Botox injection)
o Intrathecal baclofen
 Anticholinergic (trihexyphenidyl)
2-Surgical intervention
Selective dorsal rhizotomy
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7.2. Down Syndrome (DS)

Table 7.1
Head and neck Extremities Neonatal features
– Upslanting palpebral – Short broad hands – Flat facial profile

fissures – Incurved fifth finger – Slanted palpebral
– Epicanthic folds with hypoplastic middle fissures
– Flat facial profile/flat phalanx – Anomalous ears
nasal bridge – Transverse palmar – Hypotonia
– Folded or dysplastic crease – Poor Moro reflex
ears – Space between the – Dysplasia of middle
– Low-set small ears first and second toes phalanx of fifth finger
– Brachycephaly (sandal gap) – Transverse palmar
– Brushfield spots _ Hyperflexibility of (Simian) crease
– Open mouth Joints – Excessive skin at
– Protruding tongue - nape of the neck
Furrowed tongue – Hyperflexibility of
– Short neck joints
– Excessive skin at – Dysplasia of pelvis
nape of the neck
– Narrow palate
– Abnormal teeth

 Karyotype analysis
 Fluorescent in situ hybridization: Confirms Down syndrome
Management of Down Syndrome requires an organized approach to
ongoing evaluation and monitoring for associated abnormalities and
prevention of common disorders. as
 Plot growth on growth chart at each visit.
 Echocardiogram, typically done following delivery of the newborn,
repeated as indicated.
 Newborn hearing screen and ongoing hearing screening throughout
childhood, plus monitoring for otitis media, which is a common cause
of hearing loss in children with Down syndrome.
 An ophthalmologic assessment before six months of age and then
approximately annually to screen for ophthalmologic disorders.
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 Thyroid function testing in the newborn period with newborn screens

and repeated at 6 months of age, 12 months of age, and then yearly
thereafter.
 Monitor for symptoms of celiac disease beginning at one year of age.
Screening is recommended if signs or symptoms develop.
 CBC at birth, monitor for signs of leukemia and hemoglobin level at
one year of age for iron deficiency anemia.
 Neurologic evaluation for signs and symptoms consistent with spinal
cord injury at each health supervision visit.
 Monitoring for symptoms related to sleep apnea at health supervision
visits beginning at age one year. polysomnography or pulse oximetry
during sleep is recommended in all children with Down Syndrome by
four years of age.
7.3. Fragile X Syndrome (FXS)
The clinical features of FXS vary depending upon the mutation state.
 Facial features (onset in early childhood)
o Large prominent ears
o Long and narrow face with prominent forehead and chin
(prognathism)
 Macroorchidism with normal testicular function (postpubertal males)
 Developmental delay
 intellectual disability
 learning disability
 Behavior problems (ADHD, Autism spectrum disorder)
 DNA analysis
7.4. Williams Syndrome (WS)
7.4.1 Definition:
Rare genetic disorder that affects many parts of the body.
 Facial dysmorphic features:
o Elfin face
o Bitemporal narrowness
o Broad forehead and flat nasal bridge
o Malar flattening
o Short nose with a long philtrum, full lips, and a wide mouth
o Strabismus
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 Cardiovascular abnormalities: (most common source of morbidity and

mortality)
o Supravalvar aortic stenosis (Most common cardiac lesion)
o Peripheral pulmonary artery stenosis, supravalvar pulmonary
stenosis
o Structural congenital heart defects such as (mitral valve
prolapse, bicuspid aortic valve, and valvular aortic stenosis)
o Hypertension
o Prolonged QT
o Sudden cardiac death
 Endocrine Abnormalities:
o Idiopathic Hypercalcemia
o Hypothyroidism
o DM type 2
o Early Puberty
o Poor growth and short stature
 Gastrointestinal abnormalities:
o Constipation, feeding difficulties, umbilical and inguinal hernias,
and diverticula.
 Renal and urinary tract abnormalities:
o Congenital anomalies of the kidney and urinary tract
o Dysfunctional voiding
o Nephrocalcinosis
o Increased risk of UTI
 Musculoskeletal:
o Hyperextensible
o Contractured joints
 Auditory abnormalities:
o Sensorineural hearing loss
o Recurrent otitis media
o Hyperacusis
 Ophthalmologic:
o Hyperopia
o Nasolacrimal duct obstruction
o Strabismus
 Dental:
o Microdontia, missing teeth, and localized enamel hypoplasia
 Neurological abnormalities:
o Axial hypotonia
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o Peripheral hypertonia
o Signs of cerebellar dysfunction, such as ataxia and tremor, may
increase with age.
 Cognitive:
o Intellectual disability (75%)
o Developmental delay
 Behaviors:
o Overfriendliness, excessive empathy, and a lack of social
inhibition
o ADHD (50%)
o Anxiety disorder
o Sleep disorder
Clinical features but must confirm with genetic testing
 Chromosomal analysis
Fluorescence in situ hybridization
 Multidisciplinary approach.
 There is no cure for WS.
7.5. Dyslexia
7.5.1 Definition:
an unexpected difficulty in reading for an individual who has the
intelligence to be a much better reader.
Difficulties in both spoken and written language so the signs of dyslexia
usually noted at school age children.
 Mispronunciations
 Lack of fluency
 Speech with many pauses or hesitations and “ums”
 Word-finding difficulties
 Inability to come up with an answer quickly.
Dyslexia is a clinical diagnosis. Depending on history, observation, and
psychometric assessment
7.5.4 Management plan
Evidence-based reading intervention methods and programs
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7.6. Autism Spectrum Disorder (ASD)

7.6.1 Definition:
Autism is a complex neurodevelopmental disorder. It has a range of
abilities and disabilities. Characterized by intellectual disability,
communication and social impairments, and unusual behaviors.
Symptoms must be present in the early developmental period.
Deficits in social communication and social interaction
Restrictive, repetitive patterns of behavior, interests, or activities
History and examination by DSM-5 criteria
Lab : CBC, lead, iron studies, TSH, Chromosomal microarray and fragile
X-testing
 AAP Recommendations ASD screen between 18-24 months
Evidence-based interventions
 Behavioral interventions
 Speech/language therapy
 Occupational therapy
 Augmentative and alternative communication
 Risperidone and aripiprazole: Administration for irritation or
aggression in ASD, but they can cause extrapyramidal symptoms
(e.g., tardive dyskinesia) and excessive weight gain.
 Sleep disturbance is common: This can be improved by behavioral
intervention, parent education and melatonin use.
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Chapter 8: GROWTH AND PUBERTY

PROBLEMS
8.1. Short Stature
8.1.1 Definition:
 Less than 5th percentile for the height or Deceleration of previously
standard growth curve (growth of <5 cm/year).
8.1.2 Etiology:
1-Familial short stature
 Normal bone age and normal growth velocity
 Puberty occurs at the expected time.
 The final height is usually less than the 5th percentile.
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2-Constitutional delay
 Delayed bone age (consistent with height age) and normal growth
velocity
 Puberty is significantly delayed.
 The final height is usually normal.
3- Pathologic cause
present with diminished growth velocity.
 Proportionate (affects all bones) or disproportionate (affects bones
predominantly).
 Proportionate short stature:
o Growth hormone deficiency
o Primary hypothyroidism
o Cushing’s Syndrome
o Precocious puberty
o Malnutrition
o Psychosocial deprivation
o Chronic systemic diseases
 Disproportionate short stature
o Rickets (Vitamin D deficiency)
o Achondroplasia
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Serial measurements of growth are an essential parameter in monitoring
the health of children.

1-For familial and constitutional short stature, reassurance is the main
management. Other treatment is
 Treat the underlying case in pathological short stature.
 Growth hormones
 Recombinant human insulin-like growth factor 1 (rhIGF-1)
 Aromatase inhibitors
 Oxandrolone
 Estrogen
2- Referral to a Pediatric Endocrinologist in children with short stature.
Indication:
 Children with intrauterine growth retardation who do not catch up to
the growth curve by 2 years of age.
 Height more than 3 standard deviations below the mean for age
 Growth velocity < 5 cm (2 in) per year
 No onset of puberty by 14 years of age for boys or 13 years of age for
girls
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 Projected height more than 2 standard deviations (10 cm [4 in]) below

the midparental height
 Bone age more than 2 standard deviations below chronologic age
 Diagnosis of conditions approved for recombinant growth hormone
therapy.
8.2. Tall Stature
8.2.1 Definition:
Tall stature is defined as a height more than two standard deviations
above the mean for age (greater than the 97th percentile).
 Insulin-like growth factor 1
 Karyotyping
 Serum luteinizing hormone, follicle-stimulating hormone, testosterone
 Thyroid-stimulating hormone, free thyroxine

Management in extreme cases or other causes of rapid growth in which
the underlying disorder cannot be corrected.
Management include:
 Sex hormones
 Epiphysiodesis
 Treat underlying disorder
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8.3. Growing Pains (Benign Nocturnal Limb Pain)

8.3.1 Definition:
 Growing pains are crampy pains of the thigh, shin, and calf usually in
children 4-6 years of age.
 In the absence of any objective manifestations of musculoskeletal
abnormalities and generally without any limitations of activity.
 Mild, nocturnal, and frequent pain relieved by rest, massage, and
simple analgesics.
 It worsens with activity or by the end of the day. but does not limit
physical activity.
 Negative findings: no joints swelling or redness, no bony tenderness,
normal range of motion, normal strength, normal growth pattern, no
fever or weight loss.
 Normal CBC/ESR and normal radiographic findings
Diagnosis is based on clinical information
*Labs are not routinely recommended
 If severe pain, fatigue, joint pain, swelling, weight loss, fever, bony
tenderness or muscle weakness, limiting normal physical activity,
further workup is warranted such as:
 CBC, ESR, CRP, imaging.
 Symptomatic including education and reassurance.
8.4. Muscular Dystrophy
8.4.1 Definition:
Muscular dystrophies are genetic disorders affecting the muscles. Can
be divided into:
 Becker Muscular Dystrophy
 Congenital Muscular Dystrophy
 Duchenne Muscular Dystrophy
 Spinal Muscular Atrophy
Evaluate for any gross motor delay, check CK and thyroid function test to
r/o congenital hypothyroidism.
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8.4.3 Duchenne muscular dystrophy (DMD)

Age 6–7 years, boys start falling, early fatigue, and will develop calf
pseudohypertrophy.
8.4.4 Symptoms & signs:
Key diagnostic factors from history and examination
 Presence of risk factors
 Imbalance of lower limb strength
 Lower extremity musculotendinous contractures
 Delayed motor milestones
 Calf hypertrophy
 Ambulation difficulty and falls
 Diminished muscle tone and deep tendon reflexes
 Nonnal sensation
Other diagnostic factors
 Gowers’ sign ; Child uses hands to “climb up” the legs to move from a
sitting to a standing position
 Toe walking (Note: isolated toe walking is often normal before age 2
years)
 Hypotonia
 Hyperactivity
 Urinary and bowel incontinence
 Mild to severe mental retardation
 Serum creatine kinase (CK) (50-100x normal)
 Genetic testing
 Investigations to consider electromyogram (EMG)
 Muscle biopsy
 Neurology referral
 Supportive (e.g., physiotherapy, wheelchairs, braces)
 Prevent obesity.
 Cardiac health monitoring and early intervention
 Bone health monitoring and intervention (vitamin D, bisphosphonates)
 Steroids (e.g., prednisone)
 Surgical (for scoliosis
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Chapter 9: APPROACH TO COUGH:

9.1. Background:
 Cough is an airway protective reflex involving a forceful expulsion of
air from the lungs and it is an important symptom as a manifestation
of respiratory diseases.
 Cough is usually classified by: (A) Duration of cough: Acute: <2-3
weeks, Subacute :3-8 weeks, Chronic: >8 weeks (B)
Cough character: Dry, Wet/ Productive (C) Possible etiology:
Specific, Non- specific.
 Acute cough in children is mostly caused by viral upper respiratory
tract infections (URTIs)
 Chronic cough can be associated with an underlying serious
disorder and, hence, requires systematic and thorough clinical
evaluation.
9.1.1 Clinical Assessment:
9.1.2 History:
Table 9.1
Cough Onset Likely Diagnosis
While after feeding Aspiration, tracheoesophageal fistula,
laryngeal clefts
Seasonal Cough Allergic rhinitis, postnasal drip,

allergen exposure
Acute onset, choking risk Foreign body aspiration

Productive morning cough Bronchiectasis, sinusitis, reflux,
recurrent pneumonia,
cystic fibrosis
Barking cough present only Psychogenic cough, behavioral
while awake
Exercise-induced cough Air hyperreactivity
Nighttime cough Asthma (late night), GERD when
lying, postnasal drip (
early at night)
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9.1.3 Physical exam:

General appearance/ respiratory distress/ dysmorphic features
Vital signs and growth parameters, Eczematous skin changes/ viral
exanthem/ skin rash
ENT / chest / cardiac/ abdomen (cystic fibrosis)/ lower limbs edema or
clubbing
CXR if history and physical exam are inconclusive.
CBC, blood/ sputum/ nasopharyngeal culture, PPD for suspected
infectious etiology.
Consider spirometry, sweat chloride, immunoglobulins as appropriate.
9.2. Upper Respiratory Tract Infections (URTI):
9.2.1 Symptoms and signs:
 Acute cough that lasts for 1-3 weeks but can persist longer.
9.2.2 Investigation and monitoring:
Clinically. Self-limiting.
9.2.3 Management Plan:
Supportive care only. No good evidence of the effectiveness of over-the-
counter cough medication.
9.3. Respiratory Syncytial Virus Bronchiolitis:
9.3.1 Definition:
Bronchiolitis is a common lower respiratory tract
infection in infants and young children, and respiratory syncytial virus
(RSV) is the most common cause of this infection. RSV is transmitted
through contact with respiratory droplets.
 Upper respiratory tract symptoms (fever, rhinorrhea, and congestion)
for two to four days, followed by lower respiratory tract symptoms
(increasing cough, wheezing, and increased respiratory effort).
 Physical exam: wheezing and crackles on auscultation and may
include evidence of increased respiratory effort (grunting nasal flaring,
or retractions)
CXR: not recommended routinely. If obtained the findings include
peribronchial markings, hyperinflation, and atelectasis.
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 Mostly supportive (maintain nutrition and hydration status, Maintain
oxygen saturation>90%)
 Admission to hospital is required with these Red flags (Younger age,
dehydration, increased respiratory effort, tachycardia (HR >97% for
age))
 Therapies not routinely recommended: antibiotics, bronchodilators,
chest physiotherapy, Epinephrine, excessive nasal suction of
secretions, nebulized hypertonic saline (if the hospital stay <3 days),
systemic or inhaled corticosteroids.
 Prevention: (1) Educating parents of strict hand hygiene is one of the
most important things to help prevent RSV infection. (2) Minimize
passive exposure to cigarette smoke. (3)
Immunoprophylaxis with Palivizumab in the first year of life is
recommended for infants at risk of severe lower respiratory tract
infection (infants under one year of age with: Hemodynamically
significant heart disease or chronic lung disease of prematurity. Born
before 29 weeks of gestation.
9.4. Croup:
9.4.1 Definition:
 Upper airway obstruction resulting from swelling of the larynx,
trachea, and bronchi, leading to inspiratory stridor hoarseness and
a barking cough.
 Caused by Parainfluenza virus (types 1 to 3)
 Similarly to an upper respiratory infection; low-grade fever, and
coryza for12 to 72 hours. Exacerbated by emotional distress, are
worse at night, and peak between 24 and 48 hours.
 Typically resolves spontaneously within 48 hours to one week;
however, the abrupt onset and harsh cough can be worrisome.
 Physical exam: Visual inspection can reveal clues to the severity of
illness. Retractions and nasal flaring and occasionally cyanosis
indicate more severe cases.
 Croup is primarily a clinical diagnosis.
 Labs: CBC may help distinguish croup from bacterial etiologies of
stridor (e.g., bacterial tracheitis, epiglottitis, peritonsillar abscess,
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retropharyngeal abscess), but it is nonspecific. Lymphocytosis may

suggest a viral etiology.
 Corticosteroids (dexamethasone) should be used in patients with
croup of any severity.
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9.5. Chronic Bronchitis or Protracted Bacterial

Bronchitis:
9.5.1 Definition:
 Persistent bacterial infection and neutrophilic inflammation in the
airways that leads to increased mucus production, airway
inflammation, and chronic cough.
9.5.2 Symptoms and Physical exam signs:
 Common cause of isolated chronic wet/productive cough in children
 Chronic (>4 weeks) wet or productive cough that resolved within 2-4
weeks after taking oral antibiotic course.
Diagnosed clinically when all 3 of the following criteria are met:
 Presence of chronic (>4 weeks) wet or productive cough
 Absence of specific cough pointers (i.e. symptoms or signs which
could suggest other causes of wet or productive cough), and
 Resolution of cough following 2-4 weeks course of an appropriate oral
antibiotic (usually amoxicillin-clavulanate).
 Antibiotics (usually amoxicillin- clavulanate); prolonged (2 weeks)
course.
9.6. Breath Holding Spells:
9.6.1 Definition:
 Holding breath unintentional; they result from an involuntary reflex,
and the child can’t control them.
Types: There are 2 known types of breath-holding spells:
 Cyanotic breath-holding spell (most common); facial cyanosis is
noticed after the child stops breathing.
 A pallid breath-holding spell; sudden scare to the child, and he or she
becomes extremely pale during the spell.
 Episodes are described as infants crying for up to a minute, and while
crying excessively, they will hold their breath to a point at which they
might lose consciousness.
 A seizure might be witnessed immediately after the infant loses
consciousness; soon thereafter, the infant will usually regain
consciousness and breathe normally.
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 Rule out true seizure episode by detailed family history (of similar
episodes), a detailed description of the spell, and the account of an
initial cry with lack of postictal phase of lethargy are all factors that
help to determine the diagnosis of a breath-holding spell.
 Many episodes of breath-holding are associated with an inciting
incident in which the infant is irritated, is being disciplined, or is angry.
 Occur mostly among children 6 to 18 months of age.
 Clinical diagnosis
 CBC and Iron study: (High frequency of anemia among children with
breath-holding spells) to test of anemia
 The key task when a child experiencing a breath-holding spell to the
clinic is to differentiate the episode from a seizure or an apparent life-
threatening event.
 If confirmed diagnosis: Blowing air forcefully on the face of the infant
will usually terminate the episode early on, but not for all children.
 Reassure the parents, as well as to explain the condition and its
differential diagnosis.
 Treatment empirically for iron deficiency anemia is recommended.
Chapter 10: ACUTE ABDOMINAL PAIN

10.1. Acute Abdominal Pain
Signs Indicating the possible need for surgery in patients
with acute abdominal pain:
 Absent bowel sounds
 Bilious vomiting
 Bloody diarrhea or occult blood in stool
 Elevated temperature (≥ 100.4°F- 38.0°C)
 Rebound tenderness.
 Rigidity (involuntary guarding)
 Voluntary guarding
10.1.1 Constipation
Definition:
 infrequent bowel evacuations, large stools, and difficult or painful
defecation.
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Symptoms & signs:

 Presence of risk factors like low fiber intake, poor diet and obesity
 Difficult or painful defecation
 Long interval between stools
 Fecal incontinence
 Small-volume, soft, incontinent stool
 Palpable fecal mass per abdomen
 ROME IV criteria
 No initial test
 Abdominal ultrasound
 Abdominal x-ray
Management plan:
 Dietary modification (increased intake of fluids and dietary fiber)
 osmotic laxative:
o lactulose: 1 mL/kg orally once or twice daily 1 mL = 0.7 g.
or
o fecal softener:
o docusate sodium:
 children <3 years of age: 10-40 mg/day orally given in 1-4
divided doses.
 children 3-6 years of age: 20-60 mg/ day orally given in 1-4
divided doses
10.1.2 Acute appendicitis
Symptoms & signs:
 Sharp or stabbing periumbilical pain that migrates to the right lower
quadrant (RLQ)
 Anorexia, fever, vomiting, and/or diarrhea may be present; occurs in
all age groups but is rare in infants.
 Patient lies still, tries not to move.
 Positive McBurney’s sign (RLQ pain and tenderness to palpation at a
point two-thirds along a line from the umbilicus to the anterior superior
iliac spine).
 Positive Rovsing’s sign (pain in the RLQ in response to left-sided
palpation, suggesting peritoneal irritation).
 Positive psoas sign (pain in the RLQ when child placed on left side
and right hip gently hyperextended, suggesting irritation to the psoas
fascia and muscle).
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 Positive obturator sign (RLQ pain on internal rotation of the flexed

right thigh); rectal tenderness and/or palpable abscess in RLQ.
 CBC
 Urinalysis
 Urine pregnancy test
 CT scan abdomen and pelvis or MRI
Management plan:
 For severe pain, opiates should be used and will not delay or affect
the accuracy of diagnosis.
 Urgent surgical consultation should not be delayed while awaiting
diagnostic workup.
10.1.3 Intussusception
Definition:
 Invagination part of the bowel into itself
 More common at the ileocecal junction
 Most common obstruction in child 6 – 36 months
 Males more than females (3:1)
 Colicky abdominal pain, fever, lethargy, and vomiting (usually in
infants between 3 months and 12 months of age)
 Henoch-Schoenlein purpura (HSP) may be an initiating factor in an
older child (usually <11 years of age).
 Gross or occult blood that may be mixed with mucus and have ‘red
currant jelly ‘appearance, abdominal tenderness, and palpable
abdominal mass.
 Signs of HSP may be present in older children (rash of palpable
purpura, blood in the stools).
 CBC
 Barium enema: (diagnostic and therapeutic): filling defect or cupping
in the head of contrast as it advances to the site of the
intussusception
Management plan:
 Barium and water-soluble contrast enemas,75-90% successful.
 Surgery for failed cases.
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10.1.4 Mesenteric lymphadenitis

Definition:
 Non-specific inflammation in the mesenteric lymph node provokes a
mild peritoneal reaction and stimulates painful peristalsis in the
terminal ileum.
 Commonly presents with viral upper respiratory tract infection.
 abdominal pain: usually in the right lower quadrant, sometimes
mimics appendicitis and intussusception.
 Abdomen ultrasound shows abdominal lymph nodes (greater than 8
mm in diameter)
Management plan:
 Self-limited condition
 Pain management and adequate hydration.
 Children with prolonged symptoms or those with weight loss or other
systemic symptoms may warrant evaluation for inflammatory bowel
disease, tuberculosis, or malignancy.
10.2. Recurrent Abdominal Pain

Definition:
Recurrent abdominal pain” is classically defined by four criteria:
 ≥3 episodes of abdominal pain
 Pain sufficiently severe to affect activities
 Episodes occur over ≥three months
 No known organic cause
10.2.1 Functional Dyspepsia
At least two months with ≥ 1 of the following bothersome symptoms on
≥four days per month:
 Postprandial fullness
 Early satiety
 Epigastric pain or burning that is not associated with defecation.
Management plan:
Antacids, H2 antagonists, and proton pump inhibitors.
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10.2.2 Irritable Bowel Syndrome (IBS)

In addition to the universal criterion, ≥two months with abdominal pain
associated with one of the following on ≥four days per month:
 Related to defecation
 Change in frequency of stool
 Change in the form of stool
 Pain does not resolve with the resolution of constipation (resolution of
pain indicates functional constipation)
Management plan:
 Dietary modification: increased intake of fluids, fiber, fruit juices.
 Behavioral intervention: scheduled toilet times, stool diary, reward
system.
 Polyethylene glycol (Miralax)
 Severe constipation: manual dis-impaction, enemas, suppositories,
non–polyethylene glycol laxatives.
10.2.3 Abdominal Migraine
In addition to the universal criterion, all the following:
 Paroxysmal episodes of an intense, periumbilical, midline, or diffuse
abdominal pain lasting ≥1 hour at least twice within six months
 Episodes are separated by weeks or months
 The pain interferes with normal activities
 Stereotypical pattern and symptoms in the individual patient
 Pain is associated with ≥2 of the following:
 Anorexia
 Nausea
 Vomiting
 Headache
 Photophobia
 Pallor
10.2.4 Functional Abdominal Pain -Not Otherwise
Specified
In addition to the universal criterion, all the following:
 Occurs ≥four times per month for ≥two months
 Episodic or continuous abdominal pain that does not occur during
physiologic events (e.g., eating, menses)
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 Insufficient criteria for irritable bowel syndrome, functional dyspepsia,

or abdominal migraine.
Management plan:
Cyproheptadine improves patient and parent assessment of abdominal
pain. Famotidine (Pepcid), an H2 antagonist, subjectively improves pain.
10.2.5 Functional constipation
In addition to the universal criterion, ≥2 of the following occurring ≥one
time per week for > 1 month with insufficient criteria for a diagnosis of
irritable bowel syndrome:
 ≤ Two defecations in the toilet per week.
 ≥ 1 episode of fecal incontinence/ week
 History of retentive posturing or excessive volitional stool retention
 Presence of a large fecal mass in the rectum History of large
diameter stools that can obstruct the toilet.
Chapter 11: DIARRHEA IN CHILDREN

Definition:
An increase in the number of stools (3 or more) or the presence of
looser/ watery stools. Acute diarrhea is defined as when diarrhea lasts 3
weeks or less, and chronic if more than 3 weeks.
Symptoms & signs:
 Urgency, Abdominal pain and/or bloating, Rectal pain, Nausea and/or
vomiting, Weight loss, Fever, blood in stool.
 Signs of dehydration include: decrease in urine output, dry lips and
mouth, lack of tears when crying, increased irritability and fussiness,
increased sleepiness/decreased energy level, Tachycardia, Sunken
Eyes
Investigations:
 Acute Diarrhea:
o Diagnosed clinically not required a diagnostic test.
o Blood tests are requested to check for dehydration, not for the
cause.
o Stool cultures are done to identify the specific cause of diarrhea
like bacteria, viruses, or parasites.
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 Chronic Diarrhea:
o A confirmatory test may be required to establish the causes of
chronic diarrhea. A stool culture is required to R/O infectious
pathogen causing chronic diarrhea.
o We need to role out other causes like anemia, inflammation,
Celiac disease, IBD, and lactose intolerance.
o Upper GI endoscopy and colonoscopy with biopsy help to
definitively diagnose Celiac disease and inflammatory bowel
disease, If suspected.
o Lactose breath hydrogen test to diagnose lactose intolerance.
Management:
Ensure Adequate Hydration is the mainstay of treatment.
Some guidelines recommend the antiemetic ondansetron (Zofran) as an
option to improve success rates of oral rehydration.
In cases of mild -moderate dehydration:
 Treat dehydration with liquids or oral rehydration therapy (ORT)
 Children with mild dehydration should receive half-strength apple
juice followed by preferred fluids (regular juices, milk).
Patients with more severe diarrhea, and unable to tolerate fluid orally
with dehydration plus an antiemetic will require intravenous fluids in the
hospital.
 Antibiotics can be with specific bacterial or parasitic illnesses,
although in most cases, antibiotics do not affect duration and severity.
 Anti-diarrheal agents to stop motions are not recommended.
 Hand hygiene
Chapter 12: INFANTILE COLIC

Definition:
Infantile colic is self-limiting episodes of inconsolable crying of a healthy
infant. It peaks around six weeks of age and resolves by 3-6 months of
age. It usually happens in the evening and without triggers. It leads to
parental distress and multiple medical visits. It occurs equally between
males and females, and no association was found between colic and the
type of infant feeding, gestational age, socioeconomic status, or season
of the year.
 Detailed history and physical examination are crucial in infantile colic
to rule out red flags and further tests and management.
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Red flags
 Distended abdomen: Abdominal mass, hepatosplenomegaly,
Hirschsprung disease, intestinal malrotation with volvulus, necrotizing
enterocolitis
 Fever: Acute otitis media, appendicitis, bacteremia, endocarditis,
meningitis, osteomyelitis, pneumonia, sepsis, UTI, viral respiratory
infection
 Lethargy: Hydrocephalus, meningitis, sepsis, subdural hematoma
Diagnosis
Investigations:
 Infantile colic is a diagnosis of exclusion after ruling out serious
diseases by history and physical examination.
 "Rule of three" is the criteria used to help in the diagnosis, and it
includes crying more than 3 hours per day, more than three days per
week, for longer than three weeks in a healthy infant of less than
three years of age.
Management
 As infantile colic has a self-limiting course, the most significant step in
the management is parental reassurance.
 Probiotic Lactobacillus reuteri (strain DSM 17938) can improve the
symptoms of colic, mainly in breastfed babies.
 Breastfeeding should be continued. We suggest changes to feeding
technique and/or experimenting with a number of techniques to
soothe the infant (e.g., rubbing the infant's abdomen, providing "white
noise," etc.) as first- line interventions.
 Simethicone and proton pump inhibitors are no better than placebo in
treating colic; while dicyclomine is helpful but it should be avoided as
it is contraindicated in infants less than six months of age because of
side effects (apnea, seizure, and coma).
 Restricting allergens (e.g., cow's milk, eggs, fish, peanuts, soy, tree
nuts, and wheat) from the diet of breastfeeding mothers. In bottle-fed
infants, changing the formula to hydrolyzed type reduces colic
symptoms.
 Chiropractic or osteopathic manipulation, infant massage, swaddling,
acupuncture, or herbal supplements have no evidence to be used in
the management of infantile colic.
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Chapter 13: PEDIATRICS AND

ADOLESCENTS MUSCULOSKELETAL
PATHOLOGIES
13.1. Spine Conditions:
13.1.1 1-Adolescent Idiopathic Scoliosis:
Definition:
Spine deformity with lateral curvature >10°.
Symptoms and physical examination signs:
 Commonly asymptomatic. Most common in female.
 Positive Adams forward bending test on physical exam.
Investigation and monitoring:
X-ray of spine (standing AP and lateral): Measure cobb angle, assess
skeletal maturation and potential pathologies.
Management plan:
 If spinal in curves <25°: observation alone with serial radiographs to
monitor progression.
 If spinal curves >25° but <45°: bracing.
 If spinal in curves >45°: surgical fixation
 Referral to orthopedic: Should be considers for younger individuals
with curves >20° due to risk of progression.
13.1.2 2.Spondylolisthesis:
Definition:
Anterior slippage of the vertebral body in relation to the vertebra below.
 Localized back pain (at vertebrae) that worsen with any activity that
involves the extension of the back, +/- radiation of symptoms distally.
 On exam: Positive stork test. Always assess for any neurological
compromise.
X-ray of spine:
 Lateral view: to assess the severity of spondylolisthesis.
 Oblique views: to evaluate pars interarticularis
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Management plan:
 Conservative management (rest, ice, NSAIDs)
 Physical therapy focusing on core strength, and activity
modifications.
 Referral to orthopedics: consider it for those with red flags or if
slippage >50% of the vertebral body. Further management might
include bracing and surgery if indicated.
13.2. Hip Conditions:
13.2.1 Developmental Dysplasia of the Hip
Definition:
Abnormal development of the femoroacetabular joint due to inadequate
femoral head pressure into the acetabulum leads to dysplasia,
subluxation, or dislocation due to a shallow socket.
 Most common orthopedics disorder in newborn.
 Commonly asymptomatic, affecting left hip.
 Abnormal gait patterns or dislocation if not recognized early in life.
 Risk factors: breech presentation, female sex, family history, and first-
born child.
 Physical exam: asymmetric thigh skin folds, positive clunk with
Barlow and Ortolani maneuvers
 Physical exam screening is recommended for all newborns by the
American Academy of Pediatrics
 Ultrasound screening for high-risk newborns or equivocal provocative
testing (at 4–6 weeks of age). Don’t do ultrasound after 6 months of
age.
Management plan:
 Management is better handled with pediatric orthopedics.
 Start with a Pavlik harness with hips in abduction
13.2.2 Legg-Calvé-Perthes Disease
Definition:
Idiopathic avascular necrosis of the proximal femur.
 Limp with or without pain that could involve the hip, thigh, or knee.
 Age 4-8 years in boy.
 Risk factors: family history, low birth weight, and abnormal birth
presentation.
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 Physical exam: Trendelenburg gait and loss of abduction and internal

rotation.
 X-ray of affected site: (monitor the natural progression of the disease)
 Occult disease stages: Not noticeable during the first 6 months of the
disease. MRI can be used if indicated.
 Fragmentation stage: last up to 2 years.
 Ossification stage: for 18 months after fragmentation stage.
 Healing and remodeling stage: final stage.
Management plan:
 Referral to pediatric orthopedics is appropriate.
 Goals of management include symptomatic relief in the early stages
with NSAIDs and crutches followed by early physical therapy to
improve ROM and preserve the hip joint.
13.2.3 Transient Synovitis
Definition:
Inflammation of the joint’s synovium.
 Pain of the affected joint and adjacent soft tissues +/- mild fever.
Commonly affects the hip
 Can be attributed to a recent viral illness, trauma, allergic reaction, or
others.
Age 4-8 years in boy.
 Physical exam: Limited ROM of affected joint. If hip involves, will be
at the position of abduction and external rotation.
 Emergent laboratory studies (CBC, CRP, ESR, and synovial fluid
analysis) To role out septic arthritis.
 X-ray of joint: Normal.
 Ultrasound: effusion within the affected joints.
Management Plan:
 Conservative (NSAIDs and close observation). Limiting weight-
bearing.
 Improvement of symptoms usually takes about 2 days and resolution
of symptoms in 1–2 weeks.
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13.2.4 Slipped Capital Femoral Epiphysis

Definition:
Proxima femoral apophysis disruption leads to metaphyseal slippage of
the femoral.
 Insidious pain at the hip or knee with limping to acute post-traumatic
pain.
 Commonly seen in overweight adolescents ages 11–13 years with
more male prevalence. Associated with endocrine disorders.
 Physical exam: Antalgic gait with an externally rotated hip is a
common exam finding.
 X-ray of BOTH joints (AP and frog-lateral views): an ice-cream cone
slipping off its cone.
 Grades: based on slippage into grades I, II, and III with the latest
being >50% slippage and is the most severe.
Management Plan:
 Orthopedic referral: Surgical with percutaneous pinning, consider
crutches and non-weight bearing.
13.2.5 Hip Septic Arthritis
Definition:
Surgical emergency. Bacterial joint infection.
Causes: <2 years: group B streptococcal species. >2 year of age:
Staphylococcus auras. Adolescent: gonococcal infection.
 The pain of the affected joint with fever, fatigue, or malaise should
raise suspicion.
 Physical exam: Swelling and limited ROM are common exam
findings.
 Arthrocentesis with laboratory studies (CBC, blood cultures, ESR,
and CRP).
 Modified Kocher Criteria used for diagnosis.
 X-ray: inconclusive but can identify widening of joint space.
Management Plan:
 Orthopedic referral: surgical drainage and washout with broad-
spectrum IV antibiotics narrowed to a specific pathogen once cultures
are available.
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13.3. Knee Conditions:

13.3.1 Juvenile Idiopathic Arthritis:
Definition:
Chronic inflammatory arthritis: symptoms lasting at least 6 weeks in ages
<16 years.
 Joint pain and swelling, fever, rash, and visual changes. More than
one joint.
 Subtypes: systemic JIA (Still Disease), polyarticular (>5 joints), and
pauciarticular (1-4 joints).
 Physical exam: MSK: Joint effusion, limited ROM. Extra-MSK: rash,
and iridocyclitis.
 Laboratory studies (ESR; elevated, rheumatoid factor; negative, ANA;
positive in polyarticular and pauciarticular subtypes).
 X-ray of joints: Commonly negative in early disease. Juxta-articular
osteopenia and joint destruction in advanced disease.
 Monitoring: Ocular exams every 4 months (with ANA+ individuals)
Management Plan:
 Symptoms usually improve with NSAIDs and age and can resolve
after puberty.
 DMARDs can be recommended to prevent progressive articular
destruction.
13.3.2 Osgood Schlatter Disease:
Definition:
Traction apophysitis of the anterior tibial tuberosity due to overuse.
 Pain is worse with jumping or running.
 More common in male athletes in ages 10-15 years.
 Physical exam: Tenderness and swelling +/- redness at the patellar
tendon attachment to the tibial tuberosity.
 X-ray of knee (lateral view): rupture of the growth plate at the tibial
tuberosity.
Management Plan:
 Supportive measures (rest, ice). Physical therapy: stretching and
strengthening of both the quadriceps and hamstrings.
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 If severe pain, immobilize the knee in a hinged brace for a short

period of time until symptoms improve.
13.3.3 Sinding Larsen Johansson’s Disease
Definition:
Irritation of the growth plate at the distal pole of the patella
 Knee pain is worse with jumping or running.
 Also referred to as jumper’s knee in children.
 Physical exam: Localized tenderness to palpation at the proximal
patellar tendon attachment to the patella.
 X-ray of knee: show signs of apophysitis
Management Plan:
 Managed with ice packs, rest, and NSAIDs.
13.3.4 4- Osteochondritis Dissecans (OCD)
Definition:
Disruption of the portion of the chondral surface with the underlining
articular bone.
 Joint pain and swelling are common presenting symptoms. Most
commonly knee pain.
 Can be precipitated by trauma but mostly of unknown etiology.
Serious condition.
 Physical exam: check for any mechanical symptoms.
 X-ray of knee (tunnel views): OCD is usually visible.
 MRI might provide a better definition and whether a joint loose body is
present.
Management Plan:
 Small OCD lesions in skeletally immature individuals can be closely
monitored with caution to avoid high-impact activities to allow for new
bone formation.
 If a loose body is present within the joint or in skeletally mature
individuals, consider referral to orthopedics for surgical evaluation.
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13.3.5 Stress Fractures:

 Gradual onset of pain with activity that improves with rest. Mainly
affects weight-bearing bones and the tibia is commonly involved.
 Secondary to overuse.
 Physical exam: Tenderness can be elicited over affected bone with a
positive hop test.
 X-ray of affected bone: Early presentation: negative (findings lag 2–3
weeks behind symptoms onset).
 MRI can identify pathology in the early stages.
Management Plan:
 Rest for 6–8 weeks with cross-training is the recommended
management approach.
 Stress fracture management can be lengthy and setting expectations
with affected individuals is crucial.
13.3.6 Bone Tumors:
 The majority of bone tumors are benign in nature.
 Types: Primary Benign: Osteochondroma, giant cell tumor, and
osteoblastoma are the most common benign tumors respectively.
 Primary malignant: osteosarcoma (MCC; about 35% of all malignant
bone tumors) followed by chondrosarcoma and Ewing sarcoma
respectively.
 The most common presenting symptoms include bone pain which
could be nocturnal, swelling, weakness, fatigue, weight loss, and
pathological fracture.
 Presenting symptoms can be non-specific and can delay diagnosis.
 X-ray of affected bone: can be sufficient to promptly identify tumors
and refer to orthopedics and oncology specialists if indicated.
 Advanced imaging and bone biopsy can be required if the diagnosis
is uncertain.
Management Plan:
 Management will range depending on tumor type from serial follow-
ups and imaging, to using neoadjuvant and adjuvant chemotherapy in
combination with surgery.
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 Survival rates can be up to 80% with early recognition and

management of osteosarcoma/ Up to 95% of affected individuals do
not end up requiring amputation.
 In the delayed presentation, metastatic osteosarcoma and Ewing
sarcoma can lower the five-year survival rates to 20%.
13.4. Elbow Conditions:
13.4.1 Nursemaid’s Elbow:
 Commonly affects children 1–4 years of age. A “pop” might be felt or
heard by the individual pulling the child.
 The affected child is usually apprehensive to use the affected arm
and holds the elbow in flexion and pronation. Tenderness to palpation
can be felt over the radial head.
Diagnosis and management
 Radiographs are not required to make the diagnosis. Gentle reduction
is recommended with either supination and full flexion or
hyperpronation techniques.
 No need to immobilize the elbow afterward and symptoms usually
resolve after reduction.
13.4.2 Medial Epicondyle Apophysitis :
Symptoms and exam:
 Overuse injury in young athletes who throw leads to pain over the
medial epicondyle due to inflammation of the growth plate.
 During the exam, ensure ligamentous and neurovascular integrity.
Diagnosis and management:
 A radiograph is reasonable if concerned about a fracture.
 Activity modification and limiting throwing is the mainstay of
treatment.
13.5. Foot Conditions :

13.5.1 Sever’s Disease:
Symptoms and exam:
Inflammation of the growth plate in the heel due to overuse leads to
calcaneal apophysitis. Pain is localized to the posterior heel with
tenderness to palpation and limited foot dorsiflexion due to pain.
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Radiographs are sufficient to make the diagnosis with increased density
of the calcaneal epiphysis. Manage conservatively with rest, NSAIDs,
activity modification, Achilles stretches and heel pads for comforts.
13.5.2 Metatarsus Adductus:
Symptoms and exam:
 a benign congenital deformity of the feet in which the forefoot
deviated inwards.
 Can be associated with other anomalies such as DDH in up to 20% of
cases.
 Diagnosed clinically during newborn screening.
 Management is mostly conservative with parent education that the
deformity will likely correct itself by age 4 years.
 Management options can range from observation and stretching in
flexible deformities, to serial casting in rigid deformities and surgical
intervention is rarely needed.
13.5.3 Congenital Talipes Equinovarus (Clubfoot) :
Symptoms and exam
 the most common musculoskeletal birth anomaly.
 The foot is usually turned inward and downward with a combination of
plantar flexion, adduction, and inversion.
 Diagnosed during the newborn physical exam and can be noted
during intrauterine ultrasound evaluation.
 Management begins with parent education, foot stretches, serial
casting using the Ponseti technique, or surgical intervention if
indicated with persistent deformities despite conservative measures
and casting.
13.5.4 Pes Planovalgus (Flat Feet):
Symptoms and exam:
 an idiopathic condition in which there is a loss of the foot medial arch,
hindfoot valgus, and forefoot abduction.
 It is usually asymptomatic but can have foot or arch pain later in life.
 The exam is important to thoroughly inspect the feet for laxity of the
medial arch during standing and with heel raises.
 Flexible deformity will likely correct itself with heel raise, while rigid
deformity will persist.
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 Radiographs can be obtained to evaluate for a tarsal coalition (fusion)
in rigid deformity.
 Management is mostly conservative including parent education,
stretching, orthotics, and shoe wear modification.
 Surgery might be indicated in symptomatic individuals with no
response to conservative measures.
13.5.5 Physeal Fractures (Growth Plate Fractures):
 Fractures usually involve the physis with or without the adjacent
metaphysis or epiphysis. Early recognition and proper management
are crucial when evaluating physeal injuries. A missed diagnosis can
cause growth arrest in the affected bone leading to shortening and
deformity later in life.
 Physeal injuries are commonly classified using Salter-Harris
Classification (Table 13.1). Follow-up is important to ensure proper
radiographic healing.
Table 13.1 – Salter-Harris Classification
Type Description of fracture Management Prognosis
I Through the growth Closed reduction and Good

plate immobilization
II Through the growth Closed reduction and Good

plate and the immobilization
metaphysis
III Through the growth Refer to orthopedics Varies

plate and the epiphysis
IV Through all three Refer to orthopedics Varies

elements
V Compression of the Refer to orthopedics Poor

growth plate
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Chapter 14: FAILURE TO THRIVE AND

DEVELOPMENTAL DELAY
Table 14.1
Poor nutritional Increase metabolic
Malabsorption
intake demands
Insufficient Inborn errors of Chronic infections
breastfeeding metabolism
Chronic lung
Poor latching Iron deficiency disease of
/feeding behaviors anemia prematurity
Inadequate formula Celiac disease Congenital heart

preparation disease
Hyperthyroidism
Cow milk allergy
Cleft lip/palate
Asthma
Irritable bowel
Difficulty in oral syndrome
muscle coordination Inflammatory bowel
disease
Cystic fibrosis
GERD Child abuse
Renal failure
Biliary atresia
Lead poisoning
Malignancy
Pancreatic
polycystic problems
Infections
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14.1. Failure to thrive

14.1.1 Definition:
There is no agreement on the definition of childhood FTT, but many
supportive definitions exist that include the following:
 Children with weight below the 5th percentile for sex and corrected
age.
 Weight for length below the 5th percentile.
 Body mass index for age below the 5th percentile.
 History, physical examination, and measurement of serial growth
parameters over time are crucial to confirm FTT.
 In physical examination, it is essential to look for any genetic
dysmorphic features, developmental abnormalities, signs of acute or
chronic disease, and to assess the degree of undernutrition.
 There are no specific diagnostic labs recommended for FTT.
 initial test can reasonably include CBC, electrolytes, urine analysis,
thyroid function, and testing for celiac disease.
14.1.4 Management plan :
 Most cases of FTT can be treated as an outpatient with a primary
care physician. However, referral to other specialties that include
dietician, social worker, dentist, or lactation specialist can be helpful.
 Treatment of dental caries or sleep problems if present and providing
good family counseling regarding a balanced diet are all important
aspects of FTT management.
 Assessment of breastfeeding and increase formula concentration
from 19 to 24 kcal per oz can establish the appropriate nutrition intake
in breast and formula-feeding infants, respectively. It
 is also important to advise for healthy three primary meals with two
snacks among toddler and older children.
 Children with FTT should be followed up from weekly to every few
months with a more frequent assessment of infants than other
children.
 Weight must be measured on consistent technique every day to
weeks but not daily.
 After successful treatment, growth acceleration of weight needs to be
maintained for 4–9 months.
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 Weighting height above the 10th percentile with normal weight gain
on two assessments at least one month apart is a way to ensure
effective management.
14.1.5 Indications of hospitalization:
 Failure of outpatient treatment after 3–4 months
 Severe underlying disease in a child
 Poor relationship between the child and the parent
 Parent psychiatric disease that interferes with child safety
 The need for an accurate record of calorie intake
 Severe undernutrition/ dehydration
14.2. Developmental Delay
14.2.1 Causes:
 Speech and language delays, it can be primarily related to
developmental delay or expressive/receptive language disorder, and it
can be secondary to hearing difficulty, physical speech problems,
intellectual disability, autism spectrum disorder, or selective mutism.
 Motor delays can be due to central causes such as cerebral palsy or
peripheral etiology as neuromuscular diseases.
 It is crucial to be familiar with the normal developmental milestones in
children to detect alarming signs in development and to interfere with
inappropriate times for a better prognosis (Tables 14.2 – 14.3).
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Table 14.2- Speech and language developmental milestones in

children
Age Receptive Expressive
6 months Turns to a rattling Laughs
sound Vocalizes (cooing)
Turns to voice
9 months Babbles, single syllables
Says “mama” or “dada,”
nonspecific
Waves “bye-bye”
12 months Follows one-step Babbles
command Imitates vocalizations and
sounds
Says one word
Waves “bye-bye”
15 months Says one word
Says three words
Waves “bye-bye”
18 months Points to at least one Says three words
body part Says six words
2 years Points to two pictures Combines words
Follows two-step Names one picture
command
2.5 years Points to six body parts Knows two actions
Names one picture
Speech half understandable
3 years Knows two

adjectives
Names four
pictures
Names one
color
Speech all understandable
4 years Defines five words
Names four colors
Speech all understandable
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14.2.2 Red Flags

Table 14.3 – Alarming signs in pediatric language
development
Age Receptive Expressive
12 months Does not babble, point, or
gesture
15 months Does not look at or point to Does not use at least three
5 to 10 objects or persons words
when named by parents
18 months Does not follow one-step Does not say “mama,”
directions “dada,” or other names
2 years Does not point to pictures Does not use at least 25
or body parts when named words
2.5 years Does not verbally respond Does not use unique two-
or nod/shake head to word phrases, including
questions noun-verb combinations
3 years Does not understand Does not use at least 200
prepositions or action wordsDoes not ask for
wordsDoes not follow a things by name
two-step directions Repeats phrases in response
to questions(echolalia)
At any age Has regressed or lost
previously acquired
speech/language milestones
 Creatine phosphokinase.
 Thyroid function.
 Chromosomal analysis for peripheral motor delays.
 EEG and brain MRI for central motor delays.
 Early recognition of pediatric developmental delays is important for
timely referral and interventions.
 Speech and language delays, referral to a speech therapist and
audiology is essential, although close observation can be an option in
some suspected cases.
 Speech-language therapy is an effective method in the management
of speech and language delays, especially for those with an
expressive language disorder.
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 Motor delays, early intervention programs and referral to a pediatric

neurologist and physical and occupational therapist should be
considered.
References
A TQM Approach to the Measurement of Information Quality with
Implications to Concurrent Engineering,
web.mit.edu/tdqm/papers/other/evans.html.
“Depression Screening.” AHRQ, www.ahrq.gov/ncepcr/tools/healthier-
pregnancy/fact- sheets/depression.html.
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Section 4: Obstetric and Gyn

Chapter 1: OBSTETRIC CARE
1.1. Prenatal care:
primary care physicians will make the diagnosis of pregnancy with:
 History of a missed period
 Positive home urine pregnancy test
 Detection of HCG in maternal blood or urine 8–9 days after ovulation
 Ultrasound recognition of gestational yolk sac or embryo
1.1.1 Initial Prenatal Visit:
The primary goals of the initial prenatal visit are:
 To define the health status of the patient and fetus
 To determine the gestational age of the fetus
 To initiate a plan for continuing obstetrical care
Recommended components of the initial prenatal visit care
(ACOG):
 Risk assessment to include genetic, medical, obstetric, and
psychological factors.
 Estimated due date
 General physical examination
 Laboratory tests
 Patient education
1.1.2 Assessment of Gestational Age:
The duration of pregnancy from the first day of the last normal menstrual
period (LMP) is 280 days or 40 weeks. Naegele’s rule can be used to
estimate the expected date of delivery (EDD):
Add 7 days to the date of the first day of the LMP and count back 3
months (example: LMP=20 September, therefore EDD=27 June)
Indications of early ultrasonography:
 The patient has irregular cycles or bleeding
 The patient is uncertain of the timing of their last menstrual period
 There is a discrepancy in the size of her uterus compared with the
gestational age
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1.1.3 Initial Prenatal visit lab tests:

 Blood group/Rh status
 Administration of Rho (D) immune globulin markedly decreases the
risk of all immunization in RhD-negative women carrying an RhD-
positive fetus.
 Hemoglobin & hematocrit (screening for anemia)
 Screening and treatment of iron deficiency anemia can reduce the
risks of preterm labor, intrauterine growth restriction, and perinatal
depression.
 Sickle cell screen (as needed)
 G6PD (as needed)
 Cervical cytology (as needed)
 Gestational diabetes (GDM) screening (as needed at the initial exam)
 Routine 24–28 weeks
 Urine culture
 To evaluate for asymptomatic bacteriuria
 Group B streptococcus
 Routine 35–37 weeks
 STI
 Gonorrhea and chlamydia
 HIV screening
 Varicella screening
 Rubella antibody titer
 Syphilis screen
 Hepatitis B virus surface antigen
 Specific genetic testing (based on the family histories of the patient
and their partner)
 Vaccination for influenza
 Folic acid supplementation as early as possible to prevent neural tube
defects (preferably before conception)
1.1.4 Physical Examination and Counseling:
Standard elements of prenatal care include
A routine physical examination, including a pelvic examination at the
initial visit
useful in detecting reproductive tract abnormalities and screening for
sexually transmitted infections.
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Maternal weight at all visits:

Early body mass index (BMI) measurement using pre-pregnancy height
and weight is important to guide further nutritional counseling and to
address the risks of obesity and diabetes
Measure blood pressure at every visit
Auscultate fetal heart rate (FHR) after 10 to 12 weeks gestation
with a doppler monitor or after 20 weeks gestation with a fetoscope.
Assess fundal height after 20 weeks gestation at each visit
Palpate the abdomen using Leopold maneuvers to assess fetal
presentation starting at 36 weeks gestation
Promotion of breastfeeding
Papanicolaou smears should be offered during prenatal care at
recommended intervals.
1.2. Counseling Topics in Pregnancy:
 Air Travel
Generally is safe for pregnant patients up to four weeks before their due
date.
 Breast Feeding
should be recommended as the best feeding method for most infants,
Structured behavior counseling increase breastfeeding success.
 Exercise
At least 30 minutes of moderate exercise on most days of the week is a
reasonable activity level,avoid activities with risk of falls or abdominal
injurie.
 Seatbelt use
Should use a three-point seat restraint
 All immunization
The risk of all immunization for an RhD-negative patient carrying an RhD
positive fetus is approximately 1.5%, can be reduced to 0.2% with
Rho(D) immune globulin (RhoGam). Testing for ABO blood group and
RhD antibodies should be performed early in pregnancy.
Rho(D) immune globulin, 300 mcg, is recommended for non-sensitized
patients at 28 weeks gestation and again within 72 hours of delivery if
the infant has RhD-positive blood.
 Thyroid test
Thyroid-stimulating hormone levels should be measured in women with a
history of thyroid disease or symptoms of disease in pregnancy.
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 Infectious diseases
Bacterial vaginosis
Universal screening for bacterial vaginosis is not supported by current
evidence.
Rubella
Pregnant patients should be screened for rubella immunity during the
first prenatal visit, ideally before conception when vaccination is safe.
Varicella
Maternal varicella (chickenpox) can have significant fetal effects,
congenital varicella syndrome (low birth weight and limb, ophthalmologic,
and neurologic abnormalities) and neonatal varicella infection can occur
from five days before to two days after birth.
Asymptomatic bacteriuria
All pregnant patients should be screened between 11- and 16-weeks
gestation for asymptomatic bacteriuria and treated if positive to reduce
the risk of recurrent urinary tract infection, pyelonephritis, and preterm
labor.
Influenza
Physicians should recommend that all pregnant patients receive
vaccination for influenza.
Tetanus and pertussis
Patients should receive the Tdap vaccine during each pregnancy. The
best time for vaccination is between 27 and 36 weeks of gestation for
antibody response and passive immunity to the fetus.
Group B Streptococcus
causes significant neonatal morbidity and mortality. All pregnant patients
should be offered screening at 35 to 37 weeks gestation and treatment
with intrapartum antibiotic prophylaxis (penicillin or clindamycin if allergic)
for those who are positive.
 Psychosocial issue
Domestic violence
The U.S. Preventive Services Task Force (USPSTF) recommends
screening women of childbearing age for intimate partner violence, such
as domestic violence, and provide intervention services or a referral if
positive.
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Depression screening
The American College of Obstetricians and Gynecologists (ACOG)
supports depression screening during pregnancy. Perinatal depression is
underdiagnosed. Complications include prematurity, low birth weight,
neurodevelopmental delays, and issues with maternal/infant bonding.
Chapter 2: BREAST PAIN
2.1. Breast Pain:
2.1.1 History:
 Onset, Duration, Severity, Site, Characteristic, Unilateral or bilateral,
Aggravating or relieving factors, Relation to menstrual cycle
 Is it associated with the use of oral contraceptive pills or hormone
replacement therapy?
 Did it begin after a recent birth or pregnancy loss or termination?
 Is it related to vigorous or repetitive use of the pectoral muscle group?
 Is there a concurrent neck, back, or shoulder problem?
 Are there systemic or other local symptoms, such as fever or
erythema?
 Is there a recent trauma to the chest?
 Does the pain affect her ability to perform daily activities?
 Medical history
 Surgical history
 Breast cancer risk should be assessed
2.1.2 Red flags:
 Palpable breast mass
 Skin changes
 Bloody nipple discharge
 High risk for breast cancer
2.1.3 Physical examinations:
The four breast quadrants, subareolar areas, axillae, and supraclavicular
and infraclavicular areas should be systematically examined with all
positions (Lying, sitting with her hands on her hips and then above her
head).
 Check for skin changes, the symmetry and contour of the breasts,
nipples position, scars, dimpling, edema, erythema, skin retraction,
ulceration or crusting of the nipple, and changes in skin color.
 Check for enlarged or tender lymph nodes like supraclavicular,
axillary, or infraclavicular.
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 Describe and comment on breast masses.

 Check for any discharge from the nipple.
 Take special attention to any localized tenderness and relate them to
areas of pain.
 Chest wall: Physical exam should also aim at differentiating true
breast pain from extra mammary pain.
Table 2.1 Classification of breast pain
Cyclical – Associated with hormonal fluctuations of the
menstrual cycle.
– Presents in the week prior to the beginning of
menses.
– Bilateral, diffuse, mostly in the upper outer
quadrant.
– Can also be associated with hormonal agents
(COCP, HRT).
Non-cyclical – Pain is not related to the menstrual pattern.
– May be constant or intermittent.
– Unilateral and variable in location.
Possible causes:
– Large pendulous breasts.
– Lifestyle (high fat diet smoking, and caffeine
intake).
– Hormonal replacement therapy.
– Breast cysts.
– Ductal ectasia.
– Mastitis.
– Inflammatory breast cancer.
– Hidradenitis suppurativa.
– Pregnancy.
– Thrombophlebitis (Mondor’s disease).
– Trauma.
– Medications (hormones, antidepressants,
cardiovascular agents, and antibiotics).
Extramammary – Referred from sources other than the breasts.
– Unilateral and brought on by activity.
– Located very lateral or medial in the breast.
– Reproducible by pressure on a specific area of
the chest wall.
Possible causes:
– Chest wall pain.
– Spinal and paraspinal disorders.
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– Trauma.
– Post-thoracotomy syndrome.
2.1.4 Management:
Cyclical:
 Reassurance
 Physical support (well-fitting bra, sport bra during exercise)
 Warm or ice compresses
 Acetaminophen or NSAIDs (topical NSAIDs can be useful)
Non-cyclical:
 Treat as cyclical mastalgia
 Treat the underlying cause
2.2. Costochondritits:
2.2.1 Definition:
 Inflammation of costochondral junctions of ribs or chondrosternal
joints, usually at multiple levels and without obvious swelling or
induration.
2.2.2 Physical Examinations:
 Palpating the affected cartilage segments might produce pain and
may radiate on the chest wall.
 Should do chest radiography if history of fever, cough, chest wall
swelling, or other respiratory findings in examination.
 Should do EKG +/- chest radiography if age older than 35 years,
history or risk of coronary artery disease, and patients with cardio-
pulmonary symptoms.
2.2.4 Management:
 Pain relief with analgesics, heat compressors/pads, decrease
activities that provoke the symptoms, consider cough suppressant if
needed, consider physical therapy.
 Reassurance (Self-limited, benign condition).
2.3. Mastitis:
2.3.1 Symptoms:
 During first 6 weeks post-delivery.
 More during lactation, results in prolonged engorgement or poor drainage.
 Complaining of pain, fever, redness, malaise, myalgia, chills, and flu like
symptoms.
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 Clinical diagnosis.
 Consider culture of breast milk to guide the selection of antibiotics,
especially in the setting of severe infection, hospital-acquired, or
unresponsive to initial antibiotics.
 Consider imaging if 2 to 3 days no response to supportive care and
antibiotics.
2.3.3 Management:
 Initially: conservative treatment to control pain and swelling with non-
steroidal inflammatory agents, cold compresses, and complete
emptying of the breast (by ongoing breastfeeding, hand expression,
and/or pumping).
 If persistent symptoms are beyond 12 to 24 hours, with fever, the
addition of antibiotic therapy with activity against S.aureus for 5-7
days should be started.
 If recurrent mastitis in the same location and/or does not respond to
antibiotic therapy, consider investigations for inflammatory breast
carcinoma.
2.4. Breast abscess:
2.4.1 Definition:
 It is a localized collection of pus in the breast tissue. Develops when
mastitis does not respond to antibiotic treatment.
2.4.2 Symptoms and physical examinations:
 Localized, painful inflammation of the breast associated with fever
and malaise.
 On examination: fluctuant, tender, palpable mass.
 Ultrasound imaging may be used for confirmation and guided
aspiration of the collection.
2.4.4 Management:
 Drainage and empirical antibiotic therapy (activity against S. aureus).
 Initial drainage should be performed by needle aspiration with
ultrasound guidance.
 Surgical drainage is indicated for patients who present with the
compromise of the overlying skin and for patients who do not respond
to aspiration.
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 Women should be encouraged to continue breastfeeding following

breast infection and during treatment for lactation-associated breast
infections. If there is difficulty with breastfeeding, hand expression or
breast pumping can be effective for maintaining the milk supply until
nursing can resume.
2.5. Inflammatory Breast Cancer (IBC):
2.5.1 Definition:
 A rare and aggressive form of breast cancer, characterized by diffuse
dermatologic erythema and edema (peau d'orange), common
between age of 59-66 years.
 Diagnostic Criteria of IBC:
o Rapid onset of breast erythema, edema and/or peau d'orange,
and/or warm breast, with or without an underlying palpable mass.
o Duration of history no more than six months.
o Erythema is occupying at least one-third of the breast.
o Pathologic confirmation of invasive carcinoma.
2.5.2 Symptoms and physical examinations:
 Patients typically present with breast pain or a rapidly growing, self-
diagnosed breast lump. They may also report a tender, firm, or
enlarged breast or itching of the breast.
 Some women may report swollen lymph nodes or localizing pain and
symptoms depending on the location and extent of metastatic
disease.
 On physical exam, the skin over the breast in IBC is typically warm
and thickened, with a peau d'orange(skin of an orange) appearance.
 Nipple involvement may present as flattening, erythema, crusting,
blistering, or retraction of the nipple.
 A discretely palpable lump may or may not be present.
 Diagnostic mammogram on the affected side and screening
mammogram on the contralateral side, with accompanying ultrasound
of the breast and regional lymph nodes.
 A core needle biopsy of the area of concern in the breast should be
obtained to make the initial diagnosis of invasive carcinoma.
 If (suspected) on the basis of history, physical, and core needle
biopsy procced to a full-thickness skin punch biopsy.
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 After diagnosing IBC, CT scans with IV contrast of the chest,

abdomen, and pelvis and a bone scan should be obtained as many
patients have metastatic disease at presentation.
 For women with palpable or suspicious axillary lymph nodes, an
ultrasound-guided fine-needle aspiration (FNA) and/or a core needle
biopsy of the suspicious nodes should be done to make a more
accurate determination of the tumor stage.
2.5.4 Management:
 After staging, Chemotherapy, endocrine therapy for hormone
receptor-positive disease, modified radical mastectomy, and
postmastectomy radiation therapy are the treatment options.
Chapter 3: LOWER ABDOMINAL PAIN

IN FEMALES
3.1. Ectopic Pregnancy
3.1.1 Definition:
It’s the product of conception implanted outside the endometrial cavity.
The most common site is the fallopian tube, but can occur elsewhere.
Ectopic pregnancy has the most important cause of maternal deaths that
occur in the first trimester, of which non-tubal ectopic pregnancy deaths
account for a higher rate than tubal pregnancy deaths.
Ectopic pregnancy (EP) has multiple risk factors ranging between high,
moderate to low risk. The highest risk factors include: previous EP,
previous tubal surgery or pathology, sterilization, and current use of IUD.
Moderate to low risk factors include: pelvic inflammatory disease,
increased maternal age, STD, assisted conception (IVF), Hx of induced
abortion, current oral contraceptive pills use, past or current smoking.
3.1.2 Presentation:
The symptoms and signs of ectopic pregnancy can resemble the
common symptoms and signs of other conditions, for example,
gastrointestinal conditions or urinary tract infections. Presentations
include:
 Amenorrhea or a history of an abnormal last menstrual period – in
75–90% of cases (about 6 weeks on average).
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 Vaginal bleeding – from spotting to the equivalent of a normal

menstrual period – in 50–80% of cases; is due to low production of
hCG by the ectopic trophoblast.
 Abdominal pain – from vague lower abdominal discomfort to
generalized abdominal pain – in 90% of cases.
 Failure of B-HCG to rise appropriately.
 Lower abdominal and adnexal tenderness
 Cervical motion tenderness
 Peritoneal signs
 Adnexal masses (palpable in less than 10% of patients)
 Symptoms of hemodynamic compromise (hypotension, shock – now
seen less commonly due to early detection of ectopic pregnancy)
3.1.4 Acute (ruptured) EP:
About 15–20% of ectopic pregnancies present acutely. A ruptured
ectopic pregnancy is usually dramatic and often not forgotten. Features
include:
 Severe pain in the pelvis and lower abdomen.
 Tenesmus might be present.
 Collapse and eventual hypovolemic shock.
 Vaginal examination is extremely painful, especially on moving the
cervix. It may provoke further bleeding and should be kept to a
minimum.
Chronic or Un-ruptured ectopic pregnancies are extremely
variable in their presentation:
 Most patients are afebrile
 Abdominal pain is moderate, intermittent, and usually unilateral
 90% have abdominal tenderness
 Pain on defecation (due to blood in the pouch of Douglas)
 Pelvic examination reveals a palpable adnexal mass in 50% of
cases, half of which occur contralateral to the ectopic pregnancy,
representing the corpus luteum.
 The uterus is usually soft and of normal size or only moderately
enlarged.
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 Urine beta-hCG is essential to help determine further management.
If the diagnosis is in doubt, then serial serum beta-hCG measurements
are taken to distinguish between a potentially viable intrauterine
gestation, a resolving spontaneous abortion, and ectopic pregnancy.
 If the rise is less than 50% in 48 hours, it is almost always associated
with a nonviable pregnancy (either intrauterine or extrauterine).
 A transvaginal ultrasound is the standard method of investigation.
It may reveal viable or nonviable intrauterine pregnancies, ectopic
pregnancies, or no visible pregnancies
 Laparoscopy is of little value in a ruptured ectopic pregnancy.
3.1.6 Management:
Can be surgical, medical, or occasionally expectant management.
Page | 338
Management of
EP
Surgical management
Observation Medical management criteria
management criteria criteria Advanced ectopic
B-hcg < 1,000 mlU/ml B-hCG < 2,000 m pregnancy (high B-
decreasing adenaxal IU/ml hCG, large mass,
mass <3 or not Adnexal mass < 3.5 cm embryonic cardiac
detected. or not detected activity)
No embryonic activity No medical Uncertain diagnosis or
or evidence of tubal contraindications unreliable patient
upture No embryonic cardiac Contraindication to
Minimal pain or no activity methotrexate
bleeding (hematologic
No evidence of tubal dysfunction, liver,
The patient is reliable rupture kidney or pulmonary
to f/u Patient is reliable for disease, alcohol abuse,
follow up peptic ulcer,
immunodeficiency)
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3.2. Endometriosis
3.2.1 Definition:
Endometriosis is an estrogen-dependent condition predominantly
affecting reproductive-aged women and causes estrogen-dependent
chronic inflammatory process, it is characterized by the presence and
growth of endometrial glands and stroma outside of the endometrial
cavity. It is a benign condition however it has distressing
symptomatology, the association with infertility, and the potential for
invasion of the gastrointestinal and/or urinary tracts.
3.2.2 Diagnosis:
Diagnosis can only be made definitively by laparoscopic visualization of
the pelvis, but US can assist in the diagnosis.
3.2.3 Risk factors
 Mullerian anomalies
 Prolonged exposure to endogenous estrogen (early menarche, late
menopause, or obesity)
 Prolonged menstruation (> five days) and/or shorter menstrual cycles
(< 28 days
 First-degree relative with endometriosis
 Nulliparity
 Shorter lactation intervals
 Low body mass index
3.2.4 Protective factor
 Current/recent use of the combined oral contraceptive (COC),
smoking, and exercise may have a protective effect
3.2.5 Presentations:
The clinical presentation of endometriosis is highly variable and ranges
from debilitating pelvic pain and infertility to no symptoms. Suspect
endometriosis in in women (including young women aged 17 and under)
presenting with any of the following:
 Secondary dysmenorrhea: the most common presenting symptom is
seen in around 85% of patients.
 Deep dyspareunia: (deep pain during or after sexual intercourse).
 Chronic pelvic pain, Variable in severity and location
 Pain at the time of ovulation
 Infertility
 Cyclical or perimenstrual symptoms affecting the bowel or bladder
with or without abnormal bleeding or pain.
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3.2.6 Physical examination

An abdominal and pelvic examination should be offered to women with
suspected endometriosis to identify abdominal masses and pelvic signs
such as:
 reduced organ mobility and enlargement
 tender nodularity in the posterior vaginal fornix
 visible vaginal endometriotic lesions
Laparoscopic visualization is considered the gold standard
investigation unless visible lesions are seen in the posterior vaginal
fornix or elsewhere.
Ultrasound
Sometimes we might see changes suggestive of endometriosis,
preferably through transvaginal ultrasound scan (TVUS).
Do not exclude the possibility of endometriosis if the abdominal or pelvic
examination, ultrasound, or MRI are normal. If clinical suspicion remains
or symptoms persist, consider referral for further assessment and
investigation.
3.2.8 Management:
Management options can be medical or surgical, The treatment strategy
for a patient with endometriosis depends on whether the patient has
infertility or secondary dysmenorrhea (pelvic pain
 Medical treatment: In cases of pelvic pain being the primary
complaint it should be treated even if only mild disease was detected
on laparoscopy. A prolonged period of medical treatment (hormonal
treatment) is required to treat endometriosis. In general, a treatment
period of at least 6 months is undertaken.
 Surgical treatment: In cases of subfertility associated with
endometriosis, there is no evidence that medical therapies improve
fertility. The limited data available suggests that surgery can improve
a patient’s chances of conceiving. Surgical treatment aims to remove
or destroy endometriotic lesions. The chance of conception is
greatest in the two years following surgery.
3.2.9 Referral criteria
Consider referring women to a gynecology service for an ultrasound or
gynecology opinion if:
 They have severe, persistent, or recurrent symptoms of
endometriosis
 They have pelvic signs of endometriosis
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 Initial management is not effective, not tolerated, or is

contraindicated.
 If they have suspected or confirmed deep endometriosis involving the
bowel, bladder, or ureter.
3.3. Pelvic inflammatory disease
3.3.1 Definition:
Pelvic inflammatory disease (PID) refers to an acute infection of the
upper genital tract structures in women, involving any or all of the uterus,
fallopian tubes and ovaries. It can result in endometritis, salpingitis,
oophoritis, peritonitis, perihepatitis, and/or tubo-ovarian abscess.
3.3.2 Causes
Most common causative organisms are Chlamydia
trachomatis and Neisseria gonorrhea, and potentially Mycoplasma
genitalium, as well as the vaginal microflora, including anaerobic
organisms, enteric gram-negative rods, streptococci, genital
mycoplasmas, and Gardnerella vaginalis. PID represents a spectrum of
infection and there is no single diagnostic gold standard.
3.3.3 Risk factors
 Sex is the primary risk factor for pelvic inflammatory disease (PID)
 Women with multiple sexual partners are at the highest risk
 Younger age- PID occurs in highest frequency among those 15 to 25
years of age
 Past infection with chlamydia
 A partner with a STI
 Previous PID
3.4. Ovarian and Fallopian Tube Torsion
3.4.1 Definition:
Ovarian torsion is the complete or partial rotation of the ovary on its
ligamentous supports, which results in partial or complete obstruction of
its blood supply.
The right ovary appears to be more likely to be affected by torsion
compared with the left.
3.4.2 Risk factors:
 Ovarian cysts and neoplasms
 Pregnancy
 Prior ovarian torsion
 Tubal ligation
Page | 342

It can mimic:
 Ruptured ovarian cyst
 Ectopic pregnancy
 Tubo-ovarian abscess
 Appendicitis
The classic presentation of ovarian torsion:
 Acute onset of moderate to severe pelvic pain (90%), either diffuse or
localized to one side
 Nausea and vomiting (47 to 70%)
 Adnexal mass (86 to 95%)
 Fever (2 to 20%)
 History of strenuous physical activity or a sudden increase in
abdominal pressure may dispose to acute torsion
 Pelvic and/or abdominal tenderness
 Palpable pelvic mass may be felt
 Peritoneal signs indicate adnexal necrosis
 Low-grade fever
 Labs (maybe normal in many patients, do b-hcg to rule out EP)
 Ultrasound
 Surgical evaluation offers a definitive diagnosis
3.4.6 Management
After detorsion in an adult patient with a first episode of ovarian torsion
and normal contralateral ovary the following should be considered:
 Salpingo-oophorectomy is considered in the following clinical settings:
 Nonviable ovary
 Suspicion for malignancy
 Postmenopausal patients: to prevent a recurrence
Prevention of recurrence
 Suppression of the formation of new ovarian cysts through using low-
dose estrogen-progestin contraceptives (formulations containing <50
mcg estrogen) in postmenarchal patients without contraindications to
a combination pill.
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3.5. Rupture of ovarian cyst:

The rupture of an ovarian cyst is a common occurrence in females of
reproductive age. The right ovary is more commonly affected. The
average age of occurrence is 27 years old.
3.5.1 Presentation:
It varies between asymptomatic and excoriating pain based on the type
of ruptured cyst. Rupture of simple cyst can be asymptomatic while
rupture of dermoid cyst can be severely painful.
Patients can present with:
 Sudden onset of unilateral, lower abdominal pain
 Character of the pain is typically sharp and focal
 Shoulder pain or upper abdominal pain may be present in cases of
massive hemorrhage
 Intensity may be moderate or severe
 Often following strenuous physical activity (e.g., sexual intercourse,
exercise)
 A history of ovarian cysts
 Pain exacerbated with sitting position, due to psoas muscle irritation.
Page | 344
3.5.2 Risk Factors:

 Conditions that predispose a patient to ovarian cyst formation – (e.g.,
ovulation induction, prior history of ovarian cysts) increase the risk of
cyst rupture
 Current, known cyst – Patients with current, known cysts (e.g.,
endometrioma, teratoma, tubo-ovarian abscess) are at an increased
risk of rupture.
 Vaginal intercourse – Vaginal intercourse appears to be a risk factor
for ovarian cyst rupture
 Vital signs- most patients have stable vital signs, low-grade fever may
be present
 Hemodynamically instability should be ruled out
 Abdominal examination
o One side of the lower abdomen is often tender to palpation; the
right lower quadrant is more commonly affected.
o The release of sebaceous material or blood into the abdomen
may cause overt peritonitis with rigidity of the abdominal wall and
rebound tenderness.
o Intra-abdominal hemorrhage may also be associated with
Cullen’s sign (i.e., periumbilical ecchymosis).
 Pelvic examination
o Bimanual examination may reveal adnexal mass
o Cervical motion tenderness.
 Laboratory tests, CBC with differentials, blood type & cross matching
 B-hCG
 Imaging studies, Pelvic ultrasound is the mainstay of evaluation.
 Definitive diagnosis is by surgical exploration
 Adnexal torsion
 Appendicitis
 Pelvic inflammatory disease (PID)
 Tubo-ovarian abscess (TOA)
 Ovarian hyperstimulation syndrome (OHSS)
Page | 345
3.5.6 Management
Management can be observation or surgery. Patients managed surgically
are typically seen for a postoperative visit in the office within two to six
weeks after surgery.
For patients managed with observation, after discharge evaluate in the
office within one week, or sooner if they are having any symptoms of
worsening pain or lightheadedness. Non-hemorrhagic cyst fluid (from
follicular or corpus luteum cysts) is usually reabsorbed within 24 hours
and symptoms typically resolve within a few days. By contrast, a large
volume hemoperitoneum may take several weeks to resolve.
3.6. Intrauterine Adhesions (IUAs)
3.6.1 Definitions:
 Intrauterine adhesions (IUAs) is a condition in which scar tissue
develops within the uterine cavity, bands of fibrous tissue that form in
the endometrial cavity, often in response to a uterine procedure.
 IUAs that are accompanied by symptoms (e.g., infertility,
amenorrhea) are referred to as Asherman syndrome.
IUAs changes account for menstrual abnormalities, frequent
dysmenorrhea, infertility, and recurrent pregnancy loss.
3.6.2 Risk factors:
 Pregnancy (repeated curettage).
 Intrauterine procedures.
 Inflammation or infection.
 Uterine compression sutures.
 Ovulatory patient who develops secondary amenorrhea or
hypomenorrhea after an intrauterine procedure, particularly if the
procedure was performed on a gravid uterus.
 Abnormal uterine bleeding
 Infertility
 Cyclic pelvic pain or dysmenorrhea
 Recurrent pregnancy loss.
3.6.4 Evaluation:
 Ask about intrauterine procedures that happened before symptoms
started. Ask about menstrual symptoms and any previous
pregnancies.
 Physical examination is usually normal
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 Pelvic ultrasound may demonstrate an unusually thin endometrial

lining, a thin endometrial lining (<4 mm) can indicate IUAs.
 The first step a pelvic ultrasound
 Hysteroscopy is the gold standard for the diagnosis.
3.6.6 Management:
surgical intervention
Chapter 4: COMMON PREGNANCY

COMPLAINS
4.1. Early pregnancy bleeding.
 Miscarriage
 Gestational trophoblastic disease
 Infection of the vagina or cervix
 Sub-Chorionic Hemorrhage
 Vaginal Trauma
 Other causes
Miscarriage (spontaneous abortion)
4.1.2 Spontaneous abortion is influenced by:
 Maternal age Earlier miscarriages are more likely
 Smoking
 Alcohol Caused by a chromosomal
 Radiation exposure abnormalities.
 Parity
 Spacing of pregnancies
 Previous fetal loss
 Previous termination
Page | 347
4.1.3 Assessment of single episode:

Table 4.1
History Examination Investigation
Last Menstural Cardiovascular status – Pregnancy test

period(LMP), evidence of shock? US
amenorrhea, regularity Abdominal examination - CBC,blood group
of cycle, any other tenderness and rebound and cross match if
episodes of vaginal tenderness, uterine size indicated
bleed Speculum, vaginal and
Amount of bleeding, cervical examination
degree of pain, onset of (open or closed, any
pain and bleeding, any visible products)
products passed,
shoulder tip pain.
Table 4.2
Type of Presentation Examination Diagnosis Management
abortion
Threatened - PV bleed Cervix is Pregnancy - Bed rest,
- Generally, closed test, fetal sedation
no pain may No heart - Rhesus
be discharge of sounds, fetal prophylaxis
discomfort POC movements, - Progesterone
and probably
ultrasound effective
Inevitable - Dilated Either
Considerable cervix complete or
PV bleed incomplete
- Lower may result
abdominal
pain
- POC may
have been
passed
Incomplete - PV bleed Dilated - ERPC
- Abdominal cervix - In acute
pain presentation:
Immediate
Page | 348
- Some POC Bulky transfusion or

passed tender Ergometrine to
uterus control PV
bleed
Complete - All POC Closed Transvaginal - ERPC may
passed cervix US not be
- PV bleed Small firm Showed no necessary
gradually nontender retained - Prophylactic
ceases uterus POC and use of
endometrial Ergometrine or
thickness < anti-D rhesus
15 mm AB as indicated
Missed - Fetal death Uterus Pregnancy - Assess
before 24 small for test either clotting status
weeks of dates +ve or -ve - ERPC
gestation Cervix FH, FM and - Rhesus
and is not closed US evidence prophylaxis if
lost from of fetal life indicated
uterus absent - High dose
- prostaglandin
Questionable -
PV bleed Antiprogestrone
Septic - High Vaginal
Spontaneous Very ill Swab, MSU, - Closely
Abortion with Generalized blood monitor
infected peritonitis culture , RF,
uterus Offensive LFT,
- Fever vaginal coagulation
- Can lead to discharge studies
sepsis and
Renal failure
POC (products of conception), FH (fetal heart), FM (fetal movements),

ERPC (evacuation of retained product of conception), RF (renal
function), LFT (liver function test), MSU (mid-stream urine).
4.2. Hydatidiform mole
Benign tumor arising from trophoblast. About 2% of moles develop into
choriocarcinomas.
4.2.1 Risk factors
 Previous molar pregnancy
 Age < 20 y old and > 40 y old
Page | 349
 Racial origin as Asian and Taiwanese

 Diet low in folic acid and beta carotene
 Immunologic
4.2.2 Presentation
 Heavy irregular vaginal bleed following period of amenorrhea
 Usually painless but may be associated with uterine contraction
 Hyperemesis gravidarum – excessive nausea and vomiting
 Pre-eclampsia – dizziness, irritability, photophobia
4.2.3 Examination
 Large uterus for dates
 Absence of fetal heart sounds
 Uterus tend to be doughy
 Evidence of Metastasize
4.2.4 Investigation & monitoring
 Serum BHCG levels, FBC, Coagulation studies, fibrinogen and
 ECG and chest-x-ray.
 US showed “snow storm pattern”.
 Fetal Doppler -ve.
 Monitor beta-hCG for the next 1–2 years
4.2.5 Management
 Evacuation.
 Chemotherapy if metastasize is detected.
 Rarely hysterectomy.
 Avoid pregnancy usually for 1-2 years and using contraceptive pills
until BHCG is undetectable.
4.3. Late pregnancy bleeding.
4.3.1 Causes:
 Placental abruption 15%.
 Placenta Previa 10%.
 Vasa Previa.
 Incidental hemorrhage from lesion from the cervix or vagina -
infection, carcinoma, polyp and ectropion.
 Other causes as rectal bleeding, bleeding diatheses and hematuria.
Page | 350
4.3.2 Risk factors for the main causes:

Table 4.3
Placenta Previa Placental abruption Vasa Previa
- Chronic HTN. - Chronic HTN. - Uterine fibroids.

- Multiparity. - Multiparity. - IVF.
- Multiple gestations. - Previous abruption. - Multiple gestations.
- Older age. - PET. - Marginal cord
- Previous cesarean - Short umbilical cord. insertion.
delivery. - Sudden - Succenturiate lobed
- Tobacco use. decompression of an and
- Uterine curettage. over-distended uterus. bilobed placenta.
- Thrombophilia. - Low lying and
- Tobacco, cocaine, or second
methamphetamine trimester - placenta
use. Previa.
- Trauma.
- Unexplained
elevated maternal
AFP.
- Uterine fibroids.
IVC (inferior vena cava), IVF (in vitro fertilization), AFP (alpha-fetoprotein
level), PET (Pre-eclampsia).
Table 4.4
Main presentation Examination Diagnosis Management
causes
Placenta - Placenta is - Uterus is - Routine -
Previa situated in relaxed. US, Asymptomatic,
the lower - Presenting commonly repeat US at 28
uterine part not before 20 weeks.
segment. engaged. weeks’ - Symptomatic
- Degrees - Do not gestation. Tocolytic agents
revealed in perform a In 90% of For preterm
Figure 1, vaginal patients it contractions,
linked with examination. ultimately Corticosteroids
increasing resolves. at 24-34 weeks
need for CS. - CBC, estimated
- Recurrent blood group gestations.
painless cross match - Immediate
vaginal as steps include:
bleeding indicated. admission to
Page | 351
usually the hospital,

unprovoked, bed rest,
it may follow Transfusion and
intercourse CS as
with Highly Indicated.
Variable
Amount.
Placental - - Grades of - US (to - Do not
abruption Pathological hemorrhage: localize perform a
separation of 1- Mild - placenta) digital
the placenta blood loss < - FBC, examination.
before 200 ml with Blood group - Mild cases:
delivery. abdominal cross Admit to the
- 3 types of discomfort. match, hospital, Bed
presentation: 2- Moderate coagulation rest, IV line in
Concealed – up to 1/3 of studies, situ, Inspection
(no bleeding the placenta fibrinogen of the cervix
seen), separates, - High with speculum,
Revealed blood loss frequency 4-5 days after if
(bleeding 200-600 ml uterine bleeding
seen) and with contractions doesn’t recur
Mixed (most abdominal of low tone. can be d/c with
common) pain and - Fetal close
tachycardia distress. monitoring and
and FH +ve. intercourse
3- Severe - > should be
1/2 of the avoided.
placenta - Moderate
separates, cases:
severe The same as
abdominal mild but patient
pain, uterus should not be
tender and d/c from the
rigid, FH hospital.
reduced or - - labor if there
ve and are signs of
patient may fetal distress.
be in - severe
hypovolemic cases:
shock. Admit, insert
CVPL, IV-line,
urinary
catheter, fluid,
Page | 352
transfusion
cross-match 4-6
units as
indicated,
analgesics,
monitor with
CTG, labor or
be delivered by
LSCS if there
are signs of
fetal distress, if
fetus is dead
vaginal delivery
preferred.
Vasa - - - If FH - Delivery in
Previa Velamentous Hemorrhage tones are case of:
insertion of is fetal blood. re-assuring: sever
UC into -average blood Hemorrhage or
membranes blood volume sample FH tones are
in the lower of a term from non-reassuring.
uterine fetus is 250 vaginal
segment ml. vault can be - Screening can
resulting in checked for be done for
the presence fetal blood women at high
of fetal cells or fetal risk and
vessels Hg and cesarean
between the Apt test. delivery at 37-
cervix and 38 weeks using
presenting transvaginal
part. color-Doppler.
- Uncommon
- Onset
hemorrhage
at the time of
amniotomy
or SROM.
d/c (discharge), CVPL (central venous pressure line), CTG

(cardiotocography), IV (intravenous), CS (cesarean section), UC
(umbilical cord), SROM (spontaneous rupture of membranes), FH (fetal
heart), Hg (hemoglobin).
Page | 353
Minor Previa
reaching the internal cervical os
Major Previa
completely crossing the os
Figure 1
4.4. Preeclampsia
Table 4.5
Chronic Gestational PET PET
HTN HTN Superimposed
Upon Chronic
HTN
Definition High BP in High BP in High BP in When PET
pregnancy pregnancy after pregnancy diagnostic
before 20 20 weeks after 20 criteria occur in
weeks on without weeks with a woman who
at least 2 proteinuria or Systolic is diagnosed
occasions other BP >= 140 with chronic
or persist signs/symptoms or diastolic HTN.
longer than of PET related >= 90 mm
12 weeks end organ Hg on at
postpartum. dysfunction. least 2
or even occasions,
before taken at
pregnanc. least 4
hours
apart and:
Page | 354
Target BP -new onset

IS 110- proteinuria.
135/85 -and/or >1
mmHg. sever
feature.
PET (Pre-eclampsia), EC (Eclampsia), ER (Emergency), HTN

(Hypertension).
4.4.1 Risk factors Pathophysiology of PET

High
Believed to be related to under-
 Autoimmune disease
perfusion to the placenta due to
 Chronic hypertension
the early abnormal placental
 Type 1 or 2 diabetes
vascular development with
 History of pre-eclampsia
subsequent release of
 Multifetal gestation
 Renal disease antiangiogenic factors, which
Moderate causes Hypertension with
unknown triggers.
 Age >= 35 years old
 Sociodemographic characteristics
(low SES)
 Family history of pre-eclampsia (mother or sister)
 Personal history factors (e.g., Low birth weightor small for gestational
age, previous adverse pregnancy outcome,> 10-year pregnancy
interval
 Obesity (BMI >30 Kg/m2)
 Nulliparity
4.4.2 Screening and Prevention
 Screen pregnant women by measuring their BP at each visit. (Grade
B recommendation)
 Start aspirin at 81 mg/day between 12 and 28 weeks of gestation for
women with 1 high or 2 moderate risk factors.
 Ca supplementation may decrease the incidence of PET, HTN and
mortality among high-risk women with low ca intake.
Page | 355
Table 4.6
Sever features of PET Complications
- Sever BP elevation - Eclampsia

Systolic BP ≥160 or diastolic BP - Stroke
≥110 mmHg on 2 - PE (pulmonary edema)
occasions, 4 hours apart while the - HELLP syndrome
patient is on bed 1-Hemolytic anemia
rest. LH>600 U/L
- Symptoms of CNS dysfunction PBS schistocytes, helmet cell
New-onset cerebral or visual Serum bilirubin 1.2 mg/DI or more
disturbance, such as: 2-Elevated liver enzymes
Severe headache and Photopia. Transaminases levels >= 2 times
- Hepatic abnormality ULN
Transaminase concentration >2 3-Low PLT < 100 x103
times ULN or - PRES
severe persistent RUQ or epigastric Posterior Reversible
pain. Leukoencephalopathy
- Thrombocytopenia Syndrome
<100,000 platelets/microL - Obstetric complications as IUGR,
-Renal abnormality placental
Serum Cr >1.1 mg/dL or a doubling abruption, fetal demise.
in the level.
- Pulmonary edema
ULN (Upper Limit of the Normal), LH (Lactate Dehydrogenase), PBS

(Peripheral Blood Smear), BP (Blood Pressure), Cr (Creatinine).
Table 4.7
Presentation Examination Diagnosis Management
PET Pregnant Check for: Check BP and High risk
women might - proteinuria in patient.
develop any Hyperreflexia each visit. - She has to be
of the - RUQ referred to an
following tenderness. Proteinuria can OBGYN or
alarming - Bruises be measured by pregnancy high-
symptoms: - Peripheral either one of the risk clinic.
- Severe or edema and following:
persistent sudden and • 300 mg of PET without
headache rapid weight protein in a 24- severe
gain. features:
Page | 356
- Visual hour urine - Twice-weekly

disturbances sample BP monitoring
- AMS • Urinary - Antenatal
- New protein/creatinine testing for fetal
dyspnea, ratio of 0.3 or well-being by
orthopnea greater. Fetal ultrasound
- Chest pain • Two urine and Uterine and
- Upper dipstick umbilical artery
abdominal measurements Doppler.
pain of at least 1+ (30 - Delivery by 37
- Epigastric mg per dL), six weeks’
pain hours apart. gestation.
- Oliguria
Investigations PET with any
include: severe feature:
-CBC - Immediate
-PBS stabilization and
-RFT admission
-LFT - Medication:
-CP 1- magnesium
- Chest-x-ray sulfate
'batwing' pattern 2-
with air Antihypertensive
bronchograms drugs as IV
sometimes labetalol or
present. hydralazine or
oral nifedipine.
3-
Corticosteroids
for fetal lung
maturity if < 34
weeks’ gestation
- Delivery plan.
AMS (Altered Mental Status), PP (Postpartum), RUQ (Right Upper-

Quadrant), CP (Coagulation Profile), PBS (Peripheral Blood Smear),
PET (Pre-Eclampsia), BP (Blood Pressure).
Page | 357
4.5. DM in pregnancy
Table 4.8
Definition Pre-Conception Complications Management
Care
Pregnant - Need - Congenital - Insulin is the
women with multidisciplinary anomalies preferred agent,
preexisting DM. care including - PET, they used as MDI or
DM care, should be IPT in DM1
educator, prescribed low patients.
dietitian and dose aspirin
endocrinologist. 100-150 mg/ - In early
day starting at pregnancy,
- Achieve 12 to 16 weeks insulin
glycemic targets of gestation to requirements
1-FBG < 95 lower the risk of are lowered to
mg/dl (5.3 PET. avoid
mmol/L). - Macrosomia hypoglycemia
2-1 hour post - Preterm birth due to
prandial BG < - Embryopathies enhanced
140 mg/dl (7.8 include: insulin
mmol/L). Anencephaly sensitivity.
3-2 hour post Microcephaly Approaching 16
prandial BG<120 CHD weeks, insulin
mg/dl (6.7 Caudal resistance starts
mmol/L). regression to increase.
4-A1c <6%. Renal
anomalies - In DM1
- Screen for DM patients,
comorbidities Hypoglycemia
and and DKA
complications. prevention,
recognition,
- Counseling and treatment
about DM education is
retinopathy risk important,
of development ketone strips
and progression should be
along with prescribed.
Dilated eye exam
before pregnancy - In DM2
or during first patients, control
Page | 358
trimester, then weight gain

every trimester, within the
and for 1 year recommended
postpartum. range.
(15-25 Ib for
- CGM, in overweight)
addition to (10-20 Ib for
SMBG in patient obese). May
with DM1, reduce require higher
macrosomia and insulin doses in
neonatal compare to
hypoglycemia. DM1 pregnant
patients.
CGM (Continue Glucose Monitoring), SMBG (Self-Monitoring of Blood
Glucose), BG (Blood Glucose), CHD (Congenital Heart Disease),
MDI (Multiple Daily Injections), DKA (Diabetic Ketoacidosis),
PET(Preeclampsia), IPT (Insulin Pump Technology).
Postpartum care
The initial few days postpartum, Insulin sensitivity increases gradually,
reaching pre-pregnancy levels over 1-2 weeks. Therefore, Insulin
requirements need to be evaluated as they will be nearly half the pre-
pregnancy requirements initially and adjusted thereafter.
4.6. Gestational Diabetes Mellitus (GDM)

4.6.1 Definition
ACOG defines GDM as a "condition in which carbohydrate intolerance
develops during pregnancy”.
It is diagnosed in the second or third trimester of pregnancy that was not
overt diabetes before 24 weeks of gestation.
4.6.2 Screening
1-For women with risk factors for DM2, test at first prenatal visit for DM2
using the standard diagnostic criteria.
2-For women with no risk factors or not previously found to have
diabetes for gestational diabetes, test at 24 to 28 weeks’ gestation of
using one step or two step strategy.
ACOG (American College of Obstetrics and Gynecology), IUFD

(Intrauterine Fetal Death), GI (Glucose Intolerance).
Page | 359
4.6.3 Diagnosis of GDM
Table 4.9
One Step Strategy Two Step Strategy
Perform a 75-gram OGTT, with BG Step 1:

measurements when patient is Perform 50-gram GCT non-fasting
fasting (at least 8 hours) at one and with BG measurements at one
two hours, at 24 to 28 weeks of hour, at 24-28 weeks of gestation
gestation and woman not and women not previously
previously diagnosed with DM. diagnosed with DM.
If BG values is >= 130,135,140
The diagnosis of GDM is made mg/dl, proceed to steps 2 (100-
when the following BG values are gram OGTT).
met or exceeded: Step2:
- Fasting: 92 mg/dl The 100-gram OGTT done when
- One hour: 180 mg/dl the patient is fasting.
- 2 hours: 153 mg/dl The diagnosis of GDM made when
at least 2 of the following 4 BG
levels (measured fasting and at 1,
2, and 3 hours) are met or
exceeded:
- Fasting: 95 mg/dL
- 1 hour: 180 mg/dL
- 2 hours: 155 mg/dL
- 3 hours: 140 mg/dL
BG (Blood Glucose), GCT (Glucose Challenge Test), OGTT (Oral

Glucose Tolerance Test).
4.6.4 Management
Table 4.10
Lifestyle Pharmacotherapy Referral Postpartum
Management Indications Care
- calorie - Insulin is the - Controlled - Test for pre-
consumption first-line agent GDM on a diabetes or
of 1800- when target diet can be diabetes at 4-
2500 glucose levels are followed up in 12 weeks
kcal/day and exceeded PHC. postpartum,
diet low in despite nutritional using a 75-g
saturated fat therapy. oral glucose
Page | 360
and sugar- - Uncontrolled tolerance test

sweetened - Types of insulins GDM on a (OGTT) and
beverages. that can be used diet can be clinically
safely: Rapid- initiated on appropriate
- Physical activity acting insulin insulin in PHC non-
- Weight analog (aspart, if a pregnancy
management. lispro), Long- diabetologist diagnostic
acting insulin or an criteria.
analog (detemir) experienced
and NPH insulin. provider is - Screen for
available in diabetes or
- Directing the the center pre-diabetes
insulin regimen to and the at least every
correct specific absence of 3 years.
hyperglycemias is maternal or
the preferred fetal risks or - Postpartum
method when high-risk women with
isolated abnormal pregnancy GDM and pre-
values are found until an diabetes
at a specific time Endocrinology should
of the day. SMBG appointment receive
is recommended 4 is available. intensive LM
times/day fasting and/or
and after each - GDM metformin to
meal. women who prevent
have maternal diabetes.
- When initiating or fetal risks
basal analog or or with a high- - They should
bedtime NPH risk seek pre-
insulin, start 10 IU pregnancy conception
a day or 0.1-0.2 should be screening and
IU/kg a day. When referred to a care for DM.
Titrating, choose specialized
an evidence- center - Encourage
based titration offering team- breastfeeding,
algorithm, e.g., based care as screen for
increase 2 units soon as depression.
every 3 days to possible.
reach FPG target
without
hypoglycemia.
Page | 361
- When initiating
Prandial insulin,
start with 4 IU a
day or 10% of
basal insulin dose.
Increase dose by
1-2 I or 10-15%
twice weekly while
titrating prandial
insulin.
- Metformin and
glyburide
Should not be
used as first-line
agents, as they
both cross the
placenta to the
fetus and the long-
term safety data
for offspring is of
some concern.
- Other oral and
noninsulin
injectable glucose-
lowering
medications lack
long-term safety
data.
MNT (Medical Nutrition Therapy), PHC (Primary Health Care), LM
(Lifestyle Modification).
Below Some conditions that necessitate referral
Table 4.11
Maternal factors Pregnancy-related Fetal related factors
factors
- Preexisting maternal - PET - Macrosomia or
medical conditions - Placenta Previa history of
(ex. Poorly controlled - Acute fatty liver of macrosomia in
asthma or complicated pregnancy previous pregnancies.
chronic HTN) - Anticipated - Large for Gestational
- Cardiac disease complicated Age
cesarean delivery
Page | 362
- Coagulation - Polyhydramnios (LGA) or small for

Disorders which can result in gestational age (SGA).
- Complex preterm labor - Congenital
hematologic or Anomalies
autoimmune disorders - History of IUFD or
- Pulmonary HTN stillbirth
- Unstable conditions
that require an organ
transplant
- previous history of
Placenta Previa,
accerta, percreta and
uterine surgery.
- Recurrent
hypoglycemia
PET(Pre-Eclampsia), IUFD (Intrauterine Fetal Death), HTN
(Hypertension).
Pregnancy and drug considerations
The following medications should be stopped in pregnant women at
conception and
avoided in sexually active women of childbearing age who are not using
reliable contraception:
 ACE inhibitors
 Angiotensin receptor blockers
 Statins
Effective and safe antihypertensive medications in pregnancy include:
 Methyldopa
 Nifedipine
 Labetalol
 Diltiazem
 Clonidine
 Prazosin
Atenolol is not recommended, but other b-blockers may be used if
necessary.
Page | 363
Chapter 5: FAMILY PLANNING

5.1. Contraception choices
5.1.1 Reversible Contraception
 Fertility awareness
 Barrier Methods
 Progestogen-only pills
 Combined (estrogen and progestogen) pills
 Combined transdermal patch
 Combined vaginal ring
5.1.2 LARC (Long-Acting Reversible Contraception)
 Injectable contraceptives
 Subdermal implant
 Copper intrauterine device (IUD)
 Progestogen-only intrauterine system (IUS)
5.1.3 Permanent
 Vasectomy; reversal can be attempted
 Tubal occlusion with clips/rings
5.1.4 Natural Family Planning
 The limitations of NFP are related to the requirement of periodic
abstinence.
 Any illness, disrupted sleep, and the use of medications can alter or
interfere with the observation and interpretation of some biological
markers.
 Perfect use is 95 % effective in preventing pregnancy.
 The effectiveness of typical use is 76 %.
Natural Methods
 Basal body temperature charting: An increase of at least 0.4°F
(0.2°C) above the baseline temperature
 Cervical mucus monitoring: Tracks cyclical changes in the amount
or consistency of cervical secretions
 Calendar Calculation: Based on the relative consistency in the
length of the luteal phase of the reproductive cycle
 Symptothermal method
 Lactational Amenorrhoea Method (LAM): temporary postnatal
contraceptive method, over 98% effective at preventing pregnancy.
Page | 364
5.1.5 Barrier Method of Contraception

 With perfect use, male condoms are 98% effective and female
condoms 95% effective at preventing pregnancy.
 When used consistently and correctly and with spermicide,
diaphragms and cervical caps are estimated to be between 92% and
96% effective at preventing pregnancy
5.2. Combined Hormonal Contraception (CHC)
5.2.1 Combined transdermal patch (CTP)
 They are applied weekly on the same day for three weeks. This is
followed by one patch-free week.
 Very effective method of contraception in women weighing less than
90kg.
 There is an FDA safety warning as it contains 60% more estrogen per
cycle as compared to 35mcg OCP, leading to 3x more risk of VTE.
5.2.2 Combined vaginal ring (CVR)
 The soft vaginal ring releases 15 mcg Ethinyl estradiol and 120 mcg
etonogestrel daily.
 Three weeks of continuous vaginal use followed by a seven-day ring-
free interval
 It should be stored in a pharmaceutical fridge, as the ring has only a
four months active life following dispensing.
Possible side effects with CTP/CVR
 Specific to CTP: Skin reaction to the adhesive/material of the patch
and skin discoloration around the patch site
 Specific to CVR: Vaginitis, awareness of CVR during intercourse,
foreign body sensation and ring expulsion
5.2.3 Combined oral contraceptive pill (COC)
 COCs are a highly effective form of contraception with a typical-use
failure rate of approximately 8 percent.
 Missed pills are a common cause of contraceptive failure. back-up
contraception should be used for seven days after two missed pills,
regardless of the dose
 The metabolism of COCs is not affected by antibiotics, except for
rifampicin.
 COCs: most commonly contain ethinylestradiol (range from 20–40
micrograms) and Levonorgestrel or norethisterone.
Page | 365
Possible Side Effects

 Breast tenderness/enlargement, bloating, nausea, increased non-
infective vaginal discharge, headache, chloasma (skin pigmentation),
acne, greasy skin/hair, hirsutism, depression, loss of libido, Rarely
Venous thromboembolism, breast cancer risk and cervical cancer
Non-contraceptive Benefits of CHC
 help to regulate menstruation and decrease menstrual blood loss.
 The incidence of benign ovarian cysts and functional ovarian tumors
is reduced.
 Reduction in hirsutism, acne and seborrhoea
 Reduction in risk of: Ovarian cancer, endometrial cancer and
colorectal cancer
5.2.4 Contraindication
USMEC 4
Current & breast cancer, acute DVT, history of DVT with high risk for
recurrence, major surgery with prolonged immobilization, Postpartum:
‹21 days, smoking Age ≥35, ‹15 cigarettes/day, Solid-organ
transplantation: complicated, History of CVA, SLE with positive ( or
unknown) antiphospholipid antibodies, Thrombogenic mutations,
migraine with aura or without if age≥ 35, DM with (
Nephropathy/retinopathy/neuropathy ) or >20 years' duration) or with
vascular disease, Hypertension ( systolic ≥160 or diastolic ≥100) or with
vascular disease, Peripartum cardiomyopathy, Acute porphyria, Severe
Cirrhosis adenoma, Malignant liver tumors, complicated Valvular heart
disease, acute or flare-up of viral hepatitis
Initiation of Combined hormonal contraception
 Starting COC in the first 5 days OR anytime if pregnancy can
reasonably be ruled out starting on day 6 of the cycle or later. Extra
precautions (barrier methods) are necessary during the first 7 days.
Missed Pill Rule:
 ONE pill has been missed (48 – 72 hours since the last pill in the
current packet or 24- 48 hours late starting the first pill in the new
pack)
 TWO or MORE pills have been missed (>72since last pill in the
current packet or >48 hours late starting the first pill in the new
packet)
Page | 366
5.3. Progesterone Only Contraception

General features regarding progesterone-only contraception
 Progestin-only contraceptives are recommended for women with
contraindications to estrogen.
 All Progesterone only contraception is long-acting reversible
contraception (LARC), with the exception of POP (progesterone-only
pill)
 Hepatic enzyme-inducing anti-epileptic medications, including
phenytoin, carbamazepine, topiramate, and barbiturates; and the
antituberculosis drug rifampicin may reduce the efficacy of POPs.
Contraindication
USMEC 4: current breast cancer
USMEC 3 conditions include:
 Multiple risk factors for cardiovascular disease
 Vascular disease
 Stroke
 Current and history of ischaemic heart disease
 Past history of breast cancer
 Cirrhosis - severe (decompensated)
 Malignant liver tumor or hepatocellular adenoma
 Unexplained vaginal bleeding
5.3.1 Progesterone only pill
 Should be taken every day nearly same time, 12 hours safety window
 The typical user failure rate with POPs is estimated to be over 9
percent
Progesterone Side effects
 POPs after one year of use, approximately:
 5 in 10 can expect amenorrhoea or infrequent bleeding
 4 in 10 can expect regular bleeding
 1 in 10 can expect frequent bleeding
 Mood change
 Acne and breast tenderness have been reported
Page | 367
Missed Pill Rule:

Table 5.1
Type of pill Missed pill Missed pill advice
POP that works by a >3 hours late (i.e., 27 The same advice
cervical mucus effect hours since the last pill applies to both types
was taken) of POP:Take the
missed pill as soon as
possibleIf more than
one pill is missed,
simply take one
pillTake the next pill at
the usual time, even if
it means two pills in
one dayUse condoms
or abstain from sexual
intercourse (SI) for 48
hours
Desogestrel >12 hours late (i.e., 36
containing POP hours since the last pill
taken)
5.3.2 LARC (Long-Acting Reversible Contraception)

Progesterone only injection
Multiple formulations available Depo-Provera is commonly used in KSA
 DMPA is formulated for deep intramuscular (IM) injection as Depo-
ProveraTM: 150mg medroxyprogesterone acetate in 1ml an aqueous
solution in a pre-filled syringe
Side Effects with injectable progesterone
 Altered bleeding pattern includes amenorrhoea, infrequent bleeding,
spotting, and prolonged bleeding.
 Weight gain..
 Injection site reactions (induration, scarring, and atrophy)
 Acne
 Breast tenderness is rare, but galactorrhoea is a recognized side
effect, and serum prolactin should be checked if it occurs.
Page | 368
Recommendations for late injectable progesterone:

Table 5.2
Contraceptive Duration Recommendations Transition
since the to next
method
last dose cycle
Injectables (i.e., < 2 weeks Proceed with Not
depot medroxy- late (< 15 injection applicable
progesteroneacetate weeks after
[Depo-Provera]) the
previous
injection)
≥ 2 weeks Treat as a new Not
late start. applicable
Red flags
 There may be a delay in the return of fertility after stopping
progestogen-only injectables used for up to one year.
 A weak association between the current use of DMPA and breast
cancer. Any increased risk is likely to be small and reduce with time
after stopping.
 Prolonged use of DMPA (over five years) has a weak association with
the occurrence of cervical cancer, which may reduce with time after
cessation.
Progesterone implant
Subdermal implant (Nexplanon)
 SDI is a single non-biodegradable flexible rod measuring 40mm long
by 2mm diameter
 Contains 68 mg of etonogestrel
Nexplanon insertion recommendations
 Should be at the inner side of non-dominant upper arm about 8-10 cm
above the medial epicondyle of humerus, avoiding the sulcus
between biceps and triceps muscle, where neurovascular bundle lies
SDI Benefits
 Highly effective
 Long action (3 years)
 Quickly reversible
 Estrogen-free
Page | 369
 No relevant effects on metabolism (lipids, clotting, blood pressure)

and therefore no increased risk of thrombotic events or decrease in
bone mineral density
 Relief of dysmenorrhoea and ovulatory pain
Risks
 Change in bleeding pattern
 Weight Issues
 Mood Issues
 Acne
 Headache
 Skin Atrophy
 An increased risk of breast cancer cannot be completely excluded;
any increased risk is likely to be small and is likely to reduce with time
after stopping.
 Infrequent bleeding, amenorrhoea, prolonged or frequent bleeding
Risks of implant insertion
 Non-insertion or failure
 Deep insertion
 Nerve or vascular injury
Starting SDI
 Can be inserted day 1-5 of the woman’s natural cycle: no additional
precautions required.
Pearls
 In women weighing over 70 kg, SDI efficacy may be reduced at the
end of the 3yrs, yet no strong evidence. But if in doubt or previous
high fertility, it can be replaced earlier.
Intrauterine Devices
Available IUDs
 Copper -Releasing Intrauterine Contraceptive
 Levonorgestrel-Releasing Intrauterine System LNG-IUS
Contraindications
USMEC3/4
 Distorted Uterine cavity
 Breast cancer current /treated
 Cervical cancer
 Endometrial cancer
 Gestational Trophoblastic Disease
Page | 370
Complications and precautions with IUD insertion

 Uterine perforation
 Expulsion
 Change in bleeding pattern
 Pelvic infection
 Hormonal side effects
Mirena IUS
 Contains 52mg levonorgestrel-releasing approximately 20mcg/day
 Contraception failure rate <1 % in 5 yrs
 Has retrieval thread
 Irregular erratic bleeding initially but by 1yr infrequent bleeding or
amenorrhea.
 progestational side effects acne, breast tenderness, mood changes
and headaches, mostly reduce with time.
 if a woman gets pregnant with Mirena in situ, there is an increased
risk of that pregnancy being ectopic.
Mirena Use
 For contraception
 For gynecological conditions: heavy periods, pelvic pain,
endometriosis, adenomyosis and primary dysmenorrhea
 For progestogenic component HRT
LARC, Intrauterine Contraception Problems
 Low lying device
 Pregnancy
 Actinomycoses
 Lost Thread
5.4. Emergency Contraception
 Emergency contraception decreases the risk of unintended
pregnancy after unprotected sexual intercourse or after the suspected
failure of routine contraception (e.g., a condom breaking).
 Use after implantation does not interrupt an established pregnancy
 EC is best used ASAP after unprotected sexual intercourse
 Any EC may be used in a woman with contraindication to CHC –C
Page | 371
Table 5.3 – EC methods

Method Dosage Timings after UPSI
Combined oral 100 mcg of Ethinyl 5 days
contraceptive estradiol plus 0.5 mg
of levonorgestrel; two
doses are taken 12
hours apart.
Levonorgestrel, split 0.75 mg; two doses 3 days
dose taken at the same time
or 12 hours apart
Levonorgestrel, single 1.5 mg, single dose 3 days
dose
Ulipristal (Ella) 30 mg, single dose 5 days
Intrauterine copper Single device 5 days
device
Page | 372
Chapter 6: COMMON
GYNECOLOGICAL CONDITIONS
6.1. Amenorrhea
6.1.1 Definition:
Amenorrhea is defined as the absence of menstruation in non-
physiological events. It’s classified as either primary or secondary
amenorrhea.
 Primary Amenorrhea: Absence of menarche at the age of 15 years in
presence of secondary sexual characteristics or at the age of 13
years in absence of secondary sexual characteristics. Most common
causes are:
o Gonadal dysgenesis : (e.g., Turner syndrome, 45X0)
o Mullerian agenesis : (i.e., absence of vagina with/without a
uterus)
o Other anatomical defects: transverse vaginal septum or
imperforate hymen
 Secondary Amenorrhea: Cessation of regular menses for three
months, or cessation of irregular menses for six months. Most
common causes are:
o Pregnancy
o hypothalamic-pituitary-ovarian dysfunction : (e.g.,
Hyperprolactinemia, Thyroid dysfunction)
o Intrauterine adhesions
Clinical assessment of the patient includes:
History : Recent pregnancy test, OB and GYN history, Medical History,
History of radiation or chemotherapy, Vasomotor and estrogen deficiency
symptoms, Headache, blurred vision, or presence of galactorrhea,
Symptoms of excess androgen like hirsutism, acne, change in voice,
Symptoms were suggestive of thyroid dysfunction, Family history, Mental
health and Medication use.
Physical examination: Starting with a general examination, Dysmorphic

features, Thyroid examination, Tanner staging, Signs of excess
androgen, Abdominal examination, and Genital examination.
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primary amenorrhea : Pregnancy test, FSH, karyotype, Pelvic ultrasound
Secondary amenorrhea: Pregnancy test, FSH, LH, prolactin, TSH, total

testosterone, dehydroepiandrosterone sulfate, 17-hydroxyprogesterone,
Complete blood count and metabolic panel.
primary amenorrhea (Primary ovarian insufficiency) :
 Hormonal therapy (HT) until the average age of natural menopause
(age 50–51 years) for prevention of osteoporosis, cardiovascular
disease, and urogenital atrophy and to improve the quality of life.
6.2. Dysmenorrhea
6.2.1 Definition:
Painful cramps that occur with menstruation onset.
Primary dysmenorrhea: recurrent pain during menstruation in the

absence of underlying disorders that could account for these symptoms.
Secondary dysmenorrhea: Presence of underlying disorders that could

be responsible for the pain symptoms during menstruation.
Causes of Secondary dysmenorrhea:

 Gynecological: Endometriosis, Adenomyosis, Fibroids, Ovarian cyst,
Pelvic inflammatory disease, Cervical stenosis, Intrauterine or pelvic
adhesions
 Non-gynecological: Inflammatory bowel disease, Irritable bowel
syndrome, Ureteropelvic junction obstruction, Psychogenic disorder.
Clinical assessment of the patient includes:
History: Menstrual history, Pain (Timing , Characteristics and severity),
Associated symptoms, Sexual History, Obstetrics history, Past medical
history, History of pelvic surgery.
Physical examination: Vital Signs, BMI, Pelvic examination

laboratory testing, imaging, and/or diagnostic laparoscopy can be
performed to diagnose secondary dysmenorrhea, but they are not
required for the diagnosis of primary dysmenorrhea
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Non-pharmacological: Patient education and reassurance, Behavioral
counseling, Regular Exercise, Topical heat pads, Acupuncture, and Diet
and vitamins
Pharmacological: Acetaminophen, NSAIDs, Hormonal contraception.
6.3. Abnormal Uterine Bleeding
6.3.1 Definition:
AUB is the overarching term for bleeding from the uterine corpus that is
abnormal in regularity, volume, frequency, or duration in the absence of
pregnancy. It might be acute or chronic.
Table 6.1 – Normal menstruation parameters
Parameter Normal Abnormal
Frequency >24 and < Absent (no bleeding):
38days amenorrheaInfrequent
(>38 days)
Duration <8 days Prolonged (>8 days)
Regularity Regular: shortest Irregular: shortest to
to longest cycle longest cycle variation
variation: < 7to 9 >10 days
days
Flow volume Patient Patient considers
considers normal light/heavy
Intermenstrual bleeding None Either random or
cyclical (early, mid, or
late cycle)
Unscheduled bleeding on None Present
contraceptive
pills/rings/patches/IUD/injections
Acronym for etiologies of AUB is: PALM–COEIN: Polyp, Adenomyosis,

Leiomyoma, Malignancy and hyperplasia, Coagulopathy, Ovulatory
dysfunction, Endometrial, Iatrogenic, and Not otherwise classified.
Clinical assessment includes:
History: bleeding details, Associated symptoms, gynecological history,
medical history, Personal or family history (coagulation factor
deficiencies and hemophilia), Trauma (sexual intercourse or abuse), and
medications (anticoagulants or chemotherapeutic)
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Physical examination: Sings of (hypovolemia and anemia) by vital signs

and general appearance, and pelvic examination (a speculum
examination and a bimanual examination).
Acute AUB: Complete blood count, Blood type and crossmatch,
Pregnancy test, Partial thromboplastin time disorders of hemostasis,
Prothrombin time, Activated partial thromboplastin time, Fibrinogen.
Based on the clinical presentation: a workup for: TSH, Serum iron, total
iron-binding capacity, ferritin, Liver function tests, Chlamydia trachomatis,
Pap smear, and Endometrial tissue sampling.
Acute AUB: Refer patient to the emergency department for stabilization
and further assessment and management either with medical or surgical
intervention (e.g., dilation and curettage, endometrial ablation, uterine
artery embolization, or hysterectomy).
Chronic AUB: Manage treatable causes like hypothyroidism, STI, or
contraceptive-induced AUB or refer the patient to a gynecologist for
further assessment and management.
6.4. Uterine Fibroids
6.4.1 Definition:
Uterine fibroids (also known as uterine leiomyomas or myomas) are the
most common benign gynecological tumors. Most fibroids shrink after
menopause since the growth is dependent on the ovarian steroid
estrogen and progesterone.
Table 6.2 – Factors that affect the risk of uterine fibroids
Decreased risk Increased risk
Increased parity African descent

Late menarche (older than 16 Age greater than 40 years
years) Early menarche (younger than 10
Smoking years)
Use of oral contraceptives and Family history of uterine fibroids
progestin-only injectable Nulliparity Obesity
Excessive consumption of beef
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Symptoms: majority are asymptomatic, heavy menstrual bleeding,
Abdominal bloating, Pelvic pressure symptoms, Pelvic pain, Infertility.
Signs: Very large fibroids may be palpated abdominally. Vaginal

examination usually reveals – a firm, irregularly enlarged uterus that is
non-tender; an exception is one undergoing red degeneration, which
may be very tender
Complete blood count including hemoglobin, urine analysis, abdomen/
trans vaginal US, Saline infusion sono-hysterography, Pelvic MRI.
Treatment options for patients with fibroids depend on the size and
location of the tumors, patient age, symptoms, desire to maintain fertility,
access to treatment, and the physician’s experience.
Medical treatment: NSAIDs, Antifibrinolytic agents, levonorgestrel

releasing intrauterine device, gonadotropin-releasing hormone agonists,
oral contraceptives, danazol (rarely used due to the side effects)
Surgical treatment: Myomectomy, Hysterectomy, Uterine artery

embolization.
6.5. Vaginitis
6.5.1 Definition:
Vaginitis is a broad term for vaginal disorders that include inflammation,
infection, or other changes that may occur in the normal vaginal flora.
The causes of vaginitis can be infectious and non-infectious:
 Non-infectious: Atrophic, Irritant and allergens, Foreign body,
Systemic medical disorders
 Infectious: Bacterial vaginosis, Candida vulvovaginitis,
Trichomoniasis, Sexually transmitted diseases (Neisseria
gonorrhoeae, Chlamydia trachomatis, Mycoplasma genitalium).
Clinical assessment includes:
History: presenting symptoms (Dysuria, Burning, Irritation, Pruritus,
Erythema, Dyspareunia, Spotting, Change in vaginal discharge color,
odor or volume), Associated symptoms, Contraceptive methods,
Systemic review, Medication history, Past medical history, Menstrual
history, Past surgical history, Sexual history.
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Examination: Vital signs, Pelvic examination, Vulvar examination, Low

vaginal swab, Speculum examination.
 Identifying the etiology is mandatory before initiating therapy.
Diagnostic testing enables targeted treatment, increases therapeutic
compliance, and increases the likelihood of partner notification.
Empiric blind therapy can aggravate symptoms, cause misdiagnosis,
and result in inappropriate therapy.
 Referral to a specialist in vulvovaginal disease for individuals whose
symptoms persist in the absence of abnormal diagnostic tests and for
those who experience persistent symptoms or frequent symptom
recurrence following diagnostic test-directed therapy (assuming lack
of compliance has been excluded).
6.6. Bacterial Vaginosis
6.6.1 Prevalence and Risk Factors:
The most common cause of vaginitis among females aged 14–49, with
prevalence reaching up to 50% of all vaginitis courses affected by
differences in age, race, and ethnicity.
Risk factors includes: Vaginal douching, Smoking, Multiple sex partners
with unprotected intercourse, HIV infections, Gonorrhea infections,
Chlamydia infections, Herpes infections, Trichomoniasis infections.
6.6.2 Diagnosis:
Amsel criteria: At least 3 must be present for the diagnosis of BV:
 Homogenous, thin, gray discharge
 Vaginal PH > 4.5
 Positive whiff- amine test
o Whiff test positive- a fishy odor after adding KHO drops to
vaginal discharge
 Clue cells on saline wet mount
o Clue cells- vaginal epithelial cells covered by bacteria; it’s the
most important indicator for BV
Gram stain: gold standard, but requires more time, resources, and
expertise.
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Initial regimens
 Metronidazole tablet, 500 mg PO x BID x 7 days
 Metronidazole 0.75% gel, vaginally HS x one full applicator (5 g) x 5
days
 Clindamycin 2% cream, vaginally HS x one full applicator (5 g) x7
days
 No need to treat the partner
Pregnancy
 Metronidazole, 500 mg PO x BID x 7 days
Recurrence
 First time recurrent: retreat with the same treatment or an alternative
treatment regimen.
 Multiple recurrences: Metronidazole 0.75% gel, vaginally x twice
weekly x 4-6 months.
6.7. Candida Vulvovaginitis
It is one of the most common causes of itchiness, erythema, and vaginal
discharge, with a prevalence of 20% to 25%. Candida Albicans is
responsible for more than 80% of candida vulvovaginitis.
Risk factors includes: Recent antibiotic treatment, Pregnancy,

Immunocompromised patients with AIDS, poorly controlled diabetes
mellitus, and corticosteroids are more prone to having a complicated
infection.
6.7.2 Diagnosis:
 Characteristic of the Discharge: thick, whitish discharge with a cheesy
appearance associated with no odor
 Vaginal pH: Normal (4-4.5)
 Gold standard test: culture*
 Microscopy: can be diagnosed by seeing the yeast hyphae on KOH
preparation in a patient with typical symptoms.
 Blood antigen or DNA probe testing, with sensitivities of 77% to 97%
and specificities of 77% to 99%, in comparison to culture
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Topical azole therapy
 Clotrimazole 1% cream, 5 g vaginally daily x 7- 14 days
 Clotrimazole 2% cream, 5 g vaginally daily x 3 days
 Miconazole 2% cream, 5 g vaginally daily x 7 days
 Miconazole 4% cream, 5 g vaginally daily x 3 days
 Miconazole 100 mg vaginal suppository, HS x7 days
 Miconazole 200 mg vaginal suppository, HS x 3 days
 Miconazole 1,200 mg vaginal suppository, HS x1 day
Pregnancy: Topical azole therapy (clotrimazole or miconazole) applied x
7 days, vaginally
Severe: Topical azole therapy x 7-14 days or Fluconazole, 150 mg orally
every third-day x 2-3 doses
Recurrence
 Induction phase:
o Fluconazole 150 mg every third-day x 3 doses
o If not available: Topical azole 10 to 14 days, Alternate oral azole
(e.g., itraconazole)
 Maintenance phase:
o Fluconazole 150 mg once per week for 6 months.
o If not available, topical maintenance therapy:
 vaginal cream twice weekly x 6 months
 vaginal suppository once weekly x 6 months
No need to treat the partner
6.8. Trichomoniasis
Trichomoniasis is one of the most common sexually transmitted diseases
(STD) that is not caused by a virus but rather caused by a protozoan
infection. Usually, the infection is asymptomatic, but it may cause
vaginitis in 15% to 20% of the patients causing vaginal discharge,
dysuria, vaginal pain, and or soreness.
Risk factors includes:
 Drug use
 Smoking
 Multiple sex partners and unprotected intercourse
 Other sexually transmitted infections
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6.8.2 Diagnosis:
 Characteristics of the discharge: Foul odor, greenish or yellowish,
frothy appearance.
 Vaginal PH: > 4.5
 Gold standard test: Nucleic acid amplification test PCR, are highly
sensitive and specific, limitation of use is due to the limitation of
availability.
 Microscopy: motile, flagellated protozoa, sensitivity 60 to 70 % within
10–20 min; can be performed on either vaginal, endocervical, or urine
specimens, or on liquid-based Pap test samples.
 Vaginal culture: has high sensitivity and was previously considered
the gold standard diagnostic test but has been replaced by nucleic
acid amplification testing.
 Rapid antigen and DNA hybridization probes: useful in areas of high
prevalence where microscopy or culture is not available.
It is recommended to do a follow-up test as early as two weeks and
within three months due to high rates of reinfection.
Treat the partner and advise the partner to avoid sexual activity until
symptoms resolution.
Initial regimens:
 Metronidazole, 2 g orally, single, or divided dose on the same day
 Tinidazole, 2 g orally, single dose
 Other alternative regimens:
Metronidazole 500 mg orally twice daily for seven days
Pregnancy: Metronidazole, 2 g orally, single dose in any stage of
pregnancy
Recurrence or persistent
 If metronidazole, 2-g single dose fails: Trial of metronidazole, 500 mg
xBID x 7 days
 If metronidazole, 500 mg twice daily for seven days fails: Trial of
metronidazole, 2 g daily x 7 days.
Atrophic Vaginitis:
 Presentation
thin, clear discharge associated with vaginal dryness, dyspareunia,
itching with vaginal mucosa Inflamed, thin, and friable.
Page | 381
 Treatment
Hormonal treatments: local low-dose vaginal estrogen creams, tablets, or
rings. Systemic estrogen therapies in the patient with vasomotor
Symptoms
Nonhormonal treatment: Recommendations include vaginal lubricants
and moisturizers.
6.9. Recurrent urinary tract infection.
6.9.1 Definition:
Urinary tract infections (UTIs) are one of the most frequent clinical
bacterial infections in women. Around 50–60% of women will develop
UTIs in their lifetimes. Escherichia coli is the organism that causes UTIs
in most patients. Types of UTI includes:
Uncomplicated UTI (simple cystitis): Occurs in a healthy host in the

absence of structural or functional abnormalities of the urinary tract.
Recurrent uncomplicated UTI: Two separate culture-proven episodes of

acute bacterial cystitis and associated symptoms within six months or
three episodes within one year in a healthy host in the absence of
structural or functional abnormalities of the urinary tract.
Reinfection is a recurrence with a different organism or the same

organism in more than 2 weeks of a sterile culture.
Persistent infection warrants more extensive urologic evaluation
Risk factors: Frequent sexual intercourse, Age at first UTI at or before 15

years of age, Maternal history of UTIs, New sex partner in the past year,
Spermicide uses in the past year.
 History: Symptoms of the lower urinary tract (LUTs) (Dysuria,
urgency, frequency, a sensation of incomplete emptying, unpleasant
smell, nocturia, acute onset of incontinence), Associated symptoms,
Red flags (fever, chills, night sweats, weight loss, anorexia,
hematuria), Relation to sexual activity, history of STI in both couple,
Past medical history, Past surgical history, OB/Gyn History, Social
history, Medication History.
 Physical examination: General examination, Pelvic examination.
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 Urine culture and sensitivity (To define pathogen and antibiotic
susceptibility/resistance)
 KUB ultrasound +/- CT scan (if indicated)
 Education and reassurance:
 Conservative measures (increase fluid intake, postcoital voiding)
 Pharmacological approach: first-line therapy (i.e., nitrofurantoin, TMP-
SMX, fosfomycin) is dependent on the local antibiogram for the
treatment of symptomatic UTIs in women.
 Indications for referral to a Urologist/ Urogynecologist: Women with
risk factors for complicated UTI (i.e., acute UTI accompanied by signs
or symptoms that suggest the extension of infection beyond the
bladder), Women who have voiding issues (i.e., symptoms suggestive
of incomplete voiding, incontinence, prolapse), Elderly, Urinary tract
anomalies, Urinary tract instrumentation, Neurogenic bladder,
Nephrolithiasis, Immunocompromised patients, e.g., (DM, renal
transplant, immunosuppressant medications), Surgical correction of a
cause of UTI, Persistent/ Relapsing UTI.
Chapter 7: INFERTILITY
Definition:
Infertility is the failure of conception in a couple having regular,
unprotected coitus
for one year with an exception to Females more than 35 years of age: 6
months.
 Primary Infertility: infertility in a patient who has never been pregnant.
 Secondary Infertility: infertility in a patient who has had one or more
previous pregnancies.
Etiology :
 Combined factors 40%.
 Male factors 26-40%.
 Ovulatory dysfunction 15-20%.
 Tubal factors 14-20%.
 Endometriosis 6%.
 Others (e.g., cervical factors, peritoneal factors, uterine
abnormalities)10-13%.
Page | 383
 Unexplained 25-28%.
 Multiple factors are present in 15% of cases.
Symptoms & physical examination :

Table 7.1
Assessment of Assessment of male
female factor factor infertility :
Infertility :
History Duration of Duration of infertility

infertility Medical and surgical
Medical and surgical history
history: (including including testicular
chemo+/- trauma or surgery,
radiotherapy) chemo+/-radiotherapy.
Obstetrics history: Sexual
number and outcome developmental
of any prior history
pregnancies (including including testicular
ectopic and descent, pubertal
miscarriages) developmental, loss of
Gynecologic body hair.
History:
-History of PID, STI,
fibroids,
endometriosis,
cervical dysplasia, or Sexual History:
any uterine
anomalies. Sexual dysfunction or
-Pelvic or abdominal changes in libido.
pain (endometriosis). Frequency of
-Diethylstilbestrol intercourse, use of
exposure in utero. lubricants.
-Contraception Previous infertility
methods use. testing and therapies.
Menstrual history: Family history of
-age at menarche, birth defects,
cycle length, and intellectual disability,
regularity. (ovulatory or reproductive failure
dysfunction). Psychosocial history
Page | 384
-Presence of -including life

vasomotor symptoms stressors or marital
(e.g., hot flashes). conflicts.
-Dysmenorrhea -Environmental and
(endometriosis or occupational
uterine abnormalities). exposures
-Frequency of
intercourse, use of ICEE : Ideas,
lubricants, concerns, and
dyspareunia or post- expectations.
coital bleeding.
-Previous infertility
testing and therapies.
Associated
symptoms:
-Abnormal hair
growth, changes in
body weight or voice..
-Symptoms
suggestive of thyroid
disease.
-Symptoms
suggestive of pituitary
adenoma or
hyperprolactinemia.
Family history of
birth defects,
intellectual disability,
or reproductive failure.
Psychosocial history
including life stressors
or marital conflicts.
Exercise and dietary
history
-Environmental and
occupational
exposures
ICEE: Ideas,
concerns, and
expectations.
Page | 385
- BMI. -BMI.
Physical Examination -Signs of insulin -Skin examination
resistance or (any
hyperandrogenism hyperpigmentation in
(i.e., acne, hirsutism, case of iron overload)
androgenic alopecia, -Signs of Cushing’s
or acanthosis syndrome (secondary
nigricans). hypogonadism)
-Thyroid -Thyroid examination
examination. -Gynecomastia
-Breast examination. (primary
-Pelvic and abdominal hypogonadism)
examination. -External genitalia
-Adnexal masses (abnormal, loss of
and/or tenderness. secondary sexual
characteristics,
varicocele ).

 Investigation for Female factor :
o TSH.
o Fasting prolactin.
o Day 3 of menstrual cycle: FSH (Normal <10 mIU/mL) and
estradiol (Normal <80 pg/mL ) suggestive adequate ovarian
reserve.
o Day 21 of menstrual cycle (mid-luteal phase) : Progesterone
level > 5 ng/mL indicates recent ovulation.
 Investigation for male factor :
o Semen analysis
 Hormonal assessment:
TSH, fasting Prolactin, LH, FSH, and morning testosterone.
Page | 386
Management plan:
Female infertility
 Ovulatory dysfunction – clomiphene citrate, gonadotropins,
pulsatile GnRH, bromocriptine.
 Luteal phase deficiency – progesterone, clomiphene.
 Tubal damage – surgery.
 Cervical factor – bicarbonate douches, intrauterine insemination.
 Endometriosis – laparoscopic ablation may increase fecundity in the
short term .
Unexplained infertility
 Do not offer oral ovarian stimulation agents (such as clomiphene
citrate, anastrozole or letrozole) to women with unexplained infertility.
 Offer IVF treatment to women with unexplained infertility who have
not conceived after 2 years .
Intrauterine insemination
 For people with unexplained infertility, mild endometriosis, or mild
male factor infertility, who are having regular unprotected sexual
intercourse:
Male infertility
 Reduction of smoking and drinking
 Avoidance of saunas, hot baths, the wearing of tight underwear, and
other situations in which scrotal temperature may be raised.
 An infection should be treated.
 Low semen volume may produce insufficient contact with the cervical
mucus for adequate sperm migration, and may be overcome by
artificial insemination with the partner’s semen.
 High semen volume but low sperm numbers may be overcome by
concentrating the semen .
 Oligospermia may respond to treatments such as clomiphene or
interferon – although this condition is now not a hurdle to successful
in-vitro fertilization.
 Clomiphene citrate is a well-established agent that has been
described to empirically treat idiopathic oligospermia.
 Azoospermia due to mechanical blockage may respond to an
epididymovasostomy. There is a 50% success rate provided that
underlying spermatogenesis is normal.
 When semen quality cannot be improved, intrauterine insemination
timed to coincide with ovulation may be successful.
Page | 387
When to Refer:
 A patient of reproductive age who has not conceived after 1 year of
unprotected vaginal sexual intercourse.
 A patient of reproductive age who is using artificial insemination to
conceive should be offered further clinical assessment and
investigation if she has not conceived after 6 cycles of treatment.
 Offer an earlier referral for specialist consultation to discuss the
options for attempting conception for whom :
o The patient is aged 35 years or over.
o There is a known clinical cause of infertility .
Chapter 8: MENOPAUSE &

HORMONAL REPLACEMENT
THERAPY
8.1. DEFINITON:
Menopause:
 The cessation of the menstrual cycle for 12 months in the absence of
other biological or physiological causes.
 It occurs in normal women at a median age of 51.4 years, and it is the
result of ovarian follicular depletion.
Perimenopause “menopausal transition." :
 The period of change in intermenstrual interval with or without
menopausal symptoms.
8.2. SYMPTOMS & PHYSICAL EXAMINATIONS:
Table 8.1
Vasomotor Symptoms Hot flushes:
● The most common symptom
● It is defined as transient
episodes of flushing,
perspiration, and sensations of
heat, with or without night
sweats.
● As a result of loss of
production of estrogen by
ovaries.
Page | 388
● Risk factors include: Higher

BMI, Current cigarette smoking
and Low physical activity.
Genitourinary Syndrome of Vulvovaginal symptoms:

Menopause (GSM) ● Vaginal dryness and itching.
● Recurrent vaginitis.
● Dyspareunia.
Urinary symptoms:
● Urinary urgency / frequency.
Recurrent UTI.
Other symptoms ● Sleep disturbance.
● Mood changes (depression).
● Sexual dysfunction.
● Cognitive changes (memory
loss and difficult
concentration).
● Joints pain.
● Breast tenderness.
Menstrual migraines.
Long-term consequences of Mostly all the complications are a
menopause result of estrogen deficiency:
● Cardiovascular disease
(CVD):Increase in the risk of
developing CVD, which is due
to:
- Decrease in estrogen.
- Increased total
cholesterol, LDL and
Triglycerides levels.
- Decreased HDL.
● Bone loss.
● Dementia
● Osteoarthritis.
Skin changes: aging and wrinkling
of the skin.
Page | 389
8.3. MANAGEMENT:
Genitourinary Syndrome of Menopause (GSM):
 First line: lubricants and vaginal moisturizers.
 Second line: Low dose vaginal estrogen therapies. (Table 8.2)
Table 8.2
Treatment Dosage
Estradiol (0.01%) Vaginal Starting dose: 2 to 4 g applied daily
cream (Estrace) for 1-2 weeks.
Maintenance dose: 1 g applied 1-3
times/ week.
Conjugated estrogen Vaginal It contains 0.625 mg of conjugated

cream (Premarin) equine estrogen / 1g.
Starting dose: 0.5 to 2 g / day for 21
days, followed by 7 days off therapy.
Maintenance dose: 1-3 times
/week.
Vaginal Moisturizer (Raplens) Applied 3 times /week
Estradiol vaginal ring (Estring) It contains 2 mg estradiol, releases

7.5 mcg/day.
Duration: 3 months.
Estradiol Vaginal Tablets It contains 10 mcg estradiol.
(Vagifem) Dose: 1 tablet inserted into vagina
dailyX 2 weeks, then twice weekly.
Vasomotor symptoms:
 Hormonal Therapy (HT): Oral Hormonal Therapy (Table 2)
 Non-Hormonal Therapy.
Table 8.3
Hormonal Therapy (HT)
 The most effective therapy in the absence of contraindications
 Women less than 60 years of age or within 10 years after the start
of menopause who have hot flashes or night sweats are most likely
to benefit from hormonal therapy.
 A Cochrane review that included 24 RCT reported that estrogen
alone or in combination with progesterone could decrease the
weekly frequency of hot flashes by 75% and the severity by 87%.
Page | 390
Candidate for HT: - Age < 60

- Within 10 years of
menopause.
- Moderate to severe hot
flashes.
- No response to behavioral
interventions.
- Primary ovarian
insufficiency or early
menopause.
Healthy without contraindications.
Contraindications for HT Use: - Active liver disease.
- Current, past, or
suspected breast cancer
- Porphyria cutanea tarda
(absolute
contraindication).
- Known or suspected
estrogen-sensitive
malignant conditions.
- Undiagnosed genital
bleeding/Untreated
endometrial hyperplasia
- Untreated hypertension
- Hypersensitivity.
- Recent or active arterial
thromboembolic disease
(angina, myocardial
infarction)
- Current venous
thromboembolism or
Previous idiopathic (deep
venous thrombosis,
pulmonary embolism)
Long-Term Menopausal Combined estrogen-progestin

Hormonal Therapy In Women's therapy:
Health Initiative (WHI): - Increase risk of CHD
events, stroke, venous
thromboembolic (VTE)
disease and breast
cancer.
Page | 391
- Reduction of the fracture

and colorectal cancer
risk.
- The risk of CHD appears
to depend upon the timing
of exposure, with no
excess risk observed in
younger (<60 years of
age) menopausal women.
- Inconsistent risk of ovarian
cancer, a possible
increase in ovarian
epithelial tumors after
more than 10 years of
therapy.
Unopposed estrogen therapy:
- Associated with the
development of
endometrial cancer.
Therefore, a
progestational agent
should be used to prevent
hyperplasia and
endometrial cancer.
- No increase in either CHD
or breast cancer; in fact, a
possible reduction in
breast cancer risk was
observed.
- Taking estrogen and
smoking simultaneously
increases the risk of VTE
disease.
Recent research suggests that
transdermal estrogen may be the
safest option in a VTE high-risk
group.
Discontinuation of Hormonal
Therapy - The ACOG recommends
against routine
discontinuation based on
age or treatment duration
and advises that the
Page | 392
decision to continue or
stop hormone therapy
should be individualized
based on the patient's
symptoms and medical
history.
Table 8.4
Oral Hormonal Therapy
Treatment Dosage
Common Estrogen choices
Oral and transdermal estrogens relieve hot flashes and night sweats at
standard doses observed within 2 weeks.
Conjugated equine estrogen or 0.3 to 0.625 mg.
synthesized conjugated
estrogen
Micronized 17B- estradiol orally 0.5 to 1 mg.
or intramuscularly
Common Progestogens Choices
Progestogens (synthetic progestins and progesterone) are used in
women with an intact uterus to protect against uterine cancer.
Medroxyprogesterone 2.5 or 5 mg daily, 10-12

days/month.
Micronized progesterone 100 or 200 mg daily, 10-12
days/month.
Norethindrone 0.35 or 5 mg daily, 10-12
days/month
Drospirenone 3 mg daily.
Levonorgestrel 0.75 mg daily.
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Table 8.5
Candidate for Non-Hormonal Therapy:
 Age ≥60
 > 10 years from menopause at the initiation of therapy.
 History of pulmonary embolism, myocardial infarction, or stroke.
 High risk of heart disease, breast cancer, or VTE.
 Estrogen-sensitive cancer or precancerous.
 Undiagnosed genital bleeding/ untreated endometrial hyperplasia.
 Untreated hypertension.
 Porphyria cutanea trada.
Patient preference not to use hormonal therapy.
Non-Hormonal Therapy
 Lifestyle modifications, avoid these triggers:
o Stress.
o Caffeine.
o Alcohol.
o Spicy foods.
o Tight clothing.
o Heat.
o Cigarette smoking.
 Keeping the bedroom cool at night. Using fans during the day.
Wearing light layers of clothes with natural fibers such as cogon.
 Phytoestrogens:
o Black cohosh, 40mg orally daily.
o Soy.
 Medications: (Table 5)
Medications (Table 5)
SSRIs - Paroxetine, 10 to 25
mg/day.
- Escitalopram, 10 to 20
mg/day.
- Citalopram, 10 to 20
mg/day.
Fluoxetine, 20 mg/day.
SNRIs - Venlafaxine, 37.5 to 75
mg/day.
Desvenlafaxine, 75 mg once or
twice daily.
Gabapentinoid - Pregabalin, 75 to 150 mg
twice daily.
Gabapentin, 300 mg nightly / up to
900mg divided doses.
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Clonidine patch 0.3 mg, 0.2 mg, or 0.1 mg weekly.
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Section 5: Psychiatry
Chapter 1: SLEEP DISORDERS
1.1. Insomnia:
1.1.1 Definition:
Insomnia is defined as having trouble initiating or maintaining sleep,
associated with daytime consequences, not attributable to environmental
circumstances or inadequate sleep opportunities.
International Classification of Sleep Disorders (ICSD-3) typed insomnia
into:
 Chronic insomnia disorder; lasting >3 months.
 Short-term insomnia disorder; lasting <1 month.
 Other insomnia disorders.
1.1.2 Red flags:
 Increased risk for suicide
 Substance use relapse
 Excessive daytime impairment results in a risk of harm to self or
others
 Mood disorder
 GAD or panic attacks
1.1.3 Mnemonic for the diagnostic criteria of insomnia:
Table 1.1 Mnemonic for the diagnostic criteria of insomnia
SLEEP
Sleep quantity or quality dissatisfaction is associated with one or more
difficulties initiating, maintaining, and returning to sleep
Lasting for at least three months, occurring at least three times a week
despite adequate opportunity for sleep, causing significant distress or
impairment
Exclude this diagnosis if a disturbance occurs exclusively during the course
of another sleep-wake disorder
Exclude the complaint of insomnia not being due to coexisting mental and
medical disorders
The Physiological effects of a substance do not contribute to insomnia
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1.1.4 Non-pharmacological Management:

 Cognitive-behavioral therapy for insomnia (CBT-I)
o Combines cognitive therapy and behavioral treatments (e.g.,
stimulus control, sleep restriction) with or without relaxation
therapy.
o It has strong evidence for the management of chronic insomnia
in the long term.
 Stimulus control.
 Relaxation therapy.
 Sleep restriction.
 Sleep restriction initially limits the time in bed to the total sleep time,
as derived from baseline sleep logs.
 Paradoxical intention.
▪ A specific cognitive therapy in which the patient is trained to
confront the fear of staying awake and its potential effects.
The objective is to eliminate a patient’s anxiety about sleep
performance.
 Biofeedback therapy.
 Sleep hygiene therapy.
o Instructions include, but are not limited to, keeping a regular
schedule, having a healthy diet and regular daytime exercise,
having a quiet sleep environment, and avoiding napping,
caffeine, other stimulants, nicotine, alcohol, excessive fluids, or
stimulating activities before bedtime.
1.1.5 Pharmacological Management:
 The following medications are not recommended to treat insomnia
primarily unless indicated by preexisting conditions that require these
medications: sedating antihistamines, atypical antipsychotics, and
antiepileptic medications.
 When discontinuing medications, it needs to be tapered off gradually
to avoid rebound insomnia and withdrawal symptoms.
 Follow-up should be on a regular basis during the initial period in
order to assess and reassess the effectiveness of the treatment,
possible side effects of the medications, and if there is a need to
continue medicating the patient.
 A referral to a sleep specialist or psychiatrist is indicated if there is no
improvement within 2–4 weeks.
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1.2. Narcolepsy:
1.2.1 Definition:
Narcolepsy is a chronic sleep disorder characterized by overwhelming
daytime drowsiness and sudden attacks of sleep.
If narcolepsy is suspected, patients should be referred to a sleep
specialist for further evaluation, including polysomnography (PSG)
followed by mean sleep latency test (MSLT). PSG ensures enough sleep
(≥ 6 hours) and rules out other sleep disorders like OSA.
1.2.2 Non-pharmacological:
 Regular sleep schedule.
 Adequate sleep at night.
 Scheduled napping (strategic naps).
 Address safety issues like driving and operating heavy machinery.
 Avoidance of alcohol.
 Avoid any medication that could cause sleeping, e.g., some allergy
medications.
 Medications are usually initiated by a sleep specialist.
 These may include stimulants such as Modafinil, Methylphenidate,
and anti-cataplectic effects like TCA and SSRIs. Other medications
are used for both symptoms like sodium oxybate.
1.3. Parasomnia:
1.3.1 Definition:
Parasomnias are undesirable physical events or experiences that occur
during entry into sleep, within sleep, or during arousal from sleep.
Parasomnias may occur during non-rapid eye movement sleep (NREM),
rapid eye movement sleep (REM) stage of sleep, or during transitions to
and from sleep.
1.3.2 Types:
Non-REM parasomnia
 Confusional arousals.
 Sexsomnia.
 Sleep walking (somnambulism).
 Sleep-related eating disorder (SRED).
 Sleep terrors.
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REM parasomnia
 RBD (REM sleep Behavior Disorder).
 Nightmare disorder.
 Recurrent isolated sleep paralysis.
Normal variant
 Sleep talking (somniloquy)
1.3.3 Non-pharmacological interventions:
 Screen and avoid any precipitating factor.
 Maintenance of a regular sleep schedule and sleep hygiene.
 Universal safety precautions:
o Removal of sharp objects.
o Lowering the mattress to the floor level.
o Cover sharp obstacles
o Window/door alarms and locks.
o Lock firearms.
1.4. Obstructive sleep apnea:
1.4.1 Definition:
Obstructive sleep apnea (OSA) which is a sleep-related breathing
disorder that involves a decrease or complete halt in airflow despite an
ongoing effort to breathe. This leads to partial reductions (hypopneas)
and complete pauses (apneas) in breathing that last at least 10 seconds
during sleep.
1.4.2 Physical Exam:
 Neck circumference (≥ 17 inches/43 cm in men and ≥ 16 inches/41
cm in women).
 Body mass index (BMI) ≥ 30 kg/m2.
 The Mallampati score is a simple classification tool to describe the
crowdedness of the airway.
 Craniofacial abnormalities: retrognathia, micrognathia, lateral
peritonsillar narrowing, macroglossia, tonsillar hypertrophy,
elongated/enlarged uvula, high arched/narrow hard palate.
 Nasal abnormalities: polyps, deviation, valve abnormalities, turbinate
hypertrophy, and overjet.
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1.4.3 Diagnostic tools:

The patient should be referred to a sleep specialist to confirm the
diagnosis of sleep apnea.
 Polysomnography (PSG)
o If positive, proceed with treatment based on severity.
o If negative, OSA is ruled out, consider an alternative diagnosis.
 Home sleep apnea test (HSAT): This might be indicated for
uncomplicated adults with suspected moderate-to-severe OSA.
o If positive, proceed with treatment based on severity.
o If negative, consider an In-lab PSG.
1.4.4 Management:
 Continuous positive airway pressure (CPAP)
 CPAP is the standard treatment option for moderate to severe cases
of OSA.
 Positional therapy and weight loss
 Oral appliances
 Surgery
 The most common surgical methods:
o Adenotonsillectomy: surgical removal of the tonsils and
adenoids, the most common treatment option for children with
OSA.
o Maxillomandibular advancement: aims to bring forward the
maxilla and mandible and subsequently increase the airway
space. It is helpful primarily in non-obese and young individuals.
 Drowsy driving and motor vehicle crashes.
 Neuropsychiatric dysfunction.
 Cardiovascular and cerebrovascular morbidity.
 Pulmonary hypertension or right heart failure.
 Metabolic syndrome and type 2 diabetes.
 Nonalcoholic fatty liver disease (NAFLD).
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1.5. Restless Leg Syndrome:

1.5.1 Definition:
RLS is defined by sensory symptoms, not movements, based on
essential features of the sensory symptom.
 The four essential diagnostic criteria for RLS start with the primary
symptom of akathisia, or an urge to move focused on the legs. The
urge to move is often accompanied by strange, unpleasant
sensations that patients have trouble describing.
 Three critical factors must affect the expression of the primary RLS
sensations:
o Onset associated with rest, usually sitting or lying down;
o at least partial or complete relief with movement;
o a circadian pattern with symptoms worse in the evening and
night.
1.5.2 Work up:
Lab work to rule out any secondary cause of RLS as the patient clinical
picture dictates:
 Ferritin level
 Vitamin D level
 Vitamin B12 level
 HbA1C
Patients with RLS symptoms should be referred to a sleep specialist to
start the approved medication for RLS.
1.5.3 Behavioral Management:
 Sleep hygiene, regular activity, reduction of situations prolonging
inactivity
 Avoid medications that exacerbate RLS.
 Treat medical problems exacerbating or causing RLS as appropriate
 Check the iron status: Serum ferritin <50 µg/L; consider oral iron
1.5.4 Pharmacologic Management:
Usually initiated by a sleep specialist.
 Dopaminergic medications (Pramipexole, ropinirole, rotigotine)
 α2δ Anticonvulsants (Gabapentin enacarbil, pregabalin).
 Lower-potency opioids
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Chapter 2: DEPRESSIVE DISORDERS

2.1. Depression:
Unipolar Major Depression is diagnosed in patients with at least one major
depressive episode and have no prior history of mania or hypomania .
2.1.1 Secondary depression:
General medical disorders
 Neurologic disorders, Infectious disorders, Cardiac disease,
Endocrine and metabolic disorders , Inflammatory disorders,
Neoplastic disorders, Medications :
o Narcotics
o Antineoplastic agents
o Sedative hypnotics
o Centrally acting antihypertensives
2.1.2 Whom to screen:
Adults
All adults older than 18 years.
The PHQ-2 has a similar sensitivity to PHQ-9.
The specificity of PHQ-9 is higher at 91–94% as compared to 78-92% for
the PHQ-2.
Children and adolescents
at 12–18 years of age.
Screening tools: PHQ-2 and PHQ -9
Pregnant and Postpartum
all postpartum women and once during the perinatal period.
Screening tools: PHQ-2, PHQ-9, or Edinburgh Postnatal Depression
scale.
Patients with Chronic Medical Conditions
Consider screening all patients with chronic medical conditions
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2.1.3 How to screen:

Table 2.2 PHQ-2 screening for depression
Source: American Academy of Family Physicians
Over the past 2 Not More than
weeks how often at Several half the Nearly
have you— all days days every day
Had little interest or 0 1 2 3
pleasure in doing
things?
Felt down, 0 1 2 3
depressed, or
hopeless?
A score of 3 or
higher is considered
a positive result.
Table 2.3 PHQ-9 screening for depression

Source: American Academy of Family Physicians
Over the past 2 Not More than
weeks how often at Several half the Nearly
have you— all days days every day
Had little interest or 0 1 2 3
pleasure in doing
things?
Felt down, 0 1 2 3
depressed, or
hopeless?
Had trouble falling 0 1 2 3
asleep, staying
asleep, or sleeping
too much?
Feeling tired or 0 1 2 3
having little energy?
Poor appetite or over 0 1 2 3
feeding?
Feeling bad about 0 1 2 3
yourself, or that
you’re a failure, or
that you let people
down?
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Trouble 0 1 2 3
concentrating on
things?
Other people noticed 0 1 2 3
you are moving
or speaking too
slowly?
Thoughts that you 0 1 2 3
could be better off
dead, or hurting
yourself or others?
A score of 3 or
higher is considered
a positive result.
2.1.4 Diagnosis:
DSM-5 Diagnostic Criteria for Major Depressive Disorder
 Five (or more) of the following symptoms have been present during 2-
week period and represent a change from previous functioning; one
of the symptoms is either (A)or(B).
o Depressed mood, in children and adolescents (It can be irritable
mood)
o diminished interest
o Significant weight loss or weight gain
o Insomnia or hypersomnia.
o Psychomotor agitation or retardation
o Fatigue or loss of energy.
o Feelings of worthlessness or excessive or inappropriate guilt
o Diminished ability to think or concentrate,
o Recurrent thoughts of suicide (not just fear of dying), recurrent
suicidal ideation without a specific plan, or a suicide attempt or a
specific plan for committing suicide.
 The symptoms cause significant functional impairment.
 The episode is not due to the physiological effects of a substance or
to another medical condition.
o Criteria 1 through 3 represent a major depressive episode.
o Responses to a significant loss (e.g., bereavement, financial ruin,
losses from a natural disaster, a serious medical illness or
disability) may include the feelings of intense sadness,
rumination about the loss, insomnia, poor appetite, and weight
loss noted in Criterion 1, which may resemble a depressive
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episode. Although such symptoms may be understandable or

considered appropriate to the loss, the presence of a major
depressive episode in addition to the normal response to a
significant loss should also be carefully considered. This decision
inevitably requires the exercise of clinical judgment based on the
individual’s history and the cultural norms for the expression of
distress in the context of loss.
 The occurrence of the major depressive episode is not better
explained by schizoaffective disorder, schizophrenia,
schizophreniform disorder, delusional disorder, and other psychotic
disorders.
 There has never been a manic episode or a hypomanic episode.
o This exclusion does not apply if all of the manic-like or
hypomanic-like episodes are substance-induced or
are attributable to the physiological effects of another medical
condition.
2.1.5 Red Flags for Depression:
 Insomnia
 Fatigue
 Chronic life changes or stressors
 Fair or poor self-rated health
 Unexplained physical symptoms
2.1.6 Treatment:
Psychotherapy
Behavioral activation
Cognitive behavior therapy (CBT)
Interpersonal and problem-solving therapy (IPT)
Patient education
Pharmacotherapy/medication selection (Table 2.3)
All modern antidepressants are equally effective. Therapy choice is
based on cost, patient preference, adverse effect profile (Table 4), history
of any previous response to a particular medication, response of first
degree relative to a specific medication, patient’s age, coexisting medical
conditions like cardiovascular disease and chronic pain, symptoms like
poor sleep, poor appetite and weight loss, smoking and whether the
patient is in the perinatal period. Begin with an SSRI as they have fewer
side effects, no titration is required 80% of the time, once a day dosing,
and are safe in overdose. Start with one antidepressant.
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2.2. Depression in Special Population:

2.2.1 Depression in children and Adolescent:
Diagnosis
If there is a positive screen for depression, apply DSM-5 Diagnostic
Criteria.
A few key points need to be considered in this special population.
 Pediatric patients express themselves with an irritable mood, show a
negative attitude, are argumentative, and pick fights easily.
 They may have a preoccupation with body weight and image
 They may present with insomnia, hypersomnia, or significant shifts of
sleep pattern over the diurnal cycle.
 Psychomotor agitation may present as hand wringing, inability to sit
still, to pace, pulling, or rubbing clothes or skin.
 Parent-adolescent conflicts can result if parents attribute lack of
energy and motivation to laziness, an oppositional attitude, or
avoidance of responsibility.
 Feelings of worthlessness or guilt may present as a negative self-
perception with feelings of inadequacy, inferiority, and or failure.
Evaluation of these symptoms is challenging as many youths do not
directly acknowledge such negative self-perceptions.
 They can have problems with attention, concentration and memory.
 May present with psychosis
 They can experience recurrent thoughts of death or suicide or attempt
suicide.
Treatment
 Psychotherapy
 Pharmacotherapy, first line is Fluoxetine; the second line is Sertraline.
 Combination of the above two
 For mild depression: psychotherapy
 For moderate to severe depression: combine pharmacotherapy and
psychotherapy (combination Fluoxetine + CBT)
2.2.2 Antenatal depression:
Definition:
Unipolar major depression (major depressive disorder) is diagnosed in
patients who have suffered at least one major depressive episode and
have no history of mania or hypomania during pregnancy.
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Screening:
The 10-question Edinburgh Postnatal Depression Scale (EPDS)
Patients who score above 13 are likely to be suffering from a depressive
illness
Table 2.4 Edinburgh Postnatal Depression Scale
Name: ________________________Address: ____________
Your date of birth: __________________________________
Baby’s date of birth: ______________ Phone: ____________
As you are pregnant or have recently had a baby, we would like to know
how you are feeling. Please check the answer that comes closest to how
you have felt in the past seven days, not just how you feel today.
Here is an example, already completed.
I have felt happy:
❏ Yes, all the time
❏✓ Yes, most of the time (This would mean: “I have felt happy most of the
time” during the past week.) ❏ No, not very often
❏ No, not at all
Please complete the other questions in the same way.
In the past seven days:
1. I have been able to laugh and see 2. I have looked forward with
the funny side of things enjoyment to things
❏As much as I always could ❏As much as I ever did
❏Not quite so much now ❏Rather less than I used to
❏Definitely not so much now ❏Definitely less than I used to
❏Not at all ❏Hardly at all
3. I had blamed myself 4. I have been anxious or worried
unnecessarily when things for no good reason ❏ No, not at
went wrong all
❏Yes, most of the time ❏Hardly ever
❏Yes, some of the time ❏Yes, sometimes
❏Not very often ❏Yes, very often
❏No, never
5. I have felt scared or panicky for 6. Things have been getting on top
no very good reason ❏ Yes, quite a of me
lot ❏Yes, most of the time, I haven't
❏ Yes, sometimes been able to cope at all ❏Yes,
❏ No, not much sometimes I haven’t been coping as
❏ No, not at all well as usual
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❏No, most of the time, I have coped

quite well
❏No, I have been coping as well as
ever
7. I have been so unhappy that I 8. I have felt sad or miserable
have had difficulty sleeping ❏Yes, most of the time
❏Yes, most of the time ❏Yes, quite often
❏Yes, sometimes ❏Not very often
❏Not very often ❏No, not at all
❏No, not at all
9. I have been so unhappy that I 10. The thought of harming myself
have been crying has occurred to me
❏Yes, most of the time ❏Yes, quite often
❏Yes, quite often ❏Sometimes
❏Only occasionally ❏Hardly ever
❏No, never ❏Never
SCORING
QUESTIONS 1, 2, and 4 (without an *) Are scored 0, 1, 2, or 3, with the top
box scored as 0 and the bottom box scored as 3. QUESTIONS 3, 5-10
(marked with an *) Are reverse-scored, with the top box scored as a three
and the bottom box scored as 0. Maximum score: 30
Possible Depression: 10 or greater
Always look at item 10 (suicidal thoughts)
Diagnosis
If there is a positive screen for depression, apply DSM-5 Diagnostic
Criteria for Major Depressive Disorder.
Treatment
multidisciplinary team, including obstetrician, family physician, and
psychiatrist.
The appropriate setting is important, outpatient versus inpatient.
Pharmacotherapy or psychotherapy used successfully for treatment in
the past is used during pregnancy.
psychoeducation
Routine monitoring
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Mild to Moderate Antenatal Depression

Initial treatment antidepressants or psychotherapy.
The choice depends on patient’s history, patient’s preference, and
availability of treatment.
prior history of unipolar major depression: antidepressant.
no prior history of unipolar major depression: structured psychotherapy is
the first-line treatment.
Severe Antenatal Depression
refer to a psychiatrist.
Postpartum Blues
postpartum period defined as : the first 12 months after
delivery. Postpartum blues are a transient condition characterized by
several mild depressive symptoms
Onset
2–3 days post-delivery, and resolve within two weeks of onset.
Diagnosis:
diagnosis is made if 3 or 4 depressive symptoms are present.
Management
 Reassurance
 Adequate time for a patient to sleep and rest
 Support for the woman and family
 If symptoms of postpartum blues worsen or persist beyond two
weeks,or if there is suicidal ideation the patient needs further
evaluation for major postpartum depression
2.2.3 Postpartum Depression:
depression that begins within 12 months of childbirth.
Onset
occur before or during pregnancy in roughly 50%
Diagnosis
The Diagnostic criteria for major postpartum depression are the same
that are used to diagnose non-puerperal major depression. Apply the
DSM-5 criteria along with the specifiers with peripartum onset for
episodes that arise within four weeks postpartum. For episodes of
postpartum depression present more than four weeks after delivery, no
modifier is available in DSM-5.
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Assessment
As part of the initial assessment, it is important to ask patients about:
 their attitude towards the pregnancy and infant
 their functioning
 alcohol and drug abuse
 psychosocial stressors
 support systems
 intimate partner violence
Treatment
mild to moderate : outpatient or partial (day) hospital setting.
As initial therapy, psychotherapy is suggested.
SSRIs, SNRIs, bupropion and mirtazapine are a reasonable alternative
severe postpartum depression: refer to a psychiatrist
2.2.4 Postpartum Psychosis:
Onset
within two weeks of childbirth.
Presentation/Diagnosis
hallucinations and delusions, thought disorganization and/or bizarre
behavior. typically accompanied by symptoms of a mood disorders,
severe insomnia, rapid mood changes, anxiety, irritability, and
psychomotor agitation.
patients with postpartum psychosis are assigned a diagnosis based on
their primary mental disorder (e.g., bipolar disorder), with the addition of
the specifier “with per partum onset” if onset was during pregnancy or
within four weeks postpartum.
Treatment
A woman experiencing psychosis should usually be hospitalized until
stable.
First-line treatment : second-generation antipsychotic :quetiapine,
risperidone, or olanzapine
All psychotropic medications are passed on to the nursing infant. The
benefits of medication for the mother need to be weighed against risks to
the infant from exposure.
The effects of second-generation antipsychotics, benzodiazepines,
valproate, and antidepressants on the infant are clinically insignificant.
Treatment should be continued for at least one year to reduce the risk of
relapse; some patients will merit lifetime prophylaxis due to the potential
for relapse
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Chapter 3: ANXIETY DISORDERS

3.1. GAD:
3.1.1 Definition:
Excessive concern and anxiety about various activities and situations are
characteristics of GAD. In all individuals with symptoms of GAD, assess
symptoms using the GAD-7 scale for diagnosis and follow up
According to DSM-5 there are specific criteria to diagnose GAD
 Excessive anxiety and worry occurring more days than not for at least
6 months, about a number of events or activities (such as work or
school performance).
 The individual finds it difficult to control the worry.
 The anxiety and worry are associated with three (or more) of the
following six symptoms (with at least some symptoms having been
present for more days than not for the past 6 months); Note: Only one
item is required in children:
o Restlessness or feeling on edge.
o Being easily fatigued.
o Difficulty concentrating or mind going blank.
o Irritability.
o Muscle tension.
o Sleep disturbance (difficulty falling or staying asleep, or restless,
unsatisfying sleep).
 The anxiety or physical symptoms cause clinically significant distress
or impairment in social, occupational, or other important areas of
functioning.
 The disturbance is not attributable to the physiological effects of a
substance medication) or another medical condition .
 The disturbance is not better explained by another mental disorder
Perform general laboratory testing to screen for underlying medical
disorders in people with suspected physical causes of anxiety (such as
people with weight loss, cognitive impairment, or shortness of breath or
above 65 years) Labs : CBC , chemistry , TSH, urinalysis, Urine
toxicology (If suspected) and ECG (in patients over 40 with chest
discomfort or palpitations).
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For minimal and mild GAD:
The two major treatments for anxiety are medicines and cognitive
behavioral therapy (CBT). Medication and CBT may work better together
than they do separately.
The preferred first medications are selective serotonin reuptake inhibitors
(SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs):
 citalopram (cause QTc prolongation ,avoid in people who are
sensitive to weight gain )
 fluoxetine; (for people who are sensitive to weight gain)
 paroxetine (avoid in people who are worried about sexual
dysfunction, give duloxetine).
 start low dose to avoid initial insomnia, agitation, or other early side
effects. If tolerated, increase every three to four days to the
therapeutic dosage range. Allow four to six weeks for effect
3.1.5 Assessment of pharmacological response:
 Full response: Continuing treatment for at least 12 months
 Partial response
o Add CBT if not already done.
o or Augmentation of the SSRI/SNRI with buspirone (1st option) or
gabapentin (2nd choice).
 No response:Trial of a different SRI
3.2. Panic disorder
3.2.1 Definition:
Panic attacks are defined as discrete episodes of abruptly escalating
anxiety or fear, associative by a sense of impending doom. These
attacks are characterized by symptoms such chest tightness or
discomfort;(see the criteria ) it happens unexpectedly, in which the
beginning of the attack is not related with an evident trigger. The term
panic disorder describes frequent, unexpected panic attacks.
If suspect medical condition ECG, CBC TSH , chemistry ,urine test and
toxicology
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History, physical examination and mental status examination remain the
diagnostic cornerstones for panic disorder. It The diagnosis of panic
disorder is made based on DSM-5 diagnostic criteria:
 Recurrent unexpected panic attacks. A panic attack is an abrupt
surge of intense fear or intense discomfort that reaches a peak within
minutes, and during which time four (or more) of the following
symptoms occur: Note: The abrupt surge can occur from a calm state
or an anxious state.
o Palpitations, pounding heart, or accelerated heart rate.
o Sweating.
o Trembling or shaking.
o Sensations of shortness of breath or smothering.
o Feelings of choking.
o Chest pain or discomfort.
o Nausea or abdominal distress.
o Feeling dizzy, unsteady, light-headed, or faint.
o Chills or heat sensations.
o Paresthesia (numbness or tingling sensations).
o Derealization (feelings of unreality) or depersonalization (being
detached from one-self).
o Fear of losing control or “going crazy.”
o Fear of dying.
 At least one of the attacks has been followed by 1 month (or more) of
one or both of the following:
o Persistent concern or worry about additional panic attacks or
their consequences
o A significant maladaptive change in behavior related to the
attacks.
 The disturbance is not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication) or another medical
condition (e.g., hyperthyroidism, ).
 The disturbance is not better explained by another mental disorder
 Once panic disorder has been identified, the next stage is to decide
whether therapy is necessary based on clinical evaluation of the
illness’ severity, the degree of discomfort or impairment, and the
preferences of the patient
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 The gold standard instrument to assess severity is the Panic Disorder

Severity Scale (PDSS); for mild cases; follow up with these
individuals every three to six months
 (SSRIs), (SNRIs), (TCAs), (MAOIs), and benzodiazepines have all
demonstrated comparable efficacy for the symptoms of panic disorder
 For some patients, the clinical response can take up to 8 to 12 weeks.
3.3. specific phobia:
3.3.1 Definition:
 A clinically significant anxiety of a specific object, which often results
in avoidance behavior. The five categories of specific phobia include
animal, natural environment, blood-injection-injury, situational, and
other.
The main components of diagnosis are history, physical examination,
mental state assessment, and should follow DSM-5 diagnostic criteria
 Marked fear or anxiety about a specific object or situation (e.g., flying,
heights, animals, receiving an injection, seeing blood). Note: In
children, the fear or anxiety may be expressed by crying, tantrums,
freezing, or clinging.
 The phobic object or situation almost always provokes immediate fear
or anxiety.
 The phobic object or situation is actively avoided or endured with
intense fear or anxiety.
 The fear or anxiety is out of proportion to the actual danger posed by
the specific object or situation and to the sociocultural context.
 The fear, anxiety, or avoidance is persistent, typically lasting for 6
months or more.
 The fear, anxiety, or avoidance causes clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
 The disturbance is not better explained by the symptoms of another
mental disorder.
Cognitive-behavioral therapy (CBT) with exposure is the first line of
treatment for the majority of patients with new-onset specific phobias,
while a benzodiazepine is alternative.
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3.4. Agoraphobia:
3.4.1 Definition:
agoraphobia as fear or anxiety about and/or avoidance of situations
where help might not be available developing panic-like symptoms, as it
could co-exist with panic disorder or it might not.
A patient with suspected agoraphobia should undergo a thorough
psychiatric evaluation that includes the patient’s main source of fear, the
variety of fearful events, intentions for avoidance and the variables that
affect the type and degree of fear.
The Diagnostic Assessment Research Tool (DART), is one of the simple
screening tools to implement into primary care, then establish diagnosis
using DSM-5 criteria:
 Marked fear or anxiety about two or more of the following situations:
o Using public transportation (eg, automobiles, buses, trains)
o Being in open spaces (eg, parking lots, marketplaces, bridges)
o Being in enclosed places (eg, shops, theaters, cinemas)
o Standing in line or being in a crowd
o Being outside of the home alone
 The individual fears or avoids these situations because of thoughts
that escape might be difficult or help might not be available in the
event of developing panic-like symptoms or other incapacitating or
embarrassing symptoms (eg, fear of falling in older adults or fear of
incontinence).
 The agoraphobic situations almost always provoke fear or anxiety.
 The agoraphobic situations are actively avoided, require the presence
of a companion, or are endured with intense fear or anxiety.
 The fear or anxiety is out of proportion to the actual danger posed by
the agoraphobic situations and to the sociocultural context.
 The fear, anxiety, or avoidance is persistent, typically lasting for six
months or more.
 The fear, anxiety, or avoidance causes clinically significant distress or
functioning.
 If another medical condition (eg, inflammatory bowel disease,
Parkinson disease) is present, the fear, anxiety, or avoidance is
clearly excessive.
 The fear, anxiety, or avoidance is not better explained by the
symptoms of another mental disorder.
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Pharmacotherapy and/or psychotherapy are typically used in conjunction
for treatment, CBT for agoraphobia is often given during 10 to 20 weekly
therapy sessions
An SSRI is the medication of choice for treating agoraphobia.
Consider adjusting the dose of the SSRI every 2 weeks, and assess
response after 6 weeks. If minimal or no response then switch to a
different SSRI, or to a different class such as SNRI, TCAs, or MAOIs.
If a patient responds well; treatment should be continued for another 9 to
12 months.
A benzodiazepine (BZD) may be considered while the SSRI is taking
effect if the patient experiences regular panic episodes and has no
history of substance misuse.
3.5. Social anxiety disorder (SAD):
3.5.1 Definition:
Social anxiety disorder (formerly known as social phobia) is one of the
most common psychiatric disorders,
3.5.2 Screening:
The three-question Mini-Social Phobia Inventory seems to be a useful
screening tool for SAD (Mini-SPIN) :1 Fear of embarrassment causes me
to avoid doing things or speaking to people.,2 I avoid activities in which I
am the center of attention,3 Being embarrassed or looking stupid are
among my worst fears.
According to DSM-5, there are 2 subtypes of SAD:
 SAD: A marked, ongoing anxiety of one or more social or
performance circumstances involving exposure to strange people or
potential for public scrutiny is the main criteria for SAD.
 SAD- performance only: a subtype of SAD individuals who only have
symptoms when performing.
3.5.3 Monitoring:
Once SAD has been diagnosed using DSM-5 criteria, it is helpful to
define the breadth of social concerns by thoroughly examining anxiety
and avoidance in common social, professional, and academic
circumstances.
The most popular SAD monitoring is the Liebowitz Social Anxiety Scale,
a 24-item measure of fear and anxiety in a variety of typical social and
performance contexts.
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DSM5 criteria:
 Marked fear or anxiety about one or more social situations in which
the individual is exposed to possible scrutiny by others. Examples
include social interactions (e.g., having a conversation, meeting
unfamiliar people), being observed (e.g., eating or drinking), and
performing in front of others (e.g., giving a speech). Note: In children,
the anxiety must occur in peer settings and not just during interactions
with adults.
 The individual fears that he or she will act in a way or show anxiety
symptoms that will be negatively evaluated (i.e., will be humiliating or
embarrassing: will lead to rejection or offend others).
 The social situations almost always provoke fear or anxiety. Note: In
children, the fear or anxiety may be expressed by crying, tantrums,
freezing, clinging, shrinking, or failing to speak in social situations.
 The social situations are avoided or endured with intense fear or
anxiety.
SAD can be effectively treated with either pharmacotherapy or
psychotherapy for initial 8- to 12-week trial.
For patients who prefer psychotherapy for SAD; first line treatment is
CBT:
 Good response: to continue maintenance sessions, two or three visits
per year.
 Partial response: to substitute or add SSRI/SNRI.
 No response: to reassess for comorbidities such as depression,
complicated grief, or substance use.
For patients who prefer medication for SAD, first-line treatment is SSRI
or SNRI; (Paroxetine or sertraline)
For patients with performance-only SAD; choose treatment depend on
frequency of events;
 If frequent: CBT
 If non-Frequent: Beta blockers as Propranolol (An initial dose of 10 or
20 mg of can be administered orally 30 to 60 minutes before the
event.), or Benzodiazepine.
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3.6. Separation Anxiety Disorder:

3.6.1 Definition:
Separation Anxiety Disorder is the most common anxiety condition in
children under the age of 12. The onset of separation anxiety disorder
may start as early as preschool age, may occur at any time during
childhood, and rarely in adolescence. Children with separation anxiety
disorder may avoid school. Adults with the condition are frequently overly
worried about their spouses and children, and they feel intensely
uncomfortable when they are apart from them.
Use DSM-5 to establish diagnosis
 Developmentally inappropriate and excessive fear or anxiety
concerning separation from those to whom the individual is attached,
as evidenced by at least three of the following:
o Recurrent excessive distress when anticipating or experiencing
separation from home or from major attachment figures.
o Persistent and excessive worry about losing major attachment
figures or about possible harm to them, such as illness, injury,
disasters, or death.
o Persistent and excessive worry about experiencing an untoward
event (e.g., getting lost, being kidnapped, having an accident,
becoming ill) that causes separation from a major attachment
figure.
o Persistent reluctance or refusal to go out, away from home, to
school, to work, or elsewhere because of fear of separation.
o Persistent and excessive fear of or reluctance about being alone
or without major attachment figures at home or in other settings.
o Persistent reluctance or refusal to sleep away from home or to go
to sleep without being near a major attachment figure.
o Repeated nightmares involving the theme of separation.
o Repeated complaints of physical symptoms (e.g., headaches,
stomachaches, nausea, vomiting) when separation from a major
attachment figure occurs or is anticipated.
 The fear, anxiety, or avoidance is persistent, lasting at least four
weeks in children and adolescents and typically six months or more
in adults.
 The disturbance causes clinically significant distress or impairment in
social, academic, occupational, or other important areas of
functioning.
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 The disturbance is not better explained by another mental disorder.

Depending on how severe the symptoms are, separation anxiety
disorder must frequently be managed and treated appropriately.
If the symptoms are mild: patient and parent information, support, and
encouragement may be enough.
Psychotherapeutic or psychopharmacological treatments may be
necessary when symptoms are moderate or severe.
SSRIs/SNRIs are typically recommended for at least six months after the
initial reaction before being gradually stopped.( Due to the lack of FDA-
approved drugs for children under the age of six, offer only CBT.)
3.7. Selective mutism:
3.7.1 Definition:
Selective mutism typically begins before the age of five, however the
disorder may not come under clinical observation until starting school,
when social interaction and performance tasks, such reading aloud, may
cause social impairment because children could be too anxious to
interact with other children in a reciprocal way
DSM-5 diagnostic criteria of selective mutism
 Selective Mutism: Consistent failure to speak in specific social
situations in which there is an expectation for speaking (eg, at school)
despite speaking in other situations.
 Disturbance interferes with educational or occupational achievement
or with social communication.
 The duration of the disturbance is at least one month (not limited to
the first month of school).
 The failure to speak is not attributable to a lack of knowledge of, or
comfort with, the spoken language required in the social situation.
 The disturbance is not better explained by a communication disorder
(eg, childhood-onset fluency disorder) and does not occur exclusively
during the course of autism spectrum disorder, schizophrenia, or
another psychotic disorder.
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CBT is preferred over SSSRIs/SNRIs or other treatments as the primary
line, The S-CAT principles comprise a three-session CBT intervention for
the child and parent at home, which is then expanded to include school-
based CBT. The overall treatment principle contained six core
components:
 Sit alongside the child rather than across from them.
 concentrating on the child instead of getting everyone’s attention by
employing an activity they both like.
 using “think aloud” instead of directly questioning the child.
 Don’t speak on behalf of the child; instead, give them enough time to
answer.
 to carry on the conversation even if the child doesn’t respond vocally.
 to try to get a verbal response in a nonjudgmental manner as
opposed to complimenting the child.
Chapter 4: ACUTE STRESS DISORDER
4.1. Acute Stress Disorder:
4.1.1 Definition and symptoms:
Acute stress disorder (ASD) occurs within a month after a person
exposure to a traumatic event (e.g., sexual abuse, car accident, or
sexual violation).
Patients experience extreme fear and anxiety when exposed to trauma
reminders. They may have dissociative symptoms, re-experiencing the
event, and avoidance behaviors.
4.1.2 Diagnosis:
DSM-5 Diagnostic Criteria for ASD should be used for diagnosis
Table 4.5 Acute stress disorder (ASD) diagnosis criteria from DSM-5
A. Exposure to actual of threatened death, serious injury, or sexual
violation in one (or more) of the following ways:
 Directly experiencing the traumatic events
 Witnessing, in person, the event as it occurred to others
 Learning that the events occurred to a close family member or
close friend: In cases of actual or threatened death of a family
member or friend, the event must have been violent or accidental.
 Experiencing repeated or extreme exposure to aversive details of
the traumatic events (e.g., first responders collecting human
remains, police officers repeatedly exposed to details of child
abuse);
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This does not apply to exposure through electronic media, television,

movies, or pictures, unless this exposure is work- related.
B. Presence of nine (or more) of the following symptoms from any of the
five categories of intrusion, negative mood, dissociation, avoidance, and
arousal, beginning or worsening after the traumatic events occurred:
Intrusive symptoms
 Recurrent, involuntary, and intrusive distressing memories of the
traumatic events.
 Note: in children, repetitive play may occur in which themes or
aspects of the traumatic events are expressed.
 Recurrent distressing dreams in which the content and/or effect of
the dream are related to the events. Note: in children there may be
frightening dreams without recognizable content.
 Dissociative reactions (i.e., flashbacks) in which the individual feels
or acts as if the traumatic events were recurring.
 Note: in children trauma specific reenactment may occur in play.
 Intense of prolonged psychological distress or marked physiological
response to internal or external cues that symbolize or resemble an
aspect of the traumatic events.
 Negative mood
 Persistent inability to experience positive emotions (e.g., inability to
experience happiness, satisfaction, or loving feelings.
 Dissociative symptoms
 An altered sense of the reality of one’s surroundings of oneself
(e.g., seeing oneself from another’s perspective, being in a daze,
time slowing)
 Inability to remember an important aspect of the traumatic events
typically due to dissociative amnesia and not to other factors such
as head injury, alcohol, or drugs.
 Efforts to avoid distressing memories, thoughts, or feelings about or
closely associated with the traumatic events.
 Efforts to avoid external reminders (people, places, conversations,
activities, objects, situations) that arouse distressing memories,
thoughts, or feelings about or closely associated with the traumatic
events.
Arousal symptoms
 Sleep disturbance (e.g., difficulty falling or staying asleep, restless
sleep)
 Irritable behavior and angry outbursts (with little or no provocation),
typically expressed as verbal or physical aggression toward people
or objects
 Hypervigilance
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 Problems with concentration

 Exaggerated startle response
C. Duration of the disturbance (symptoms in criterion B) is three days to
one month after the trauma exposure.
 Symptoms typically begin immediately after the trauma, but
persistence for at least three days and up to a month is needed to
meet disorder criteria.
D. The disturbance causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning
E. The disturbance is not attributable to the psychological effects of
substance (e.g., medication or alcohol) or another medical condition
(e.g., mild traumatic brain injury) and is not better explained by brief
psychotic disorder
4.1.3 Management:
 Trauma-focused Cognitive behavioral therapy is the first-line
treatment of patients with ASD.
 SSRIs have no benefit in treating ASD.
 Benzodiazepine can be used for short-term (up to 4 weeks) for
patients with ASD and intense anxiety, agitation, or sleep disturbance.
 Beta-blockers may be helpful for sympathetic symptoms, decrease
trauma conditioning, memories and prevent the development of
PTSD.
 Morphine is good for pain control which is helpful in preventing PTSD.
 Referral is required if patients have prolonged symptoms that cause
distress or affect social life or daily functioning.
4.2. Obsessive-Compulsive Disorder (OCD):
Obsessive-compulsive disorder (OCD) is a chronic neuropsychiatric
disorder characterized by recurrent, unwanted distressing thoughts with
repetitive responses to relieve the distress.
4.2.2 Diagnosis:
DSM-5 Diagnostic Criteria for OCD should be used for diagnosis
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Table 4.6 Edinburgh Postnatal Depression Scale

A. Presence of obsessions, compulsions, or both:
Obsessions are defined by 1 and 2:
 Recurrent and persistent thoughts, urges, or images that are
experienced, at some time during the disturbance, as intrusive and
unwanted, and that in most individuals cause marked anxiety or
distress.
 The individual attempts to ignore or suppress such thoughts, urges
or images, or to neutralize them with some other thought or action
(i.e., by performing a compulsion).
Compulsions are defined by 1 and 2:
 Repetitive behaviors for example hand washing, ordering, checking
or mental acts for example praying, counting, repeating words
silently, that the individual feels driven to perform in response to an
obsession or according to rules that must be applied rigidly
 The behaviors or mental acts are aimed at preventing or reducing
anxiety or distress, or preventing some dreaded event or situation;
However, these behaviors or mental acts are not connected in a
realistic way with what they are designed to neutralize or prevent or
are clearly excessive.Note: young children may not be able to
articulate the aims of these behaviors or mental acts
B. The obsessions or compulsions are time consuming, take up more
than one hour per day, or cause clinically significant distress or
functioning.
C. The obsessive-compulsive symptoms are not attributable to the
psychological effects of a substance drug abuse, a medication, or other
medical condition.
D. The disturbance is not better explained by symptoms of another
mental disorder.
Specify if:
With good or fair insights: the individual recognizes that obsessive
compulsive disorder believes are definitely or probably not true or that
they may or may not be true.With poor insight the individual thinks
obsessive compulsive disorder believes are probably true.With absent
insight\delusional beliefs: the individual is completely convinced that
obsessive compulsive disorder’s beliefs are true.
Specify if:
Tic-related: the individual has current or past history of tic disorder.
4.2.3 Management:
OCD can be treated by CBT as well as SSRI or both (Algorithm 4.1).
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4.3. Posttraumatic Stress Disorder (PTSD):

Posttraumatic Stress Disorder (PTSD) is characterized by exposure to
traumatic events and the subsequent development of four general
symptom domains:
 Intrusion symptoms.
 Avoidance symptoms.
 Negative cognitions and mood symptoms.
 Arousal and reactivity changes.
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4.3.2 Diagnosis:
A diagnosis of PTSD is made only after a month has passed since the
traumatic event. Prior to that time, patients with PTSD-like symptoms are
diagnosed with acute stress disorder.
History of exposure to actual or threatened death, serious injury, or
sexual violence the diagnosis of PTSD can be made if the adult has all of
the following for at least one month:
 At least one re-experiencing symptom:
o Recurrent, involuntary, and intrusive distressing memories of the
traumatic event.
o Recurrent distressing dreams in which the content and/or effect
of the dream are related to the traumatic event
o Dissociative reactions (e.g., flashbacks) in which the individual
feels or acts as if the traumatic event(s) were recurring.
o Intense or prolonged psychological distress at exposure to
internal or external cues that symbolize or resemble an aspect of
the traumatic event(s)
o Marked physiological reactions to internal or external cues that
symbolize or resemble an aspect of the traumatic event(s).
 At least one avoidance symptom:
o Staying away from places, events, or objects that are reminders
of the traumatic experience
o Avoiding thoughts or feelings related to the traumatic event
 At least two arousal and reactivity symptoms:
o Being easily startled
o Feeling tense or “on edge.”
o Having difficulty sleeping
o Having angry outbursts
o Problems with concentration.
o Sleep disturbance (e.g., difficulty falling or staying asleep or
restless sleep).
 At least two cognition and mood symptoms:
o Trouble remembering key features of the traumatic event
o Negative thoughts about oneself or the world
o Distorted feelings like guilt or blame
o Loss of interest in enjoyable activities
o Feelings of detachment or estrangement from others.
o Persistent inability to experience positive emotions
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 The disturbance usually causes clinically significant distress or

functioning.
 The disturbance sometimes is not attributable to the physiological
effects of a substance (e.g., medication, alcohol) or another medical
condition.
4.3.3 Management:
 The choice between medication and trauma-focused psychotherapy
depends on patient preference and treatment availability.
 SSRI/SNRI: need 6-8 weeks to achieve full therapeutic benefit
 Switching to another medication if no improvement after 8 weeks of
therapy.
 SSRI/SNRI should continue for at least 6-12 months to prevent
relapse or recurrence.
 Adjunctive treatment with prazosin is recommended for patients with
PTSD who have sleep disturbance.
 Augment SSRI/SNRI with antipsychotic medications in patients with
psychosis.
Chapter 5: OTHER PSYCHOLOGICAL

DISORDERS
5.1. Bipolar disorder:
5.1.1 Definition:
manic or hypomanic episodes sometimes, but not necessarily,
accompanied by depressive episodes.
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5.1.2 Types of Bipolar disorders:

Table 5.6 Types of bipolar disorder
Cyclothymic
Bipolar I Bipolar II disorder
At least one manic At least one hypomanic Doesn’t meet criteria
episode ± major episode + major of manic, hypomanic,
depressive episode depressive episode or depressive episode
Episode lasting at Episode lasting at least Symptoms on and off
least four days seven days for at least two years
Manic Hypomanic Never free of
symptoms for more
than two consecutive
months
Social and/or NO social and/or Social and/or
occupational occupational occupational
dysfunction dysfunction dysfunction
± Psychosis Social and/or
(delusions and/or occupational
hallucinations) NO psychosis dysfunction
5.1.3 Diagnostic criteria :
Bipolar Major Depressive episode
5 of the following symptoms, presenting for at least two weeks, and at
least one symptom being either depressed mood or loss of interest.
 Depressed mood, nearly every day
 Loss of interest
 Unintentional weight loss or weight gain (5% of body weight in 1
month) or changes in appetite
 Insomnia/hypersomnia
 Fatigue
 Psychomotor agitations
 Feeling worthlessness, excessive guilt
 Inability to concentrate
 Suicidal ideation with or without a specific plan
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Manic episode
At least a 7-day period of abnormally elevated, irritable, or expansive
mood nearly every day; in addition to 3 of the following symptoms (4 if
the mood is irritable):
 Distractibility
 Impulsivity/injudiciousness (poor judgment, shopping sprees,
hypersexual activity)
 Grandiosity
 Flight of thoughts
 Psychomotor agitation (increased goal-directed activities)
 Decreased need for sleep
 Pressured speech
For both manic and depressive episodes, the symptoms cause marked
social and occupational dysfunction, and they are not better explained by
any other conditions or substance use.
Hypomanic episode
At least 4 days of abnormally elevated, irritable, or expansive mood
nearly every day; in addition to 3 of the following symptoms (4 if the
mood is irritable):
 Distractibility
 Impulsivity/injudiciousness (poor judgment, shopping sprees,
hypersexual activity)
 Grandiosity
 Flight of thoughts
 Psychomotor agitation (increased goal-directed activities)
 Decreased need for sleep
 Pressured speech
Hypomania doesn’t cause significant social or occupational dysfunction,
and the symptoms must not be better explained by any other condition or
substance use.
One manic episode is enough to diagnose bipolar disorder.
No laboratory or radiological imaging is required to diagnose bipolar
disorders.
 Non pharmacological :
 Behavioral: cognitive behavioral therapy, psychoeducation
 Pharmacologic treatment:
Page | 429
Table 5.7 Acute treatment of bipolar disorders

MANIA Initial Lithium or valproate + antipsychotic
(aripiprazole, haloperidol, risperidone,
quetiapine, olanzapine)
Switch valproate to lithium, or vice
versa
Modification Change to different antipsychotic
HYPOMANIA 1st line Risperidone
Olanzapine
Alternatives Lithium, valproate, quetiapine,
aripiprazole, haloperidol
BIPOLAR 1st line Quetiapine
MAJOR Lurasidone
DEPRESSION
2nd line Olanzapine + Fluoxetine
Valproate
Quetiapine or lurasidone + Lithium or
Valproate
Lithium + valproate or lamotrigine
3rd line Lamotrigine
Lithium
Olanzapine
Carbamazepine
Olanzapine + lithium or valproate
Lithium or valproate + antidepressant
Second generation antipsychotic +
antidepressant
 Maintenance therapy:
o 1st line: same medication used for an acute episode
o 2nd line: lithium, valproate, lamotrigine, quetiapine
o 3rd line: olanzapine, risperidone, aripiprazole
 Regular follow-up with a focus on the progress of symptoms, suicide
risk, and side effects of medications.
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5.2. Intimate partner violence:

5.2.1 Definition:
threat of or actual violent behavior from a current or previous partner.
Violent behavior may be :
 Physical: Use of force with the intention of harm, with or without the
use of weapons.
 emotional/psychological: intent of physical or sexual violence, social
isolation, economic control and stalking.
 Sexual: Forcing an individual into a sexual act against their will or
they are unable to vocalize their unwillingness for any given reason
o Abusive sexual contact
o or any combination of them.
5.2.2 Screening and screening tools:
 The U.S. Preventive Services Task Force recommends routine
screening of all women of childbearing age.
Table 5.8 IPV screening tools
HITS Hurt you physically?
Questions Insult you or talk down to you?
Threaten you with harm?
Scream or curse at you?
Scoring: never = 1, rarely = 2, sometimes = 3,
fairly often = 4, frequently = 5.
A score of 10 is a positive screen.
Partner Have you experienced physical violence within the
Violence Scale past year? If yes, from whom?
Do you feel safe in your current relationship?
Is there a previous partner that makes you feel
unsafe?
A positive answer to any of these questions is a
positive screen.
HARK Humiliation – humiliated or emotionally abused by
Questions your partner or previous partner?
Afraid – afraid of your partner or previous partner?
Rape – raped or forced to have any kind of sexual
activity by your partner or previous partner?
Kick – kicked, hit, slapped, or otherwise physically
hurt by your partner or previous partner?
positive screen.
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Stat Questions Has your partner ever:

 Pushed or s lapped you?
 Threatened you with violence?
 Thrown, broken, or punched things?
positive screen.
Asking open-ended questions and showing empathy while avoiding
being judgmental, hesitant, or uncomfortable can help the patient open
up.
Table 5.8 History and Physical examination findings in IPV

History Physical
Inconsistent explanation of Refusal of the Physical exam
injuries Delaying Treatment Injuries of the head , neck , teeth
Frequent E R visits Missed , and genital area Wounds
appointments Medication Bruising (different colors)
compliance In pregnancy late Forearm fractures or wounds
prenatal care Recurrent (defensive wounds) Evidence of
abortions Any of the health sexual assault Signs of STI
effects mentioned above
Appropriate laboratory or radiological studies are to be carried out as
indicated by the patient’s presentation.
 Showing support, expressing empathy, and offering assistance
 Assessment of their stage of readiness Before referring the patient
for counseling.
 Assessing safety.
 If any risk factors of escalating abuse exist, advise patients to make a
safety plan:
o An emergency kit and a place to go to in case of emergency.
o In case of danger, alert the authorities.
 When possible, Document everything by photographing.
o Omission of history of violence from the documentation if
that’s the patient’s wish.
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o Cases where it’s mandatory to report domestic violence, despite

the patient’s autonomy, are when children or weapons are
involved.
 Follow up :
Close and frequent follow-up.
5.3. Schizophrenia:
5.3.1 Definition:
Schizophrenia is a prevalent psychotic disorder.
5.3.2 Diagnostic criteria:
According to DSM-5:
 Two or more of the following each present for a significant period of
time during a one month period (or less if successfully treated). At
least one must be 1, 2, or 3:
o Delusions
o Hallucinations
o Disorganized speech for example frequent derailment or
incoherence
o Lead disorganized or catatonic behavior
o Negative symptoms for example diminished emotional
expression or avolition
 For a significant portion of the time since the onset of the disturbance,
level of functioning in one or more major areas, such as work,
interpersonal relations, or self care, is markedly below the level
achieved prior to the onset
 Continuous signs of the disturbance persist for at least six months.
This six month period must include at least one month of symptoms
or less if successfully treated that meet criteria on A and may include
periods of prodromal or residual symptoms. During these prodromal
or residual periods, the signs of the disturbance may be manifested
by only negative symptoms or by two or more symptoms listed in
criterion A present in an attenuated form.
 Schizoaffective disorder and depressed or bipolar disorders with
psychotic features have been ruled out because either:
o 1. no major depressive or manic episodes have occurred:
currently with the active phase symptoms, or
o 2. if mood episodes have occurred during active phase
symptoms, they have been present for a minority of the total
duration of the active and residual periods of the illness.
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 The disturbance is not attributable to the psychological effects of a

substance for example drug abuse or a medication or another
medical condition
 If there is a family history of autism spectrum disorder or a
communication disorder of childhood onset, the additional diagnosis
of schizophrenia is made only if prominent delusions or hallucinations,
in addition to the other required symptoms of schizophrenia, are also
present for at least one month or less if successfully treated
 Antipsychotics are the first-line and they should be initiated after
consulting a psychiatrist.
 At least four weeks of therapeutic dose should be started. If they
report symptom relief, they should be placed on maintenance therapy.
 The goal of treatment is remission for six months of no symptoms or
mild symptoms for six months that do not interfere with the patient’s
behavior
 Adjunctive therapy like CBT should be used.
1st generation antipsychotic and side effects
Chlorpromazine, Haloperidol, Perphenazine, Thiothixene
Drowsiness, dry mouth, extrapyramidal symptoms, hypotension (Except
Perphenazine and Thiothixene) tachycardia, neuroleptic malignant
syndrome, tardive dyskinesia
2nd generation antipsychotic and side effects
Aripiprazole, Clozapine, Olanzapine, Quetiapine, Risperidone
anxiety, Constipation, dizziness, headache, metabolic changes, nausea,
vomiting, weight gain, agranulocytosis, neuroleptic malignant syndrome,
tardive dyskinesia
5.3.4 Monitoring for side effects:
 Those on 2nd generation antipsychotics have a weekly CBC for six
months, then monthly as they are prone to get agranulocytosis. And
they should also be monitored for metabolic changes.
5.4. Sexual abuse:
5.4.1 Definition:
engaging in a sexual act without obtaining consent from the other
individual, or when the other individual cannot give consent for any given
reason (e.g., intoxication, unconsciousness). It is recognized as one of
the types of intimate partner violence.
Page | 434
5.4.2 Screening:
 The U.S. Preventative Services Task Force recommends the same
screening methods for IPV to be used for sexual assault in all women
of reproductive age.
 The Two-Question Screening Tool is validated for use in primary care:
1st question for IPV:
Have you ever been kicked, slapped, hit, or physically hurt by your
partner?
2nd question for sexual violence:
Have you ever been forced to have sexual activities?
History taking:
 Name of the assailant, time, location, date of the assault.
 Use of weapons.
 Loss of consciousness/ memory loss.
 Details of means of sexual assault.
 Use of drugs or alcohol by the victim or assailant.
 Details regarding the use of barrier method.
 Location of trauma. Bleeding by victim or assailant for hepatitis B and
HIV risk
detailed physical examination is extremely important
 Patient’s emotional state during physical examination
 Any evidence of trauma
 Including photographs, with the consent of the patient
 Bruises, abrasions, erythema over the surface of the skin
 Males :Thighs, penis and glans, urethral meatus, scrotum, perineum
and rectum
 Females :Breasts, rectum, vagina, anus, external genitalia and
posterior fourchette
 X-rays should be obtained for any areas subjected to trauma.
 Work up for STI: the CDC recommends nucleic acid amplification
testing for chlamydia, gonorrhea, and trichomoniasis.
 Wet mount for bacterial vaginosis.
 Serum HIV.
 Serum hepatitis B antigen.
 Serum rapid plasma reagin for syphilis.
Page | 435
 Urine pregnancy tests for females.

 Drug screening: flunitrazepam, gamma-hydroxybutyrate,
benzodiazepines, alcohol, ketamine.
Initial management includes managing fractures and soft tissue injuries.
 Sexually transmitted infections:
o Empiric treatment:
 Chlamydia and gonorrhea coverage: Ceftriaxone 500 mg
I.M. once + Azithromycin 1 g P.O. once.
 Trichomoniasis: metronidazole 2 g PO once.
 Hepatitis B: management for hepatitis B will depend on the patient’s
vaccination status and documentation of immunity.
 HIV: Initiation of antiretroviral drugs for PEP in sexual assault cases
presented within the first 4-72 hours from the assault ( Specialists
should be consulted )
 HPV: follow the same recommendations for vaccination.
 Tetanus booster if immunization status is unknown for ten years.
 Pregnancy: emergency contraception can be offered.
o Levonorgestrel 1.5 mg up to 72 hours after the assault
o Copper IUD within five days of the assault
 Psychosocial: offering support and empathy, providing a referral to
mental health services or professionals.
 Documentation: incident forms.
 Follow up:
o Offer close follow-up after 1-2 weeks.
o At one week follow-up, repeat testing for STI and pregnancy
should be performed even when the patient received emergency
contraception.
o Abstain from sexual intercourse until prophylaxis for HIV is
completed.
o Repeat HIV testing at one month and three months follow up.
5.5. Somatic symptom disorder:
5.5.1 Definition:
Psychological or emotional distress manifested in the form of physical
symptoms that are otherwise medically unexplained. These disorders
can start in childhood, adolescence, or adulthood, with an estimated
female-to-male ratio of 10:1
Page | 436
5.5.2 Etiology:
The etiology of the somatic disorder is unclear.
Somatic symptoms may result from a heightened awareness of certain
bodily sensations, combined with a tendency to interpret these
sensations as indicative of a medical illness.
5.5.3 Diagnosis and screening:
Screening : by Somatic Symptom Scale-8.
5.5.4 DSM-5 Criteria:
 One or more somatic symptoms that are distressing or result in
significant disruption of daily life:
o Excessive thoughts, feelings, or behaviors related to these
somatic symptoms or associated health concerns as manifested
by at least one of the following:
o Disproportionate and persistent thoughts about the seriousness
of one’s symptoms.
o Persistently high levels of anxiety about health or symptoms.
o Excessive time and energy devoted to these symptoms or health
concerns.
 Although any one somatic symptom may not be continuously present,
the period of being symptomatic if it is persistent is typically more than
six months.
 Specify if:
o With predominant pain: this specifier is for individuals whose
somatic symptoms predominantly involve pain.
o Persistent: a persistent course is characterized by severe
symptoms, marked impairment, and long duration more than six
months.
 Specify current severity:
o Mild: only one of the symptoms specified in criterion B is fulfilled.
o Moderate: two or more of the symptoms specified in criterion B
are fulfilled.
o Severe: two or more of the symptoms specified in criterion B are
fulfilled, plus there are multiple somatic complaints, one or one
very severe somatic symptoms
Page | 437
 Subclass Characteristics of somatic symptom disorder:

o Conversion disorder: one or more symptoms of altered
voluntary movement or sensory function inconsistent with a
known condition
o Factitious disorder: falsification of physical or psychological
symptoms, or induced injury or disease, although not for
personal gain as with malingering
o Illness anxiety disorder: preoccupation with getting or having
serious medical disorder.
o Psychological factors affecting other medical conditions:
medical condition must exist and psychological factors must
negatively affect the condition
o Other specified somatic symptom and related disorders:
symptoms consistent with somatic symptom disorder are
present, but do not meet full criteria for any of the above
disorders
o Unspecified somatic symptom and related disorders:
symptoms consistent with somatic symptom disorder are present
but do not meet criteria for any of the above disorders.
The management requires a multifaceted approach tailored to the
individual patient.
 General treatment:
o Scheduling regular, short-interval visits (5 minutes might be
enough)
o Acknowledging and legitimizing symptoms once the patient has
been evaluated for other medical and psychiatric diseases
o Reassuring the patient that serious medical diseases have been
ruled out
o Educating patients about coping with physical symptoms
o Limiting diagnostic testing
o Setting a treatment goal of functional improvement rather than
cure;
o Minimize polypharmacy
o Taper and discontinue medications with high potential for abuse
o Appropriately referring patients to subspecialists and mental
health professionals
o Creating a collaborative, therapeutic alliance with the patient
Page | 438
 Other Modalities:
 Non pharmacological
o Cognitive behavioral therapy
o Mindfulness-based therapy
o St. John’s wort
 Pharmacological
o Amitriptyline
5.6. Personality Disorders:
5.6.1 Definition:
 a repetitive, pervasive, rigid, and maladaptive pattern of thoughts,
feelings, and behaviors associated with the environment and oneself
that cause severe suffering and/or functional impairment
 Incidence age: late infancy through early adolescence. Males,
young, uneducated, and the unemployed are more likely to be
affected
5.6.2 Types:
 The disorders are grouped into three clusters:
Table 5.9 Personality disorders defined by DSM-5 diagnostic criteria
Family
Personalit history
Characteristi y associat
Prevalence c behavior disorders ion
Cluster 5%Increased Odd ParanoidSc Psychoti
A if there is a Eccentric hizoidSchiz c
family history Unable to otypal disorder
of form close
schizophrenia interpersonal
relationships
No psychosis
Cluster 2% Dramatic Borderline Mood
B Emotional HistrionicA disorder
ntisocial
Narcissistic
Cluster 5% Fearful AvoidantDe Anxiety
C Avoidant pendnt disorder
Anxious Obsessive-
Compulsive
personality
disorder
Page | 439
5.6.3 Diagnosis:
Diagnosis of personality disorder is based on DSM 5 Criteria:
At least two or more of the following deviate from cultural expectations:
 Cognition (e.g., perceives events, self, or other in an inappropriate
way)
 Interpersonal functioning
 Affectivity
 Impulse control
 Begins in early adulthood and progresses steadily
 This leads to significant impaired functioning and distress in important
areas of life (e.g., social, occupational)
 Isn’t the result of another mental illness, substance misuse, or
medical condition.
 It can be diagnosed in those under the age of 18 if symptoms have
been present for at least a year (except antisocial personality
disorder).
Page | 440
5.6.4 Diagnosis of each type based on DSM 5 criteria:

Table 5.10 CLUSTER A
Paranoid personality Schizoid personality Schizotypal
disorder: at least 4 of disorder: at least 4 of personality disorder:
the following criteria the following criteria at least 5 of the
have to be met: have to be met: following criteria
have to be met:
Pervasive distrust of Voluntary Odd and eccentric
others. detachment from behavior or physical
social relationships appearance
Unjustified fear that Enjoys few activities Magical thinking
others will use
information against
them.
Unjustified Prefers solitary Social awkwardness
suspicions about activities
loyalty of
friends/family.
Suspicions of No or little interest in Excessive social
infidelity in sexual sexual relationships anxiety
partners.
Disproportionate Lacks people to trust Ideas of reference
reactions to or close friends
perceived attacks.
Perceives benign Indifferent to praise Unusual perceptual
remarks as hidden or criticism experiences
humiliations.
Holding grudges. Restricted emotional Bizarre
expression, flattened thinking/speech
affect.
Paranoia and
suspicion of others
Constricted affect
Few or no close
friends
Social anxiety
Page | 441
Table 5.11 CLUSTER B

Antisocial personality disorder: 3 Borderline personality disorder:
or more of the following of at least 5 of the following criteria
conduct are present from at have to be met:
least 15 years of age.
Deceitfulness, manipulation Unstable mood
A history of hostility and Intense anger is difficult to
repeated aggression control
Repeated engaging in criminal Feeling of emptiness
activity Self-damaging acts
Impulsivity or failure to plan Self-harm, suicidal behavior
ahead Unstable self-image
A reckless disregard for the Suspicion about what others
safety of others and one’s own think of them
safety as well Unstable personal relationships
Fear of abandonment
Histrionic personality disorder: at Narcissistic personality disorder:
least 5 of the following criteria at least 5 of the following criteria
have to be met: must be met:
Attention seeking Fantasizes disproportionately
Exaggerated emotional about success, power, etc.
expression Excessive sense of self-
Uses dramatic speech importance
Feelings are often shallow and Believe in being special and a
unstable feeling of superiority
Uncomfortable not being the Expecting favorable treatment
center of attention from others
Exhibiting inappropriate, Great need for admiration
sexually provocative The exploitation of others to
Easily influenced by others achieve their own goals
Overestimating the degree of Often envious of others
intimacy in relationships Lack of empathy
Often behaves arrogant and/or
snobbish
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Table 5.12 CLUSTER C

Avoidant personality Obsessive- Dependent
disorder: at least 4 of compulsive personality disorder:
the following criteria personality disorder: at least 5 of the
have to be met At least 4 of the following criteria
following criteria must be met.
must be met:
Avoidance of Excessive Disproportionate
interpersonal contact preoccupation with need for support
due to fear of rules, lists, details
criticism or rejection
Restrained in Perfectionism often Avoids disagreeing
intimate relationships interferes with task with others due to
due to fear of being completion fear of losing their
shamed support
Only interacts with Obsession with work Difficulty making
people if certain of and productivity often everyday decisions
being liked by them occurs at the
expense of
occupational
success, social
relationships
Preoccupation with Great fastidiousness Makes extreme
and hypersensitivity and efforts to obtain
to criticism conscientiousness, support from others
inflexible about
matters of morality or
ethics
Low self-esteem Unwillingness to Difficulty initiating
delegate work or to projects, lack of self-
collaborate with other confidence
people
Feelings of Cling to worn Urgently seeking
inadequacy resulting out/worthless items. new relationships
in involuntary social when one fails
withdrawal
Avoids taking risks Often show Feelings of
and seldomly miserliness helplessness when
engages in new alone
activities
Rigid routines Both are afraid of
being abandoned
Page | 443
and afraid to
abandon their
partner
 No specific physical examination
 Psychological testing: For DSM 5, the Minnesota multiphasic
personality disorder questionnaire, we can employ a structured
clinical interview (best-known test)
 The following tests can be used to make a diagnosis: toxicology
screen, HIV, and other STD screening.
 Non-pharmacological:
o Psychotherapy is the first line of treatment.
o It consists of: psychodynamic, interpersonal, CBT, and supportive
 Pharmacological:
o Avoid using medications on a regular basis.
o Applied to specific behaviors:
o Antidepressants (SSRI): anger, mood swings, OCD
o Mood stabilizers (valproate, topiramate, and lamotrigine):
irritability, mood swings
o Buspirone: anxiety
 Consultation and follow-up:
o consider psychiatric consultation
o If a patient is discharged a follow-up appointment with a
psychiatrist should be scheduled within 24–48 hours.
Page | 444
Section 6: Geriatrics and Palliative

care
Chapter 1: PALLIATIVE CARE
1.1. Background:
1.1.1 Definitions:
Palliative Care: "Palliative care means the specialized care of people
who are dying – care aimed at alleviating suffering (physical, emotional,
psychosocial or spiritual), rather than curing.
Commonest symptoms among patients in palliative care:
 Pain
 Constipation
 Dyspnea
 Nausea & Vomiting
1.2. Pain:
1.2.1 Definitions:
 Pain "is an unpleasant sensory and emotional experience associated
with actual or potential tissue damage or described in terms of such
damage."
 Background pain is pain present for twelve or more hours per day
during the previous week or presents if not taking analgesia.
 Breakthrough pain (BT) is a transient exacerbation of pain that occurs
spontaneously or in relation to a trigger, despite adequately controlled
background pain.
 Physical dependence: a normal physiological response to the
pharmacological effects of chronic opioid administration. It is only
seen when the administration of the opioid is abruptly stopped or an
antagonist is administered.
 Withdrawal syndrome: Typically characterized by sweating tremors,
agitation, muscle cramps, tachycardia, fever, and dilated pupils.
 Addiction (psychological dependence): This is a pathologic
psychological condition that includes a compulsion to take a specific
drug (e.g., opioid) to experience its psychic effects.
Page | 445
 Tolerance: A normal physiological phenomenon in which increasing

doses of an opioid are required overtime to produce the same
analgesic effect.
1.2.2 Assessment:
 Detailed History
 Physical Examination
 Diagnostic test: Depend on pain site, type, and etiology.
1.2.3 Management:
 Non-Pharmacologic
o Message, application heat/cold, Positioning, Relaxation or
cognitive therapy.
 Pharmacologic
o Follow Patient preference in drug selection.
o Consider the patient situation, e.g., organ impairment, medical
condition, performance status, and allergies.
o Initiate analgesic: start low, go slow, by mouth, by a clock, follow
WHO ladder.
o Mild pain 1-4/10: use Acetaminophen or non-steroidal anti-
inflammatory drugs (NSAIDs) +- adjuvant therapy.
o Moderate 5-6/10: Start weak opioid +- adjuvant therapy
o Severe 7-10/10: Use strong opioid +- adjuvant therapy
o Adjuvant analgesics are medication used for a purpose other
than pain and give analgesic effect; They include: anticonvulsant,
antidepressant, corticosteroid, muscle relaxants, topical
NSAIDS/opioids, bone modifying drugs.
1.2.4 Breakthrough pain:
 Use 10% of the total regular daily opioid dose and increase it if the
patient needs 3 or more breakthrough doses / 24h Starting doses:
o Morphine 5mg q4h regularly and 2.5mg or 5mg PO 1qh PRN for
breakthrough pain.
o Hydromorphone 1mg q4h regularly and 0.5mg q1h PO PRN.
o Oxycodone 5mg q4h PO regularly and 5mg q1h PO PRN.
1.2.5 Opioid Side effects:
 Nausea, vomiting, Myoclonus (jerking of limbs or facial muscles),
Constipation, Hyperalgesia/allodynia, Somnolence, Delirium,
Xerostomia, Hallucinations, Pruritus, Cognitive impairment.
 Consider antiemetic regularly first 3-4 days and laxative.
Page | 446
1.2.6 Opioid toxicity:

 Manage by switching one opioid to another opioid agonist, hydration,
and reducing opioid dose if possible.
 Monitor for excessive opioid-induced drowsiness; use pasero Opioid-
Induced sedation scale.
1.3. Constipation:
1.3.1 Definition:
"The passage of small, hard feces infrequently or with difficulty, and less
often than is normal for that individual."
1.3.2 Causes:
 Drugs: opioid, antimuscarinic drug, iron, antihypertensive agent,
serotonin antagonist, diuretic, somatostatin analogs, and antacids.
 Concurrent disease: IBS, IBD, neurological disease, hemorrhoid.
 Direct effect of tumor: spinal cord compression, bowel obstruction,
radiation, chemotherapy.
 Metabolic: hyperglycemia, DM, hypothyroidism, hypokalemia.
 Others: inactivity, lack of toilet privacy, inadequate diet, painful
defecation, confusion, dehydration, fever, vomiting.
1.3.3 Prevention:
 Prescribe laxative when starting opioid (e.g., bisacodyl, lactulose).
 Encourage mobility if possible.
 Encourage regular bowel habits.
 Provide toilet privacy.
 Treat causes, if possible, e.g., hemorrhoids, anal fissure.
 Encourage fiber and fluid intake.
1.3.4 Treatment:
 Aim to prevent complications (e.g., intestinal obstruction, urinary
retention, fecal retention or incontinence, increase agitation, pain,
fecal impaction, seizure).
 Consider patient preference of laxative.
 Aim to formed stool every 2-3 days; more than 3 days required
intervention.
 Metoclopramide used in nausea and vomiting can increasing
peristalsis in the digestive tract.
 Avoid bulk-forming (fiber) in a patient with poor oral intake.
Page | 447
 Combination of stimulant and softener: Senna 2-4 tablets or

Bisacodyl 5-10mg, at bedtime in combination with docusate sodium
100mg capsule, twice daily.
 Severe, intractable opioid-induced constipation: we can use
peripheral opioid receptor antagonists (e.g., Methylnaltrexone).
1.3.5 Important points:
 Avoid rectal agent in neutropenia or thrombocytopenia, never given in
inadequate prescription of oral laxative.
1.4. Dyspnea:
1.4.1 Definition:
"Dyspnea (Shortness of Breath): Is a subjective experience of breathing
discomfort that that vary in intensity."
1.4.2 Causes:
 Pulmonary: pleural effusion, COPD, pneumonia, PE, fibrosis, airway
obstruction.
 Cardiac: CHF, pericardial effusion, CAD, arrhythmia, primary or
metastatic tumor.
 Systemic: anemia.
 Neurological: ALS, muscle weakness, CVA.
 Psychological: anxiety.
 Others: ascites, infection, carcinomatosis, hepatomegaly.
1.4.3 Screening:
 Screen outpatient at each clinic visit and daily for inpatients.
1.4.4 Diagnosis:
 Depend on the patient's situation and prognosis. Provide CBC,
Electrolyte, renal function, oxygen saturation, and chest x-ray if
indicated.
1.4.5 Management:
Behavioral and supportive intervention
 Position: sitting upright supported by a pillow, avoid compression of
chest and abdomen, elevate the head of bed 15-45 degrees.
 Small meal.
 Breath control methods, Pulmonary rehabilitation.
 Non-pharmacology Anxiety management and relaxation.
 Avoid trigger.
Page | 448
Oxygen is used in hypoxic patients.
 Mild dyspnea 1- 3/10:
o Opioids are the first line that starts with morphine 2.5mg IR Orally
Q4h PRN OR hydromorphone 0.5 mg IR orally q4h PRN.
o Bronchodilator if needed, e.g., salbutamol, ipratropium for
asthma, COPD.
 Moderate dyspnea 4-6/10:
o Start opioid in regular doses with PRN
 Morphine orally 5mg IR q4h regular and 2.5mg q2h PRN Morphine
parenterally:
o 3mg q4h regular 2mg SC q1h PRN.
Or
 Hydromorphone 0.5mg orally q4h or Hydromorphone 0.25 mg SC or
IV every 4 hours.
 Short course of corticosteroid dexamethasone 8m/day PO or IV or SC
or prednisone 50mg/day PO in case of major airway obstruction,
lymphangitis carcinomatosis, radiation or drug-induced pneumonia,
endotracheal and bronchial tumors for 5 days trial.
 A limited course duration will likely reduce the risk of adverse effects.
 Provide benzodiazepines for anxiety or panic or chlorpromazine 7.5-
25mg PO q6-8h regular PRN Severe dyspnea 7-10/10:
o A Use combination opioids and adjunctive anxiolytics/sedatives.
o An Opioid naïve: use morphine 5 mg SC or IV bolus every 30
minutes, double dose every 2-3 doses if no benefit.
o An Opioid tolerant: give full regular opioid dose SC or IV every 5
to 10 minutes, double dose every 2- 3 doses if no benefit.
o Midazolam 2.5 to 5 mg SC or IV, OR lorazepam 5 mg SC or IV
every 5 to 15 minutes PRN in combination with an opioid in an
anxious patient.
1.5. Nausea/Vomiting:
1.5.1 Definition:
 Nausea: "Is expressed as an unpleasant subjective sensation as a
result from stimulation of the gastrointestinal lining, the
chemoreceptor trigger zone in the base of the fourth ventricle, the
vestibular apparatus, or the cerebral cortex."
Page | 449
 Vomiting: "Is an observable neuromuscular reflex that constitutes a

final common pathway after stimulation of one or more of these
regions. Vomiting can occur without nausea, and nausea does not
always lead to vomiting".
1.5.2 Causes:
 Chemical, Cortical, Cranial, Vestibular, Visceral or serosal, Gastric
Stasis.
1.5.3 Assessment History &Examination:
 Assess dehydration, fever, Jaundice, Drug toxicity.
 Abdominal +- rectal examination.
 Neurological examination: signs of a cranial lesion or raised
intracranial pressure.
 CBC and differential, calcium, glucose, renal, and liver function, Urine
culture.
 Abdominal imaging: X-ray, ultrasound, CT/MRI.
 Endoscopy
1.5.5 Management Non-pharmacological:
 Oral care, Prevent constipation, Consult a dietitian if required,
Aromatherapy e.g., peppermint, Use wrist band, acupressure.
 Select antiemetics according to the etiology of nausea and vomiting
and start with a single agent.
 Metoclopramide: usually the first choice treats common causes of
nausea, avoid use with complete bowel obstruction.
 Haloperidol.
 Methotrimeprazine
 Ondansetron: useful in chemotherapy-induced nausea is considered
as a fourth-line therapy in chronic nausea.
 If nausea persists for 48h consider the use of a combination
antiemetic with different receptors.
Page | 450
1.6. Depression (Psychosocial):

1.6.1 Background:
 Depression is commonly present in people with advanced illness of
any etiology; Studies estimate that 15% - 30% of palliative patients
develop a major depressive disorder and, patients with pancreatic
cancer have higher rates, up to 40. Up to half of the palliative patients
are diagnosed with an adjustment disorder, and 30% may develop
major depression.
 Antidepressant medication requires 3-6 weeks for full effect; consider
prognosis before initiating medication
1.6.2 Assessment:
 Assess for signs and symptoms of depression:
o Depressed mood (ask if he/she is feeling depressed most of the
time – highly sensitive and
o the efficient way of screening for depression in this population)
o Tearfulness
o Hopelessness, helplessness, worthlessness
o Social withdrawal
o Guilt
o Suicidal ideation/wishing to die soon/request
o Profound anhedonia
 Assess for Risk Factors for Depression e.g. Uncontrolled pain and
other symptoms, Advanced malignant or chronic disease, Medications
(e.g., steroids), Prior personal and family history of depression, social
stress, suicide attempts, substance use, and abuse, Presence of
delirium or mild dementia, Past losses and ineffective coping
strategies history of psychiatric disorders, Lack of social support.
1.6.3 Management:
 Assess for and Treat Clinical Conditions that may Mimic depression
e.g. Delirium (especially the hypoactive form), hypercalcemia,
hypothyroidism and Medications that may contribute to depression
(e.g., anticonvulsants, Baclofen, betablockers, corticosteroids,
tamoxifen, cyproterone acetate)
 Expressive/Supportive Therapy.
o SSRIs: e.g., citalopram, fluvoxamine
o Tricyclic antidepressants: e.g., nortriptyline, desipramine
o Psychostimulants: e.g., methylphenidate
Page | 451
 Suicide Risk Intervention: Contact Palliative care Team for support.

1.7. Spirituality:
1.7.1 Background:
It is often referred to as a person's relationship with God or a higher
being.
Spiritual pain:
"Spiritual pain" or "Soul pain" has multiple definitions. Basically, it is
agony that arises from a source that has a relation to spiritual, religious,
or existential matters. It refers to a person's perception of pain along with
an aspiration to surpass the physical world.
Spiritual needs of terminally ill patients:
 To find a motive in life, To reflect on the meaning of suffering and
death, To achieve peace of mind, To be able to accept and forgive, To
be able to give and receive love.
1.7.2 Signs and symptoms of spiritual pain:
 The patient is unresponsive to conventional pharmacological
measures that would normally relieve the target symptoms.
 Lack of organic cause.
 Intense feelings of anxiety, emptiness, detachment from the world
and/or God, injustice, meaninglessness as to why this is happening to
them, and fear of God and the afterlife.
 The clinician's feelings of uneasiness when approaching the patient.
 Scoring high on ESAS-r symptom scale.
1.7.3 Basic of spiritual Assessment:
 Several tools are available for physicians to conduct a spiritual
assessment.
 FICA Spiritual History Tool HOPE Questions for Spiritual Assessment
(2) The Open Invite Mnemonic (3)
1.7.4 Management of spiritual pain:
 Acknowledge and respect the patient's spiritual beliefs
 Be present with the patient and do not feel the need to answer all
questions and resolve spiritual suffering.
 Be aware of your biases and emotions.
 Listen attentively in a non-judgmental way.
 Help the patient in accessing appropriate support based on the
spiritual Assessment.
 Seek advice from a chaplain to explore the spiritual and religious
requirements thoroughly.
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 Implement an interdisciplinary approach

1.7.5 Drawbacks in discussions about spiritual/religious
matters:
 Going beyond one's area of expertise
 Force one's religious or spiritual ideas on the patient
 Attempting to find a solution to unanswerable questions
 Giving false hope by giving early reassurance
1.7.6 Two principles that are important in palliative care:
 The sacredness of life (any approach to speed up a death are strictly
forbidden)
 Preservation of hope
1.8. Social Issues in palliative care:
1.8.1 Background:
Psychosocial care, defined by the National Council for Hospice and
Specialist Palliative Care Services as care concerned with the
psychological and emotional wellbeing of the patient and their
family/caregivers, including issues of self-esteem, insight into an
adaptation to the illness and its consequences, communication, social
functioning, and relationships.
1.8.2 Assessment:
Considerations for a comprehensive assessment within the context of
the patient's lifelimiting illness may include but is not limited to:
 Ecological factors e.g. marital status, family, pattern and style of
communication.
 Psychological factors e.g. self-esteem, coping abilities, response to
previous losses.
 Cultural factors e.g. beliefs, rituals, and values.
 Social factors e.g. education, employment, housing, financial.
 Spiritual factors: meaning applied as to what gives purpose, hope.
1.8.3 Indicators for Specialized Consultation (social
worker):
 Emotional anguish experienced by the patient and/or family.
 Feeling overwhelmed and/or unable to make decisions.
 No caregiver in the home or caregivers' ability is compromised.
 Language, cultural considerations.
 Guardianship with children, young children in the home.
 Unresolved grief from previous and/or traumatic losses.
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 Concerns regarding abuse and/or neglect

 Financial and practical stressors.
1.9. Emotional care in palliative medicine:
1.9.1 Background:
 Providing emotional and spiritual support to patients and their families
suffering from incurable, life-limiting illnesses is a difficult challenge.
 Assessment starts with detailed history from the patient, family, and
friends regarding the social, psychological status of the patients and
their families. Involvement of multidisciplinary team: Social worker,
Spiritual educator, Psychologist.
 Advanced communication skills are necessary at each step of the
Assessment, management, and follow-up after providing emotional
care.
 Listen to them
 Be ready to share their upsetting thoughts and feelings
 Ask what might make things easier
 Suggest some enjoyable activities
 Encourage them to be involved in day-to-day things such as news
and social activities.
1.9.2 Maladaptive Patient coping:
Patient at high risk of poor coping: Lack of support from at least one
loved person, previous unresolved loss, history of multiple losses, history
of unsuccessfully handled stressful events in the past, history of mental
illness, express severe emotional reaction, poor communication or bad
relationships with family.
1.9.3 Strategies to help patients cope:
 Help the patient to express emotions
 Facilitate empowerment by providing information that he needs
 Encourage the patient to find their own coping way
 Support each own patient strategies for empowerment
 help maintain or strengthen relationships with significant others
 encourage patient to adopt a tutoring role when previous roles cannot
be maintained Adaptive coping results in enhanced functional,
emotional, spiritual wellbeing in spite of progressive illness.
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1.9.4 Communicating with families at the time of death:

 Allow for silence
 Encourage the family to express their feeling
 Give family time alone with the deceased
 Offer support to the family and ask if they need help
 Help them to make their requests regarding the treatment of the body
after death
Chapter 2: COMMON GERIATRICS
PROBLEM
2.1. Delirium:
2.1.1 Definition:
Delirium is a condition characterized by an acute, fluctuating syndrome
of altered attention, cognition, and awareness, which is precipitated by
an underlying condition or event in a vulnerable patient.
2.1.2 Types of delirium:
There are three delirium subtypes: hypoactive, hyperactive, and mixed
2.1.3 History:
past medical history, medications, recent falls, recent surgery, recent
febrile illness, history of organ failure, history of alcoholism or drug
abuse, recent depression
2.1.4 Examination:
 Vital signs, the state of hydration, skin condition, and potential
infectious foci.
 Assessment of visual fields and specific cranial nerve and motor
deficits are essential to identify individuals with a higher likelihood of
focal neurologic disease
 Assess cognition objectively using the mini-mental status examination
(MMSE) or the confusion assessment method (CAM)
2.1.5 Invstigation :
All patients presenting with delirium require a basic workup including:
 complete blood count
 measurement of electrolyte levels
 urinalysis
 renal and liver panel
 ECG
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Further evaluation should be individualized based on the patient’s chief

concern, current illness, medical history, and physical examination
findings
Table 2.1 Evaluation of medical conditions that may lead to delirium
Signs and Symptoms Evaluation
Cardiovascular: chest pain, ECG, troponin and myoglobin
shortness of breath, diaphoresis levels, d-dimer test
Endocrine: temperature TSH and serum glucose levels,
intolerance, unintentional weight measurement of serum cortisol
gain/loss, anxiety/depression, level or ACTH stimulation test
unexplained diaphoresis,
dysphagia, palpitations, signs,
and symptoms of hypo- or
hyperglycemia
Environmental exposure: Measurement of patient’s core
shivering, hypo- or hypertension, temperature
brady- or tachycardia,
vasoconstriction, low or high
respiratory rate.
Gastrointestinal: abdominal Liver function tests, measurement
distention, abdominal pain, of lipase and ammonia
history of cirrhosis
Infection suspected Blood cultures, CBC, chest X-ray,
CT, LP, UA and Urine C/S, skin
examination
Malnutrition, social isolation Vitamin B12, folate, albumin, and
prealbumin levels
Neurologic: focal neurologic Neurologic examination, CT of the
deficits, seizure head, EEG
Pain, recent trauma, or surgery Pain assessment scale
Pharmacologic: addition or Medication reconciliation
change to medication regimen,
patient, or caregiver unable to
convey medication administration
details
Renal: history suggestive of Serum chemistries, blood urea
impaired kidney function or nitrogen/creatinine ratio
electrolyte disturbance
Respiratory distress, hypoxia Pulse oximetry, ABG
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Rheumatologic: fatigue, ESR and CRP level

intermittent fevers, myalgias,
arthralgia
Substance abuse, suicide, empty Review of social history and
pill bottles found at home occupational or other exposures,
urine drug screen, salicylate,
measurement of serum alcohol, and
acetaminophen levels
Volume depletion (dehydration or CBC, urine-specific gravity test,
blood loss): fatigue, light- serum osmolarity measurement,
headedness, falls, syncope, BUN/creatinine ratio
pallor, melena/hematochezia,
decreased intake, diarrhea,
nausea/vomiting, decreased skin
turgor, dry mucous membranes,
orthostasis, tachycardia
2.1.6 Diagnosis and screening:
4RT tool is a short and validated tool that can be used in screening
Table 2.2 DSM-5 delirium diagnostic criteria
A A disturbance in attention (i.e., reduced ability to direct, focus,
sustain, and shift attention) and awareness (reduced orientation to
the environment).
B The disturbance develops over a short period of time (usually hours
to a few days), represents a change from baseline attention and
awareness, and tends to fluctuate in severity during the course of a
day.
C An additional disturbance in cognition (e.g., memory deficit,
disorientation, language, visuospatial ability, or perception).
D The disturbances in Criteria A and C are not explained by another
pre-existing, established, or evolving neurocognitive disorder and do
not occur in the context of a severely reduced level of arousal, such
as a coma.
E There is evidence from the history, physical examination, or
laboratory findings that the disturbance is a direct physiological
consequence of another medical condition, substance intoxication or
withdrawal (i.e., due to a drug of abuse or to a medication), or
exposure to a toxin, or is due to multiple etiologies.
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2.1.7 Prevention:
Non-pharmacologic prevention strategies consist of:
 Orientation and therapeutic activities
 Early and recurrent mobilization
 Minimizing the use of psychoactive drugs
 Encourage normal sleep-wake cycles.
 Allowing easy access to adaptive equipment for sensory impairment
(e.g., hearing aids and glasses)
 Preventing dehydration
 Treatment in various settings
2.1.8 Management:
Once delirium is diagnosed, it is crucial to identify and treat the
underlying causes. After the causative factors are managed:
Non-pharmacologic:
 Treat Cognitive impairments or disorientation
 Dehydration/constipation
 Hypoxia
 Immobility or limited mobility
 Infection
 Pain
 Poor nutrition
 Sensory impairment
 Sleep
Pharmacological management:
Table 2.3 Pharmacologic management of delirium
Drug Class Dose / route Common ADRs
Haloperidol First-generation 0.25 mg–0.5 Hypotension,
antipsychotic mg po or IM constipation,
twice daily xerostomia,
as needed akathisia,
extrapyramidal
disease (frequent),
somnolence, blurred
vision
Quetiapie Second- 25 mg once Orthostatic
generation daily titrated hypotension,
antipsychotic up to 50 mg constipation,
Q12h as xerostomia
needed increased liver
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enzymes, asthenia,
dizziness
extrapyramidal
disease headache,
somnolence, fatigue
Risperidone Second- 0.25–0.5 mg Constipation,
generation po Q4h PRN akathisia,
antipsychotic somnolence, blurred
vision, anxiety,
nausea
Olanzapine Second- 2.5–5 mg Orthostatic
generation po or IM hypotension,
antipsychotic Q12h constipation,
PRN xerostomia,
akathisia,
asthenia,
dizziness,
somnolence,
tremor
2.1.9 Urgent evaluation:
Medical events
 Systolic BP< 90 mm Hg, heart rate < 50 beat/min or > 120 beat/ min,
respirations > 30 breath/ min, temperature < 96°F (36°C) or > 101°F
(38°C)
 New-onset focal deficits
 New-onset respiratory distress, with increasing hypoxia and dyspnea
 Signs indicating a serious underlying condition causing delirium (e.g.,
chest pain, stroke, haematuria)
Psychiatric or behavioral events
 Escalating physically aggressive behavior or threats of violence
 Persistent danger to self or others
2.2. Elder Abuse:
2.2.1 Definition:
Intentional actions that cause harm or create a serious risk of harm (even
if no harm is intended) to a vulnerable elder by a caregiver or other
person who stands in a trusted relationship with the elder that include
Physical, Emotional or psychological abuse, Financial or material
exploitation, Neglect or abandonment and Sexual abuse
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2.2.2 Screening:
There are no clear guidelines regarding routine screening of abuse in
older adults. However, physicians may be faced with situations that raise
suspicion of abuse. In these situations, the Elder Abuse Suspicion Index
(EASI) is a useful tool.
2.2.3 Approach:
It is important to conduct a comprehensive history and physical
assessment of functional and cognitive assessment with special attention
to warning signs.
2.2.4 History:
 Medication history: asking who manages the medication, medication
adherents, use of anticoagulants
 Full history of injuries
 Family history of the caregiver (abuser): history of mental illness, drug
or alcohol abuse, employment of the abuser
 Social history: functional status (ADLs and IDALs), relation with a
caregiver, living situation
2.2.5 Examination:
 Once the abuse is suspected, a full head-to-toe exam is required
2.2.6 Laboratory studies:
 CBC
 Renal function and electrolytes
 Urinalysis
 Serum levels of relevant medications
 Urine drug screen
 Ethanol level
2.2.7 Imaging studies:
 X-rays of relevant body parts used to detect fractures
 CT head can be used to detect intracranial bleeding
2.2.8 Treatment:
 An essential step is reporting the abuse, even if it is only suspected
and not yet proven.
 Correct the acute presenting problem or injury.
 Address the social and psychological components of elder abuse.
 If the patient is in immediate danger, it is vital to protect the patient by
multidisciplinary team.
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2.2.9 Consultations / Referral:

 Psychiatry consultation.
 Geriatrics or internal medicine consultation.
 Neurology or neurosurgical consultation.
 Orthopedics consultation.
 Social services.
2.2.10 Prevention:
 Listen to the elderly and caregivers to understand challenges and
provide support.
 Report suspected abuse to adult protective services.
 Recognize and learn how signs of abuse differ from the normal aging
process.
 Check-in elderly with few friends or family member support.
 Provide over-burdened caregiver support.
2.3. Tremor:
2.3.1 Definition:
Tremor is a rhythmic, oscillatory involuntary movement of a body part.
The most common tremors seen in primary care are enhanced
physiologic tremor, essential tremor ( most common pathologic tremor) ,
and parkinsonian tremor, all of which are more common in older age.
2.3.2 Types:
According to movement:
Table 2.4 Broad classification of tremo
Tremor type Description
Resting (less  Seen in a body part that is completely supported
common) against gravity and is relaxed.
 Enhanced by mental stress or movement of
another body part.
 Diminished by voluntary movement.
 Parkinsonism is the most common cause.
Action (more  Occurs when a muscle is voluntarily contracted.
common)  Includes postural, isometric, and kinetic tremors.
Postural  Occurs when a body part is kept against gravity
voluntarily.
 It includes essential, physiologic, cerebellar,
dystonic, and drug-induced tremors.
Isometric  Occurs when muscle contracts against a rigid
stationary object. (e.g., when making a fist)
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Kinetic  Occurs with any kind of voluntary movement

(target-directed movement).
 Includes classic cerebellar, dystonic, and drug-
induced tremors.
Intention  As the target is approached, this subtype of
kinetic tremor is intensified.
 It implies that the cerebellum or its pathways are
disrupted.
According to conditions:
Table 2.5 Features of common tremor syndromes
Tremor
conditio Diagnostic
n Clinical features tests Management
Cerebell Intention tremor, Head CT or MRI Treat underlying
ar ipsilateral involvement cause, deep
tremor to lesion, imbalance, brain stimulation
abnormal finger-to-
nose and heel-to-shin
tests
Enhance Postural tremor of low History of Treat underlying
d amplitude, a side caffeine use or cause,
physiolo effect of exacerbating anxiety, glucose reassurance
gic medication (in case of
tremor hypoglycemia),
TSH, LFT
Essentia Postural tremor, No specific test, Propranolol,
l tremor symmetric, involving CBC, TFT, primidone,
the head, serum chemistry surgery
hands/wrists, lower profile may rule
extremities, or voice, out other
positive family history, diseases.
improvement with
small amount of
alcohol intake
Parkinso Resting tremor, No specific test, Dopamine
nian asymmetric, involves PET or single- agonists,
tremor distal extremities, photon emission anticholinergics,
decreases with CT for atypical surgery, deep
voluntary movement, presentation brain stimulation
postural instability,
bradykinesia and
rigidity
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Psychog Abrupt onset, Careful history Mental health

enic spontaneous counseling
tremor remission changing
tremor characteristics,
extinction with
distraction
Drug- careful attention paid Example: trial
induced to any medications Amiodarone, discontinuation
tremors taken prior to the Hypoglycemic of that
onset of the tremor agents, medication
Atorvastatin, should be
Metoclopramide, attempted if
Thyroid clinically
hormones, etc possible
Metaboli symptoms and Ammonia level Treat underlying
c- causes of metabolic Calcium level cause.
induced tremor varies Blood glucose
tremors Sodium level
Mg + level
TSH
Parathyroid
Vitamin B12
level
Wilson autosomal recessive serum Chelation
disease and life-threatening ceruloplasmin therapy
disorder level and 24-
Usually those affected hour urinary
are 5 to 40 years of copper excretion
age
2.3.3 Approach:
History:
 onset of symptoms. Keep track of how the symptoms develop.
 Behavioral changes, difficulties with behaviors like eating or getting
out of chairs, or personality changes.
 Family history of similar symptoms.
 medical history, medication and over-the-counter drugs (OTC).
 Look into drug abuse and herbicide or pesticide exposure, particularly
in patients under 55 years old.
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Examination:
Check temperature, pulse, respiratory rate, blood pressure, and weight:
Orthostatic hypotension should be noted.
Inspect
 Look at the overall appearance.
 Observe any tremor at rest.
 Look for subtle facial masking, frequency and amplitude of eye blinks.
 Changes in stance or gait: Festination, or shuffling, progressively
small steps, turning difficulty; freezing, or inability to move.
Palpate
 Check for increased tone in resting muscles by palpating the
extremities.
Neurologic examination
 Examine all the cranial nerves. Examine the deep tendon reflexes
(DTRs).
 Evaluate alternating fast gestures. Rapid alternating motions.
 Examine the cogwheel effect, Best tested in wrists.
 Perform mental status examination.
2.4. Parkinson's Disease:
2.4.1 Definition:
Neuro-degenerative disease that causes severe morbidity and mortality.
Degeneration of dopaminergic neurons in the substantia nigra leads to
the formation of Lewy bodies in the remaining dopaminergic neurons.
2.4.2 Sign and symptoms:
 History of bradykinesia and rigidity, Difficulty turning over in bed,
Difficulty opening jars, Difficulty rising from a chair.
 Poor heel-to-toe gait, History of shuffling gait, Loss of balance
 Rigidity as a sign.
 History of tremor Distal resting tremor as a sign.
 History of micrographia
2.4.3 Diagnosis:
The appearance of the cardinal features of bradykinesia, rigidity, tremor,
and postural instability, along with the development of symptoms and
sustained response to levodopa therapy, are used to diagnose
Parkinson’s disease.
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Table 2.6 Diagnosis of Parkinson’s disease

Relative Inclusion Criteria Supportive of Relative Exclusion
Criteria the Diagnosis Criteria
•Bradykinesia •Gradually progressive •Focal brain lesions
•Rigidity course within the basal ganglia
•Rest tremor •Good response to •Recent history of
•Asymmetric onset dopaminergic therapies neuroleptic medication
(++) (++) use
•Motor fluctuations •Severe dysautonomia
(+++) unrelated to
•Dyskinesias (+++) medications
•Motor symptom •Supranuclear gaze
duration > 5 years palsy
Prominent postural
instability at initial
presentation (–)
•Prominent cerebellar
atrophy on MRI (–)
Freezing of gait
developing within 3 y of
motor symptom onset
(–)
2.4.4 Imaging Modality:
MRI : to differentiate Parkinson’s disease (PD) from multi-system atrophy
Single-photon emission CT : to differentiate Parkinson’s disease from
essential tremor
2.4.5 Secondary Parkinsonism:
disorders that are similar to Parkinson’s disease but have different
causes
 Medication (drug-induced parkinsonism or pseudoparkinsonism)
 Metabolic disorders
 Toxins
 Cerebrovascular disease (vascular Parkinsonism)
 CNS infections
2.4.6 Management:
Management of motor symptoms
 Early medical therapy
Referral to a neurologist to start and adjust medications as soon as a
patient develops functional impairment
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 Carbidopa/levodopa:Immediate and sustained-release

carbidopa/levodopa
 Dopamine agonists:
o Nonergot: Pramipexole, Ropinirole
o Ergot: Bromocriptine, Pergolide
o Monoamine oxidase-B inhibitors : Selegiline, Rasagiline
o Catechol O-methyltransferase inhibitors : Entacapone, Tolcapone
o Injectable dopamine agonist : Apomorphine
o N-methyl-D-aspartate receptor inhibitor : Amantadine
o Anticholinergics : Benztropine, Trihexyphenidyl
 Late medical therapy
As Parkinson’s disease progresses, initial therapy becomes less
successful, and additional motor complications, such as dyskinesias and
motor fluctuations, emerge,
 Surgery
When disabling symptoms develop despite optimal medical therapy,
deep brain stimulation, targeting either the subthalamic nucleus or the
globus pallidus interna.
 Physical, occupational, and speech therapy.
Management of nonmotor symptoms
Fatigue and sleep disturbance: Methylphenidate may improve fatigue in
patients with Parkinson’s disease, but melatonin is not effective. Educate
and encourage patients about good sleep hygiene, as excessive daytime
sleepiness is quite common in patients with Parkinson’s disease.
2.4.7 Psychiatric disorders:
Tricyclic antidepressants are not recommended as they can cause
anticholinergic adverse effects and should not be used in patients with
cognitive impairment. Other antidepressant, risks and benefits should be
calculated.
Clozapine is effective in managing psychosis, manifested by visual or
auditory hallucinations and delusions.
2.4.8 Dementia:
Always evaluate patients for other causes of dementia and consider
discontinuing anticholinergic or dopaminergic medications that may
contribute to cognitive impairment.
 Rivastigmine : improve in cognitive, clinical, and activities of daily
living but adversely caused increased tremor and vomiting
 Donepezil: increase cognitive function
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2.5. Polypharmacy:
Regular use of at least five medications increases the risk of adverse
medical outcomes. A study found that the prevalence in the elderly
ranges from 50–90%.
 The most common medications associated with polypharmacy and
adverse outcomes are:
 Cardiovascular drugs,
 Diuretics,
 NSAIDs,
 Antidiabetics,
 Second-generation antipsychotics,
 Anticoagulants,
 Antiplatelet agents.
Principles of prescribing for older adults
 Non-pharmacologic approaches should always be considered first.
 Consider the patient's life expectancy and the time required to
achieve therapeutic benefit.
 Consider whether the benefits outweigh the risks of the medication.
 Consider whether one medication can be used to treat multiple
conditions.
 Consider whether medication is being used to treat adverse events of
another medication.
 Determine if the patient can comply with necessary monitoring (blood
tests for anticoagulants, diabetes, anticonvulsant medications, etc.).
 Educate the patient and caregiver about the medication, dose,
frequency, duration, side effects, compliance, and monitoring needed.
Approach to deprescribing
A process of tapering, discontinuing, or withdrawing medications to
improve outcomes and treat polypharmacy:
 Count all medications and the indication for each medication.
 Consider the harm of each medication to determine the priority of
deprescribing.
 Assess each drug’s expected benefit and possible burden or harm.
 Prioritize drugs for discontinuation with the lowest benefit-harm ratio
and the lowest likelihood of adverse withdrawal reactions or disease
rebound syndromes.
 Implement a discontinuation plan and monitor the patient closely for
withdrawal symptoms or loss of medication benefits.
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Choosing Wisely® pharmacotherapy recommendations

Choosing Wisely is an initiative to advance a national dialogue on
avoiding unnecessary medical treatments and procedures. One of the
recommendations of this initiative for the geriatric population is to only
prescribe medication after conducting a drug regimen review.
Resources to help primary care physicians prevent
polypharmacy.
 Medstopper.com https://medstopper.com
o It helps determine the best way to taper off the medication over a
period. It also gives information on stop priority, taper approach,
expected harm, and possible withdrawal symptoms.
 Epocrates or Lexicomp website phone application
https://www.epocrates.com, www.online.lexi.com
o It gives accurate dosing based on the GFR, liver function, and
each indication. Also, it lists medication contraindications and
expected adverse events. Moreover, it has drug-drug and drug-
food interaction checkers.
2.6. Major Depressive Disorder in Older Adults:
Depression in older adults is often overlooked and/or undertreated.
Depression has a severe impact on the quality of life. Most older adults
with depression initially presented to primary care with somatic
complaints. Depression can present atypically with cognitive, functional,
or sleep problems and complaints of fatigue or low energy. A
retrospective study found a 70% increase in developing dementia among
older subjects with depression.
2.6.1 Physical examination, Screening, and Diagnosis:
Depression in older adults is a clinical diagnosis.
 Mental Status Examination (MSE) is an excellent way that provides
essential information for diagnosis: Appearance, Motor, Speech,
Affect, thought content, Thought process, Perception, Intellect, and
Insight.
 The initial two questions (PHQ-2) have high sensitivity and specificity
and are considered appropriate for community-based setting use:
 Over the past two weeks, did the patient had
o Little interest or pleasure in doing things?
o Feeling down, depressed, or hopeless?
 PHQ-2 score ranges from 0–6. A score of 3 is considered the cut-off
for positive depression screening.
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 Diagnosis of major depressive disorder should be made based on

DSM-5 diagnostic criteria, which are outlined below:
At least 5 of the following symptoms must have been present for two
weeks (and at least 1 of the symptoms must be diminished
interest/pleasure or depressed mood):
 Depressed mood
 Diminished interest or loss of pleasure in almost all activities
 Significant weight change or appetite disturbance
 Sleep disturbance
 Psychomotor agitation or retardation
 Fatigue or loss of energy
 Feelings of worthlessness
 Diminished ability to think or concentrate; indecisiveness.
 Recurrent thoughts of death, recurrent suicidal ideation without a
specific plan, or a suicide attempt or specific suicide plan.
2.6.2 Management:
Pharmacological and psychotherapy are considered first-line treatments.
Selective serotonin reuptake inhibitors (SSRIs) are considered the first
line for treating depressive disorders. Side effects of antidepressants are
one of the main reasons for discontinuing the treatment and should be
regarded as in antidepressants medications selection. The resolution of
depressive symptoms takes longer in the geriatric age group. The
duration of therapy is usually 6–12 months. Relapse is more common
among older adults than younger adults, which might warrant a longer
period of treatment and symptom monitoring after discontinuation of
therapy. Psychotherapy should be utilized when available. Cognitive-
behavioral therapy (CBT) is the most studied and used among all types
of psychotherapy. CBT can be more effective when the depression is
minor or refractory. Combining both psychotherapy and treatment is
superior to psychotherapy or treatment alone.
2.7. Falls in the Elderly:
Is coming to rest inadvertently on the ground or at a lower level. Fall and
fall-related consequences are considered one of the major reasons for
morbidity and mortality in the elderly internationally. A study estimated
the prevalence of falls to be 31.6% among the Saudi elderly. Advanced
age, age-related changes, polypharmacy, and other environmental
causes were listed as risk factors for falling in the elderly.
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2.7.1 Age-related changes that increase the risk of falls:

 Visual changes and reduced ability to discriminate edges (e.g., stairs)
 Sensory deficits like the reduced peripheral sensation
 Slower reaction times
 Muscle weakness
2.7.2 Screening:
US Preventive Services Task Force (USPSTF):
 Recommends exercise interventions to prevent falls in community‐
dwelling adults 65 years or older at increased risk.
 Recommends against vitamin D supplementation to prevent falls in
community-dwelling adults 65 years or older.
2.7.3 Risk factors:
Non-modifiable:
Advanced age, Female gender, Personal history of falling and/or
fractures, Cognitive impairment/dementia, History of stroke/transient
ischemic attacks, history of arthritis, or Recent hospital discharge (within
one month).
Modifiable:
Cardiac diseases (e.g., arrhythmias), Environmental hazards (poor
lighting, lack of appropriate railings, elevated seats, loose carpet, low-
lying objects, pets), Medication use (polypharmacy: taking four or more
medications), Metabolic (e.g., diabetes, low BMI), Musculoskeletal
(balance impairment, gait impairment, foot problems), Neurological
disorders (cerebrovascular, Parkinson’s disease), Psychological
disorders or Sensory impairment (e.g., visual impairment).
2.7.4 Complications of falls:
 Medical consequences (Fractures etc.)
 Psychological issues (Fear of further falling (3 F syndrome)).
 Social problems (Dependence).
 Immobilization can lead to
o Loss of muscle tone and strength.
o Increase the risk of thromboembolic events (DVT/PE).
2.7.5 Assessment:
 History of any acute compliant or acute illness.
 Circumstances of fall.
 Fall history.
 Medical history.
 Surgical history/history of fracture.
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 Family history.
 Medication history (Neuroleptics, Benzodiazepines, Vasodilators,
etc.).
 Social and functional history.
 General appearance.
 Assess for any injuries.
 Vital signs (blood pressure sitting and standing to rule out postural
hypotension, pulse).
 Cognitive Screening (three-item recall at 3 minutes).
 Visual acuity testing using the Snellen chart.
 Cardiovascular examination (heart rate and rhythm).
 Neurological examination (gait, muscle strength, balance, reflexes,
focal deficits, neuropathy, tremor, rigidity).
 Foot and footwear examination.
 Particular test to assess the risk of falls among the elderly–The Timed
Up and Go (TUG) test: If the patient needs ≥ 12 seconds to complete
the TUG test, this is associated with an increased risk of falls in older
people
2.7.7 Management:
Multifactorial assessments and interventions are appropriate in the
elderly based on their individualized risk. Patients with no gait, strength,
or balance problems and no history of falls or fall-related injuries are
considered moderate risk. Patients with a history of two or more falls or
at least one fall-related injury are considered high risk.
 Moderate‐ risk patients should receive the following:
o Medication review.
o Referral for physical therapy.
o Vitamin D should be prescribed if there is a deficiency.
 High-risk patients should receive the following:
o Medication review.
o Exercise program with muscle strengthening and gait/balance
training.
o Vitamin D supplementation 800 IU +/- calcium.
 Home environment modification
 Management of medical problems
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2.7.8 Red flags:

Require further assessment and specialist referral.
 Abnormal gait and balance
 Possible loss of consciousness to rule out cerebrovascular and
cardiovascular causes
 Dizziness as a precipitating factor
 When medical conditions contributing to the falls could be optimized
(postural hypotension, Parkinson’s disease)
 Recurrent unexplained falls in patients with normal gait and balance
2.8. Urinary Incontinence (UI):
Any involuntary leakage of urine. It is not a typical result of aging; it is a
pathological condition that may lead to a significant impact on the elderly
and includes:
 Financial burden
 Decreased quality of life (QOL)
 Increased anxiety and depression among the elderly and their
caregivers
 Increased urinary tract and skin infections
 Increased risk for falls and non-spine, non-traumatic fractures in older
women
A study estimated the prevalence of UI to be 41.7%. Aging, hypertension,
and high parity were UI's most common high-risk factors.
Regular physiological changes in the urinary tract associated
with aging
 Shortening of the urethra.
 Atrophy of the vagina and urothelium due to estrogenic deficiency.
 Reduced bladder sensation.
 Reduced detrusor muscle function and urethral closure.
 Increased residual bladder volume.
2.8.1 Assessment:
 Analysis of the chief complaint (onset, duration, and nature of urinary
symptoms)
 Associated symptoms: frequency, nocturia, weak urine stream,
urinary dribbling, incomplete emptying of the bladder to rule out
urinary tract infections, and prostatic enlargement (in men)
 Medical history.
 Surgical history
 Obstetrics/Gynaecological history
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 Family history.
 Medication history (Neuroleptics, Benzodiazepines, Vasodilators,
etc.).
 Social and functional history.
 Fluid intake (3-day voiding diary) to differentiate between urge and
stress UI by measuring the amount of fluid intake and the volume of
voided urine in both continent and incontinent situations (using a
measuring cup). Loss of a large amount of urine is consistent with
urge UI, while leakage of a small amount of urine may indicate stress
UI.
In addition to general examinations to rule out the organic cause;
 Cough stress test:
o Excellent reliability, sensitivity, and specificity for identifying
stress UI
o The patient’s bladder should have at least 200–300 mL of urine
or be at symptomatic fullness
o Immediate leakage is consistent with stress UI
 Cotton swab test:
o Performed to evaluate for urethral hypermobility (usually done by
an expert physician)
o A change in cotton swab angle more than 30 degrees from the
resting position is considered positive, indicating urethral
hypermobility.
 Measurement of post-void residual volume (PVR)
o Normal PVR < 50 ml, borderline if PVR 100-200 ml and needs to
be repeated, suggestive for overflow if PVR >200 ml.
Laboratory tests and imaging
 Urinalysis to rule out diabetes or infection
 Fasting blood sugar and HbA1C if you suspect diabetes
 Renal function test (if there is a concern for obstruction)
 Other than ultrasound to assess post-void residual, routine imaging
should not be performed in the initial assessment of uncomplicated
UI.
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2.8.4 Management:
Stepwise approach:
 Conservative management
o Appropriate fluid intake
o Timed voiding (voiding at regular intervals)
o Reduction of caffeinated and carbonated beverages
o Smoking cessation
o Regular moderate physical activity
o Weight loss if the patient is overweight or obese
o Avoid aggressive fluid restriction
o Medication adjustment
o Pelvic floor muscle exercise such as Kegel exercise, especially in
stress UI
o Continue the regimen for at least 15 to 20 weeks
 Physical devices and medications
 Surgical interventions
2.8.5 Red Flags:
Should prompt referral
 Complicated UI including pain, persistent haematuria, or proteinuria,
pelvic organ prolapses
 Previous pelvic surgery or radiation
 Suspected fistula
 Elevated post-void residual (> 200 ml)
 Stress UI when there is no improvement in behavioral modifications
after 6-8 weeks or severe symptoms
 Uncertain diagnosis
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Chapter 3: DEMENTIA &

ALZHEIMER’S DISEASE
3.1. Dementia:
3.1.1 Definition:
Dementia (or major neurodegenerative disorder in DSM-5) is a disorder
that is characterized by a Significant progressive decline in cognition
affecting one or more cognitive domains (learning and memory,
language, executive function, complex attention, perceptual-motor, social
cognition). This deficit must represent a decline from the previous level of
function and be severe enough to interfere with daily function and
independence. Other medical and psychiatric conditions, including
delirium, have been excluded.
Mild cognitive impairment (MCI) is defined as an intermediate clinical
state lying between normal cognition and dementia. Overall function
(ADLs) is not impaired in MCI compared to dementia. MCI can progress
to dementia at a rate of 10–15% per year.
3.1.2 Common causes of dementia:
 Alzheimer disease-AD (60-70%):
o Most common age-related neurodegenerative disease.
o Incidence doubles every five years beyond the age of 60.
o Short-term memory impairment is early and prominent in most
cases.
o Variable deficits of executive function, visuospatial function, and
language.
 Vascular dementia (10-20%):
o A progressive accumulation of cognitive deficits in association
with repeated strokes.
o Symptoms depend on the localization of strokes.
 Dementia with Lewy bodies
o Cognitive dysfunction, with prominent visuospatial and executive
deficits.
o Psychiatric disturbance, with anxiety, visual hallucinations, and
fluctuating delirium.
o Parkinsonian motor deficits with/or after other features.
 Parkinson’s disease with dementia
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 Frontotemporal dementia (FTD):

o Peak incidence in the sixth decade.
o Familial cases result from mutations in genes for tau,
progranulin, or others.
o Behavioral variant FTD: Deficits in empathy, social comportment,
insight, abstract thought, and executive function. Behavior is
disinhibited, impulsive, and ritualistic, with prominent apathy.
o Semantic variant primary progressive aphasia: Deficits in word-
finding, single-word comprehension, object and category
knowledge, and face recognition
o Non-fluent/agrammatic variant primary progressive aphasia:
Speech is effortful with dysarthria, phonemic errors, sound
distortions, and poor grammar
 Mixed pathology is common, e.g., Alzheimer’s with vascular dementia
 About 10-20% of cases of cognitive impairment are due to potentially
reversible causes, such as thyroid disease, drug toxicity, subdural
hematoma, normal pressure hydrocephalus, vitamin B12, folate, and
thiamine deficiency.
3.2. Approach to diagnosis of dementia:
3.2.1 History:
 Changes in cognition, personality, language skills, and behavior
 Any changes in activities of daily living (eating, bathing, dressing,
toileting, transferring, and continence) or instrumental activities of
daily living
 Family history
 Drug and alcohol use
 Past medical history of systemic illness
 Risk factors for stroke (previous history of stroke, transient ischaemic
attacks, hypertension, coronary artery disease, and atrial fibrillation)
 History of Parkinson’s disease
3.2.2 Brief Initial Screening Tests for Cognitive
Impairment:
 To assess the need for further evaluation, brief screening tests are
useful such as Mini-Mental State Examination (MMSE), Mini-Cog,
Ascertain Dementia 8-Item, Montreal Cognitive Assessment (MoCA),
and Saint Louis University Mental Status Examination
 The Ascertain Dementia 8-Item Informant Questionnaire is a quick,
sensitive, and validated screening tool.
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 Guidelines advocate combining the Mini-Cog with The Ascertain

Dementia 8-Item Informant Questionnaire.
 Dementia severity can be categorized by MMSE, MoCA, or clinical
dementia rating (CDR) scores as mild, moderate or severe dementia.
 Patients with confirmed cognitive impairment should be screened for
depression. They should have laboratory tests to rule out other
common disorders that can cause cognitive impairment and should
undergo imaging of the brain.
 Routine cerebrospinal fluid (CSF) analysis and genetic testing are not
recommended, but these tests may be appropriate in some patients.
3.2.3 Investigation and Evaluation:
 CBC, TSH, Vitamin B12 level
 Comprehensive chemistry panel including renal function and liver
function tests
 Lumipulse G β-Amyloid ratio 1-42/1-40 (Fujirebio Diagnostics) test
 Neuroimaging is indicated in patients with acute onset of cognitive
impairment or dementia. CT brain is generally sufficient, but MRI
provides much more information.
 Genetic testing should be considered in patients with multiple family
members with Alzheimer’s disease diagnosed at a young age.
 Non-pharmacologic therapy for cognitive, functional symptoms, and
behavioral disturbance includes the following:
o Enjoyable leisure activities
o Mental stimulation programs (e.g., puzzles, gardening, word
games, baking)
o Occupational therapy training in coping strategies and cognitive
aids
o Structured physical exercise programs
o For behavioural disturbance, it is more effective than
pharmacologic and should be tried first. Provide education and
support for caregivers and avoid environmental triggers,
physiological triggers and communication triggers.
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 Pharmacotherapy for cognitive, functional symptoms, and behavioural

disturbance includes the following:
o Unfortunately, there are no curative therapies for Alzheimer’s
disease and other common aetiologies of dementia. The goal of
currently available pharmacologic therapies is to delay the
progression of symptoms of neurocognitive and physical decline
o Consider a trial of cholinesterase inhibitors (such as Donepezil,
Galantamine, Rivastigmine) for mild-to-moderate AD
o Consider a trial of memantine (N-methyl-D-aspartate receptor
antagonist) for moderate-to-severe AD
o Aducanumab (new medication) is an Anti-amyloid monoclonal
antibody given IV infusion
o For behavioural disturbance, it includes treatment of depression,
psychosis, aggressive behaviour or sleep disturbance
o For Depression, use Antidepressants.
o For Psychosis, anger, and physical aggression, use low dose for
short term of antipsychotic e.g., Aripiprazole, haloperidol,
o For Manic like behavior, use Mood stabilizers e.g., Depakote.
o For Disturbance of sleep cycle, use Melatonin, Mirtazapine,
Trazodone
o For Dangerous and aggressive sexual behavior, use
Antidepressants e.g., sertraline, or Antiandrogens e.g., oral
progesterone.
3.2.5 Prognosis of dementia:
AD progresses inexorably. Some studies have found that patients
decline 3 to 3.5 points on average on the MMSE each year, with a
minority (<10 percent) having a more rapid decline of 5 to 6 points on
annual MMSE. After a diagnosis of AD, the average life expectancy has
been reported to range between 8 and 10 years but may range from 3 to
20 years. This depends heavily on how impaired the person was when
they were diagnosed.
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Section 7: Dermatology
Chapter 1: PRIMARY VS SECONDARY
SKIN LESIONS
1.1. Primary Skin Lesions
1.1.1 Macules
skin discoloration less than 1 cm
Macule more than 1 cm is a patch
1.1.2 Papules
Circumscribed solid elevation of skin less than 0.5cm in diameter
1.1.3 Nodules
Circumscribed solid elevation more than 0.5 cm in diameter
1.1.4 Plaques
Raised surface of skin with change in skin texture or consistency
1.1.5 Vesicles
Elevation of skin containing fluid less than 0.5 cm
1.1.6 Bullae
Elevation of skin containing fluid more than 0.5 cm
1.1.7 Comedones
Closed comedones = whitehead which is yellowish papule
Open comedones = blackhead
1.1.8 Hives
Primary lesion of urticaria
Edematous elevation of the skin of variable size
Itching is usually present
1.2. Secondary Skin Lesions
1.2.1 Pustules
Papules filled with pus
1.2.2 Scales
Dry greasy laminated keratin seen on the surface of primary lesions
papules, plaques
1.2.3 Crust
Dry material on skin such as serum, pus or blood
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1.2.4 Erosions
Partial or total loss of epidermis not reaching to the dermis so heal
without a scar
1.2.5 Scars
Hypertrophy at the place of surgical scar
1.2.6 Fissures
Linea cleft in epidermis extending into dermis
1.2.7 Ulcers
Round or irregularly shaped excoriation than extends into epidermis and
sometimes dermis
1.2.8 Petechiae
Circumscribed deposition of blood less than 0.5cm in diameter
1.2.9 Purpura
Circumscribed deposition of blood greater than 0.5 cm in diameter
1.2.10 Telangiectasias
Superficial dilated capillaries
1.2.11 Cysts
Circumscribed lesion with wall and lumen.
Cavity may have fluid or solid
Chapter 2: SKIN CANCER
2.1.1 Types of Skin Cancer
 Non-melanoma or keratinocytes carcinoma
 Melanoma
Non-melanoma skin cancers are the most common human malignancy
and can be divided into two major subtypes:
Basal Cell Carcinoma (BCC)
Squamous Cell Carcinoma (SCC)
2.1.2 Basal Cell Carcinoma (BCC)
BCC is the most common invasive malignant cutaneous neoplasm of
adults, especially the elderly.
The main risk factor for the development of BCC is ultraviolet light
exposure.
Risk factors
Fair skin, blonde or red hair, light eye color, poor tanning ability, and sun-
damaged skin are at greatest risk.
Types of BCC
It is further characterized based on its appearance into 4 subtypes
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Nodular BCC (Nodular BCC is the most common subtype, most common
on the head, neck, and upper back. )
Infiltrative micronodular BCC
Morpheaform BCC
Superficial BCC
Clinical assessment
It presents with shiny, pearly, white nodules and open, non-healing
ulcers. The traction on the surrounding skin accentuates the pearly
border. The growth pattern is irregular, forming an oval mass whereby
the surface may become multinodular.
Diagnosis
Multiple biopsy techniques or Complete excision may be an appropriate
initial diagnostic procedure.
Treatment:
Mohs micrographic surgery
Electrodesiccation and curettage
cryotherapy
radiotherapy
Topical imiquimod (Aldara)
2.1.3 Squamous Cell Carcinoma (SSC)
second most common skin cancer overall.
This tumor typically is aggressive and with a high risk of metastasis.
Mostly seen in irradiated skin, thermal injury, chronic ulcers, chronic
sinuses.
Risk factors
Common risk factors are
actinic keratosis, cutaneous horn, Bowen’s disease, chemical exposure,
tar and arsenic, leukoplakia lichen sclerosis, site of chronic infection,
ulcers, chronic sinus tracts, and radiation damaged skin.
Clinical assessment
The most common presentation is a firm, smooth, or hyperkeratotic
papule or plaque, that may have central ulceration.
Diagnosis
Mostly clinical, once suspicion arises need to refer for biopsy, mostly
based on surgical pathology.
Treatment
Wide local excision with histological confirmation, electrodesiccation, and
curettage excision. Mohs micrographic surgery has the lowest
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recurrence rate among treatments but is best considered for large, high-
risk tumors or tumors in sensitive anatomic locations.
2.1.4 Melanoma
This is a malignancy arising from melanocytes, which can arise from
mucosal surfaces, the eyes, and leptomeninges. Survival improves with
early melanoma detection. 30% of melanomas develops in pre-existing
nevus and the rest arise de novo. Any suspicious pigmented lesion
should be biopsied to confirm the diagnosis.
Types of Melanomas
 Melanoma in Situ
 Superficial Spreading Melanoma
 Nodular Melanoma
 Lentigo Maligna Melanoma
 Amelanotic Melanoma
 Acral Lentiginous Melanoma
 Subungal Melanoma
Multiple irregular shaped variable-coloured lesions should be suspected
for melanoma.
Important characteristics of melanoma:
Table 2.1 – Important characteristics of melanoma
A Asymmetry One-half of the lesion
does not look like the
remaining half.
B Border irregularity The border is scalloped or
has a focal “pseudopod”
extension into the
surrounding skin.
C Color variegation Lesions can have varying
hues and varying colors.
D Diameter >6 mm The longest axis of the
lesion is measured.
Risk of melanoma:
family or personal history of melanoma, atypical nevus, previous non-
melanoma skin cancer, chronic tanning with UV light, skin exposure.
Diagnosis
Skin biopsy is necessary to confirm melanoma diagnosis. Sentinel lymph
node biopsy is performed for lesions greater than 1 mm in thickness.
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Treatment
Surgical removal is the primary treatment for cutaneous malignant
melanoma.
2.2. Bowen’s Disease
Also called superficial type of SCC in situ. Mostly occurs on the head,
neck, trunk, and arms. Can be present on the genital area as well.
Usually presents as a single lesion on extremities, mostly hands.
Bowen’s disease is usually the result of damage due to chronic sun or
other carcinogenic exposure such as human papillomavirus (HPV).
Prognosis is very good
The clinical presentation early in the disease includes erythematous, dry
skin, scaly plaque, or patch with irregular, sharply demarcated border.
Later the scaly patch can become hyperkeratotic, fissured, crusted or
ulcerated
2.2.2 Diagnosis
Biopsy and histopathology
2.2.3 Treatment
Excisional surgery, electrodesiccation, cryosurgery, 5% imiquimod cream
once daily application for 16 weeks, 5-FU.
2.3. Keratoacanthoma
It is a relatively common skin tumor that occurs in pilosebaceous glands.
Commonly occurs in sun-exposed surfaces of the face and dorsum of
the upper extremities. A distinguishing feature of KA is a clinical course
characterized by rapid initial growth followed by a variable period of
lesion stability and subsequent spontaneous resolution.
2.3.1 Risk Factors
Predisposing factors are UV light or site of previous trauma but can
occur in any area including anal area, chemicals carcinogen, drugs,
HPV.
2.3.2 Clinical Presentation
Presents with solitary, smooth, dome-shaped red papules or nodules
resembling molluscum with central keratin plug. Rapidly increases in size
to 1–2 cm and retains its smooth surface. When untreated, growth
restricts in 6 weeks and slowly regresses in 2-12 months.
2.3.3 Diagnosis
Requires a pathological diagnosis to differentiate from SCC, some
studies classify them as a variant of invasive SCC.
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2.3.4 Treatment
Electrodesiccation and curettage, blunt dissection, topical and
intralesional 5-fluorouracil imiquimod, intralesional methotrexate.
2.3.5 Follow Up for Skin Malignancies
 Screening of patients with new primary skin malignancies should be
performed once every year.
 After more than one diagnosis, the five-year risk probability increases
to 82%.
 Studies found the five-year probability of a subsequent keratinocyte
carcinoma after a first diagnosis was 40.7%
Chapter 3: Hair Disorder
3.1. Hypertrichosis (Too Much Hair)
Hypertrichosis can be congenital (e.g., trisomy 18 and porphyria) or
acquired, and refers to excessive hair growth which may be localized or
universal. There are two causes 1-drugs (e.g., cortisone, penicillamine,
psoralens, phenytoin, diazoxide, minoxidil, cyclosporine, streptomycin),
2- repeated or chronic dermal inflammation (e.g., chronic rubbing,
burns).
3.1.1 Hirsutism (Hair in the Wrong Spot)
 Clinic assessment: Signs of amenorrhea, virilization, and endocrine
problems such as polycystic ovarian syndrome or congenital adrenal
hyperplasia. Morning blood testosterone levels should be measured
in a severe case.
 Treatment: hypertrichosis and hirsutism are directed at the
underlying cause (e.g., ceasing a drug, treating thyroid condition).
Hyperandrogenic hirsutism may also respond to cyproterone acetate
and spironolactone. Symptomatic options include bleaching agents,
depilatory creams, shaving, waxing, and electrolysis.
3.2. Androgenetic Alopecia
 There are 2 types, first male pattern affects the frontotemporal areas
progressing to the vertex and the entire scalp may be bald and the
second female pattern widening occurs of the central part of a
“Christmas tree”.
 Treatment:
o Females: 1st line minoxidil topical. 2nd line spironolactone orally
o Males: finasteride (Propecia®) 1 mg/day over topical minoxidil
5%.
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o Hair transplant.
3.3. Telogen Effluvium (decrease hair in resting stage)
 Clinical Assessment: +ve pulling hair test (painless large amount of
telogen hair).
 Investigations: rule out underlying conditions such as thyroid
disease, iron deficiency, and protein deficiency.
 Treatment: based on identifying underlying causes
3.4. Anagen Effluvium (decrease hair in the growth
stage)
 Treatment: Elimination of the offending agent.
3.5. Alopecia Areata (nonscarring hair loss)
 Clinical assessment: discrete areas of complete hair loss,
exclamation mark, and May be associated with pernicious anemia,
vitiligo, thyroid disease, and Addison’s disease. Has 2 types Alopecia
totalis: complete loss of hair on the scalp and alopecia universalis:
complete loss of scalp hair, eyelashes, eyebrows, and body hair.
 Diagnosis: history and physical examination. Biopsies if you are not
sure.
 Treatment: Topical corticosteroids and intralesional triamcinolone
acetonide (corticosteroids). Immunomodulatory (diphencyprone,
anthralin)
3.6. Cicatricial Alopecia (irreversible scarring hair loss)
 Investigations: biopsy from active legion.
 Testament: Infections: treat the underlying infection. Inflammatory:
topical/intralesional steroids, anti-inflammatory antibiotics, and
antimalarials.
3.7. Trichotillomania (hair-pulling disorder)
 Diagnosis: the affected area is asymmetrical (often to the side of
hand dominance), revealing twisted and fragmented broken hairs of
differing lengths.
3.8. Pediculosis (Lice)
 Clinical Presentation: Either asymptomatic or pruritus. Lice can be
seen with the naked eye.
 Diagnosis: by direct visualization on clinical examination.
 Treatment: Permethrin 1% cream rinse repeated within 7 days.
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3.9. Cradle cap

 Clinical Presentation: first month of life, No pruritus, and thick
greasy scaling and crusting
 Treatment: conservative, soft brush with mineral oil, selenium, and
ketoconazole 2% shampoo.
Chapter 4: NAIL DISORDERS
4.1. Paronychia
4.1.1 Acute Paronychia (less than 6 weeks)
 Clinical assessment: pain, erythema, and inflammation of the nail
folds
 Treatment: warm soaks, topical antibiotics, and drainage.
4.1.2 Chronic Paronychia (more than 6 weeks)
 Treatment: Avoid triggers (trauma water etc.), topical steroids, and
antifungals.
4.2. Onychomycosis
 Clinical assessment: there are 2 types 1- DLSO will present with
discolored, thickened, and separation of nails .2- SWO will present
with a white, dry, and powdering of the nail.
 Diagnosis: KOH prep, fungal culture, and nail clippings for a PAS
stain.
 Treatment: First line is Terbinafine if there is CI uses itraconazole.
 DDX: Onycholysis has pitting nail, Lichen planus appear as
longitudinal ridges and grooves, and splitting of the nail.
4.3. Subungual Hematoma
 Clinical assessment: painful, dark red to black discolorations
caused by bleeding.
 Treatment: drilling a hole through the nail into the hematoma to
relieve the pressure.
4.4. Longitudinal Melanonychia
 Clinical assessment: hyperpigmented ventricle bands that occur as
normal variants in 90% of black people.DDX from subungual
melanomas has HX of melanoma and Hutchison’s sign.
4.5. Ingrown Toenails
 Treatment: wide or open toe box, warm water before topical
antibiotic, drainage, and surgery in case of laceration, glomus tumor,
and chronic paronychia.
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4.6. Onychogryphosis (Ram’s horn nail)

 Clinical assessment: hypertrophy and excessive curving of the
nails.
 Treatment: conservative for high-risk patients or by an electric drill,
burn chemical, and surgery for removal of subungual keratosis.
4.7. Brittle Nail Syndrome (fragility of the nail)
 Clinical assessment: onychorrhexis (longitudinal ridging of the nail)
and onychoschizia (lamellar splitting of the distal free edge of the nail
plate).
 Diagnosis: based on HX and EX if not certain basic labs and culture.
 Treatment: underlying the causes. May consider biotin or
moisturizers for the primary cause.
Chapter 5: HERPES SIMPLEX

5.1. Herpes Libialis
5.1.1 Definition:
Non-genital herpes simplex virus type 1 (HSV-1) is a common infection
usually transmitted during childhood via nonsexual contact but can be
acquired through sexual contact in adulthood. Most of these infections
involve the oral mucosa or lips (herpes labialis). Although genital herpes
simplex virus type 2 (HSV-2) also can affect the oral mucosa, this is
much less common and does not tend to become recurrent.
May range from asymptomatic to very painful
Recurrent infections cause cold sores that can affect appearance and
quality of life. The mouth lesions (herpetic gingivostomatitis) consist of
painful vesicles on a red, swollen base that occurs on the lips, gingiva,
oral palate, or tongue. The lesions ulcerate and the pain can be severe.
Refusal to eat or drink may be a clue to the presence of oral HSV. The
lesions usually heal within 10 to 14 days.
In recurrent herpes labialis, symptoms of tingling, pain, paresthesia,
itching, and burning precede the lesions in 60 percent of persons. The
lesions then appear as clusters of vesicles on the lip which subsequently
ulcerates and crusts. Healing begins in 3-4 days.
5.1.3 Diagnosis:
clinically made by the appearance of the lesions (grouped vesicles or
ulcers on an erythematous base) and patient history.
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Primary infection
We recommend antiviral therapy for patients with evidence of primary
gingivostomatitis who present within 72 hours of symptom onset.
Acyclovir: 400 mg orally three times daily or 200 mg five times daily
Famciclovir: 250 mg three times daily or 500 mg twice daily
Valacyclovir: 1 g twice daily
Pain relief can be achieved via mouth rinses with viscous lidocaine or
topical benzocaine.
Recurrent infection
Acyclovir (400 mg three times daily for five days)
Famciclovir (750 mg twice daily for one day or 1500 mg as a single dose)
Valacyclovir (2 g twice daily for one day)
Prophylaxis in case of recurrent disease
Acyclovir 400 mg twice daily
Valacyclovir 500 mg daily
5.2. Genital Herpes
5.2.1 Definition:
Genital herpes is caused by the herpes simplex virus (HSV) and is
characterized by lifelong infection and periodic reactivation. Although
HSV-1 and HSV-2 are indistinguishable visually, they exhibit differences
in behavior that may affect management.
A visible outbreak consists of single or clustered vesicles on the
genitalia, perineum, buttocks, upper thighs, or perianal areas that
ulcerate before resolving.
5.2.3 Diagnosis:
Diagnosis is usually made clinically. Polymerase chain reaction assay is
the preferred method of confirming HSV infection in patients with active
lesions.
Pregnancy
Antiviral prophylaxis with acyclovir is recommended from 36 weeks of
gestation until delivery in women with a history of genital herpes. Elective
cesarean delivery should be performed in laboring patients with active
lesions to reduce the risk of neonatal herpes.
Treatment can be extended for 10 days if healing is incomplete after 10
days.
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 Acyclovir 400 mg TID 7-10 days

 Acyclovir 200 mg five times daily 7-10 days
 Famciclovir 250 mg TID 7-10 days
 Valacyclovir 1 gm BID 7-10 days
Episodic treatment
Requires the initiation of treatment preceding outbreaks or within 1-2
days with the onset of lesion. The patient should be provided a
prescription for treatment
 Acyclovir 400 mg TID X 5 DAYS
 Acyclovir 800 mg BID x 5 days
 Acyclovir 800 mg TID x 5 days
 Famciclovir 1 gm BID x 1 day
 Valacyclovir 1 gm BID x 3 days
 Valacyclovir 1 gm once daily x 5 days
5.2.5 Herpetic Whitlow
Definition:
Herpetic whitlow is a vesicular lesion found on the hands or digits. It
occurs in children who suck their thumbs or medical and dental workers
exposed to HSV-1 while not wearing gloves. Vesicular eruptions are
often seen on the torso but can occur in any location where skin-to-skin
contact has occurred.
5.2.6 Herpetic Sycosis
It is a follicular infection with HSV that causes vesiculopapular lesions in
the beard area. It is often caused by autoinoculation from shaving.
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5.2.7 Herpes Simplex Keratitis

Herpetic keratitis is an HSV infection of the eye. Common symptoms are
eye pain, light sensitivity, and discharge with gritty sensation in the eye.
Fluorescein stain with ultraviolet light may show a classic dendritic ulcer
on the cornea. Without prompt treatment scarring may occur which can
lead to clouding of the cornea.
5.3. Herpes Zoster

5.3.1 Definition:
Also called shingles, caused by the reactivation of the varicella zoster
virus that causes chickenpox.
Initial symptoms include malaise, headache, low-grade fever, and
abnormal skin sensations for two to three days before the classic
maculopapular rash appears. The rash is usually unilateral, confined to a
single dermatome, and typically progresses to clear vesicles that
become cloudy and crust over in seven to 10 days. Lesions usually heal
two to four weeks after onset, but scarring and pigmentation changes are
common.
Most lesions develop in the T1-L2 dermatome, although the ophthalmic
division of the trigeminal nerve is affected in 15% of cases. Adjacent
dermatomes are affected in 20% of the cases.
5.3.3 Diagnosis:
Mostly clinical, although it is not easy to diagnose during prodrome, the
appearance of typical exanthem aids in diagnosis.
Although treatment should be started within a 72 hours period of
appearance of the rash, treatment can be started outside the 72 hour
window if new lesions are developing or if ophthalmological or
neurological complications arise.
 Acyclovir 800 mg orally five times per day for seven days
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 Famciclovir 500 mg orally three times per day for seven days
 Valacyclovir (Valtrex) 1,000 mg orally three times per day for seven
day
Adjunctive therapy
Corticosteroids (e.g., prednisone, prednisolone) Prednisolone: 40 mg
orally per day (days 1 to 6),
Pain control
 Acetaminophen
 Nonsteroidal anti-inflammatory drugs (e.g., ibuprofen)
 Prednisone as discussed earlier
 Opioids
 Tricyclic antidepressants
 Gabapentin
 Pregabalin
5.4. Herpes Zoster Ophthalmicus
Headaches, nausea, and vomiting are prodromal symptoms. Ipsilateral
preauricular and, sometimes, submaxillary nodal involvement is a
common prodromal event. The rash extends from eye level to the vertex
of the skull but does not cross the midline. Vesicles on the side or tip of
the nose (Hutchinson’s sign) that occur during an episode of zoster are
associated with the most serious ocular complications, including
conjunctival, corneal, scleral, and other ocular diseases, although this is
not invariable.
5.5. Eczema Herpeticum
Eczema herpeticum is a serious complication in patients with chronic
skin disease, primarily atopic dermatitis, and is caused by herpes
simplex virus 1 infection. Mostly seen in patients with atopic dermatitis in
which there is disruption of the epidermal barrier along with cell-mediated
immunity which leads to intensely pruritic and inflamed skin which allows
microbial superinfections.
Presentation of eczema herpeticum is with herpetic vesicles, usually on
the face, neck, and upper trunk. The skin has papulovesicular lesions
that rupture to form small, punched out, crusted ulcers overlying an
erythematous base diffusely spread over the body sparing the genital
area. May present with fever, malaise lymphadenopathy. The
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complications of this condition is an ocular infection that can cause

blindness and death in severe cases
5.5.2 Diagnosis:
Mostly clinical and treatment should be initiated immediately.
Eczema herpeticum is mainly treated with acyclovir. Because secondary
bacterial infections, such as staph aureus infection, are common,
prophylactic antibiotics (e.g., cephalexin [Keflex], clindamycin,
doxycycline, trimethoprim/sulfamethoxazole) are often administered.
Chapter 6: TINEA INFECTION

6.1. Tinea Capitis and Kerion
Tinea capitis affects children aged 6–10 years old.
Typically, it only infects the hair follicles of the scalp. It presents as a
round hyperkeratotic plaque of alopecia with evidence of broken hair
shafts or black dot alopecia. A scale may be present. The area and
plaque will have a green fluorescence with Wood’s lamp examination. In
the case of a kerion it will be associated with inflamed nodes, possibly a
purulent discharge, thick plaques, crusting, and loose hairs. Tinea capitis
can present with superimposed inflammation or without. Without
inflammation, patients will complain of scalp pruritus, scaling, alopecia,
occipital or posterior auricular adenopathy. With the formation of a
kerion, the term used to describe inflammatory tinea capitis, symptoms
will include pain, crusting, and, on occasion, alopecia or purulent
discharge.
6.1.2 Diagnosis:
Diagnosis can be made from a clinical exam.
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Treatment requires oral antifungals, as topical agents alone are
ineffective. However, evidence shows that concomitant treatment with
topical agents can decrease transmission rates. These agents include
1% or 2.5% selenium sulfide (Selsun Blue) shampoo or 2% ketoconazole
shampoo. Topical treatment is only required for the first 2 weeks. If a
kerion is present, adjuvant therapy with systemic prednisone (1 mg/kg
per day for 14 days for children) can be used for painful kerions.
Ketoconazole should not be used as oral treatment because it is
associated with severe liver injury and adrenal insufficiency.
6.2. Tinea Corporis
6.2.1 Background:
Tinea corporis affects all ages, lesions in areas of the body that touch
such as the axilla or thighs can cause “kissing” lesions. It is commonly
seen in tropical and subtropical regions. People who work with animals
are also at an increased risk.
Typically, it presents as a pruritic round scaling, well-demarcated plaque.
In the neck, trunk, and extremities excluding the hands, feet, and groin.
Occasionally, vesicles or pustules will be present at the margin. There is
a central clearing. Lesions can also take on a psoriasiform plaque.
Sometimes, lesions can have a vesicular presentation.
6.2.3 Diagnosis:
Usually, topical agents are sufficient. All agents should be applied BID for
about 4 weeks.
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Table 6.2 – Treatment options of tinea corporis

Agents Options
Best Agents Terbinafine (Lamisil) 1% cream
Butenafine (Lotrimin 1% cream
Ultra)
Other Agents Imidazoles Clotrimazole
Miconazole
Ketoconazol
e
Econazole
Oxiconazole
Sertaconazole
Allylamine Naftifine
Naphthenates Tolnaftate
Substituted pyridone Ciclopirox olamine
6.3. Pityriasis Versicolor (Previously Known As Tinea
Versicolor)
6.3.1 Background:
This infection is caused by M. furfur, which is a yeast not a
dermatophyte. It typically affects patients starting at puberty, through
young adulthood, and is less common in patients over the age of 60. It is
exacerbated by warm seasons, exercises, oily skin, use of cocoa butter,
glucocorticoid treatment, and immunodeficiency. For most patients, it will
occur only in the summer months. In patients who sweat consistently,
year-round, like athletes, it can persist even in the winter months.
This infection is asymptomatic or mildly pruritic. Patients will seek care
due to discoloration of their skin. Tinea Versicolor can be found
anywhere on the body. It is most common in areas with high sebaceous
gland activity. It appears as sharp margined macules that will vary in
size. Lesions can range from light brown to dark brown, typically
becoming hypopigmented on tanned skin. There is typically a very fine
scale that can only be appreciated with scraping.
6.3.3 Diagnosis:
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Table 6.3
Agent Dose
Selenium sulfide shampoo or 2.5%. Apply daily for 1 week. Applied
lotion to lesions for 10–15 min before
showering.
Prophylaxis: 1–2 weekly
Ketoconazole shampoo Daily for 1-week Prophylaxis: 1–2
weekly
Terbinafine 1% solution BID for 7 days
Azole creams BID for 2 weeks
6.4. Tinea Cruris
6.4.1 Background:
Tinea cruris typically affects male adults. Risk factors include tight
clothing, obesity, and topical glucocorticoid application. It is most
commonly associated with a concurrent tinea pedis infection.
Tinea cruris presents with pruritus of the region but can be
asymptomatic. It is found in the groin, upper thighs, and buttocks.
Typically does not extend to the penis or scrotum The lesions are well-
demarcated, large, with scaling plaques. The color ranges from red to
brown. There is commonly a central clearing. Occasionally, pustules are
present at the edge of the lesion.
6.4.3 Dignosis:
Treatment is typically topical agents and shows a similar success profile
to those used to treat tinea corporis.
6.5. Tinea Pedis
6.5.1 Background:
Tinea pedis most commonly affects male adults aged 20–50 years old.
Risk factors include hot, humid weather, excessive sweating, occlusive
footwear, and walking barefoot on contaminated areas.
Tinea pedis affects interdigital areas and soles of the feet most
commonly. Causing peeling of skin or mild pruritus of the feet.
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6.5.3 Diagnosis:
The treatment combines a topical agent with prevention. Typically topical
agents and shows a similar success profile to those used to treat tinea
corporis.
6.6. Tinea Unguium (Onychomycosis)
6.6.1 Background:
Onychomycosis affects all ages with a minor increased prevalence
among males. Risk factors include wearing occlusive footwear and being
immunocompromised.
Most commonly affects the nail of the big toe. Feet are affected 80% of
the time. Typically presents as asymptomatic color change in the nails.
Can present with bacterial superinfection and would cause pain,
erythema, and tenderness. Typically begins with a white patch that is
noted at the edge of the nail. As the infection progresses, the nail can
become completely discolored and become eroded from the nail bed
allowing for easy removal.
6.6.3 Diagnosis:
Diagnosis cannot be made by clinical exam alone but requires fungal
culture or dermatopathology.
Treatment includes debridement, topical and systemic agents. Topical
agents include ciclopirox nail lacquer which is only successful with
concurrent debridement. Systemic treatments are listed below. Of note,
the nails will not regain their normal appearance until well after treatment
has been completed due to their slow growth.
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Table 6.4
Agent Adult Dose
Terbinafine 250 mg/day for 6 weeks for
fingernails and 12–16 weeks for
toenails
Itraconazole 200 mg/day for 6 weeks for
fingernails and 12 weeks for toenails
Fluconazole 150–400 mg given once a week or
100–200 mg daily until the nails grow
back normally
Ketoconazole Not recommended given
hepatotoxicity
6.7. Tinea Incognito
This is a confusing diagnosis that occurs when a dermatophyte is treated
with a topical corticosteroid when it is misdiagnosed as eczema or
another type of dermatitis. If you suspect tinea incognito, have the
patient stop corticosteroid. The scale should recur within a few days, and
a KOH test is performed. If positive, then the patient is treated
accordingly.
6.8. Erythrasma
Characterized by sharply delineated, dry, brown, slightly scaling patches
occurring in the intertriginous areas, especially the axilla, the genitocrural
crease, and the webs between the fourth and fifth toes and, less
commonly, the third and fourth toes. The lesions are asymptomatic
except in the groins, where there may be some itching and burning.
Patients with extensive erythrasma have been found to have diabetes
mellitus or other debilitating diseases.
Wood’s light is the diagnostic medium for erythrasma. The affected areas
show a coral-red fluorescence, which results from the presence of a
porphyrin. Washing of the affected area before the examination may
eliminate the fluorescence.
Topical erythromycin solution or topical clindamycin is easily applied and
rapidly effective.
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Chapter 7: COMMON DERMATOLOGIC

AL CONDITIONS
7.1. Acne Vulgaris
7.1.1 Definition
Acne is a multifactorial process that affects the pilosebaceous units of
the skin. It often begins in early puberty with increased sebum production
and mid-facial comedones, followed by inflammatory lesions.
7.1.2 Clinical Characteristics
 Characterized by open and closed comedones.
 Inflammatory lesions, such as papules, pustules, and nodules.
 Lesions typically occur on the face, neck, chest, and back.
7.1.3 Diagnosis
 The diagnosis of acne vulgaris rests upon the patient’s history and
physical examination.
 Laboratory tests are not necessary for most patients.
7.1.4 Management
Table 6.5 –Treatment options for acne vulgaris
Mild Moderate Severe
1st Line Benzoyl Topical Oral Antibiotic
Treatment Peroxide (BP) or Combination +
Topical Retinoid Therapy” Topical
OR BP + Antibiotic Combination
Topical or Retinoid BP Therapy
Combination or Retinoid + BP BP+ Antibiotic
Therapy + Antibiotic or Retinoid + BP
BP+Antibiotic OR or Retinoid + BP+
or Retinoid+ BP Oral Antibiotic+ Antibiotic
or Retinoid + Topical Retinoid OR
BP+ Antibiotic + BP Oral Isotretinoin
OR
Oral Antibiotic+
Topical Retinoid+
BP+Topical
Antibiotic
Alternative Add Topical Consider Consider Change
Treatment Retinoid or BP Alternate in Oral Antibiotic
(if not on Combination OR
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already) Therapy Add Combined

OR OR Oral Contraceptive
Consider Consider Change or Oral
Alternate in Oral Antibiotic Spironolactone
Retinoid OR (Females)
OR Add Combined OR
Consider Topical Oral Consider Oral
Dapsone Contraceptive Isotretinoin
or Oral
Spironolactone
(Females)
OR
Consider Oral
Isotretinoin
Recommendations for Topical Therapies
 Benzoyl peroxide or combinations with erythromycin or clindamycin
are effective acne treatments and are recommended as monotherapy
for mild acne, or in conjunction with a topical retinoid, or systemic
antibiotic therapy for moderate to severe acne.
Recommendations for Systemic Antibiotics
 Systemic antibiotics are recommended in the management of
moderate and severe acne and forms of inflammatory acne that are
resistant to topical treatments.
 Doxycycline and minocycline are more effective than tetracycline, but
neither is superior to the other.
 Although oral erythromycin and azithromycin can be effective in
treating acne, their use should be limited to those who cannot use the
tetracyclines (i.e., pregnant women or children under 8 years of age).
 Monotherapy with systemic antibiotics is not recommended.
Recommendations for Isotretinoin
 Should be initiated by a dermatologist.
 For severe nodular acne or moderate acne that is treatment-resistant
or for the management of acne that is producing physical scarring or
psychosocial distress.
 Routine monitoring of liver function tests, serum cholesterol, and
triglycerides at baseline and again until response to treatment is
established is recommended.
 Females of child-bearing potential taking isotretinoin should be
counseled for double contraceptive methods, including user-
independent forms.
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7.2. Rosacea
7.2.1 Clinical Features
 Dome-shaped inflammatory papules ± pustules (Figure 7.3).
 Flushing, non-transient erythema, and telangiectasia.
 Distribution: typically, on central face including forehead, nose,
cheeks, and chin.
 Exacerbating factors: heat, cold, wind, sun, stress, drinking hot
liquids, alcohol, and spices.
 Characterized by remissions and exacerbations.
 Exacerbating factors: heat, cold, wind, sun, stress, drinking hot
liquids, alcohol, and spices.
 Phyma: a distinct swelling caused by lymphedema and hypertrophy of
subcutaneous tissue, particularly affecting the nose (rhinophyma)
(Figure 7.5).
 Ocular manifestations: blepharoconjunctivitis, keratitis, and iritis.
7.2.2 Management
 Non-pharmacological management: Trigger avoidance and daily
sunscreen use for long-term management.
 Avoid topical corticosteroids.
 Pharmacological management
Table 6.6
1st Line 2nd Line 3rd Line
– Oral Tetracyclines – Topical Clindamycin Oral Retinoids
– Topical – Topical Erythromycin
MetronidazoleOral 2% solution
Erythromycin (250-500 – Topical Benzoyl
mg PO BID) Peroxide
– Topical Azelaic Acid – Oral Metronidazole
– Topical Ivermectin
7.3. Atopic Dermatitis
7.3.1 Clinical Manifestations
 Triggers include climate, food, contact with allergens, physical or
chemical irritants, and emotional factors.
 In Infants: Erythematous, edematous, weeping, pruritic papules and
plaques on the face, scalp, and extensor surfaces of the extremities.
The diaper area is often spared.
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 In Children: Dry, scaly, pruritic, excoriated papules and plaques in the

flexural areas and neck.
 In Adults: Lichenification and dry, fissured skin in a flexural
distribution. Often, there is hand or eyelid involvement.
7.3.2 Diagnosis
 Is a clinical diagnosis.
7.3.3 Management
 Non-pharmacological management include
o Use of non-drying soaps
o Application of moisturizers
o Avoidance of known triggers.
 Topical corticosteroids are the first-line therapy.
 Topical immunomodulators (e.g. tacrolimus, pimecrolimus) are useful
for moderate to severe eczema if the patient is > 2 years of age.
7.4. Contact Dermatitis
7.4.1 Clinical presentation
 Commonly presents with pruritus and rash
 Frequently implicated allergens include poison ivy, poison oak,
nickel, soaps, detergents, cosmetics, and rubber products containing
latex.
 Distributions are often seen where makeup, clothing, perfume, nickel
jewelry, and plants come into contact with the skin.
7.4.2 Diagnosis
 Patch testing can be used to establish the causative allergen after the
acute-phase rash has been treated.
7.4.3 Management
 Non-pharmacological management:
 Avoidance of the offending allergen.
 Cool, wet compresses to soothe crusted lesions of the skin.
 Treat with topical or systemic corticosteroids as needed.
7.5. Seborrheic Dermatitis
 A common disease that may be caused by Pityrosporum ovale.
 It has a predilection for areas with oily skin.
 Infants: presents as red rash with yellow scale, erosions, and blisters.
A thick crust (“cradle cap”) may be seen on the scalp.
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 Children/Adults: red, scaly patches are seen around the ears,

eyebrows, nasolabial fold, mid-chest, and scalp.
7.5.2 Diagnosis
 Differential diagnosis : contact dermatitis and psoriasis.
7.5.3 Management
 Selenium sulfide or zinc pyrithione shampoos for the scalp.
 Topical antifungals and/or topical corticosteroids for other areas in
adults
 Cradle cap often resolves with routine bathing and application of
emollients.
7.6. Lichen Planus
 Morphology: pruritic, well-demarcated, violaceous, polygonal, at-
topped papules.
 Common sites: wrists, ankles, mucous membranes in 60% (mouth,
vulva, glans), nails, scalp.
 Wickham’s striae: pathognomonic, reticulate white-gray lines over the
surface;.
 Mucous membrane lesions: lacy, whitish reticular network, milky-
white plaques/papules; increased risk of Squamous cell carcinoma
(SCC) in erosions and ulcers.
 Nails: longitudinal ridging; dystrophic; pterygium formation.
 Scalp: scarring alopecia with perifollicular hyperkeratosis and
erythema.
 Spontaneously resolves but may last for weeks, months, or years.
 Koebner’s phenomenon (lesions that appear at the site of trauma).
7.6.2 Diagnosis
 Consider a skin biopsy.
 Consider hepatitis C serology if the patient has risk factors.
7.6.3 Management
 Mild cases are treated with topical corticosteroids.
 Severe cases are treated with systemic corticosteroids and
phototherapy may be used.
7.7. Cutaneous Warts
 Human papillomavirus (HPV) is a dsDNA virus that infects epithelial
skin layers and mucous membranes.
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 Cutaneous warts are generally described in six categories:

o Common warts (verruca vulgaris)
o Plantar warts (verruca plantaris)
o Flat or plane warts (verruca plana)
o Intermediate warts (combined common and flat)
o Mosaic warts (or plaque)
o Periungual warts (under or around the nail bed)
7.7.1 Diagnosis
 key features such as densely packed papillae in a well-defined region
which disrupts normal skin lines
7.7.2 Management
 Salicylic Acid is a keratolytic agent that slowly eats away at the HPV-
infected skin layers.
o Side Effects: the major side effect being irritation to the skin
surrounding the wart.
o How to Use: begin by soaking the wart area with warm water for
5 minutes, and gently file down the rough area. Apply the salicylic
acid directly to the wart carefully to avoid damaging the
surrounding tissues.
 Cryotherapy:
o Liquid nitrogen (LN2) is a common treatment found in most
primary care offices
o How to Use: treatment can be repeated every 2–3 weeks until
the wart has been cleared.
7.8. Folliculitis
 Inflammation of the hair follicles
 Folliculitis
o A tiny pustule that appears at the opening of a hair follicle and
usually has hair penetrating it.
 Furuncle (boil)
o Deep infection of the hair follicle in which purulent material
extends through the dermis into the subcutaneous tissue.
 Carbuncle
o coalescence of several furuncles into a single inflammatory mass
7.8.2 Diagnosis
o Is a clinical diagnosis.
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7.8.3 Management
 Lesions may resolve spontaneously with or without drainage.
 More extensive involvement or lesions lasting for 2-3 weeks are
usually treated with antibiotics.
 Shaving should be avoided in involved areas.
 Staph folliculitis:
o Mild – topical mupirocin
o Severe or persistent lesions
Chapter 8: ACUTE ALLERGIC
REACTION
8.1. Anaphylaxis and Anaphylactic Reaction
 The most common symptoms are
o Urticaria
o Difficulty breathing
o Mucosal swelling
 The most common triggers are
o Medications
o Stinging insect venoms
o Foods
8.1.2 Diagnostic Criteria of Anaphylaxis
Anaphylaxis is highly likely when any of the following 3 criteria are met:
 Acute onset of an illness (i.e., minutes to several hours) with
involvement of the skin, mucosal tissue, or both (e.g., generalized
hives, pruritus or flushing, swollen lips, tongue, or uvula), and at least
one of the following:
o Respiratory compromise (e.g., dyspnea, wheezing,
bronchospasm, stridor, reduced peak expiratory flow,
hypoxemia).
o Reduced blood pressure or associated symptoms of end-organ
dysfunction (e.g., hypotonia [collapse], syncope, incontinence).
 Two or more of the following that occurs rapidly (i.e., minutes to
several hours) after exposure to a likely allergen for that patient:
o Involvement of the skin, mucosal tissue, or both (e.g.,
generalized hives; pruritus or flushing; swollen lips, tongue, or
uvula).
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o Respiratory compromise (e.g., dyspnea, wheezing,

bronchospasm, stridor, reduced peak expiratory flow,
hypoxemia).
o Reduced blood pressure or associated symptoms (e.g.,
hypotonia [collapse], syncope, incontinence).
o Persistent gastrointestinal symptoms (e.g., abdominal cramps,
vomiting).
 Reduced blood pressure that occurs rapidly (i.e., minutes to several
hours) after exposure to a known allergen for that patient.
8.1.3 Management
 Arrange the patient in supine position with lower extremity raised,
element the trigger.
 Monitor and support airway, breathing, and circulation.
 The most important treatment in anaphylaxis is epinephrine.
o Administer IM epinephrine on outer-mid thigh by auto-injector
0.15 mg for children less than 30 kg, and 0.3 mg for children
more than 30 kg, adolescents, or adults or 1:1000 dilution 0.05
mg per kg, max dose 0.3 mg pre-pubertal and 0.5 mg
adolescents and adults.
 Repeat in 5-15 mins if there is no response.
 For patients with hypotension, give IVF 0.9 isotonic saline 1-2 L
rapidly; for reactive airway patients, give beta-2 agonist nebulizers.
 Needs ICU admission and close monitoring.
 If symptoms improve, then the patient needs monitoring, administer
100% O2, two large-bore IV lines for maintenance fluids, consider
starting H1, H2 antagonists, and consider giving a single dose of
corticosteroids.
 If symptoms resolve, then consider observation for biphasic reaction.
o Biphasic reaction defined as the recurrence of anaphylaxis within
72 hours of the initial reaction without re-exposure to the
allergen. Observation of a minimum of 4 hours is recommended.
8.2. Angioedema and Urticaria
 Urticaria
o A common dermatologic condition that typically presents with
intensely pruritic, well-circumscribed, raised wheals ranging from
several millimeters to several centimeters or larger in size.
 Angioedema
o A localized non-pitting edema of the subcutaneous or interstitial
tissues that may be painful and warm.
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8.2.1 Etiology
o IgE-mediated: aero-allergen, food allergen, chemicals, insect
venom, medications.
o Non-IgE mediated: autoimmune mediated, bacterial infections,
fungal infections, viral infections, lymphoma, vasculitis (Figure
8.3).
o Non-immunological mediated: physical stimulus such as cold,
heat, light, pressure, vibration, medication.
o 80-90% of chronic urticaria is idiopathic.
8.2.2 Diagnosis
 The diagnosis of Angioedema and Urticaria are done by history and
physical examination.
 Lab tests are usually not indicated unless an underlying disease is
suspected. For example, a presentation that suggests urticarial
vasculitis should prompt a skin biopsy.
8.2.3 Management
 First to rule out anaphylaxis, which has findings or symptoms
involving other organ systems.
o Pulmonary (wheezing, stridor)
o CVS (tachycardia, hypotension)
o Gastrointestinal (diarrhea, vomiting, abdominal pain)
o CNS (dizziness)
 Steps in treatment of acute urticaria:
o Identify the Offending factor.
o Mild symptoms of new onset urticaria, give a non-sedating H1
antihistamine alone at bedtime.
o Moderate-to-severe new-onset urticaria, adding an H2
antihistamine.
 Steps in treatment of chronic urticaria:
o If symptoms are severe, a short course of systemic
corticosteroids can be added for 5-10 days (0.5-1mg/kg per
day) to step 1, 2, or 3.
o If systemic symptoms are suggested to give epinephrine.
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Section 8: Surgery
Chapter 1: PERIPHERAL ARTERY
DISEASE
1.1. Definition:
Atherosclerosis of the arteries of the lower extremities is defined as PAD.
An ankle-brachial index (ABI) ≤0.90 is sensitive and specific for arterial
stenosis/occlusion and diagnostic for lower extremity PAD.
 - Claudication: Exertional leg pain relieved by rest that may be
unilateral or bilateral. atypical pain such as exertional pain that does
not resolve with rest & 40% are Asymptomatic.
 -Ischemic rest pain: Very painful localized pain in forefoot & toes
Increased with raising Lower limb and relieved by walking or hanging
the foot on bed
Examination:
decreased or absent distal pulses, bruits, but can also be normal; look
for ulcers, gangrene, elevation pallor and dependent rubor, and
pulses/bruits in other vascular beds. The nails may become brittle,
hypertrophic, and ridged as well.
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Table 1.1 – High-risk features on history and physical exam

Characteristic Arterial ulcer Venous Ulcer Characteristic
Location Over toe joints, The medial and Location
malleoli (over the lateral malleolar
bony area above bony
prominence), prominence,
anterior shin, the posterior Calf,
base of the heel, maybe large,
pressure points. circumferential
Appearance Irregular margins, Irregular margins, Appearance
base dry and pink or red base
often pale or that may be
necrotic covered with
(brown/black yellow fibrinous
fibrous tissue) tissue exudate
common (maybe
heavy); ulcers
can be large,
sometimes
circumferential.
Foot Warm or cool Warm Foot
temperature temperature
Pain Yes, maybe Present Pain
severe
Sensation Variable Present Sensation
 -Patients present with gangrenous digits, forefoot, or hind foot.
Gangrene can be described as dry gangrene and wet gangrene which
is a surgical emergency.
Investigation & Monitoring
Ankle-Brachial index:
The ABI is the ratio of the highest systolic pressure in each leg, obtained
at the dorsalis pedis and posterior tibial arteries using a doppler probe, to
the higher of the right or left arm brachial artery pressures.
Table 1.2 – API Interpretation
Diagnostic Criteria for Lower Extremity Peripheral Artery Disease on
ABI testing
Normal Ankle-brachial index 1.0 – 1.3
Borderline 0.9 – 1.0
Mild 0.7 – 0.9
Moderate 0.4 – 0.7
Severe < 0.4
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 Risk factor modification: smoking cessation, control of Diabetes &
Hypertension
 Supervised exercise therapy
 Antiplatelet therapy with aspirin alone (75 to 325 mg per day) or
clopidogrel alone (75 mg per day.
 Statin therapy
 Ramipril with BP goal ≤140/90 mm Hg.
 Cilostazol
1.4. Acute Limb Ischemia
It is a medical emergency caused by obstruction in blood supply to an
extremity Present with pain, pallor, paresthesia, pulseless, and
paralysis. It is usually thrombotic, and the heart is the common source
in 80-90%.
1.5. Arterioarterial Emboli: The Blue Toe Syndrome
Cholesterol or atherothrombotic emboli and occludes small vessels
May be confused as bruising the diagnosis is confirmed by skin or
muscle biopsy and the presence of cholesterol crystals on the
fundoscopic exam.
1.6. Aortic Diseases
Abdominal aortic aneurysm (AAA)
Definition
develop as a result of degeneration of arterial media and elastic tissues.
An aneurysm is >50% in vessel diameter or a dilatation greater than 3.0
cm.
Presentation:
Usually as Pulsatile mass around the umbilicus. A bruit during abdominal
auscultation
Maybe wound incidentally during imaging.
Ruptured AAA is characterized by hypotension, shooting abdominal or
back pain, and a pulsatile abdominal mass.
Screening:
 Screen one time for abdominal aortic aneurysm (AAA) with
ultrasonography in men aged 65–75 years who have ever smoked.
 Selectively offer screening for AAA in men aged 65–75 years who
have never smoked.
 There is insufficient evidence to recommend for or against screening
for AAA in women who have ever smoked.
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 Do not screen women for AAA who have never smoked.

Surveillance
If patients are diagnosed with AAA on initial screening, regular
surveillance is needed every six months to three years, depending on
aneurysm size
Table 1.3 – Surveillance For Patients With Stable AAA
Aneurysm diameter ACC/AHA guidelines
3.0 cm No surveillance
3.0 cm to 3.9 cm Ultrasonography every two to three
years
4.0 cm to 5.4 cm Ultrasonography or computed
tomography every six to 12 months
Consider surgical consultation for
an aneurysm 5.0 cm or greater, or
if expanding at a rate greater than
expected for its size
> 5.4 cm Surgical consultation for elective
repair
Treatment Medical
Statins for CVD outcomes
Control of Diabetes and Hypertension
Surgical
Elective repair of AAA is done when the diameter of the AAA has
reached 5.5 cm.
1.7. Superficial Vein Thrombosis and Phlebitis of the
Lower Extremity
a benign condition unless it involves the accessory veins, Most often
affect the legs.
Superficial phlebitis
pain and inflammation involving a vein in the absence of thrombus.
Clinical findings of pain, tenderness, induration, and erythema along the
course of a superficial vein. It May be infected or thrombosed
Superficial thrombophlebitis
Thrombosis of the tributary veins That is confirmed by Duplex US,
Involving the axial veins (e.g., great saphenous, accessory saphenous,
and small saphenous veins).
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Causes
Varicose veins, Pregnancy, postpartum status, Systemic autoimmune
disease, Iv drug use, Local trauma or malignancy
Presentation
 Presents with localized pain and swelling in the superficial veins.
 Use the Wells criteria for clinical criteria to identify patients at the
highest risk of DVT.
 fever and/or chills May suggests septic/suppurative thrombophlebitis.
Deferential diagnosis:
Table 1.3 – Deferential diagnosis of superficial thrombophlebitis
Diagnosis Features
Cellulitis Fever, elevated WBC
Panniculitis Not limited to the superficial vein;
histopathologic diagnosis by biopsy
Deep venous Thrombosis Edema of Calf or leg, deep venous
cords; positive Doppler ultrasound
Erythema Nodosum Usually multiple nodular lesions,
not over a vein; histopathologic
diagnosis by biopsy.
Ascending lymphangitis Fever, elevated WBC
Diagnosis
 -Clinical diagnosis based on history and physical examination.
 -Diagnostic compression ultrasound if high risk for DVT or not
responding to conservative management.
Management
The goals of therapy are to relieve local symptoms, prevent recurrences,
and limit the risk of deep venous thrombosis.
Primary treatment
Usually includes NSAIDs, local heat, elevation, and support stockings.
LMWH or NSAIDs for at least four weeks are appropriate therapy.
Anticoagulants
They are started as per risk, and no anticoagulants are given if they are
low risk.
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Chapter 2: BREAST MASSES

2.1. History
 A detailed history of the breast mass should be obtained: the site,
size, onset, the character of the lump, associated symptoms, relieving
and aggravating symptoms, and the symptoms’ severity.
 Red flags should be excluded, such as: fever, weight loss, malaise,
nipple retraction, discharge, bleeding, or inversion, dimpling (Peau
d’orange), lymphadenopathy and bone pain.
 Past medical and surgical histories should be obtained.
 Family history of breast, ovarian, and colon cancer is very important.
If present, we should clarify the age of onset.
 Social history, smoking, alcohol, and drug history.
 Assess the risk factors of breast cancer: preexisting breast cancer or
a previously diagnosed high-risk breast lesion, a known underlying
genetic mutation (such as a BRCA1 or BRCA2 gene mutation), a
history of chest radiation at a young age, increasing age, and
increase estrogen exposure such as; early age of menarche, late age
of first pregnancy, nulliparity, oral contraceptive or hormone
replacement therapy, and late menopause. Other risk factors, such as
excess alcohol intake and obesity, are thought to increase
endogenous estrogens. Breastfeeding is a protective factor.
2.2. Physical examination
 Visual inspection while the patient is seated with her hands on her
hips. Any signs of nipple discharge, asymmetry, skin retraction,
bulging, edema, erythema, or skin thickening should raise concern for
malignancy.
 Palpation of the breasts should be performed with the patient in the
supine position.
 Palpation of the axillary, supraclavicular, and cervical lymph.
 Benign masses are more likely to be smaller, mobile, smooth, and
regular. However, malignant masses are typically larger, fixed, hard,
and heterogeneous in texture.
 Documentation of a mass found should include size, consistency,
distance from the areolar edge, and circumferential position on the
breast.
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2.3. Imaging
 Diagnostic mammography is the most appropriate initial imaging
modality for women 40 years and older. All mammography reports are
accompanied by a Breast Imaging Reporting and Data System (BI-
RADS) categorization to direct management (Table 2.1).
 Ultrasonography is recommended for women younger than 30 years.
Table 2.1 – Breast Imaging Reporting and Data System (BI-RADS)
Assessment Categories
BI-RADS Interpretation Recommended

category management
0 Incomplete Obtain additional
imaging
1 Negative findings Manage according to
Figures 1 and 2; no
additional imaging
necessary unless
high clinical suspicion
2 Benign findings Resume routine
screening
3 Probably benign Short-interval follow-
findings (< 2% risk of up according to
cancer) Figures 1 and 2
4 Suspicious abnormality Biopsy; referral to
subspecialist
5 Highly suggestive of Biopsy; urgent
malignancy (≥ 95% risk referral to
of cancer) subspecialist
2.4. Biopsy
 Any suspicious mass detected on physical examination,
mammography, or ultrasonography should be referred for biopsy.
 A highly suspicious breast mass found on physical examination
should be biopsied regardless of imaging findings, and suspicious
masses on imaging should be biopsied even if the physical
examination suggested benign findings.
 In most cases, a core needle biopsy should be performed with
imaging guidance for evaluation of a suspicious mass.
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Table 2.2 – Differential diagnosis of common benign breast masses
Condition Clinical findings Diagnosis tips Management

Fibroadenoma – Typically identified – Well-defined, – It can be
in young women but mobile mass on managed with
can also be physical core biopsy or
identified as a examination or a short-term (three
calcified mass in well-defined solid to six months)
older women. mass on follow-up with a
ultrasound. repeat ultrasound
– Can increase in and breast
size during – Definitive examination.
pregnancy or with diagnosis can
estrogen therapy, only be confirmed – If a biopsy-
and usually regress with a core biopsy proven simple
after menopause. or excision. fibroadenoma is
asymptomatic, it
– The mass is firm can be left in
and often mobile. place.
May be solitary,
multiple, or bilateral. – Disadvantages
of excisional
biopsy include
scarring at the
incision site,
dimpling of the
breast from the
removal of the
tumor, damage to
the breast duct
system, and
mammographic
changes.
– If fibroadenoma
increases
significantly in
size or is
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symptomatic, then
excision is
mandated to rule
out malignant
change and
confirm the
diagnosis.
Cyst – A simple cyst is a – Aspiration is an
benign, fluid-filled – appropriate first
mass that can be Ultrasonography step in the
palpated as a or aspiration must management,
component of be used to with clinical
fibrocystic changes establish a follow-up after
of the breast or as a definitive aspiration, four to
discrete, diagnosis. six weeks, to
compressible, or determine if the
ballotable solitary – Cysts require cyst has recurred.
mass. surgical biopsy
only if the – In contrast to
– Commonly found aspirated fluid is macrocysts,
in premenopausal, bloody; the nonpalpable cysts
perimenopausal, palpable identified by
and occasionally abnormality does mammography
postmenopausal not resolve and confirmed to
women completely after be simple cysts
the aspiration of by ultrasound
– Clinically, cysts fluid, or the same examination
are well demarcated cyst recurs require no
from the surrounding multiple times in a treatment, but a
breast tissue. They short period of complex cyst or
are characteristically time. cyst containing
firm and mobile and debris should
may be tender. – Routine receive further
cytologic investigation to
– On physical examination of rule out
examination, it is cyst fluid is not malignancy.
often difficult to indicated because
distinguish a cyst of the low
from a solid mass. likelihood of
cancer in the
absence of
clinical findings of
bloody fluid or a
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residual mass
after aspiration.
Fibrocystic – Common, Patients with Reassurance that
changes particularly in early fibrocystic there is no
premenopausal change show malignancy and
women small areas of over-the-counter
increased density analgesics are
– May be prominent on the enough.
and organized. mammogram.
However, the breast These are
tissue tends to be irregular and
more diffuse and scattered, with
tender and generally varying degrees
does not form a of density.
discrete or well-
defined mass.
– Most patients
present with breast
pain that may be
cyclical or constant
and may be
bilateral, unilateral,
or focal.
– The breast tissue,

particularly in the
upper outer
quadrant, may
increase in size prior
to the onset of
menses, then return
to baseline after the
onset of the
menstrual flow.
– On clinical
examination, the
breast tissue is
nodular with no
palpable mass.
Galactocele – Milk retention – Ultrasound is – In mothers with
cysts that result the primary a diagnosis of
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from a blocked milk diagnostic galactocele

duct. imaging modality confirmed by
to distinguish aspiration,
– They present as galactoceles from repeated needle
cystic, sometimes other breast aspiration or
very large masses masses, including surgical excision
during pregnancy, adenomas, is only necessary
lactation, and after fibroadenomas, if the galactocele
weaning. papillomas, is bothersome to
lipomas, the mother.
– Unless they are abscesses, and
infected, they are fibrocystic – Breastfeeding
usually painless. disease. In can continue
addition, although during aspiration
– Initially, they uncommon, or excision.
contain milky fluid, breast
but over time, malignancies can – A preoperative
contents become present as breast discussion with
thicker, creamier, or masses during the surgeon
oily as the fluid is lactation. regarding plans to
reabsorbed. continue
– Aspiration breastfeeding is
demonstrating the essential. In some
characteristic cases, surgery
milky contents can be postponed
confirms the until after the
diagnosis of infant is weaned.
galactocele and
excludes
malignancy.
Fat necrosis – A benign breast – Fat necrosis Usually does not
mass that can can often be require any
develop after blunt clinically and treatment other
trauma to the breast; even than analgesia
injection of native or radiographically and monitoring.
foreign substances difficult to However, the
such as fat or distinguish from a surgical
silicone, an malignant mass consultant should
operative procedure consider whether
such as breast – Represent as the mass is
reduction surgery or oily cysts causing the
breast (collection of patient significant
reconstruction, and liquefied fat) on
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radiation therapy to radiography. pain or cosmetic

the breast. issues
– Sometimes a
– Fat necrosis from biopsy is needed
trauma is generally to confirm the
associated with skin diagnosis.
ecchymosis.
Mammary – Non-proliferative – Initial imaging – Excluding other
duct ectasia inflammatory assessments can pathologies and
disorder of the large include bilateral symptomatic
duct (milk duct) of mammography, management
the breast; affecting and ultrasound
nipple and areola examination – Apply warm
complex. depending on the compresses over
patient’s age. the central part of
– Patients may be the breast,
asymptomatic or – MRI (more wearing a
present with rarely CT) can be supportive bra
intermittent nipple used at any age with breast pads
discharge of varying to assess cases to absorb any
colors, pain and of equivocal or nipple discharge,
tenderness of the concerning and maintaining
nipple and areola. findings. nipple and areola
hygiene.
– Other symptoms – Fine-needle
include an inverted aspiration (FNA)
nipple or a palpable cytology and
breast lump. tissue
confirmation will
also be required
in suspicious
lesions and may
be helpful in
equivocal cases.
2.5. Breast cancer screening in Saudi Arabia

 For an average risk women aged 40 to 69, screening mammography
is recommended every two years.
 For high-risk women, screening mammography is recommended
annually, at a younger age, in addition to other investigations such as
MRI.
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 Follow ‘Saudi Ministry of Health Guide of national breast cancer early

detection program’. Available
from: https://www.moh.gov.sa/Ministry/About/Health%20Policies/011.p
df for more details
2.6. The U.S. Preventive Services Task Force
recommends the following
 Routine screening for women aged 50 to 74 years with screening
mammography every two years (Grade B).
 The decision to start screening mammography in women prior to age
50 years should be an individual one. Women who place a higher
value on the potential benefit than the potential harms may choose to
begin biennial screening between the ages of 40 and 49 years (Grade
C).
 Evidence on mammography screening in women aged ≥75 years is
insufficient, and the balance of benefits and harms cannot be
determined (Grade I)
Chapter 3: HEAD INJURIES
3.1. Classification of head injuries
 Mild
o GCS 13-15
o Brief LOC, nausea, cognitive, behavioral, and emotional
disturbance
 Moderate
o GCS 9-12 after non-surgical resuscitation
 Severe
o GCS < 8 after non-surgical resuscitation
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Table 3.1 – Pediatric head CT rule

Age 2 years or older Younger than 2
years
CT head is AIMS AIMS
recommended Or Or
GCS < 15 GCS < 15
Or Or
Signs of basilar skull Palpable skull fracture
fracture
Observation Vs. History of LOC History of LOC > 5
Head CT Or seconds
History of vomiting Or
Or Non-frontal hematoma
Severe headache Or
Or not acting normally
Sever mechanism Or
Sever mechanism
Discharge No CT Required No CT Required
3.2. Decision rules for head CT imaging in adults

Table 3.2 – Decision rules for head CT imaging in adults
New Orleans Criteria – GCS 15 Canadian CT head Rules – GCS
13-15
Headache GCS <15 at 2 h
Vomiting Suspected open or depressed
skull fracture
Age >60 y Age ≥65 y
Intoxication More than one episode of
vomiting
Persistent antegrade amnesia Retrograde amnesia >30 min
Evidence of trauma above the Dangerous mechanism (fall >3
Clavicles ft or struck aspedestrian)
Seizure Any sign of basal skull fracture
3.3. Investigations
 Complete blood count
 Electrolytes
 Renal function test
 Blood glucose
 Abo blood type
 Coagulation profile
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 Toxicology
3.4. Types of Brain Injuries
3.4.1 Skull fractures
 Depressed skull fractures are classified as open or closed, depending
on the integrity of the overlying scalp.
 Although basilar skull fractures can occur at any point in the base of
the skull, the typical location is the petrous portion of the temporal
bone. Findings associated with a basilar skull fracture include
hemotympanum, cerebrospinal fluid (CSF) otorrhea or rhinorrhea,
periorbital ecchymosis (raccoon eyes), and retroauricular ecchymosis
(Battle sign).
 In children, linear skull fractures that result from a fall from a small
height (<4 ft) generally are not associated with the development of
clinically significant intracranial lesions. Significant intracranial injuries
in children often occur after falls from more extreme heights or higher
impact collisions.
3.4.2 Subdural hematoma
 A subdural hematoma (SDH), which is a collection of venous blood
between the dura mater and the arachnoid, results from tears of
bridging veins that extend from the subarachnoid space to the dural
venous sinuses.
 A common mechanism is sudden acceleration/deceleration. Patients
with brain atrophy, such as alcoholics or the elderly, are more
susceptible to SDH.
 In infants, SDH is strangely associated with nonaccidental trauma. In
acute SDH, patients present within 14 days of the injury, and most
become symptomatic within 24 hours of injury.
 After two weeks, patients are defined as having a chronic SDH.
 Symptoms may range from a headache to lethargy or coma. It is
important to distinguish between acute or chronic SDHs by history,
physical examination, and CT scan.
 An acute SDH appears as a hyperdense, crescent-shaped lesion that
crosses suture lines.
3.4.3 Epidural hematoma
 An epidural hematoma results from an acute collection of blood
between the inner table of the skull and the dura mater. It is typically
associated with a skull fracture that lacerates a meningeal artery,
most commonly the middle meningeal artery.
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 Underlying injury to the brain is not necessary to be severe.

 In the classic scenario, the patient experiences loss of consciousness
after a head injury. The patient may be present to the ED with clear
mentation, signifying the lucid interval, and then begin to develop
status deterioration in the ED. A fixed and dilated pupil on the side of
the lesion with contralateral hemiparesis is a classic late finding.
 The high-pressure arterial bleeding of an epidural hematoma can lead
to herniation within hours of injury.
 An epidural hematoma appears biconvex on a CT scan.
3.4.4 Traumatic subarachnoid hemorrhage
 This condition results from the disruption of subarachnoid vessels and
presents with blood in the CSF. Patients may complain of diffuse
headache, nausea, or photophobia.
 Traumatic subarachnoid hemorrhage may be the most common CT
abnormality in patients with moderate or severe TBI. Some cases
may be missed if the CT scan is obtained less than 6 hours after
injury.
3.4.5 Cerebral contusions and intracerebral hemorrhage
 A common location for contusions is the frontal poles, the sub-frontal
cortex, and the temporal lobe.
 Contusions may occur directly under the site of impact or on the
contralateral side (contrecoup lesion). The contused area is usually
hemorrhagic with surrounding edema and occasionally associated
with subarachnoid hemorrhage.
 Neurological dysfunction may be profound and prolonged, with
patients demonstrating mental confusion, obtundation, or coma. Focal
neurological deficits are usually present.
3.4.6 Herniation
 Diffusely or focally increased ICP can result in herniation of the brain
at several locations.
 Transtentorial (uncle) herniation occurs when an SDH or temporal
lobe mass forces the ipsilateral uncus of the temporal lobe through
the tentorial hiatus into the space between the cerebral peduncle and
the tentorium. This results in compression of the oculomotor nerve
and parasympathetic paralysis of the ipsilateral pupil, causing it to
become fixed and dilated. When the cerebral peduncle is further
compressed, it results in contralateral motor paralysis. The increased
ICP and brain stem compression resulting in a progressive
deterioration in the level of consciousness. Occasionally, the
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contralateral cerebral peduncle is forced against the free edge of the

tentorium on the opposite side, resulting in paralysis ipsilateral to the
lesion – a false localizing sign.
 Central transtentorial herniation occurs with midline lesions in the
frontal or occipital lobes or in the vertex. Bilateral pinpoint pupils,
bilateral Babinski signs, and increased muscle tone are found initially,
which eventually develop into fixed midpoint pupils, prolonged
hyperventilation, and decorticate posturing.
 Cerebellotonsillar herniation through the foramen magnum occurs
much less frequently. Medullary compression causes flaccid paralysis,
bradycardia, respiratory arrest, and sudden death.
3.4.7 Penetrating injuries
Gunshot wounds and penetrating sharp objects can result in penetrating
injury to the brain. The degree of neurological injury will depend on the
energy of the missile, whether the trajectory involves a single or multiple
lobes or hemispheres of the brain, the amount of scattering of bone and
metallic fragments, and whether a mass lesion is present.
3.4.8 Shaken baby syndrome
The potential life-threatening head injury in children <2 years is caused
by rapid acceleration and rotation of the head. Shearing injuries of the
brain or intracranial vessels and cervical spine injuries may result. Almost
half of the children found with syndrome exhibit no external signs of
trauma, so clinical vigilance must remain high.
Table 3.3 – Emergency department management, care, and
disposition
Element Comments
Initial Initiate standard protocol for evaluation and
stabilization of trauma patients. Search carefully for
other significant injuries.
Administer 100% oxygen and secure cardiac
monitoring and two IV lines; for patients with severe
TBI, endotracheal intubation (via rapid sequence
intubation) to protect the airway and prevent
hypoxemia is the top priority. Provide cervical spine
immobilization, and use an adequate
sedation/induction agent when securing the airway.
If hypotension Hypotension is associated with an increased
mortality rate. Restoration of adequate blood
pressure is vital to maintain cerebral perfusion.
Resuscitation with IV crystalloid fluid to a MAP > 80
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mm Hg is indicated; if aggressive fluid resuscitation

is not effective, then add vasopressors to maintain
a MAP MAP > 80 mm Hg.
Neurosurgical Obtain immediate neurosurgical consultation after a
consultation head CT scan demonstrating intracranial injury has
been identified.
Patients with new neurologic deficits from an acute
epidural or SDH require emergent neurosurgical
treatment.
If increased All patients who demonstrate signs of increased
ICP ICP should have the head of their bed elevated 30
degrees (provided that the patient is not
hypotensive), adequate sedation, and maintenance
of adequate arterial oxygenation. If the patient is
not hypotensive, consider administering mannitol,
0.25 to 1.0 gram/kg IV bolus.
Hyperventilation is not recommended as a
prophylactic intervention to lower ICP because of
its potential to cause cerebral ischemia. Reserve
hyperventilation as a last resort for lowering ICP; if
used, implement it as a temporary measure and
monitor the PCO2 closely to maintain a range of 30
to 35 mm Hg.
If brain Patients with signs of impending brain herniation
herniation may need emergency decompression by
trephination (burr holes) when all other methods to
control the elevated ICP have failed. CT scan prior
to attempting trephination is recommended to
localize the lesion and direct the decompression
site.
Admission Admit patients with a basilar skull fracture or
penetrating injuries (gunshot wounds or stab
wounds) to the neurosurgical service and start them
on prophylactic antibiotic therapy (e.g., ceftriaxone
1 gram every 12 hours ).
Discharge Discharge patients who have an initial GCS score
of 15 that is maintained during an observation
period and who have normal serial neurologic
examinations and a normal CT scan.
Discharge patients home with a reliable companion
who can observe them for at least 24 hours, carry
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out appropriate discharge instructions and follow

the head injury sheet instructions.
Observation Patients who have an initial GCS score of 14 and a
normal CT scan should be observed in the ED. If
their GCS score improves to 15 and they remain
symptom-free and neurologically intact after serial
examinations, they can be discharged home.
Chapter 4: ABDOMINAL PAIN

4.1. Chronic Constipation
4.1.1 Definition
Three or fewer bowel movements per week.
4.1.2 Symptoms & physical examination:
Constipation symptoms is defined by Rome III diagnostic criteria:
Table 4.1 – Rome IV Diagnostic criteria for functional constipation
1. Must include two or more of the following for the last three
months, with symptoms onset at least six months before
diagnosis:
– Straining during at least 25% of defecations
– Lumpy or hard stool in at least 25% of defecations
– Sensation of incomplete evacuation for at least 25% of defecations
– Sensation of anorectal obstruction or blockage for at least 25%
defecations
– Manual maneuvers to facilitate at least 25 percent of defecations
(e.g., digital evacuation, support of the pelvic floor)
– Fewer than three defecations per week
2. Loose stools are rarely present without the use of laxatives
3. There are insufficient criteria for irritable bowel syndrome

Diagnostic evaluation is mostly by history and physical examination. No
testing or imaging is routinely recommended in the initial evaluation of a
patient with chronic constipation unless the patient has other clinical
symptoms suggestive of medical causes.
First line: non pharmacological ( life style modification )
 Schedule toileting after meals.
 Increase fiber intake gradually
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 Increase water intake to 1.5-2 L per day.

 Exercise if possible.
4.1.5 Second line: pharmacological
 Stool softener: Docusate sodium .
 Stimulant laxatives: Bisacodyl tablets , Senna tablets
 Bulking agents: Methylcellulose powder , Polycarbophil tablets ,
Psyllium powder.
 Osmotic laxatives: lactulose solution , Polyethylene glycol ,
Magnesium citrate.
o If the symptoms improved after life style modification or
medication continue on it.
o If symptoms not improved refer to further evaluation.
o Patients with one or more of the red flag features should
undergo endoscopic/colonoscopic evaluation.
4.2. Irritable Bowel Syndrome
 Cramping abdominal pain related to defecation.
 Altered bowel habits.
 Other G.I. symptoms: Feeling of incomplete evacuation, looser stools
at the onset of pain, bloating, or a passage of mucus.
4.2.2 Diagnosis:
IBS is diagnosed with Rome IV criteria. It is defined as recurrent
abdominal pain with at least one per day per week in the previous three
months, associated with two or more of the following:
 Related to defecation (improve or worsen)
 Associated with a change in stool frequency
 Associated with a change in the stool form
If the patient meet the criteria for IBS and has no alarming features no
testing or imaging is routinely recommended.
First line: life style modification :
 Diet:
o Eating in moderation, decrease fatty and spicy food
o Avoid caffeine, soft drinks and sweeteners.
 Exercise: vigorous exercise 3-5 times per week
Second line: complementary therapy :
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 Peppermint oil.
 Antispasmodic : for pain management.
 Antidepressant: SSRI and tricyclic for abdominal pain and symptoms
score.
 Laxative, lubiprostone and neomycin: for constipation.
 Loperamide, Rifaximin and Alosetron : for diarrhea.
4.3. Celiac Disease
 Intestinal:
o Diarrhea and steatorrhea.
o Abdominal pain.
o Abdominal distention, bloating and flatulence.
o Nausea.
o Loss of appetite
o Weight loss or poor weight gain.
 Extraintestinal:
o Anemia or nutritional deficit.
o Dermatitis herpetiformis.
o Osteoporosis.
o Peripheral neuropathy, seizure and impaired cognition function.
o Aphthous ulcer and atrophic dermatitis.
 IgA tissue transglutaminase (tTG).
 Total IgA.
 Small bowel biopsy : gold stander.
 IgG deaminated gliadin peptide.
o If positive tTG and normal IgA : refer for biopsy.
o If normal tTG and IgA : consider other diagnosis.
o If IGA deficiency: order IgG deaminated gliadin peptide.
o If IgG deaminated gliadin peptide: refer for biopsy.
 Gluten - free diet is the only accepted treatment for celiac disease.
 Monitor for iron and vitamin deficiency and supplement as needed.
 Screen for osteoporosis and depression.
 For rapid control of symptoms:
Adult: Prednisolone 30-40 mg/d; taper off completely in 6-8
weeks:
 Follow up: 4-8 weeks after strict diet has been started.
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 antibodies can be followed every three to six months until

normalization.
 Referral indication:
o Endocrine: patient with Hashimoto thyroiditis.
o Gastroenterology: failed gluten -free diet and to start
corticosteroid.
4.4. Inflammatory bowel disease
4.4.1 Crohn’s disease:
Chronic inflammatory condition affecting gastrointestinal tract at any
point from mouth to anus.
Symptoms & physical examination:
 Common symptoms include:
o diarrhea, abdominal pain, rectal bleeding,
o fever, weight loss, and fatigue.
 Extraintestinal symptoms:
o episcleritis, scleritis or anterior uveitis.
o Cholelithiasis or nephrolithiasis.
o Anemia or venous thromboembolism.
o Inflammatory arthropathies or osteoporosis.
o Erythema nodosum or pyoderma gangrenosum.
 Important history elements:
o Nocturnal history, urgency or food intolerance.
o Travel history including antibiotic.
o Family history of IBD.
o Smoking history.
 Abdominal and anorectal examination :
o tenderness, distention, and/or masses.
o abscesses, fissures or fistulas.
 to rule out Crohn’s: fecal calprotectin
 to support diagnosis : CBC, ESR, CRP and stool studies for
clostridium or ova .
 to assess disease activity: CRP, fecal calprotectin, and stool
lactoferrin.
 Periodic follow up for complication:
o Anemia: hemoglobin and hematocrit.
o Nutritional deficiencies: iron, folate and vitamin D.
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 when methotrexate, thiopurines and/or biologic agents are used for

treatment: CBC, renal and hepatic panel.
 Imaging for making the initial diagnosis, monitoring disease activity,
and identifying complications:
o C.T or MR enterography.
o Standard abdominal/pelvic MRI with and without contrast.
 endoscopic procedures:
to allows direct visualization,identification of characteristic lesions,
monitoring therapy, screening for colorectal cancer and taking biopsy
and therapeutic intervention.
Management plan :
o Corticosteroid.
o Immunomodulator.
o Biological therapies.
 Surgical :
o To treat fistulas, abscess or perianal disease.
o Perforation, obstruction, malignancies.
 Other therapies:
o Enteral nutrition to induce remission in children.
 Preventative measures:
o Screen for depression and osteoporosis.
o Colonoscopy for all patient within 8 years symptoms onset and
every 1-3 years.
o Smoking cessation.
o Annual vaccination for influenza.
o In patients on immunosuppression: annual screening for cervical
cancer, consider human papillomavirus vaccine, PCV13 and
PPSV23 vaccines.
4.4.2 Ulcerative colitis:
inflammatory bowel disease that is limited to the colon.
Symptoms & physical examination:
 Common symptoms include:
o abdominal pain.
o Diarrhea and hematochezia.
 Extraintestinal symptoms:
o uveitis.
o Aphthous stomatitis .
o Arthritis or ankylosing spondylitis.
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o Primary sclerosing cholangitis.

o Erythema nodosum, psoriasis or pyoderma gangrenosum
 Important history elements:
o Bloody or small frequent volume diarrhea.
o Bowel urgency or nocturnal bowel movement.
 Elevated fecal calprotectin and lactoferrin level
 To distinguish the condition from Crohn’s disease in those with
indeterminate histology:
o Perinuclear antineutrophil cytoplasmic antibodies (ANCA)
o Anti-saccharomyces cerevisiae antibodies (ASCA).
 CRP and ESR insensitive for detecting ulcerative colitis.
 Endoscopic biopsy is used to confirm the diagnosis.
Management plan :
1. Active disease:
 For mild to moderate distal colitis:
Topical 5-aminosalicylic acid (5-ASA) (suppository and enema) for 4-6
weeks.
 For mild to moderate extensive colitis:
o Oral 5-ASA for 4-6 weeks in addition to topical.
o If no improvement: oral corticosteroid 4-6 weeks.
o If no improvement: infliximab for 4-6 weeks.
o If no improvement: IV corticosteroids, cyclosporine, or colectomy
 Sever to fulminant colitis:
Admission if needed or outpatient IV corticosteroids then,
azathioprine, cyclosporine, infliximab, or colectomy if needed.
2. Maintenance:
 the same agent is usually used to maintain remission.
3. Preventative measures:
 Screen for depression and osteoporosis.
 Colonoscopy for all patient within 8 years symptoms onset and every
1-3 years.
 Smoking cessation.
 Annual vaccination for influenza.
 In patients on immunosuppression: annual screening for cervical
cancer, consider human papillomavirus vaccine, PCV13 and PPSV23
vaccines.
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4.5. Chronic Pancreatitis

4.5.1 Definition:
irreversible and progressive disorder of the pancreas characterized by
inflammation, fibrosis, and scarring. Exocrine and endocrine functions
are lost, often leading to chronic pain.
 chronic epigastric pain radiating to the back.
 Exocrine dysfunction: malabsorption or steatorrhea.
 Endocrine dysfunction: lead to diabetes.
 Other complication my raise:
o Recurrent pancreatitis.
o Osteoporosis or osteopenia.
o Weight loss.
 Laboratory tests are ordered according to the presenting complaint of
the patient :
o If infection or abscess: CBC .
o If ductal obstruction: hepatic enzyme and total bilirubin.
o If diabetes: fasting blood sugar.
o Lipid profile: high triglyceride can cause chronic pancreatitis.
o Pancreatic function tests are not routinely recommended, can be
used if normal imaging.
 maging studies should progress from least invasive to more invasive:
o CT scan: if positive manage chronic pancreatitis.
o MRI or MRCP: if CT scan negative.
o Endoscopic ultrasonography: if negative MRI and MRCP.
o ERCP: if negative pancreatic ultrasonography and normal
pancreatic function.
The goal of treatment is to
 Improve pain and quality of life,
 Decrease morbidity and mortality from endocrine and exocrine
pancreatic dysfunction.
1. lifestyle modification:
 Low-fat diet and small meals
 Cessation of alcohol and tobacco use
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 Vitamin supplementation (A, D, E, K, and B12) to overcome patient’s

deficiency
2. pain control: stepwise approach
 Paracetamol or NSAIDS.
 Narcotics.
3. Treat comorbidities and complications.
4. Endoscopy:
 treat symptomatic strictures, stones, and pseudocysts.
5. Surgery:
 Endoscopic.
 Surgical procedures.
4.6. Chronic diarrhea
4.6.1 Definition:
Definition: predominantly loose stool lasting longer than four weeks
Table 4.2
Diagnosis Clinical features Investigations
Bacterial Can cause chronic HIV, stool test, and
enterotoxin symptoms in serology.
(e.g., cholera) immunocompromised
patients
Bile acid Similar to functional Serum C4, FGF19, 48-
malabsorption diarrhea and IBS hours fecal bile acids,
(common) trial of cholestyramine
and SeHCAT if available
Brainerd History of raw milk R/O other causes, non-
diarrhea ingestion, acute diarrhea specific
last for >= 4 weeks
Crohn’s Fever, weight loss, joint CBC, fecal calprotectin,
disease ileitis pain, abdominal pain, colonoscopy with
Anal fissure biopsy
Endocrine Fatigue, anxiety, TSH, serum electrolytes,
disorders tachycardia, dry skin adrenal hormone
stimulation test.
AlcoholismMedi Alcohol abuse, Trial off medication if
cation medication use possible, treat
alcoholism
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Microscopic Similar to functional Colonoscopy with biopsy

colitis diarrhea and IBS
(common)
Neuroendocrine Carcinoid syndrome C.T.MRI Endoscopy Hor
tumors (watery diarrhea, monal assay
flushing, bronchospasm,
hypotension, right-sided
heart failure) is usually
asymptomatic
Post-surgical Surgical history, Scars None
(cholecystecto
my,
gastrectomy,
vagotomy,
bariatric
surgery)
Vasculitis Oral and genital CBC, CRP, clinical
aphthosis, uveitis, diagnosis often needs
thrombosis, more time.
pseudofolliculitis
Carbohydrates Food trigger, family Breath testTrial of
malabsorption history certain food avoidance.
(e.g., lactose,
fructose) can
also cause fatty
diarrhea.
Celiac disease; Gluten food trigger, Tissue-transglutaminase
can also cause family history, type 1 IgA, total IgA, upper
a fatty D.M., Down syndrome, endoscopy with biopsy.
malabsorption neurological symptoms,
(common) dermatitis herpetiform,
IDA
Medications, Medications Excessive Trial off medication if
excessive sugar or sweet intake possible, decrease or
intake of certain stop causative food if
foods possible
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Table 4.3 – Rome IV Diagnostic criteria for functional diarrhea

1. Loose or watery stools without predominant abdominal pain or
bothersome bloating
2. Loose stools occur >25% of the time
3. Symptoms must be there for the last 3 months with symptoms

onset at least 6 months to diagnosis
4. Irritable bowel syndrome predominant diarrhea must be excluded

If meet Rome IV criteria and normal CBC, celiac serology,
CRP and metabolic panel:
 Diagnose IBS and treat.
If not meet the criteria :
 Positive fecal immunochemistry, calprotectin or lactoferrin: treat
inflammatory diarrhea.
 Elevated fecal fat: treat fatty diarrhea.
 Other lab abnormality : treat accordingly.
 If all negative : treat watery diarrhea.
 If no clear diagnosis or failed treatment:
o Colonoscopy with biopsy.
o Consider specialty consultation.
Chapter 5: ANORECTAL AND
COLORECTAL DISEASE
5.1. Diverticular Disease
5.1.1 Definition :
 Diverticula are saclike protrusions of mucosa through the muscular
colonic wall.
 Diverticulitis occurs when the diverticula become plugged and
inflamed.
5.1.2 Signs and Symptoms :
 Diverticulosis is usually asymptomatic
 Painless rectal bleeding
Common diverticulitis symptoms:
 Colicky abdominal pain mainly in the left lower quadrant
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 Attacks are precipitated by eating

 Constipation is common
5.1.3 Physical examination signs:
Tenderness in the left lower quadrant, or occasionally a tender palpable
loop of sigmoid colon.
5.1.4 Complications
 Bleeding from diverticulosis
 Free perforation, abscess, fistula, obstruction, or stricture
 Formation of scar tissue, leading to narrowing and obstruction of the
colonic lumen
Gold standard: CT scan of the abdomen and pelvis is the optimal
method.
Non-pharmacological
 Strict adherence to diet
 Dietary management o Nothing by mouth (NPO) status for acute
treatment
 Full-liquid diet or low-fiber diet if not on bowel rest
 Long-term dietary management o A high-fiber diet, including bran,
beans, fruits, and vegetables
 Bulk agents, if unable to tolerate bran
 Note foods to avoid such as nuts
 Acute treatment may include the following: o Nasogastric (NG) tube
placement
 Intravenous (IV) fluids
 Surgical intervention is required for abscess, peritonitis, obstruction,
fistula, or failure to improve after several days of medical
management
Pharmacological
 Diverticulitis initial attack: Ciprofloxacin (Cipro) 500 mg orally twice
daily and metronidazole (Flagyl) 500 mg orally three times daily for 7
to 14 days
 Amoxicillin/clavulanic acid or sulfamethoxazole-trimethoprim may also
be used with metronidazole
 Avoid laxatives, enemas, opiates, and NSAIDs
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Follow up
 Follow up in 2–3 days
 Colonoscopy should be performed from 6–8 weeks after recovery to
evaluate the extent of diverticulosis/rule out other manifestations
Consultation/referral
Arrange for prompt hospitalization and surgical consultation if
 the patient’s temperature rises above 38.3℃
 pain worsens, peritoneal signs develop.
 WBC continues to rise.
5.2. Anorectal Disease
5.2.1 Assessment
History and physical examination including a digital rectal examination,
and anoscopy are usually enough to reach diagnosis in most cases.
History
The patient may be presented with many symptoms (Table 5.1). Detailed
bowel movement history should be obtained, previous endoscopy or
colonoscopy, and their results may help guide you in eliminating red
flags.
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Table 5.1 – Anorectal symptoms and differential diagnosis

Symptom Differential diagnosis
Anal bleeding Anal fissuresHemorrhoids Upper or
lower GI bleeding
Incontinence Fecal impaction.Fistula.Neurologic
disease Rectal prolapseSphincter
defect
Mass Perianal abscessCondyloma or
perianal warts Hemorrhoids
Pilonidal cysts Rectal prolapse
Pain Perianal abscess Anal fissures
Fistula Proctalgia fugax Rectal
prolapseThrombosed external
hemorrhoids
Pruritus Dermatologic condition Excessive
hygiene External hemorrhoids
Infection MedicationPruritus ani
5.3. Hemorrhoids
5.3.1 Definition:
dilation of the venous plexus and connecting tissue and an outgrowth of
anal mucosa from the rectal wall.
5.3.2 Types:
 Internal hemorrhoids: develop above the dentate line are internal.
 External hemorrhoids : develop below the dentate line
5.3.3 Symptoms
Internal hemorrhoids are usually asymptomatic while external
hemorrhoids are painful.
Associated symptoms include bright red bleeding, prolapse, soiling, and
itching.
5.3.4 Physical examination :
inspection of the perineal and rectal areas for obvious external
hemorrhoids or prolapse of internal hemorrhoids.
A digital rectal examination can detect masses, tenderness, fluctuance,
and large or prolapsed internal hemorrhoids.
Anoscope may be used for better visualization.
If strangulated patients may present with acute onset of perianal pain
and a palpable perianal “lump” from thrombosis.
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Endoscopic evaluation is not needed if there are no red flags (e.g.,
weight loss, abdominal pain, fever, signs of anemia), do not have a
personal or family history of colorectal cancer or inflammatory bowel
disease, and respond to medical management.
Medical treatment
 Increase fiber in diet in addition to fiber supplementation if needed
 Increased water intake
 Warm water (sitz) baths
 Stool softeners
 Anti-hemorrhoidal creams and suppositories for temporary associated
symptomatic relief
 Benzocaine
 Dibucaine
 Pramoxine
 Hydrocortisone
 Topical nitroglycerin as a 0.4% ointment and topical nifedipine for pain
relief
Surgical treatment
 office based (banding and infrared photocoagulation) to treat grade I
to III internal hemorrhoids
 surgical hemorrhoidectomy for more complicated hemorrhoids or
medical failed treatments.
5.4. Anal Fissure
5.4.1 Definition:
tear to the anoderm within the distal half of the anal canal.
Pain that is provoked by defecation and lasts for hours afterward, often
with associated anal bleeding.
By either directly visualizing a fissure or reproducing anal pain by gentle
digital palpation of the anal verge.
5.4.4 Acute vs chronic fissure
The pathognomonic feature of an acute fissure (<8 weeks) is a
superficial tear, while a chronic fissure (>8 weeks) appears hypertrophied
with skin tags and/or papillae.
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Initial medical management
Four weeks of medical therapy with all of the following:
 Increase fiber intake and fiber supplementation may also be added
 Sitz bath.
 Stool softener for a patient with constipation
 Emollients suppository
 Topical analgesic (2% lidocaine)
If no improvement after 4 weeks
 Topical nifedipine or topical nitroglycerin
 Botulinum toxin can be injected locally into the sphincter may be
useful.
Follow up :
If the patient didn’t improve after a trial of eight weeks of medical therapy,
the patient should be referred for surgery (sphincterotomy) that rapidly
reduces symptoms.
5.5. Proctalgia Fugax
5.5.1 Definition:
is a functional anorectal disorder characterized by severe, intermittent
episodes of rectal pain that are self-limited.
recurrent attacks of severe anorectal pain that may last from a few
seconds to minutes, but the duration does not exceed 30 minutes.
5.5.3 Diagnosis:
Rome IV criteria requires all of the following criteria to be fulfilled for the
past three months, with symptom onset at least six months prior to
diagnosis:
 Recurrent episodes of pain localized to the rectum and unrelated to
defecation
 Episodes last from seconds to minutes, with a maximum duration of
30 minutes
 Absence of anorectal pain between episodes
 Exclusion of other anorectal and pelvic pathology
Mild symptoms
Reassurance and explanation.
Moderate and Severe symptoms
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 Sitz baths
 Fiber supplementation
 Topical nitroglycerin
 Topical calcium channel blockers
 Inhaled salbutamol
 Biofeedback therapy
 Botulinumtoxin A injections can be considered
5.6. Perianal Hematoma
5.6.1 Definition:
The hematoma is caused by the rupture of a blood vessel beneath the
anal skin.
blue-black bulge in the skin near the margin of the anus.
the perianal hematoma resolves over a few days, and requires only oral
analgesia. If the pain becomes intolerable, then it is possible to excise
and drain the hematoma under anesthesia.
5.7. Perianal Abscess
5.7.1 Symptoms :
painful swelling in the anal area.
redness, pain, and induration and should focus on measuring the size
and anal sphincter involvement. An opening with or without drainage
suggests a fistula formation.
MRI is advised for patients with recurrent abscess or patients who fail
initial treatment.
 A superficial abscess that does not involve the anal sphincter: incision
and drainage can be done by a Family physician in an outpatient
setting under local anesthesia with epinephrine. Packing should be
avoided as it delays healing.
 Abscess involving anal sphincter or fistulas: should be referred for
surgery.
 Follow up: abscess should be followed up postoperatively until
completely healed.
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5.8. Perianal Warts (Condyloma)

5.8.1 Definition:
Is caused by Human papillomavirus by direct skin contact.
Condylomas are at risk for anorectal cancer
Diagnosis is mostly clinical by history and physical examination.
Patient applied therapies include
 Imiquimod 5% applied three times a week.
 Podofilox 0.5% solution.
 Sinecatechins 15% ointment.
Clinicians applied therapies include
 Podophyllin.
 Trichloroacetic acid.
Destructive techniques include
 Cryosurgery.
 Electrosurgery.
 Surgical excision.
5.9. Fecal Incontinence
5.9.1 Definition:
It is a recurrent uncontrolled passage of fecal material.
 Inspection: ask the patient to strain to evaluate for prolapse.
 Digital rectal exam to assess for rectal tone and rule out impaction.
 Neurological examination: pinprick test examination in the perianal
area for sensation.
5.9.3 Investigations :
If initial treatment fails pelvic MRI or endoanal ultrasonography should be
done to assess sphincter defects.
Initial treatment
 Correcting the underlying cause if possible.
 Impaction should be treated with medical or manual disimpaction.
 Diarrhea should be treated with anti-diarrheal agents.
 Biofeedback is a first-line treatment.
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 Other treatment options include fiber supplements, a fluid

management diet, and stool diaries.
Surgical management
 Sphincteroplasty or anal bulking injections
 Colostomy in patients with severe symptoms may improve the quality
of life.
5.10. Pilonidal Disease
5.10.1 Definition:
This is a common condition of the skin and subcutaneous tissue at or
near the upper part of the natal cleft of the buttocks.
5.10.2 Symptoms:
Mainly two types
 Acute exacerbation: o Sudden onset of mild-to-severe pain
 swelling with mucoid, purulent, and/or bloody drainage.
 Fever is associated with an undrained abscess.
 Chronic: recurrent or persistent drainage and pain.
 Acute exacerbation: o Cellulitis in the natal cleft
 Tender Fluctuant mass (abscess).
 Chronic disease:
 sinus openings draining mucoid, purulent, and/or bloody fluid.
 hair protruding from a sinus opening.
clinical diagnosis depending on history and physical examination only
 Acute abscess: immediate incision and drainage.
 Chronic or recurrent disease: Surgical excision is the mainstay of
operative management.
Chapter 6: UROLOGY AND GENITAL
DISORDERS
6.1. Benign Prostatic Hyperplasia
The most common lower urinary tract symptoms are:
 Obstructive voiding symptoms (weak or intermittent urinary stream,
straining, hesitancy, and dribbling).
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 Urine storage (irritation) symptoms (urgency, frequency, nocturia, and

urge incontinence) and post micturition dribbling.
Acute urinary retention and irreversible renal insufficiency are
uncommon.
Therefore, management decisions should be based on the presence and
severity of symptoms.
Association (AUA) Symptom Index is a validated seven-question
instrument that can objectively assess the severity of BPH.
Figure 6.1 – The American Urological Association (AUA) Symptom Index
mild BPH <7

moderate BPH 8-19
severe BPH 20-35
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Physical examination findings include a non-tender, enlarged prostate on

digital rectal examination (DRE). The size of the Prostate on examination
does not correlate well with symptom severity
The AUA recommends urinalysis for all men presenting with LUTS,
Normal urinalysis findings help rule out non-BPH causes
Prostate imaging
Trans-rectal ultrasound is not needed for diagnosis. It is indicated only
when the treatment choice of LUTS/BPH is dependent on total prostate
volume, as in the use of 5-ARIs (5-Alpha reductase inhibitors) or the
selection of certain surgical techniques.
According to the AUA urinary symptom score: the patient can be classified
into:
 Less than 7 (mild): Watchful waiting
 8-19 (moderate): Alpha-1-adrenergic antagonist (monotherapy)
 More than 20 (severe ): A combination of an alpha-1-
adrenergic antagonist and 5-alpha-reductase inhibitor
 Surgical options if medical treatment failed after 12–24 months
 Nonbothersome moderate (8 to 19) to severe (20 to 35) symptoms
require no treatment.
BPH Medications
 Alpha-1 antagonists: Tamsulosin,,Terazosin and Doxazosin
 5-alpha Reductase Inhibitors: finasteride , dutasteride and epristeride
 Combination therapy may help if:
o Severe symptoms
o Large Prostate volume (>40 ml)
o Those who do not get an adequate response to maximal dose
monotherapy with an Alpha-adrenergic antagonist
o Grade 2A
 Phosphodiesterase type 5 inhibitors:
They are used for patients with BPH-related symptoms and erectile
dysfunction.
 . Tadalafil 5 mg/day has been approved for use in men with
LUTS/BPH.
Referral for surgical treatment
Once patients have failed medical management, they should be
considered for surgical therapy.
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Some indication for referral are:

 Moderate-to-severe LUTS/BPH that are refractory to medical therapy.
 Recurrent urinary tract infection attributed to BPH.
 Recurrent bladder stones and gross hematuria.
 Bilateral hydronephrosis with renal functional impairment.
Surgery
 Transurethral resection of the prostate (TURP).
 Transurethral microwave thermotherapy (TUMT)
 Water vapor thermal therapy (WVTT)
6.2. Acute Bacterial Prostatitis
Symptoms
Voiding symptoms:
 irritative (e.g. Dysuria, urinary frequency, urinary urgency)
 obstructive (e.g., Hesitancy, incomplete voiding, straining to urinate,
weak stream)
 Pain ; suprapubic, rectal, or perineal painful ejaculation,
hematospermia and painful defecation possible,
Systemic symptoms (fever, chills, nausea, emesis, and malaise).
Physical exam
The prostate is often firm, edematous, and exquisitely tender.
Investigations
Urine analysis,
elevated inflammatory markers ( ESR , CRP )
findings include peripheral leukocytosis, pyuria, bacteriuria, and,
occasionally, positive blood cultures
Elevated PSA, if serum PSA testing for prostate cancer screening is
planned, it should be deferred for one month following the resolution of
acute prostatitis.
Blood cultures to evaluate for bacteremia are warranted in patients with
signs suggestive of severe sepsis (e.g., hypotension, hematologic
derangements).
 Trimethoprim-sulfamethoxazole (one double-strength tab orally every
12 hours)
 fluoroquinolone (ciprofloxacin 500 mg orally every 12 hours or
levofloxacin 500 mg orally once daily) as empiric therapy.
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 Younger than 35 years, who are sexually active, and men older than
35 years, who engage in high-risk sexual behavior, should be treated
with regimens covering N. Gonorrhoeae and C.trachomatis:
o Ceftriaxone dose of 500 mg IM < 150 kg
o 1 g intramuscularly in a single dose for patients weighing ≥ 150
kg
o Azithromycin (1 g orally once) or doxycycline 100 mg orally twice
daily for seven days.
If cannot tolerate oral medication, demonstrate signs of severe sepsis, or
have bacteremia. In such cases, intravenous levofloxacin or ciprofloxacin
may be given with or without an aminoglycoside (gentamicin or
tobramycin 5 mg/kg daily if the creatinine clearance is normal).
Treatment duration
Mild infection is typically 10 to 14 days; 4 weeks for severe infections.
6.3. Prostate Cancer Screening
 The decision to undergo periodic prostate-specific antigen (PSA)–
based screening for prostate cancer should be an individual one.
 The USPSTF recommends that clinicians inform men ages 55–69
years about the potential benefits and harms of PSA-based screening
for prostate cancer.
 The USPSTF recommends against PSA-based screening for
prostate cancer in men aged 70 years and older. (Recommendation
grade D)
 American Cancer Society suggested screening for high risk to start at
age 40 to 45 for:
o Black men
o Men with a family history of prostate cancer, particularly in a first-
degree relative who was diagnosed at age <65 years.
 The use of digital rectal examination(DRE) is not recommended as a
screening method
 Most early prostate cancer is asymptomatic. Symptoms associated
with advanced disease may include lower urinary tract symptoms,
hematuria or hematospermia, erectile dysfunction, and bone pain.
 Clinical signs associated with prostate cancer include an elevated
prostate-specific antigen (PSA) on laboratory testing and an abnormal
prostate finding on digital rectal examination (DRE).
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 False-positive results that required additional workup: prostate biopsy.
Definitive diagnosis of prostate cancer requires histopathologic analysis
of biopsy.
Proceed to biopsy if the patient has a life expectancy of at least ten years
and one of the following:
 PSA (on initial PSA testing and on repeat a few weeks later) that is
elevated above the range for the patient’s age cohort
 An increase in the PSA of more than 0.75 ng/mL over one year
 A nodule induration or asymmetry on DRE.
If the PSA results are equivocal, adjunctive testing (e.g., PSA density,
PSA doubling time, magnetic resonance imaging [MRI]) can be useful to
better estimate the likelihood of prostate cancer. If the patient has
significant comorbidities that limit life expectancy, a prostate biopsy to
evaluate for the possibility of asymptomatic prostate cancer is usually not
warranted.
6.4. Genitourinary Disorders in Primary Care
6.4.1 Hydroceles
A hydrocele is a collection of fluid in the scrotum, usually between the
layers of the tunica vaginalis. In children, three broad categories exist for
a hydrocele:
 Communicating.
 Noncommunicating.
 Reactive.
Symptoms cystic scrotal mass (lump or swelling that is smooth and not
painful)
 Communicating Hydrocele = increase in size during the day or with
the Valsalva maneuver (Figure 6.3)
 Noncommunicating Hydrocele = are not reducible and do not change
in size or shape with crying or straining.
6.4.3 Differential diagnosis (Table 6.2)
Page | 547
Table 6.2 – Differential diagnosis of painless scrotal swelling in

children
Increase with
Valsalva
Mass Population Transillumination? maneuver?
Tumor Firm No No
Varicocel bag of worms No Yes
e
Noncomm fluid filled Yes No
unicating
hydrocele
Communi fluid filled Yes Yes
cating
hydrocele
Inguinal nontender No Yes
hernia reducible mass
without
incarcerat
ion
Scrotal bilateral scrotal No No
edema sweating, soft
Spermato small, soft, and yes No
cele localized cyst
Page | 548
The following algorithm can help you in the clinic to narrow your
differential diagnosis for patients who came with scrotal mass.
Algorithm 6.1 – Evaluation of scrotal mass

6.4.4 Diagnosis
History and by physical examination and transillumination of the scrotum
that demonstrates a cystic fluid collection.
Hydroceles can be confirmed and distinguished from hernias on
ultrasound.
Management plan:
 Many noncommunicating hydroceles will resolve spontaneously
within the first year of life.
 If hydrocele enlarges or begins to fluctuate in size, implicating the
development of a communicating hydrocele, then surgery is indicated.
 Reactive hydroceles will resolve with the primary event and do not
need attention other than treatment for the cause.
 Hydroceles of the spermatic cord do not tend to resolve
spontaneously but rarely require urgent surgery and can also be
corrected after age one year.
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 Surgical correction is similar to a herniorrhaphy: An inguinal incision is

made, the spermatic cord is identified, the hydrocele fluid is drained,
and high ligation of the processus vaginalis is performed.
6.5. Hernias
Groin hernias are caused by a defect of the abdominal wall in the groin
area (protrusions of viscera or adipose tissue through the inguinal or
femoral canal), which result in:
 Inguinal hernia (direct and indirect)
 Femoral hernia
Figure 6.5 – The inguinal (Hesselbach) triangle is an anatomic landmark

bounded by the rectus abdominis muscle medially, the inguinal ligament
inferiorly, and the inferior epigastric vessels laterally.
Swelling (bulge) in the groin area.
Pain (vague discomfort) as a dull aching, pulling, or burning sensation
But up to one-third of patients have no symptoms.
Increased intra-abdominal pressure can worsen the symptoms.
Patients may report having symptoms only at the end of the day or after
prolonged activity and that the bulge disappears when they are lying flat.
However, the absence of a reducible mass or palpable defect does not
rule out a hernia.
Severe pain could suggest that the hernia has become incarcerated and
may require emergent surgical intervention.
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An indirect hernia is often piriform in shape—broad in the scrotum and
narrow over the medial half of the inguinal ligament.
A direct hernia is globular in shape over the medial half of the inguinal
ligament and usually does not enter the scrotum.In women, groin hernias
often do not present with a visible bulge. However, a bulge can
sometimes be detected on direct palpation with the Valsalva maneuver
The diagnosis in men does not need imaging. However, imaging is often
required in women and may be helpful when a recurrent hernia, surgical
complication after repair, or other cause of groin pain (e.g., groin mass,
hydrocele) is suspected.
MRI has a sensitivity of 91%, specificity of 92%, and is superior to
ultrasonography and computed tomography in diagnosing inguinal
hernias, particularly occult hernias.
Herniography.
Recommendations from the Society of American Gastrointestinal and
Endoscopic Surgeons: Avoid the routine use of ultrasonography in
evaluating a clinically apparent inguinal hernia.
Management
The management of groin hernia can be divided into:
Conservative management
Watchful waiting is a reasonable and safe option in men if the patient’s
usual activities are not limited by pain and discomfort, and there is no
difficulty reducing the hernia. But this option is not recommended in
nonpregnant women because of the higher likelihood of femoral hernias,
which are associated with a higher risk of strangulation and for those
with an asymptomatic hernia.
Counsel patients with asymptomatic or minimally symptomatic inguinal
hernias about the expected natural course of the condition and the risks
of emergency surgery and advise them with frequent follow-up (The best
interval for follow-up during watchful waiting is unclear).
Surgical management
Surgical interventions can be categorized as open anterior repair, open
posterior repair, tension-free mesh repair, and laparoscopic repair. Mesh
techniques are strongly recommended because of lower recurrence
rates compared with non-mesh techniques (which have fallen out of
favor in the United States but are still acceptable internationally).
Page | 551
Postoperative care
 Surgeons have recommended four to six weeks of inactivity after
groin hernia repair, which was based on expert opinion.
 There is no evidence that early physical activity increases the risk of
recurrence, regardless of surgical approach.
 Most patients undergoing laparoscopic hernia repair should be
encouraged to resume physical activity three to five days after the
procedure.
 Extended periods of analgesic treatment and extended sick leave are
not supported by evidence.
6.6. Hypospadias
Hypospadias is a congenital anomaly of the male urethra that results in
the abnormal ventral placement of the urethral opening.Newborns with
hypospadias should not be circumcised because the foreskin may be
used for repair.
Figure 6.7
6.6.1 Management
Refer to pediatric urology for further assessment and surgical
intervention. The need for urologic referral is based on the severity of the
hypospadias and family preference (Table 6.4 and Figure 6.7). A urologic
referral is not needed for patients with mild defects and if surgical
reconstructions are not requested by the family.
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6.7. Circumcision and hypospadias

Neonatal Circumcision should be avoided in patients with hypospadias
where the foreskin is asymmetric with abnormal development on the
ventral aspect of the penis.
Newborns with hypospadias should not be circumcised because the
foreskin may be used for repair.
Table 6.3 – Classification of hypospadias based on physical findings

Approximat
e relative Ectopic
frequency urethral Penile Foreskin Manageme
Classification (%) location curvature appearance nt
Forme fruste 10 normal normal normal to no surgical
or location mild correction
hypospadias with a asymmetric or further
(incomplete urethral pet ventral evaluation
or partial or ectopic deficiency ( needed
presence of urethra on incomplete
hypospadias) the distal closure
glans around the
glans)
Standard 40 distal normal to ventral surgical
hypospadias urethral mild deficiency correction
with normal location on asymmetric with a in most
glans width glance or dorsal cases,
(maximal coronal hooded however
diameter 25 margin Moderate appearance families
greater than may
or equal to choose
14 mm) Proximal Ventral observation
urethra deficiency No other
moderate with a evaluation
location on dorsal
penile hooded Surgical
shaft, at the appearance correction
penoscrotal requiredNo
junction, or other
evaluation
Page | 553
within the
scrotum
Severe with 20 severe ventral surgical
an penile correction
abnormally foreskin required
small glans tethering or usually two
(maximal fusion of stage
diameter less the foreskin procedure
than 14 to the Endocrine
millimeters scrotum evaluation
to detect
disorders of
sex
developme
nt
Other 5
variants
Chordee normal mild to normal surgical
without urethral severe correction
hypospadias opening of
and glans chordeeNo
other
evaluation
Megameatus large normal normal correction
intact urethral is usually
prepuce opening at performed
the coronal based on
margin family
preference
No other
evaluation
The recommendations from the American Academy of Pediatrics (AAP)
regarding the best time for surgical intervention is between six months
and one year of age in full-term.
6.7.1 Follow-up care
Following surgical reconstruction, the urinary stream should be
observed. Initially, there may be some spraying of urine, which is normal.
This should resolve over a few months as the swelling from the operation
resolves.
Referral to pediatric urology if two urinary streams ( urinary fistula) and a
thin urinary stream ( urethral stricture).
Page | 554
6.7.2 Circumcision
Male Circumcision is a common elective surgical procedure for the
removal of the foreskin covering the glans penis.
6.7.3 Benefits
Circumcision has been associated with several medical benefits,
including lower rates of:
 Urinary tract infection (UTI)
 Sexually transmitted infections
 Penile inflammation (phimosis, paraphimosis, and balanoposthitis)
 Penile cancer
 Provides good genital hygiene
6.7.4 Disadvantages
As with any surgical intervention, some complications might occur like:
 Bleeding
 Infection
 Inadequate skin removal
 Removal of excessive skin, which may result in a denuded penile
shaft
 Skin bridges
6.7.5 Management
Technique
In brief, the three most common techniques for circumcision are:
 Mogen clamp
 Gomco clamp
 Plastibell device
Contraindications to newborn circumcision
 Anatomic contraindications
 Concealed penis
 Congenital megaprepuce
 Epispadias
 Hypospadias
 Penile torsion
 Penoscrotal webbing
 Medical contraindications
 Admission to a neonatal intensive care unit
 Age < 12 hours
 Bleeding dyscrasias (e.g., hemophilia)
 Current illness
Page | 555
 Jaundice
6.7.6 Post-procedure care
Counseling and education about post-surgical care are very important
and can prevent some complications from occurring.
 Apply petroleum jelly and gauze to the glans after the procedure to
keep the diaper from sticking to the wound during the healing period.
 The newborn can be discharged from the hospital after the
procedure.
 Advise the parents to follow up in 3 to 5 days and counsel them on
applying the dressing with each diaper change until healing is
complete or until the Plastibell falls off (which takes about seven
days).
6.8. Urolithiasis
6.8.1 Definition
Urolithiasis is a general term for stones anywhere within the urinary tract
and is usually categorized according to the anatomical location of the
stones
6.8.2 Assessment
Your history should emphasize more on the pain and the associated
symptoms in addition to the key risk factors for renal stones.
The classical renal colic (severe, acute flank pain that radiates to the
ipsilateral groin) waxes and wanes in severity and develops in waves or
paroxysms .
For those with upper ureteral or renal pelvic obstruction, the pain is
usually in the flank, whereas lower ureteral obstruction causes pain that
may radiate to the ipsilateral testicle or labium.
Other associated symptoms include:
 Nausea and vomiting (with acute episode)
 Malaise; fever and chills
 Urinary frequency and urgency (secondary to bladder irritation by a
stone passage)
 Hematuria (85% microscopic and rarely macroscopic hematuria can
present)
 Testicular pain (because of stone passage)
 Previous episodes of nephrolithiasis
 Risk factors
Page | 556
The physical examination should be directed toward excluding

differential diagnoses (e.g., urinary tract infection, musculoskeletal
inflammation or spasm, ectopic pregnancy, testicular torsion,
malignancy).
CBC, urine culture and urinalysis, serum electrolyte with urea and
creatinine, and a urine pregnancy test as well as imaging to confirm the
diagnosis of kidney stones and assess for hydronephrosis and stone
size and position.
Imaging
US and CT
Although non–contrast-enhanced CT( NCCT) of the abdomen and pelvis
has superior sensitivity and specificity, first-line US has acceptable
performance and is more cost-effective.
Per NICE, the first investigation (image) to order is NCCT scan for any
nonpregnant adult patient with suspected renal colic.
If the patient is pregnant or under 16 years of age, request an urgent
(within 24 hours of presentation) renal US.
In children and young people, consider low-dose NCCT if the diagnosis
remains uncertain after an ultrasound.
First you need to make sure that your patient is stable and does not need
immediate emergency department referral, for example:
 when medical analgesia is insufficient
 when sepsis is suspected
 when anuria, bilateral obstruction, urinary tract infection with renal
obstruction, or obstruction of the sole functioning kidney are present
 women who are pregnant or have delayed menstruation (because of
the risk of ectopic pregnancy)
 patients who have potential comorbidities or are older than 60 years,
especially those with arteriopathy (because of the risk of leaking
abdominal aortic aneurysm)
The main goals of treatment are:
 Ameliorate pain
 Relieve any renal or ureteral obstruction caused by calculi
 Prevent recurrence
Page | 557
Acute pain management and hydration

 Pain relief is the priority in the acute management of renal colic,
which can be managed conservatively with pain medication and
hydration until the stone passes.
 Nonsteroidal anti-inflammatory drugs (e.g., ketorolac, 30 to 60 mg
intramuscularly) are more effective and have fewer adverse effects
than opioids.
 If an opioid is used, meperidine (Demerol) should be avoided
because of the significant risk of nausea and vomiting.
 Neither scopolamine (Buscopan) nor increased fluid intake alleviates
renal colic. NSAIDs should be stopped three days before the
anticipated shock wave lithotripsy (SWL) to minimize the risk of
bleeding.
 Stone size is the major determinant of the likelihood of spontaneous
stone passage, although the stone location is also important.
 Most stones ≤5 mm in diameter pass spontaneously with a
progressive decrease in their pass if >5mm.
 Proximal ureteral stones (renal pelvis) are also less likely to pass
spontaneously.
Medical expulsive therapy
May be attempted with ureteral stones smaller than 10 mm in diameter
for 4 to 6 weeks if the pain is controlled, kidney function is normal, and
there is no evidence of urinary tract infection or ureteral obstruction.
Alpha-blockers facilitate stone passage by promoting ureteral smooth
muscle relaxation.
Tamsulosin 0.4 mg with radiopaque lower ureteral stones of 10 mm or
smaller PO at bedtime for 28 days or until definite stone passage (i.e.,
evidence of stone on urine straining) in addition to standard analgesia
suggest pass stones earlier.
6.8.5 Recurrence Prevention
Lifestyle modifications such as:
 increased fluid intake to reach urine volume of at least 2 L daily (total
daily fluid intake of approximately 2.5 L).
 Decreasing intake of carbonated drinks (colas).
 Diet: should be high in fiber and vegetables, with normal calcium
content (1.0 to 1.2 g/day) and limited sodium (4 to 5 g /day) and
animal protein (0.8 to 1.0 g/ kg/day).
Citrate supplementation, and medications:
Page | 558
 Thiazide diuretics, allopurinol, and citrate supplementation are

effective in preventing calcium stones even in the absence of
hyperuricemia, urinary acidosis, hypocitraturia, or hyperuricosuria.
 Unsweetened lemonade is a more palatable and less expensive
alternative for citrate supplementation.
 Advice your patient to check the potassium level(thiazide diuretics or
potassium citrate) and liver enzyme(allopurinol) before starting these
medications.
 No evidence that Cranberry juice is beneficial for stone prevention.
 No evidence that coffee, tea, and alcohol should be avoided to
prevent stone formation.
6.8.6 Interventional procedures
 Ureteroscopy
 extracorporeal shock wave lithotripsy (ESWL)
 percutaneous nephrolithotomy
These interventional options for renal stone treatment are usually
indicated in the following patients:
 Failure of conservative management
 Intractable pain or vomiting despite analgesic drug therapy
 Pregnancy, if preterm labor is detected or for intractable pain or
vomiting
 stones greater than 10 mm, and many of those between 5 and 10 mm
in size
 Stones that have not passed despite one week of conservative
management
 Stone in the setting of urinary tract infection or sepsis
 Anatomic variations (e.g., ureteral stricture, diminished lumen size)
that make spontaneous passage unlikely
 Struvite stone
6.8.7 Follow up
It is very crucial to follow up with these patients and assess their
response to dietary or medical therapy as well as the stone passage. For
those with stones greater than 5 mm, frequent follow-up is necessary to
avoid complications of infection and renal impairment.
Assessment for adverse drug effects for those patients who are on
pharmacotherapy used for prevention:
 During treatment with thiazides, monitor for hypokalemia with periodic
potassium measurements within 4 to 6 weeks after the start of
therapy and every six months thereafter.
Page | 559
 During treatment with potassium citrate, monitor for hyperkalemia

with periodic potassium measurements within 4 to 6 weeks after the
start of therapy and every six months thereafter.
 During treatment with allopurinol, monitor liver enzyme levels within 4
to 6 weeks after the start of therapy and every six months thereafter
6.8.8 Male Hypogonadism
Male hypogonadism is a clinical syndrome involving subnormal
testosterone levels and/or impaired sperm production due to dysfunction
at one or both levels of the hypothalamic-pituitary-testicular axis.
6.8.9 Types
 Primary hypogonadism (testicular dysfunction)
 Secondary hypogonadism (pituitary or hypothalamus dysfunction)
 Mixed
Table 6.4 – Causes of hypogonadism in men
Type Laboratory values Origin Possible causes
Primary Decreased total Congenital Chromosomal
serum abnormalities,
testosterone, cryptorchidism,
increased LH and Acquired FSH\ alleged
FSH receptor gene
mutation,
klinefelter
syndrome, mitotic
dystrophy
Chemotherapy,
hypothyroidism,
orchitis/epididymal
orchitis,
radiation\trauma to
testes, testicular
torsion
Secondary Decreased total Congenital Common
serum syndrome, prader
testosterone, willi syndrome,
normal or Acquired other genetic
decreased LH and abnormalities
FSH
Chronic opioid
use,
Page | 560
hyperprolactinaemi
a, pituitary tumors,
sellar radiation,
sleep deprivation,
surgery, trauma
Mixed decreased total Acquired Aging, cancer,
serum chronic
testosterone, glucocorticoid use,
variable LH and chronic kidney
FSH disease, chronic
obstructive
pulmonary
disease, cirrhosis,
diabetes mellitus,
hemochromatosis,
human
immunodeficiency
virus, obesity
6.8.10 Assessment
Depend upon the age of onset, the severity of testosterone deficiency,
and whether there is a decrease in one or both of the two major functions
of the testes: sperm production and testosterone production.
Adolescents and young adults who have not yet completed puberty
appear younger than their chronologic age and may also present with
small genitalia, difficulty gaining muscle mass despite vigorous exercise,
lack of a beard, and failure of the voice to deepen.
In adult men, several common but nonspecific symptoms such as
decreased vigor and libido and depressed mood. Decreased muscle
mass and body hair are less common but do not occur for a year or
many years. Hot flashes occur when hypogonadism is severe.
Gynecomastia, tender or not, is more likely to occur in primary than
secondary hypogonadism, as is infertility.
Page | 561
Table 6.5 – Signs and symptoms of male hypogonadism

Anemia (normocytic, normochromic) *
Breast discomfort, gynecomastia
Depressed mood *
Diminished bone density, low-trauma fractures
Diminished energy, sense of vitality, or sense of well-being *
Diminished muscle mass and strength *
Diminished physical or work performance *
Hot flashes, sweat, Impaired cognition *
Incomplete or delayed sexual development (in cases of prepubertal

onset)
Increased body fat, body mass index *
Increased fatigue *
Infertility
Loss of body hair
Sexual symptoms (decreased libido, decreased spontaneous erection)
Very small testes
* — Less specific; may be associated with other conditions

6.8.11 Diagnosis
According to guidelines from the Endocrine Society, male hypogonadism
should be diagnosed only if there are signs or symptoms of
hypogonadism and total serum testosterone levels are low on at least
two occasions.
Page | 562
Algorithm 6.2 – Evaluation of Male with Hypogonadism

Treatment with testosterone replacement therapy at hospital with
specialized physician not by family physicians.
Testosterone therapy should be initiated only after two morning total
serum testosterone measurements show decreased levels.
Several testosterone preparations are currently available or are under
development for treating testosterone deficiency
In the meantime, physicians must counsel patients that the
cardiovascular risks and benefits of testosterone therapy are uncertain
and should engage in shared decision-making.
Absolute contraindications
 Breast cancer
 Polycythemia hematocrit more than 54%
 Prostate cancer
Page | 563
 Prostate specific antigen more than 4MG per ML or presence of

nodules\ induration on digital rectal examination
o Referral to urologist is required for before considering
testosterone therapy
Relative contraindications
 Baseline hematocrit more than 50%
 The desire for fertility
o Testosterone therapy suppresses spermatogenesis
 Severe lower urinary tract symptoms
 Uncontrolled congestive heart failure
 Untreated obstructive sleep apnea
Page | 564
Section 9: Ophthalmology
Chapter 1: VISION LOSS
1.1. Media Problems:
1.1.1 Keratitis:
Definition:
Keratitis (Figure 1.1) is an inflammation of the cornea.
Risk factors:
 Trauma
 Allergy
 Dry eye
 Abrasive exposure (UV light)
 Infection (viral, bacterial, fungal, or parasite)
Symptoms:
 Red painful eye, tearing, photophobia, and foreign body sensation.
Management:
 Non-contact lens users: broad-spectrum antibiotic eye drops
 Contact lens users: discontinuation of contact lens use; topical
fluoroquinolones or aminoglycoside drops
 Infectious keratitis should be evaluated by an ophthalmologist within
24 hours, consideration of corneal culture, and requires close follow-
up.
1.1.2 Corneal abrasion:
Definition:
A corneal abrasion (Figure 1.2) is a loss or defect in the epithelial surface
of the cornea.
Risk factors:
 Mechanical trauma
 Foreign body
 Chemical and flash burn
 Contact lens use
Symptoms:
 Eye pain, tearing, sensitivity to light, and blurry vision especially with
history of trauma.
Page | 565
 Fluorescein dye under cobalt blue light (Figure 1.3):
o Loss of epithelial cells is demonstrated by corneal uptake of
fluorescein dye.
 Linear appearance if from trauma or foreign body
 Rounded if from contact lens use
 Dendritic shape suggests herpetic keratitis requires
immediate referral
 The upper eyelid should always be everted to detect foreign bodies.
Figure 1.3 – Corneal abrasion with fluorescein staining

Management:
The goals of treatment are to relieve pain, prevent bacterial
superinfection, and speed healing.
 Oral analgesics
 Topical agents, such as antibiotics, nonsteroidal anti-inflammatory
drugs (NSAIDs), and cycloplegics
 Patching is not indicated
 Analgesia:
o sufficient
o Uncomplicated cases: Topical NSAIDs (e.g., diclofenac 0.1%,
ketorolac 0.4%) used for no more than 1 to 2 days, as prolonged
use may be associated with corneal toxicity
o Severe cases: opioid analgesics may be necessary
 Topical antibiotics: Should be used in corneal abrasions caused by
contact lens use, foreign bodies, or a history of trauma with
infectious or vegetative matter, as there is a higher risk of secondary
bacterial keratitis.
o Uncomplicated abrasions: erythromycin 0.5% ophthalmic
ointment, polymyxin B/trimethoprim ophthalmic solution, and
sulfacetamide 10% ophthalmic ointment or solution.
o Contact lenses wearer: topical antibiotic with antipseudomonal
activity, such as a fluoroquinolone or an aminoglycoside due to
colonization with Pseudomonas aeruginosa and other gram-
negative organisms.
Page | 566
 Indications for referral:

o Chemical burn
o Evidence of corneal ulcer or infiltrate
o Failure to heal after 3-4 days
o Inability to remove a foreign body
o Increased size of abrasion after 24 hours
o Penetrating injury
o Presence of hyphemia or hypopyon
o Rust ring
o Vision loss of more than 20/40
o Worsening symptoms or not improved after 24 hours
1.1.3 Hyphema
Definition:
Blood in the anterior chamber of the eye is a hyphema (Figure 1.4)
Risk factors:
 May be spontaneous
o Blood thinners
o Clotting disorders
 Blunt trauma
 Poorly controlled diabetes mellitus, due to increased fragility of the
blood vessels of the iris
Management:
Patients with Hyphema should be evaluated by an ophthalmologist within
24 hours.
1.1.4 Cataracts:
Definition:
Cataracts (Figure 1.5) are opacities of the lenses.
Risk factors:
 Age (accounts for 90% of cases)
 Congenital
 Genetic
 Alcohol consumption
 Smoking
Figure 1.5
 HIV/AIDs
 Infectious
 Metabolic syndrome
 Poor control diabetes mellitus.
 Toxic
Page | 567
 Trauma from sunlight exposure, ionizing radiation or penetration.

Symptoms:
 Difficulty driving at night, reading road signs, or reading fine print.
 Painless progressive vision loss.
Physical exam:
 A comprehensive eye examination is often used to make the
diagnosis.
 A dilated fundus examination should be performed to rule out other
pathology.
Management:
 Without functional vision impairment: observation
 With functional vision impairment: phacoemulsification and intraocular
lens implantation.
1.1.5 Vitreous hemorrhage:
Definition:
It is bleeding into the vitreous humor.
Risk factors:
 Spontaneous due a retinal tear or vitreous detachment
 Trauma
 Conditions with retinal neovascularization such as poorly controlled
diabetes mellitus
Symptoms:
Painless floaters and sometimes flashes of light (Figure 1.6)
Management:
Patients suspected of vitreous hemorrhage should be referred to
ophthalmologist within 48 hours.
Figure 1.6 – Typical floaters associated with vitreous hemorrhage
Page | 568
1.1.6 Endophthalmitis:
Definition:
It is an infection affecting all intraocular tissue (Figure 1.7).
Symptoms:
Acute visual loss after recent ocular surgery.
Management:
Any patient suspected of having
endophthalmitis should be evaluated by an
ophthalmologist within 24 hours.
1.2. Retinal Problems: Figure 1.7
1.2.1 Central Retinal Artery Occlusion (CRAO):
Symptoms:
Severe, sudden, painless, central, or paracentral vision loss
Physical exam:
 On fundoscopic examination in 20% of cases embolus will be visible,
while others may show only vascular narrowing.
 After several hours, milky white retina could be seen with cherry-red
spot of the fovea (Figure 1.8).
Figure 1.8 – Normal fundus compared to the fundus appearance in

CRAO and CRVO
Management:
Patients suspected of having CRAO must be immediately referred
to emergency department for a stroke workup.
Page | 569
1.2.2 Central Retinal Vein Occlusion (CRVO):

Symptoms:
 Acute onset of painless blurred vision unilaterally.
 Typically, it is subacute in contrast to the sudden visual loss
associated with CRAO.
Physical exam:
The thrombus may result in venous stasis, which leads to disc
swelling. This causes the cotton wool spots and the classic “blood and
thunder” appearance seen on fundoscopic exam (Figure 1.8).
Management:
Ophthalmology referral should be within 48 hours
1.2.3 Retinal Detachment:
Risk factors:
 Highly myopic or nearsighted vision
 Proliferative diabetic retinopathy
 Trauma
Symptoms:
 Patients complain of a sudden onset of flashes of light, new floaters,
or black dots (Figure 1.9).
 Partial visual field loss occurs initially, which may lead to severely
compromised visual acuity once the macula has become involved.
Management:
 Requires urgent ophthalmology referral within 24 hours
 Treatment depends on several features: symptomatic vs.
asymptomatic, type and the extent of detachment, and other patient
factors
 Laser retinopexy (photocoagulation)
 Cryoretinopexy
Figure 1.9
Page | 570
1.2.4 Acute maculopathy:

Definition:
It is a disease that alters the back of the retina or the macula usually due
to chronic disease such as dry diabetic retinopathy, bleeding. Infection,
inflammation, and fluid leakage. It is progressive in nature and usually
bilateral.
Symptoms:
Patients complain of blurred vision, a central blind spot (scotoma), or
visual distortion.
Physical exam:
 Dilated fundoscopic examination.
 Optical coherence tomography (OCT)
Management:
Ophthalmology referral should be within 48 hours.
1.2.5 Retinoblastoma:
Definition:
It is a malignant tumor of the retina, the most common primary
intraocular malignancy of childhood
Physical exam:
 Leukocoria (Figure 1.10)
 Strabismus
 Red eye
 Nystagmus
 Indirect ophthalmoscopy by an ophthalmologist shows the
characteristic finding of a chalky, off-white retinal mass with a soft,
friable consistency
Management:
 Children with family history should underdo clinical screening and/or
genetic testing within the first 8 weeks of life by an ophthalmologist
(Table 1.2)
 Ophthalmology referral for complete physical examination
 Pathology is not needed to confirm the diagnosis
 Imaging studies as needed.
Page | 571
1.2.6 Retinitis Pigmentosa:

Definition:
It is a condition that comprises a group of inherited conditions that can
cause progressive retinal degeneration and affect the photoreceptors
and retinal pigment epithelium. 70 % of patients have a positive family
history.
Symptoms:
 Decreased night vision or night blindness—earliest symptom, may be
so gradual that it goes unnoticed
 Loss of peripheral vision—progressive starting in the midperiphery
and progresses more peripherally, results in a constricted visual field
 Decrease in central vision—can be early or late in the disease
process, cataract may further compromise central vision
 Color vision is intact until late
 Onset of symptoms ranges from childhood to adulthood
 Other symptoms: photopsia (sensation of sparkling lights) and
headache
Physical exam:
 Evaluation of visual acuity, visual fields, color vision, and contrast
sensitivity
 Funduscopic examination showing waxy pallor of the optic nerve
(Figure 1.11), arterial attenuation, and pigmentary changes in the
peripheral retina (Figure 1.12).
 Electroretinogram (ERG): decreased electrical activity, reflecting
declining function of photoreceptors
 Genetic testing
Page | 572
Management:
 No cure currently available
 Limited group with some forms may benefit from treatment with
vitamins (vitamin A, E and K) and nutritional supplements (Omega-3),
but for only a short duration
 New treatments in active development include gene therapy,
implanted electrical devices, and transplantation
1.2.7 Vitreous detachment:
Definition:
It is a condition in which the vitreous, a component of the eye, shrinks
and separates from the retina.
Risk factors:
 Age > 40
 Myopia (nearsightedness)
 Trauma
 Recent eye surgery
 History of previous vitreous detachment within the last year
Symptoms:
 Floaters—most common symptom
 Flashing light or lightning streaks in their peripheral vision.
 Majority will not experience any symptoms that impact their daily
Physical exam:
 A dilated eye examination
 Optical coherence tomography (OCT) or ocular ultrasound
Management:
 Vitreous detachment is not life-threatening, and most patients’
symptoms resolve.
 After three months, most patients no longer notice flashes and
floaters tend to improve.
 It does not require any special treatment. However, while
complications are uncommon, they can be serious and necessitate
immediate treatment, such as laser treatment for a retinal tear or
surgery for a retinal detachment. As a result, one or more checkups
are advised within three months of onset.
 In rare cases, the floaters may persist and vitrectomy surgery to
remove the floaters is effective.
Page | 573
1.2.8 Macular Degeneration:

Definition:
 Age-related macular degeneration (AMD) is an eye disease that can
worsen over time. It is the most common cause of severe, permanent
vision loss in people over the age of 60.
 Stargardt disease, also known as juvenile macular degeneration, is a
type of macular degeneration that affects children and young adults.
Types of age-related macular degeneration:
 Early and intermediate AMD
 Late AMD (Figure 1.13)
o Geographic atrophy (dry AMD)
o Neovascular AMD (wet AMD)
Risk factors:
 Age over 50 years
 Family history of AMD
 White skin color
 Female
 Tobacco use Figure 1.13
 Elevated blood pressure
 Elevated cholesterol level
 Obesity
 Diet rich in saturated fat
Symptoms:
Patients complain of deterioration of vision, size or color of objects
appearing different with each eye, abnormal dark adaptation.
Physical exam:
 Dilated eye exam can detect age-related macular degeneration
 Drusen (tiny yellow spots under the retina) or pigment clumping are
common early signs
 May notice some of the straight lines are wavy, or that some of the
lines are missing on an Amsler grid (Figure 1.14)
 Ophthalmologist examination using optical coherence tomography
(OCT) and optical coherence tomography angiography (OCTA)
Page | 574
Management:
 Dry AMD: currently no treatment,
taking certain vitamins and minerals
on a daily basis may help to slow the
progression of dry AMD
o Vitamin C (500 mg)
o Vitamin E (400 IU)
o Lutein (10 mg)
o Zeaxanthin (2 mg)
o Zinc (80 mg) Figure 1.14
o Copper (2 mg)
 Wet AMD: Anti-angiogenesis drugs via ocular injection aids in the
reduction of abnormal blood vessels and reduces blood vessel
leaking, laser therapy
1.3. Neural Visual Pathway Problems:
1.3.1 Ischemic Optic Neuropathy:
Definition:
It is interruption of the blood supply of the optic nerve
Risk factors:
Cardiovascular disease is a major risk factor.
Symptoms:
Patients complain of sudden, painless, severe vision loss.
Management:
Temporal arteritis or giant cell arteritis (GCA) must be ruled out and
treated to avoid complications such as contralateral vision loss.
1.3.2 Giant Cell Arteritis (GCA):
Symptoms:
 Patients complain of temporal region headache with scalp tenderness
and jaw claudication, stiffness in the shoulder, neck and hip.
 Associated with constitutional symptoms of fever, fatigue, weight loss,
and sometimes night sweats.
Investigations
 Labs may show:
o Elevated ESR or CRP
o Elevated AST, ALT, and Alkaline phosphatase
 Imaging studies such as ultrasound, MRI, and PET scan play
important role in diagnosis
 The gold standard is temporal artery biopsy
Page | 575
Management:
 Do not delay treatment to obtain biopsy
 High dose steroid therapy such as prednisone orally or high dose
solumedrol IV should be initiated emergently
 Urgent ophthalmology referral within 24 hours
1.3.3 Optic neuritis:
Definition:
It is Inflammation of the optic nerve
Symptoms:
Patients complain of reduced visual acuity, pain with eye movement, and
washed-out color vision.
Management:
Ophthalmology referral should be within 24—48 hours.
1.3.4 Acute Transient Visual Loss (Amaurosis Fugax):
Definition:
A transient loss of vision monocular or binocular which last less than 24
hours.
Symptoms:
Patients report transient visual loss either in one or both eyes.
Medications linked to vision loss
 Anticholinergics: loss of accommodation, angle-closure glaucoma
 Bisphosphonates: uveitis
 Digoxin: yellow vision
 Rifabutin: uveitis
 Sildenafil: blue vision, ischemic optic neuropathy
 Sulfonamides: myopia
 Topiramate: angle closure glaucoma
 Oral contraceptives: ischemic, retinal, or optic nerve events
 Fingolimod: macular edema
 Cancer therapy drugs: retinopathy, uveitis, acute dry eye
Psychogenic vision problems:
 Vision loss without an organic cause is functional vision loss.
 Patients who fake blindness on purpose are malingerers, whereas
those who truly have perceptual blindness have a conversion
disorder.
 The vision loss can be total or partial, monocular or binocular.
Page | 576
Table 1.1 - Visual impairment warranting referral to an

ophthalmologist
– Infectious keratitis
Within 24 hours – Hyphemia
– Endophthalmitis
– Acute retinal necrosis
– Central retinal artery occlusion
– Retinal detachment
– Ischemic optic neuropathy
– Vitreous hemorrhage
Within 24—48 hours – Central retinal vein occlusion
– Acute maculopathy
– Optic neuritis
Table 1.2 – Causes of acute persistent vision loss by presentation

Unilateral Bilateral
Painless Painful Painless Painful
● Lens ● Corneal ● Pseudotumo Keratitis from
dislocation abrasion r cerebri bilateral
● Vitreous ● Keratitis ● Metabolic or exposure
hemorrhage ● Acute toxic (contact lens,
● Acute glaucoma (hyperglyce UV light,
maculopathy● Hyphemia mia, chemical, etc.)
● Retinal ● Endophthal methanol
detachment mitis toxicity)
● Retinal ● Anterior Homonymous
artery uveitis fields loss
occlusion Optic neuritis
Ischemic optic
neuropathy
Page | 577
Page | 578
Chapter 2: RED EYES IN CHILDREN

2.1. Neonatal Conjunctivitis:
Definition:
is an eye infection that occurs within the first 30 days of life.
Symptoms & signs:
Purulent, mucopurulent, or mucoid discharge from one or both eyes
(Figure 2.1)
Previous or concurrent sexually transmitted disease in the mother
Injected conjunctiva
Swelling of the lids
History of systemic infection
The majority of neonates with sticky
discharge have a benign cause , most
commonly a blocked nasolacrimal duct
Investigation :
Microbiological investigations: conjunctival swabs
Maternal investigations: cervical swabs
Based on h&pe plus investigation
2.2. Chemical Conjunctivitis:
irritation tearing and redness
Management plan:
self limiting artificial tear
2.3. Bacterial Conjunctivitis:
Definition:
Subacute onset between the 4th and 28th day of life.
Signs & symptoms:
Presents with red eye with lid swelling and varying amounts of purulent
discharge.
2.4. Gonorrheal Infection:
Onset : Occurs 2—5 days after birth
Signs & symptoms:
 Hyperacute conjunctival injection and chemosis
 Lid edema
 purulent discharge
Page | 579
management:
 Immediate referral to ophthalmology
 1st Systemic penicillin G or a cephalosporin
 2nd topical erythromycin in addition
 3rd Frequent irrigation until discharge ceases.
Prevention:
Prophylactic ocular topical medication to prevent gonococcal ophthalmia
neonatorum (Grade A recommendation) , only use erythromycin
The USPSTF recommends screening for gonorrhea in all sexually active
women 24 years and younger and in older women at increased risk for
infection, as well as pregnant women.
2.5. Chlamydial Infection:
Onset:
5—12 days after birth, some reports of up to 28 days
Signs & symptom:
 Unilateral / bilateral
 Watery discharge that later becomes copious and purulent
 Preseptal cellulitis
 Rhinitis, otitis, and pneumonitis may be present less frequently
 Management
 Systemic erythromycin
 Topical azithromycin
2.6. Viral Conjunctivitis:
Definition:
Acute onset of serosanguinous ocular discharge, and vesicular skin
lesions. Appears 1—14 days after birth, could be unilateral or bilateral.
Page | 580
Signs & symptoms:

 Ocular
o Keratitis
o Anterior uveitis
o Cataract
o Retinitis
o Optic neuritis (rarely)
 Systemic
o Jaundice
o Hepatosplenomegaly
o Pneumonitis
o Meningoencephalitis
o Disseminated intravascular coagulation ( DIC)
Management:
Herpetic conjunctivitis: systemic and topical antivirals, e.g., acyclovir
URGENT REFERAL:
 Decreased visual acuity
 Ciliary flush
 Photophobia
 Sever foreign body sensation (patient can’t open their eye)
 Corneal opacity
 Fixed pupil
 Severe headache with nausea
 Suspicion for hyperacute bacterial conjunctivitis or epidemic
keratoconjunctivitis (EKC)
2.7. Trachoma:
Definition:
It is a bilateral infection of the eyes and is the leading cause of infectious
blindness in the world. Caused by Chlamydia trachomatis.
Signs & Symptoms:
Based on stage
Early stage:
 Redness (pink eye)
 Mild itching and irritation of eye and eyelids
 Eye discharge
Late stage:
 Pain
 Photophobia
Page | 581
 Blurred vision
Management:
 1ST Oral azithromycin as
single dose- preferred
 Topical tetracycline
 Surgery: If trichiasis develops
to prevent blindness.
Figure 2.2 – Examples of appearance of trachoma
2.8. Periorbital / Orbital Cellulitis:

Definition:
Orbital cellulitis an infection of the soft tissues within the orbit, posterior
to the orbital septum. It must be differentiated from preseptal cellulitis,
which is an infection of the anterior portion of the eyelid.
Signs & Symptoms:
 Red, swollen, tender eyelids
 Extraocular movements
limited due to pain or muscle
edema
 Vision changes, diplopia
 Fever and ill appearance in
children
Investigation:
Computed tomography CT of the Figure 2.3 – Typical appearance of
orbits with intravenous contrast periorbital/orbital cellulitis
media differentiates periorbital
cellulitis from orbital cellulitis and can detect abscess formation.
Management:
 Orbital cellulitis:
o Same day ophthalmology consultation
o Consider ENT consultation
o Inpatient antibiotic therapy
o A three-week course of systemic antibiotics (vancomycin +
ceftriaxone or cefotaxime)
o Surgical intervention if empirical antibiotic failed
o Close follow up
Page | 582
 Periorbital cellulitis:
o Same day ophthalmology consultation
o Consider ENT consultation
o Inpatient antibiotic therapy
o A three-week course of systemic antibiotics (vancomycin +
ceftriaxone or cefotaxime)
o Surgical intervention if empirical antibiotic failed
o Close follow up
Chapter 3: EYE CONDITIONS IN
CHILDREN
3.1. Amblyopia (Lazy eyes):
3.1.1 Definition:
 Amblyopia is the reduction of best corrected visual acuity caused by
abnormal vision development during childhood and adolescence. It is
commonly unilateral, but it may be bilateral.
Symptoms:
 wandering eye
 squinting of one eye
 torticollis (head tilting)
 nystagmus
 strabismus
Examination
 Ptosis
 Cataracts and corneal
opacities
 Presence of abnormal
head posture (e.g., tilt
or turn)
 Pupil examination
 Ocular motility and
alignment using
corneal light reflection,
binocular red reflex test, and cover/uncover test (Figure 3.1)
 Visual acuity
Page | 583
3.1.3 Management:
Treatment:
 Treat the cause of visual loss (e.g., cataract removal, strabismus
surgery in some cases).
 Correction of refractive
error with eyeglasses.
 Promoting use of the
amblyopic eye by:
o Patching (Figure 3.2)
for two hours a day
(as successful as
patching for six hours)
o Optical penalization of
the better eye with
atropine 1%
ophthalmic drops.
 Early detection and referral for treatment to prevent vision loss
 Preferred age for treatment is under 7 years old, though older
children can also benefit
3.1.4 Screening:
 All children <5 years old should undergo routine vision screening to
detect amblyopia
 Screening includes vision risk assessment at all health maintenance
visits and vision screening at 3, 4, and 5 years of age.
 Examination and tests done during screening include:
o External inspection of the eyes and lids
o Ocular history
o Ocular motility assessment
o Ophthalmoscopy
o Pupil examination
o Red reflex examination
o Vision assessment
o Visual acuity testing (preferred) or photo screening
Page | 584
3.2. Strabismus:
3.2.1 Definition:
 A common vision problem in
children in which the visual
axes of the eyes are not
parallel and the eyes appear to
be looking in different directions
(Figure 3.3). Caused by eye
misalignment.
 Assessment of general health
and neurological status, evaluate for the presence of abnormal head
posture
 Eye examination: should include an assessment of
o Visual function, pupillary reactivity, eyelid position, extraocular
movements (ductions/versions)
o Corneal light reflex test
o Cover/uncover test and the Bruckner simultaneous red reflex test
3.2.3 Management:
Treatment
 Correction of refractive error with eyeglasses, prisms are occasionally
used to aid in focus.
 Amblyopia treatment
 Patching or blurring with atropine drops might be recommended to
help strengthen a misaligned eye
 Surgical therapy
Indications for Ophthalmology referral
 Constant strabismus at any age
 Intermittent manifest strabismus after 4—6 months of age
 Persistent esodeviations after 4 months of age
 Corneal light reflection test or cover test demonstrates deviation
 Asymmetry of appearance on the Bruckner simultaneous red reflex
test
 Deviation that changes depending upon the position of gaze
 Torticollis that is not explained on a musculoskeletal basis
 Complaints of diplopia or asthenopia
 Parental concern about ocular alignment
Page | 585
3.3. Pseudostrabismus:
3.3.1 Definition:
 Pseudostrabismus is the false
appearance of eye crossing that occurs
in children less than 1 year old. Caused
by wide, flat nose or a skin fold at the
inner eyelid (Figure 3.4)
On examination:
 the eyes appear misaligned
 the light reflection is in the same location in both eyes.
3.3.3 Management:
 Reassurance
 Resolves spontaneously as the child grows
3.4. Nasolacrimal Duct Obstruction:
3.4.1 Definition:
 The presence of a membrane at the end
of the tear duct (Hasner’s valve), or
absent puncta (upper and/or lower
eyelids), narrow tear duct system,
infection, and incomplete development of
the tear duct that does not communicate
with the nose.
3.4.2 Symptoms & Physical examination:
 Excessive tearing
 The eyelids may become red and swollen
 Yellowish-green discharge
3.4.3 Management:
 Resolves spontaneously before the age of 8 to 10 months
 If it persists try tear duct massage, topical antibiotic eye drops, tear
duct probing, balloon tear duct dilation, or tear duct intubation.
Page | 586
Chapter 4: RED EYES IN ADULTS

4.1. Conjunctivitis:
4.1.1 Bacterial:
Symptoms & Physical examination:
 Conjunctival hyperemia
 Purulent sticky discharge
 Conjunctival papillae
 In Neisseria gonorrhoeae: copious discharge, eye pain and
decreased vision.
 If severe or recurrent: conjunctival swab
Management:
 Topical Erythromycin ointment, trimethoprim‐polymyxin
 Contact lens users: fluoroquinolone due to risk of Pseudomonas
 Follow up after 2—3 days initially then every 5—7 days until it
resolves
 Chlamydia trachomatis: Treat with Azithromycin, topical tetracycline
can be used as alternative
 Genital infection & Partner must be treated
 Hyperacute bacterial conjunctivitis (gonococcal) needs immediate
ophthalmological referral for antibiotics
4.1.2 Viral:
 Watery or mucoserous discharge,
 Burning, foreign body sensation
 Erythema of conjunctiva, &lid edema.
 The tarsal conjunctiva may have a follicular appearance
Management:
 Self-limited, supportive care with cold compresses, ocular
antihistamines, and artificial tears
Page | 587
4.1.3 Allergic:
 Bilateral Itching and tearing
 Conjunctival injection
 Cobblestone conjunctival papillae
Management:
 Avoid exposure to allergens
 Treat with artificial tears
 Over the counter antihistamine/mast cell stabilizers
 Cold compresses
Figure 4.1 – Bacterial conjunctivitis Figure 4.2 – Conjunctival papillae Figure 4.3 – Viral conjunctivitis
Figure 4.4 – Follicular appearance Figure 4.5 - Allergic conjunctivitis Figure 4.6 - Chlamydia Trachomatis
4.2. Infections of the sclera:

4.2.1 Scleritis:
 Severe constant pain, radiating to the face and periorbital region,
limits activity and prevents sleep
 Associated with violaceous redness of the eye, decreased visual
acuity
 Slit-lamp examination and ophthalmoscopy: Scleral edema with
dilatation of the deep episcleral vascular plexus
Page | 588

Management plan:
 NSAIDs: Ibuprofen, naproxen,
indomethacin
 Prompt ophthalmology referral Figure 4.7 - Scleritis
4.2.2 Episcleritis:
Symptoms & Physical examination signs:
 Abrupt onset of inflammation in the episcelra of one or both eyes
 Redness, irritation, and watering of the eye with preserved vision
Management:
 Self limiting
 Consider artificial tears Figure 4.8 - Episcleritis
 Topical NSAIDs for persistent discomfort
despite lubricants
4.3. Uveitis:
4.3.1 Symptoms:
 Red eye, photophobia, miosis, no
discharge, tearing is minimal, usually
unilateral.
 Ciliary flush (Figure 4.9).
 Inflammatory white blood cells in the Figure 4.9
anterior chamber (Figure 4.10).

4.3.3 Management:
 Topical steroids initially to decrease
ocular inflammation
Figure 4.10
 Emergent ophthalmology referral
Page | 589
4.4. Acute angle closure glaucoma:

4.4.1 Symptoms:
 Sudden severe pain, red eye, blurred vision, associated with nausea,
vomiting, headache and abdominal pain
 Halos
 Decreased visual acuity
 high intraocular pressure
 Fixed, mid-dilated pupil
 hard globe on palpation
 Ciliary injection
 Hazy cornea
4.6. Management:
 Immediate ophthalmology referral
 Timolol 0.5% then repeat after 30 minutes to decrease aqueous
humor production
 Pilocarpine 4% drop (constricts pupil)
 Acetazolamide 500 mg PO to decrease Aqueous humor production
 Methazolamide 50 mg PO instead of acetazolamide in patients with
sickle cell disease
 Head of bed at 30 degrees
 Prophylactic anti-emetics and analgesics
Page | 590
Table 4.3 Viral keratitis

Herpes simplex Herpes Zoster Ophthalmicus
Both can present with Red, eye, photophobia, decreased visual
acuity, tearing
 History of perioral cold sore
 Examination: Dendritic  Examination: Herpetic vesicles
fluorescein stain (Figure (Figure 4.13)
4.12), corneal inflammation  Corneal inflammation
 Vesical rash on the eyelid  Hutchinson’s sign (Figure
(rare) 4.14)
 Management: Topical
antivirals (ganciclovir
0.15% ophthalmic gel, or
trifluridine 1% drops) and
cycloplegics  Management: Oral antivirals
 Cold compresses (acyclovir, famciclovir,
 Ophthalmology referral valacyclovir)
 Steroids are  Immediate ophthalmology
contraindicated referral
Figure 4.12 Figure 4.13

Figure 4.14
4.7. Chemical eye injury:
 Decreased vision, moderate to severe eye
pain, blepharospasm, conjunctival
redness, and photophobia.
 In severe cases of alkali exposure, the eye
may appear white due to ischemia of the
conjunctiva and scleral vessels (Figure
4.15).
Page | 591
4.7.3 Management:
 Immediate evaluation and treatment to prevent permanent vision loss.
o Irrigation for at least 30 mins.
 With or without Morgan lens
 May need topical anesthetics
 Irrigate until pH is normal
o Remove particulate matter from the fornices
o After irrigation:
 Cycloplegic agent
 0.5% erythromycin ointment QID
 Pain management
o Immediate ophthalmologic consultation is mandatory for
significant eye exposures.
Figure 4.16 – Eye irrigation with a Morgan lens
4.8. Photokeratitis:
 foreign body sensation, tearing, intense pain
photophobia, and blepharospasm.
 Examination: Decreased visual acuity,
conjunctival injection
 Fluorescein exam: Superficial punctate
keratitis (Figure 4.17)
Page | 592
4.8.3 Management:
 Cycloplegic
 Topical broad-spectrum antibiotic
 Oral analgesics
 Symptoms should resolve in 24 hours
Chapter 5: EYELID AND LACRIMAL
DISORDERS
5.1. Dacryocystitis:
5.1.1 Definition:
 Infection due to obstruction of the nasolacrimal system
5.1.2 Classification:
Acute:
 complication of congenital nasal lacrimal duct obstruction
Chronic:
 bacterial overgrowth in the stagnant tear pool of the lacrimal sac.
 Erythema swelling, warmth, tenderness of the lacrimal sac, Purulent
discharge expressed from the punctum, history of trauma or surgery.
By Examination:
 apply gentile pressure to express the discharge, asses for pupillary
reflex, extraocular movement, proptosis, and evidence of cellulitis.
5.1.4 Management:
Acute:
 empirical systemic antibiotic with clindamycin 7—10 days ,
 if febrile/acutely ill need to consult ophthalmology and hospitalized
Chronic:
treat with topical antibiotics when discharge
copious: tobramycin sulfate 0.3%,
moxifloxacin 0.5%,
topical gentamicin, erythromycin
Page | 593
5.2. Dacryoadenitis:
5.2.1 Definition
 Inflammatory enlargement of the lacrimal gland either infectious or
due to systemic disease like sarcoidosis, Wegener’s granulomatosis,
Sjogren’s syndrome
Acute:
 rapid sever onset - Red and swollen upper eyelids, warm and
tender on palpation Conjunctival injection, chemosis , Ipsilateral
preauricular lymphadenopathy, Photophobia, tearing, discharge or a
foreign body sensation ,dry eyes
 Hx of travel systemic illness immunization
Chronic:
 Enlarged lateral upper eyelids, months to years, history of systemic
illness
 CBC for leukocytosis ,CT with contrast
5.2.4 Management:
Acute:
 viral self-limiting – bacterial with 1st
generation cephalosporin- Inflammatory
investigate for systemic underlying cause
Chronic
 referral, f\u after 2-6 weeks
5.3. Hordeolum:
5.3.1 Definition:
 Acute infection of the eyelid usually caused by staphylococcus.
5.3.2 Risk factors:
 skin conditions:(e.g., rosacea and seborrheic dermatitis)
 Eye makeup contaminated with bacteria
5.3.3 Classification:
 internal and external
 localized pain and swelling at the site of the infection
Page | 594
5.3.5 Management:
 resolves spontaneously, Warm
compresses 5-10 minutes 3-5 times a day,
Massage and gentle wiping, Discontinue eye
makeup.
 Refer if lesion does not reduce in size within
1-2weeks for possible I&D
5.4. Chalazion:
5.4.1 Definition:
 Painless localized eye swelling caused by obstruction of the gland of
Zeis or Meibomian glands.
 Non-tender rubbery nodule
5.4.3 Management:
 resolves spontaneously, Warm compresses 5-10
minutes 3-5 times a day
 Refer if lesion dose not resolved after 3—4 weeks
for I&D
 Persistent or recurring lesions, especially if
unilateral, should be assessed histopathologically for possible
carcinoma
5.5. Blepharitis:
5.5.1 Definition:
 Inflammation of the eyelid margin Can be associated with rosacea or
seborrheic dermatitis
 Red itchy or gritty eyes, with burning sensation, crusting in the
morning and excessive tearing.
By examination:
 Scaly, crusty, erythematous eyelid , Conjunctival
injection and small yellow plugs on Meibomian
glands
Page | 595
5.5.3 Management:
 lid hygiene, warm compressors, lid massage , use topical antibiotic
for sever cases .
 Refer if severe eye redness or pain, light sensitivity, impaired
vision, corneal abnormalities (e.g., erosions, ulcers, scarring),
uncertain diagnosis, concern for malignancy, or severe or
refractory symptoms
Chapter 6: REFRACTIVE DISORDERS
6.1. Emmetropia (normal refraction):
 Normal refractive state in which the image is focused on the retina
producing clear and focused image. This is 20/20 vision.
6.2. Ametropia:
 Abnormal refractive state in which image is not
focused on the retina producing a blurred image. Figure 6.1
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6.3. Myopia (Nearsightedness):

 Refractive disorder where the image is focused in front of the retina.
 Symptoms: Patient cannot see distant objects clearly.
 Management: Test visual acuity with Snellen chart and Referral to
optometrist.
 Treatment: Correction with concave refractive surface (Figure 6.2).
6.4. Hyperopia (Farsightedness):

 Refractive disorder where the
image is focused behind the
retina.
 Symptoms: Patient cannot see
close objects clearly.
 Management: Test visual acuity
with Snellen chart and Referral
to optometrist.
 Treatment: Correction with
convex refractive surface (Figure 6.3).
6.5. Astigmatism (Lack of pinpoint):
 Refractive condition in which abnormal corneal shape causes light
rays entering the eye along different planes to be focused unevenly.
 Symptoms: Patient complaint of
blurred vision at all viewing
distances.
 Management: Test visual acuity
with Snellen chart and Referral
to optometrist.
 Treatment: Correction with
Cylindrical optical surface lens
(Figure 6.4).
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6.6. Presbyopia (Aging sight):

 A non-refractive error that occurs when the lens loses its normal
accommodating power. Usually begins after age of 40 years old.
 Symptoms: Patient complaint of difficulty in reading and seeing at
arm’s length. Management: Visual acuity using Snellen eye chart
done at 20 feet, unexplained vision loss should be confirmed by using
phoropter by eye specialist which is used to measure severity of
refractive error for prescribing corrective lenses. A pinhole occluder
and retinoscope are additional devices that can be used to assess
refractive error by the eye specialist.
 Treatment: Correction with Bifocals, Trifocals or Progressive lenses.
Management of refractive errors:
 First line treatment: Corrective lenses (Eyeglasses and contact
lenses), or refractive surgery.
 Surgical procedures:
o Laser in situ keratomileusis (LASIK)
o Laser epithelial keratomileusis (LASEK)
o Photorefractive keratectomy (PRK)
o Intraocular lens implants (IOL).
 Note:Refractive surgery does not correct presbyopia in older patients.
 Preoperative Evaluation:Use of contact lenses must be discontinued
(1 to 2 weeks for soft lenses, and 3 to 4 weeks for hard lenses) so
that the corneal surface can stabilize, allowing for accurate
preoperative measurements.
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Section 10: ENT

Chapter 1: RHINITIS
1.1. Rhinitis:
It can be subdivided based on whether it is allergic or non-allergic, the
symptoms being seasonal, perennial, or episodic, and whether the
symptoms are mild, moderate, or severe
1.2. Allergic rhinitis:
1.2.1 Symptoms & Physical examination signs:
 rhinorrhea, nasal congestion, sneezing, nasal itching, and ocular
itching
 On examination, the nasal mucosa is pale and blue-hued
 Skin prick allergy tests: consider when candidate for immunotherapy.
 Allergen-specific IgE antibody serum test: useful where medication
may interfere with results of skin testing
 Sinonasal imaging: not recommended.
 Avoidance of triggers.
 First line: Intranasal steroids (INS) or antihistamines
 Oral antihistamines: second-generation antihistamines are
recommended for those with primary symptoms of sneezing and
itching
 Combination therapy: in patients who have an inadequate response.
 Second line: leukotriene receptor antagonists
 Immunotherapy: for moderate to severe symptoms not responsive to
usual treatments, may need referral to a specialist.
 Inferior turbinate reduction: where nasal obstruction with enlarged
inferior turbinates is present despite medical management.
1.3. Chronic non-allergic rhinitis:
 Symptoms include rhinorrhea and congestion but no sneezing, nasal
itching, or ocular itching.
 The examination is usually normal except for atrophic rhinitis.
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1.3.2 Investigations & monitoring

 When predominant symptoms are congestion or mixed:
o Intranasal steroids or Intranasal antihistamine
 When predominant symptom is rhinorrhoea:
o Intranasal ipratropium + Intranasal steroids or Intranasal
antihistamine
 Saline irrigation
1.4. Rhinitis medicamintosa:
1.4.1 Definition:
A form of rebound nasal congestion that occurs due to the overuse of
over-the-counter nasal decongestants
 nasal congestion
 without other symptoms of allergic rhinitis
 History of using over-the-counter nasal decongestants for more than
5-7 days and worsening symptoms when use abruptly stops.
 Examination: Erythematous nasal mucosa, Swollen inferior
turbinates , Mucoid discharge, Deviated septum or nasal polyps
 Stop the offending medication.
 Topical intranasal corticosteroids, e.g., fluticasone, may need to take
for up to one year in cases of long-term overuse.
 Oral corticosteroids, e.g., oral prednisone 0.5mg per kg for five days.
 Surgical intervention as a last resort, inferior turbinectomy may be
necessary.
1.5. Rhinosinusitis:
1.5.1 Acute rhinosinusitis
Duration: Acute: < 4 weeks – Subacute: > 4weeks but < 12 weeks
 Mucopurulent nasal discharge
 Nasal congestion
 Facial pain, pressure, or fullness
 Maxillary toothache
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in case the cause is Bacterial:

 Fever >39oC
 Failure to improve within 10 days or worsening of symptoms after
initial improvement
Management plan:
 Supportive treatment with analgesia, intranasal steroids, and saline
irrigation.
 Consider antibiotics if bacterial infection likely.
1.5.2 Chronic rhinosinusitis:
Duration: > 12 weeks
 Nasal congestion (most common)
 Facial pain, pressure, or fullness
 Mucopurulent nasal discharge
 Hyposmia
 Nasendoscopy
 CT imaging
Management plan:
 Intranasal steroids
 Saline irrigation
 Oral steroids
 ENT specialist referral
Chapter 2: DEAFNESS AND HEARING
LOSS
2.1. Deafness in Children
Symptoms:
 Otorrhea
 Recurrent ear infections
 Mouth breathing, snoring, rhinorrhoea
 Delayed speech and language developmental milestones
 Previous infections such as meningitis, congenital
 Birth history, postnatal complications
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 Family history of hearing loss

 Neonatal screening test results
 Any trauma, head injuries
Examination
Otoscope examination of the outer ear and tympanic membrane looking
for:
 Anatomical abnormalities
 Cerumen impaction
 Scarring or perforation of the tympanic membrane
 Effusions behind the tympanic membrane
 Early identification of hearing loss via newborn hearing screening by
1 month of age, diagnosis by 3 months, and early intervention by 6
months, Screening tests used:
o Otoacoustic emission testing.
o Auditory brainstem response testing.
 Play audiometry, speech perception, pure tone audiometry (when
much older), and tympanometry can be performed.
 MRI or CT scan to determine underlying causes
 Chromosomal studies may be indicated.
 Conductive hearing loss:
o Removing wax or referral for grommet insertion and/ or
adenoidectomy for middle ear effusion.
o Hearing aids in cases of bilateral effusions.
o Surgical intervention is required where there is ossicular damage
or cholesteatoma.
 Sensorineural hearing loss:
o Bilateral cochlear implants are recommended in children with
severe to profound hearing loss.
2.2. Presbycusis
2.2.1 Definition:
Presbycusis is a Bilateral, symmetric, high-frequency sensorineural
hearing loss.
 Gradual onset
 Association with old age, noise exposure, tobacco use,
cardiovascular disease
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 It may be accompanied by tinnitus

 Consideration to the risk of falls, isolation, depression, and dementia
 Audiogram
2.2.4 Management plan
 Treatment: binaural hearing aids
2.3. Noise-induced hearing loss
2.3.1 Definition:
Noise-induced hearing loss is a Sensorineural hearing loss, affecting the
higher frequencies (3kHz- 4kHz).
 Gradual onset
 Chronic exposure to excessive sounds levels
 Typically, symmetrical, but the noise from such sources as firearms or
sirens may produce an asymmetric loss.
 Audiogram
 Management includes prevention, counseling regarding noise
protection, screening, and hearing aid support.
 If the patient presents with sudden onset hearing loss within 24 hours,
they should have an immediate referral.
2.4. Otosclerosis
2.4.1 Definition:
Otosclerosis is a Primary and exclusive disease of the bony labyrinth and
footplate of the stapes. It can involve cochlea resulting in mixed hearing
loss or SNHL
 Onset 20-30 years of age
 May be bilateral
 Symptoms: hearing loss, vertigo, tinnitus
 Audiogram shows the typical Carhart’s notch at 2kHz and widening
the gap between air conduction and bone conduction in the Right ear
affected by otosclerosis.
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 Surgical intervention involves stapedectomy, where the stapes
footplate is replaced with a prosthesis.
 Alternative management options include hearing aids.
Chapter 3: PATIENT HEARING
ASSESSMENT AND ANALYSIS
3.1. Cleft Lip and Cleft Palate:
It is the most common congenital anomaly affecting the craniofacial
region. Can be present in isolation or in combination. Cleft lip with or
without palate is more common in males, while the isolated cleft palate is
more common in females. Presentation can be unilateral or bilateral.
3.1.1 Signs & Symptoms:
Ventilation and Feeding difficulty, Recurrent otitis media and hearing
loss, Speech abnormalities and Psychosocial issues.
3.1.2 Assessment:
 Prenatal screening ultrasound at 20 weeks’ gestation (low detection
rate).
 Postnatal newborn intraoral examination (inspection and finger
palpation).
 A systemic examination should be done to rule out other
malformations.
3.1.3 Management:
 Proper ventilation, feeding, nutrition, and management of recurrent
infections must be insured.
 Definitive treatment is: by surgical repair, which is done at 3 months
for cleft lip and at 8 months for cleft palate.
3.1.4 Prevention:
Folic acid supplementation (400mcg daily) is recommended to all women
of reproductive age and women with increased risk.
3.2. Facial deformity:
Asymmetry of the head is common in infants which can result from
positional deformity, congenital torticollis, simple craniosynostosis,
complex craniosynostosis, metabolic bone disease, microcephaly, and
hydrocephalus.
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Signs & Symptoms:

Can range from Asymptomatic condition with only Cosmetic changes to
Life threatening.
Investigations:
 Physical examination and radiography used for Diagnosis and to rule
out craniosynostosis. Ultrasound, CT, and MRI can be done for
confirmation.
 Physical exam includes looking for dysmorphic features, craniofacial
examination, palpate the skull to look for bony ridges at the site of the
cranial sutures, check neck range of motion, extremities, and back .
 Ask for family history of craniosynostosis and/or facial deformity for
any child with a facial deformity.
Management:
 According to the cause and symptoms.
3.2.1 Congenital torticollis:
Contracture of the sternocleidomastoid muscle on one side leading to
contralateral rotation of the face and chin. It is more common in males.
 Symptoms: Decreased range of motion and painless swelling over
the side of the neck. It can be associated with hip dysplasia and can
cause facial asymmetry and difficulty in feeding.
 Diagnosis is clinical, and ultrasound can be done to rule out a tumor.
 Treatment is: by Physical therapy.
 Surgical treatment is reserved for cases that fail conservative
treatment and for cosmetic reasons.
3.2.2 Positional flattening (positional plagiocephaly)
Flattening of one side of the head by continuous application of external
force, which occurs in the first few months after birth, resulting in
asymmetric deformity of the skull without craniosynostosis. It might be
associated with congenital torticollis.
 Signs & symptoms: Asymptomatic Cosmetic changes.
 Diagnosis: is by examination and radiography to rule out
craniosynostosis. Ultrasound, CT, and MRI can be done to confirm a
diagnosis
 Treatment:
o Mainly conservative (changing position, physiotherapy, massage,
and helmet therapy).
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3.2.3 Craniosynostosis:
A result of premature fusion of one or more cranial sutures. Synostosis of
a single suture is more common, leading to only cosmetic changes.
Synostosis of several sutures may be life-threatening and can lead to
increased intracranial pressure, papilledema, and loss of vision.
Types of deformities:
 Scaphocephaly: boat-shaped skull caused by premature fusion of the
sagittal suture, decreased width, and elongation of the anteroposterior
diameter of the cranium.
 Plagiocephaly: caused by unilateral coronal synostosis resulting in
retrusion of the forehead and upper orbit. Compensatory mechanism
results in protrusion or overgrowth of the ipsilateral occiput and
contralateral frontal bone.
Signs & symptoms:
 Asymptomatic cosmetic changes in case of single suture fusion.
 signs & symptoms of increased ICP in case of several sutures’ fusion.
Management:
 Conservative treatment in asymptomatic patients.
 Referral if Signs & symptoms of increased ICP.
3.3. Nasal disorder
3.3.1 Choanal atresia:
A congenital obstruction of the posterior nasopharynx and the most
common cause of neonatal nasal obstruction. Can be unilateral or
bilateral; unilateral is twice as common. The right side is more affected
than the left side. More frequent in girls than boys. Half to two-thirds of
patients have associated malformations, including genital hypoplasia, ear
malformations, and deafness.
Diagnosis:
 Flexible nasal endoscopy and CT.
Treatment:
 Surgical repair at 6 to 9 years old for unilateral atresia and as early as
possible for bilateral atresia.
3.3.2 Nasal dermoid:
Usually present at birth or in early infancy. More common in males. Most
cases are sporadic. However, hemifacial microsomia, cleft lip and/ or
palate, and craniosynostosis have been associated with dermoid.
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Signs & symptoms:

Patients present with nasal obstruction, difficulty in feeding and/or nasal
cosmetic deformity. Nasla dermoid is midline mass that is
noncompressible and does not transilluminate, and may be associated
with a sinus opening (may contain hair follicles, sebaceous glands, or
eccrine glands). Hair protruding through a punctum is pathognomonic. It
might be infected with intermittent sebaceous discharge. They carry a
risk of intracranial infections and associated complications.
 Diagnosis is by CT (accurate imaging for bony anatomy) and MRI
(better evaluation for soft tissue and intracranial extension).
 Management requires a Multidisciplinary approach (otolaryngology,
neurosurgery and, neuroradiology).
 Treatment is by complete surgical excision of the lesion.
3.3.3 Nasal septal deformity:
Nasal trauma during vaginal delivery or in utero can lead to septal
deformity.
 Symptoms: Most cases are asymptomatic.
 Management: self-corrected in early childhood.
 Surgical intervention is reserved for children with significant
respiratory distress using septoplasty or closed reduction.
3.3.4 Dacryocystocele:
Bluish-gray mass in the inferomedial canthus that usually appears in the
first few weeks after birth.
 Symptoms: epiphora (overflow of tears onto the face), nasal
congestion and respiratory distress.
 It may be associated with an intranasal cyst.
 Diagnosis is: by examination and nasal endoscopy.
Management:
 Conservative for uninfected cysts (massage, warm compresses, and
topical antibiotics).
 If the condition does not resolve in one month, probing and
endoscopic manipulation are performed.
3.4. Ear deformities
3.4.1 Preauricular sinus:
A congenital foramen at the anterior margin of the ascending limb of the
helix. It is isolated finding, but could be associated with extracutaneous
anomalies (renal or inner ear anomalies). More common in females and
unilateral but can be bilateral.
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 Symptoms: It is mostly asymptomatic. Symptoms are related to

infection.
 Diagnosis is: clinical.
 Renal ultrasound is indicated to rule out other anomalies in the
following conditions:
o Another malformation or dysmorphic feature
o Family history of deafness
o Auricular and or renal malformation
o Maternal history of gestational diabetes
 Treatment:
o If Asymptomatic: No treatment required unless infected.
o Recurrent or persistent infection: Surgical excision.
3.4.2 Branchial sinus, cyst and fistulae:
These are congenital anomalies, although they may not become
apparent until several years. Branchial cysts are the most common
cause of congenital neck mass. It might be associated with other
malformations (branchio-oto-renal syndrome, branchio-oculofacial
syndrome).
 Symptoms: They may present as visible punctum on the skin, cyst, or
neck masses, they are painless, mobile swellings on the lateral
aspect of the upper neck along with the sternocleidomastoid muscle;
they may swell with respiratory tract infection. Branchial sinuses and
fistulas are located at the lateral lower third of the neck.
 Diagnosis is: clinical.
 Treatment is: by surgical excision.
3.4.3 External angular dermoid:
Subcutaneous cysts are usually present at birth. They contain epidermal
and dermal tissues.
 Symptoms: Presented Commonly in anterior fontanelle, junction of
the sagittal and coronal sutures on the scalp, the upper lateral region
of the forehead near the eyebrow, and the submental area.
 Diagnosis is: by radiography, CT scan, and MRI.
 Treatment is: by surgical removal
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3.4.4 Prominent bat ear:

Ears projections more than 15-20mm or more than 21-30 degrees from
the temporo mastoid plane of the skull. Mostly are bilateral. It is an
acquired deformity in many patients, arising in the first three months of
life.
 Symptoms: There is no functional impairment and the main effect is
aesthetic and psychological.
 Treatment is: by surgical correction, which is usually done around 5
years of age.
Chapter 4: BELL’S PALSY
4.1. Definition:
 It is an acute peripheral facial nerve palsy of unknown cause.
4.2. History:
 Symptoms progress over hours to several days
 Weakness or complete paralysis of all facial muscles on one side of
the face
 Dysgeusia (impaired sense of taste)
 Hyperacusis
 Lacrimation
 Difficult to close the ipsilateral eye
 Difficulty eating
 Facial or retroauricular pain
 Synkinesis (e.g., mouth twitching while blinking or winking while
smiling)
 Ask about hearing loss, ataxia, rashes
4.3. Physical Examination:
 Head and neck
o External ear, TM, ear canal > Rule out infection, cholesteatoma,
rash (Ramsay Hunt syndrome)
o Oropharynx > Rule out herpes simplex
o Parotid Gland for any masses > Rule out tumor
 Complete neurological exam
 Cranial nerves
o Cranial nerve VII:
 Facial creases and nasolabial folds disappear
 The forehead unfurrows, if forehead spared > UMNL
 The corner of the mouth droops
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 The eyelids will not close, and the lower lid sags; on
attempted closure, the eye rolls upward (Bell’s
phenomenon)
 Normal gait
 Normal extremity motor and sensory examination
 Skin
o Vesicular rash > rule out herpes zoster
o Ramsay Hunt Syndrome
o Erythema Migrans > rule out Lyme Disease
 Lab testing not regularly indicated, rule out DM if suspected
 MRI for head and neurology referral only indicated in patients with
gradual onset (within 2 weeks), forehead sparing, bilateral palsies, or
if no improvement within the first two or three weeks after onset of
symptoms.
4.5. Management:
 Typical presentation > Within three days of symptoms start oral
steroids to improve facial nerve inflammation
 Severe presentation > Initiate antivirals for House Brackmann (H-B)
grade IV or higher
 All patients need eye care to prevent complications of corneal injury
4.6. Management plan includes:
 Prednisone 60 mg tab one time per day for one week, no need for
tapering
 It remains uncertain whether antiviral therapy adds benefit to
glucocorticoids in patients with new-onset Bell’s palsy. Absence of
high quality evidence suggest co-administration of oral antiviral
therapy along with glucocorticoids for patients with severe facial
palsy.
 Either acyclovir 400 mg 5 times per day for seven days or valacyclovir
1 g 3 times per day for one week
 Recommend artificial tears, eye protection, taping during sleep until
the facial paralysis
 No role of physiotherapy in Bell’s palsy
 Atypical presentation > Treat Underlying cause
Page | 610
4.7. Follow-up:
 2-3 weeks from the presentation to assess the improvement and
monitor for ocular complications
 If incomplete recovery within 3 to 4 months consider botulinum toxin
injection for cosmetic appearance and referral to multidisciplinary
facial nerve clinic
Chapter 5: DIZZINESS
5.1. Background:
is a feeling that is sometimes hard to describe, It is important to clarify
dizziness as a presenting symptom by taking detailed history and
examination as this will influence the differential diagnosis.
Typically, the following categories apply:
Vertigo: Sensation of movement or a spinning sensation, lasts for a few
seconds up to weeks associated with nausea and vomiting.
Light-headedness : Transiently slowed consciousness, faintness, can
progress to a loss of consciousness or syncope associated with warmth
and visual changes. Lasts for a second up to minutes ,a history of
cardiac disease, including cardiac dysrhythmias (tachycardias or
bradyarrhythmia), coronary heart disease, and congestive heart failure,
is relevant.
Disequilibrium: Difficulty maintaining balance, associated with frequent
falls without loss of consciousness. Lasts for a second up to weeks.
5.2. Initial Assessment / History:
 Hx : asking about detailed history to clarify the type of the dizziness,
Timing , triggers(change in position, trauma, coughing, weightlifting,
bowel movement) aggravating factors, concurrent symptoms, age,
and preexisting conditions , associated symptoms : Hearing loss,
tinnitus , headache , photophobia ,eye pain or redness , any
neurological symptoms
 Medication history : Alcohol ,Antiarrhythmics ,Anti-dementia
medications, Antiepileptics ,Antihistamines Antihypertensives
,Benzodiazepines.
 Past medical history : Atherosclerosis and migraine
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 Orthostatic Hypotension: BP (sitting, standing & supine), Postural
hypotension.
 Ear exam
 Neurological exam including cerebellar exam
 Gait & Romberg
 Central vs. peripheral: HINTS (Head-Impulse,Nystagmus,Test
ofSkew). The HINTS examination is sensitive and specific in
identifying stroke in patients with the acute vestibular syndrome.
 Most patients presenting with dizziness do not require laboratory
testing.
 Brain MRI +/- MRA , Audiometry if Meniere’s disease is suspect
Page | 612
5.5. Peripheral etiologies of vertigo:

5.5.1 Benign paroxysmal positional vertigo:
 Severe episodic vertigo ,provoked by change in head position,
vertical head movements, lasting for 10-20 sec,
 By examination: Dix-Hallpike maneuver elicits symptoms, Rotary
nystagmus accompanies the vertigo .have to Rule out CNS and ear
organic disease.
 Management: self limiting , resolved 4-6 weeks , head exercises to
reposition the canalith from the semicircular canal into the vestibule,
such as the Epley maneuver.
5.5.2 Vestibular neuritis and labyrinthitis:
 Self limiting Vertigo due to post-viral inflammation of the
vestibulocochlear nerve can last days to weeks
 Vestibular neuritis- vestibular branch only
 Labyrinthitis- both branches (auditory symptoms may also be present
 Treatment: Corticosteroid if less than 72 hours, or vestibular
sedatives (e.g., meclizine)
5.5.3 Meniere’s disease:
 triad of episodic vertigo lasting between 20 minutes to 12 hours,
tinnitus, and hearing loss mainly in adults between 20 and 60
years. Associated with aural fullness, progressive hearing loss, and
tinnitus which can be episodic or constant not related to the position.
 Usually its due to increased volume of a fluid called endo-lymph which
is responsible for transmitting sound waves to receptors in the
cochlea and for detecting angular acceleration within semicircular
canals.
 Management: Lifestyle changes includes Limiting dietary salt intake,
less than 1500mg and no more than 2300mg per day reduce caffeine
consumption
 Daily thiazide diuretic therapy can be added ,Symptomatic treatment
with Betahistine
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5.6. Central etiologies:

5.6.1 Vestibular migraine:
 Episodic vertigo with signs of migraine affects 10% of migraine
sufferers lasting from minutes associated with visual aura and
headache.
 Diagnosis: At least five episodes of vestibular symptoms of moderate
or severe migraine lasting a few minutes up to 72 hours, with a history
of migraine headache, one or more migraine features, and at least
50% with vestibular symptoms; and no other cause of vestibular
symptoms.
 Management : avoiding migraine triggers , Preventive medications
include anticonvulsants, beta-adrenergic blockers, calcium channel
blockers, and tricyclic antidepressants.
5.6.2 Vertebrobasilar ischemia:
 The vertebrobasilar system supplies blood to the brainstem,
cerebellum, thalamus and occipital cortex. Any major branch
occlusion can cause vertigo. Sudden onset vertigo is usually
associated with ataxia, diplopia, cranial nerve defects, and limb
weakness.
 Diagnosis relies on a history of the symptoms, such as diplopia,
dysarthria, weakness, or clumsiness of the limbs.
 Treatment
o antiplatelet therapy and reduction of risk factors for
cerebrovascular disease.
o Warfarin has been used in cases of significant vertebral or
basilar artery stenosis.
 If suspicion is there for ischemia, immediate consultation to the
neurology needed.
5.7. Management:
Treatment of the underlying cause is necessary to diminish the
symptoms of vertigo or alter the disease course. However, symptomatic
treatment may be required to suppress vestibular symptoms
1-Medication:
Three classes of drugs can be used to suppress the vestibular system:
 Antihistamines – meclizine, dimenhydrinate, diphenhydramine
 Benzodiazepines – diazepam, lorazepam, clonazepam, alprazolam
 Antiemetics – ondansetron, prochlorperazine, promethazine,
metoclopramide, domperidone
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2-vestibular rehabilitation:
Promotes recovery in patients with permanent unilateral or bilateral
peripheral vestibular hypofunction.
Chapter 6: EAR PAIN
6.1. Perichondritis:
6.1.1 Definition:
An infection and inflammatory condition of the external ear that requires
prompt diagnosis and treatment. Delays can result in cartilage necrosis
with subsequent deformities of the ear.
6.1.2 Signs & symptoms:
Initially, a dull ache that progresses to severe otalgia
Redness and swelling of the pinna with sparing of the ear lobe.
6.1.3 Management:
Includes prompt referral to ENT,
systemic antibiotics. e.g fluroquinolone ( ciprofloxacin )
Incision and drainage if there is abscess formation
6.2. Otitis Externa:
6.2.1 Definition :
Otitis externa is mainly an inflammation of the external auditory canal
(EAC) but may include the pinna or tympanic membrane.
6.2.2 Signs & symptoms :
 Rapid onset of symptoms presenting within a short time frame of 48
hours in the past 3 weeks .
 Symptoms of inflammation such as otalgia, itching, and fullness with
or without hearing loss.
 Signs including tenderness of the tragus and or pinna or ear canal
edema and/or erythema with or without otorrhea, lymphadenopathy,
tympanic membrane erythema, or cellulitis of the pinna and adjacent
skin.
6.2.3 Management :
 topical antibiotics use in uncomplicated diffuse AOE.
 Systematic antibiotics use in sever disease .
 Topical therapy can include non-antibiotic therapy such as acetic acid,
boric acid, and silver nitrate or steroids. (Duration of use is typically 5-
7 days and up to 14 days if severe infection.)
 Analgesia such as NSAID , paracetamol , opioid- based combination
depends on severity .
Page | 615
6.2.4 Important instructions :

 Avoid ototoxic preparations where there is tympanic membrane
perforation. Such as aminoglycosides and alcohol. Quinolones are
the only approved topical antimicrobials.
 Neomycin drops can cause sensitization and may require topical
steroids.
 If there is increased swelling and debris aural toilet using suction and
removal of cerumen will allow better delivery and absorption of topical
therapy.
 If there is a narrowing of EAC an ear canal wick can promote drug
delivery.
6.2.5 Prevention:
 Avoid trauma to the ear canal
 Remove obstructing cerumen to avoid moisture accumulation
 Acidifying ear drops before and after swimming and at bedtime
 Drying the ear canal with a hairdryer
 Using earplugs when swimming or swimming cap is more effective.
6.3. Otitis media:
6.3.1 Definition:
 infection to the inner ear could be in children and adult In childhood
6.3.2 Signs & symptoms:
 Ear pain- most prominent symptom
 New-onset otorrhea present in 15%-20%
 Non-verbal children: features of tugging or rubbing the ear
 Fever, irritability, sleep disturbance
 Otoscopy shows erythema, bulging opaque tympanic membrane with
loss of light reflex
 Pain on tracheal tug
Page | 616
6.3.3 Management :
 Depend on presentation, severity of symptoms and age group
 Sever symptoms ( Fever > 39◦C , Otorrhea , Moderate to severe
otalgia , Otalgia present > 48hours ).
 non sever (age 6m – 23m) bilateral all use antibiotics.
 Antibiotics 1st line.
 Amoxicillin: 80mg-90mg/kg per day in two divided doses
 2nd line
 Amoxicillin/Clavulanate: 90mg/kg 6.4mg/kg per day in two divided
doses
 Duration:10 day course if child < 24months or severe symptoms , 5-7
day course if child > 24months and does not have severe symptoms.
 Penicillin allergy you can use :
o 1st line
o Cefuroxime: 30mg/kg per day in two divided doses
o 2nd & 3rd line Ceftriaxone IM or IV: 50mg/kg per day for 1-3 days
(max dose 1g per day)
 Non-sever:
o Close follow-up within 48-72 hours.
o Start antibiotic therapy if worsening symptoms or no
improvement.
6.3.4 Prevention :
 Vaccination
 Breastfeeding for at least 6 months
 Avoid tobacco smoke exposure
Note : Otitis Media with Effusion (Watchful waiting for three months can
be applied to children who are not at risk.)
Acute Otitis Media in Adults use antibiotics directly
1st line amoxicillin
ENT referral (presenting with recurrent AOM: > 2 episodes per year or if
there is evidence of otitis media with effusion persisting for more than 6
weeks to rule out postnasal eustachian tube obstruction.)
Page | 617
Section 11: Orthopedics

Chapter 1: SPORTS MEDICINE
1.1. The Preparticipation Physical Examination
It is considered as a screening tool for early identification of at-risk
individuals for appropriate activity restrictions and to reduce the risk of
sudden cardiac death.
The goal is to screen for high-risk features on history and physical exams
(Table 1.1). The preferred time to perform a preparticipation physical
exam is about six weeks before the activity to allow enough time for
further workup if indicated.
Further evaluation is required only in high-risk groups and in most
individuals, no further blood, urine, or radiological studies are needed.
Table 1.1 – High-risk features on history and physical exam
High-risk history High-risk exam
Personal history of: – Abnormal blood pressure for age
– Syncope – Marfanoid features
– Chest pain – Visual acuity <20/40
– Active fever – Heart murmur
– Poorly controlled asthma – Respiratory distress
– Seizure – Abdominal organomegaly
– Solitary organs – Single testicle
– Monocular – Abnormal balance
– Concussion
– Menstrual dysfunction
– Eating disorder
– Sickle cell disease
Family history of:

– Hypertrophic cardiomyopathy
– Dilated cardiomyopathy
– Long QT syndrome
– Marfan Syndrome
– Arrhythmia
– Sudden cardiac death <50 years of
age
Page | 618
1.2. Concussion
1.2.1 Definition:
A concussion is a traumatic brain injury that results from mechanical
trauma to the head. It is mostly seen in sports, falls, or major accidents.
1.2.2 Symptoms:
symptoms include but are not limited to headache, confusion, blurry
vision, dizziness, nausea, amnesia, and photosensitivity, with or without
loss of consciousness.
1.2.3 Diagnosis:
Diagnosis is clinical and the SCAT-5 tool can be used to establish the
diagnosis and monitor progress.
No further workup is needed in most concussions.
Advanced imaging with CT or MRI may be indicated if there is concern
for a skull fracture, intracranial bleed, increased intracranial pressure,
focal neurologic findings, or amnesia more than 30 minutes.
1.2.5 Management & monitoring:
The first and most important step in management is early recognition.
Relative mental and physical rest is recommended until the resolution of
symptoms followed by a gradual return to activity.
Full return to sports should be guided more by symptoms and
progression than absolute timescales. Symptoms persisting for more
than 14 days in adults and four weeks in children are abnormal and the
athlete should be evaluated by a physician.
Chapter 2: GENERAL APPROACH TO
MUSCULOSKELETAL CASES
2.1. PHYSICAL EXAMINATION
A complete musculoskeletal examination should include the following:
 Inspection.
 Palpation.
 Active & passive ROM testing.
 Manual muscle testing.
 Provocative and special tests as indicated by the involved joint.
Page | 619
Note: Consider always examining the contralateral side to compare

positive findings. Different exam maneuvers have varying sensitivities
and specificities, which can be improved by using more than one exam
technique.
2.2. PRINCIPLES OF IMAGING
Different imaging modalities are frequently used. However, it is essential
to use your clinical judgment and knowledge of common tools, such as
Ottawa knee, ankle, and foot rules, to assist you when deciding whether
further imaging is needed.
2.2.1 X-Ray
 2- orthogonal radiographs should be obtained at minimum (AP and
lateral).
 When imaging pediatrics, consider a contralateral comparison image
as growth plates can look suspicious for pathology.
 Special views should be considered as indicated by the suspected
pathology.
2.2.2 Diagnostic MSK Ultrasound
 It is usually operator-dependent, which requires special training as
well as the need to understand the physics of US and MSK anatomy
to interpret imaging findings accurately.
 It has a quick and cost-effective diagnostic point-of-care evaluation
and helps guide your interventions if indicated.
2.2.3 CT SCAN & MRI
 CT is an excellent modality for preoperative planning when managing
fractures. However, MRI has the advantage of delineating underlying
soft tissue structures such as cartilage, meniscus, ligaments, and
tendons.
2.3. PRINCIPLES OF FRACTURE CARE
 Fracture management starts with early recognition, neurovascular
assessment, and protection of the affected area. This can be
accomplished via a splint initially, to allow swelling to subside,
followed by the appropriate cast of choice.
 Consider non-weight-bearing status as indicated in addition to rest,
elevation, ice, compression, and NSAIDs “ensure NO
contraindications to use.”
 Avoid using opiates except in acute pre-or post-surgical cases and
only for a few days.
Page | 620
 Recognizing fractures that require either immediate or urgent referral

to orthopedics is critical, and when in doubt, always consult your
orthopedics colleagues.
 Intra-articular fractures carry a higher risk for complications and
warrant surgical consultation. In contrast, open fractures are an
orthopedics EMERGENCY and require surgical intervention within 24
hours.
 Regular follow-up and repeat radiographs are critical aspects of
fracture care.
 Temporary joint stiffness is frequent after prolonged joint
immobilization, and patient education is important.
 Consider prescribing home exercises or referring to physical therapy
to work on range of motion and strength during recovery.
2.4. PHYSICAL THERAPY PRESCRIPTION
 Understanding the musculoskeletal pathoanatomy and formulating a
physical therapy prescription helps optimize your patient’s recovery.
 Multiple physical therapy protocols and modalities can be
incorporated into the management plan including, but not limited to,
therapeutic exercises, water therapy, therapeutic ultrasound,
phonophoresis, iontophoresis, low-level laser therapy, electrical
stimulation, heat or cold application, and soft tissue mobilization.
 Medical rehabilitation professionals, such as occupational therapists,
physical therapists, and orthotics and prosthetics specialists, all play
an important role in managing individuals with musculoskeletal
pathologies.
2.5. ULTRASOUND IN SPORTS MEDICINE
 Ultrasound has been validated as an excellent modality for evaluating
many sports injuries. It provides an affordable point-of-care window to
evaluate tissues such as fat, muscles, tendons, ligaments, joints,
bones, and neurovascular bundles.
 Ultrasound has also been used to guide interventions and has the
lead when it comes to accuracy, cost-effectiveness, and tolerability
when compared to conventional landmark-guided interventions.
 Ultrasound training is crucial as it requires an understanding of
human anatomy, ultrasound physics, and ultrasound artifacts that can
mimic pathology.
Page | 621
Chapter 3: SHOULDER PATHOLOGIES

3.1. Rotator Cuff Diseases and Impingement Syndrome
3.1.1 Definition
Impingement syndrome is a non-specific terminology that could involve
pathology of the shoulder at one or multiple potential areas depending on
the affected tendon, bursa, or ligament
3.1.2 Symptoms & sign
 Acute (injury) or insidious (tendinitis)
 Pain with above head activity is a common presentation.
 Supraspinatus tendon is the most affected tendon. It is
 More common in older individuals
 Limited active range of motion (ROM) with abduction and internal
rotation
 Jobe, Hawkins, and Neer tests
3.1.3 Investigation
 X ray for chronic degenerative changes within the tendons
 MRI is the gold standard.
 Ultrasound is an excellent emerging diagnostic modality
3.1.4 Management
 Supportive care with relative rest, ice, NSAIDs, and early home
exercises or physical therapy enrolment
 Subacromial corticosteroid injection might provide short-term relief
(when surgery is not an option)
 Surgical repair as indicated in acute full thickness tears in young
active individulas.
3.2. Adhesive Capsulitis (Frozen Shoulder)
 Pain and restricted movement are the key presenting symptoms.
 Limited active and passive range of motion.
 Risk factors include DM and prior shoulder injury, but it could be
idiopathic.
3.2.2 Investigation
 Clinical Dx
 MRI can detect glenohumeral ligament inflammation
Page | 622
3.2.3 Management
 Patient education (full recovery can take up to 2 years)
 NSAIDs and early rehabilitation focusing on ROM (Initial
management)
 Glenohumeral corticosteroid injection
 Hydrodilation of shoulder capsule.
 Surgery is rarely required.
3.3. Acromioclavicular (AC) Joint Pathology
 Pain over the AC joint with or without a deformity.
 Arthritis is a common pathology that might predispose to
supraspinatus injury
 AC joint separation related to trauma (Rockwood Classifications)
3.3.2 Investigation
 X ray In traumatic injuries, distal clavicle displacement above the
acromion may be noted.
3.3.3 Management
 Conservative Management in most cases
 Supportive care and topical NSAIDs.
 Subacromial corticosteroid injection (bursitis).
 Surgery might be indicated for persistent symptoms (supraspinatus
injury).
 Type I and II AC separation conservative management (sling and
rehabilitation).
 Type III is controversial, (trial of conservative followed by surgical)
 Types IV-VI often require surgical fixation.
3.4. Glenohumeral Dislocations
 Anterior dislocation is far most common dislocation (trauma)
 Posterior dislocation (electrical shock or grand mal seizure).
 Patient cannot move the Joint
 Anterior dislocation presents with an abducted and externally rotated
arm.
 Posterior dislocation present with an adducted and internally rotated
arm.
 Deformity
 Apprehension & sulcus sign are frequently present on the exam.
Page | 623
3.4.2 Investigation
 Shoulder 4-view radiographs (especially Y and axillary views)
3.4.3 Management
 Attempted reduction with gentle force is recommended.
 Neurovascular evaluation pre- and post-reduction.
 Reduction under sedation (if delayed presentation).
 Arm sling for 4 weeks followed by physical therapy for strengthening.
 Referral to orthopedics as indicated (high recurrence rate).
3.5. Labral Lesions
3.5.1 Definition
The shoulder labrum is a cup-like rim of cartilage that lines and
reinforces the humeral head within the glenoid fossa
 Posttraumatic pain
 Catching or popping sensation in the shoulder
 Positive O’Brien’s active compression test on exam.
3.5.3 Investigation
 MRI +/- arthrogram can aid in the diagnosis
3.5.4 Management
 Conservative (NSAIDs and rehabilitation)
 Surgery (persistent symptoms or instability)
3.6. Sternoclavicular Injuries
 Usually traumatic but can be degenerative.
 Pain, clicking, redness
 Deformity with occasional popping
 Can lead to anterior or posterior dislocation.
 Posterior dislocation more risky (carotid and subclavian arteries).
 Pain with cross-body arm adduction.
3.6.2 Investigation
 Radiographs and CT angiogram as indicated are the modality of
choice in the acute setting.
3.6.3 Management
 Chronic anterior dislocation (arthritis) can be managed
symptomatically.
 Acute posterior dislocations need referral to the emergency room.
Page | 624
 Traumatic posterior SC dislocation is a surgical emergency.

3.7. Myofascial Pain Syndrome (Trigger Points)
3.7.1 Definition
Chronic pain disorder caused by focal areas of painful and tender taut
bands within skeletal muscles due to repetitive use and stress of
muscles
 Commonly involves the neck, shoulders, or pelvic girdle muscles
 Focal tenderness with areas of stiffness within the affected muscle.
3.7.3 Investigation
Diagnosis is clinical
3.7.4 Management
 Conservative (hydration, heat pads, NSAIDs, deep massage)
 Physical therapy
 Trigger point injections if indicated.
3.8. Clavicle fractures
 Usually due to traumatic falls
 Middle third of the clavicle most common
3.8.2 Investigation
 Radiographs
3.8.3 Management
 Arm sling or figure of eight harnesses for 4–6 weeks
 Range of motion and strengthening exercises
 Surgical management :
o Open fracture
o neurovascular compromise
o shortening >20 mm
o displacement >10mm
3.9. Scapula Fractures
 High impact injury
3.9.2 Investigation
 X ray
Page | 625
3.9.3 Management
 Arm sling for protection and early rehabilitation
 Surgical referral
o intra-articular fracture
o displaced scapular neck fracture
o shoulder instability
3.10. Humeral Fractures
 Bimodal age distribution (high energy trauma in the young and low
energy trauma in the elderly)
 Swelling and deformity
3.10.2 Investigation
 X ray
3.10.3 Management
 Conservative for closed nondisplaced fractures with an arm sling
 Surgical consultation
o open fracture
o neurovascular compromise
o compartment syndrome
Chapter 4: ELBOW AND FOREARM
PATHOLOGIES
Symptoms:
Pain at tendon origin:
- Medical epicondyle Golfer’s Elbow
- Lateral epicondyle Tennis Elbow
Examination:
Localized tenderness at tendon origin, might radiate to forearm.
Diagnosis:
Clinically and imaging (MRI or US) when indicated.
Management:
Physical therapy: eccentric exercises.
NSAIDs.
Counterforce brace.
Corticosteroid injection (controversial)
Page | 626
4.1. Cubital Tunnel Syndrome

4.1.1 Definition:
Neuropathy is caused by the entrapment of the ulnar nerve at the
posterior elbow (ulnar nerve impingement)
4.1.2 Symptoms:
Pain at the elbow radiates distally with numbness and tingling at the
ulnar nerve distribution.
4.1.3 Examination:
Weakness of the hand’s intrinsic muscles.
Positive Tinel Test over the cubital tunnel.
4.1.4 Diagnosis:
Clinical, nerve conductive study aids the diagnosis.
MRI or ultrasound can reveal structural causes.
4.1.5 Management:
Limit full flexion of elbow.
Night splints.
Surgical decompressions if no improvement.
4.2. Olecranon Bursitis
4.2.1 Symptoms:
Swelling of the olecranon.
Septic bursitis should be excluded.
4.2.2 Examination:
Swelling of the posterior elbow.
4.2.3 Diagnosis:
Radiographs if fracture is suspected.
4.2.4 Management:
Protection, compression, ice and NSAIDs.
Bursa aspiration and empiric antibiotics are indicated if septic bursitis is
suspected.
4.3. Distal Biceps Avulsion
4.3.1 Definition:
Compromised distal biceps tendon attachment leading to retraction or
tearing of the tendon.
Usually results from a sudden vigorous eccentric contraction, more with
anabolic steroid use and smoking.
Page | 627
4.3.2 Symptoms:
Reverse Popeye deformity.
4.3.3 Examination:
positive provocative hook test.
4.3.4 Diagnosis:
Clinical and MRI or ultrasound if indicated
4.3.5 Management:
Surgical consultation to evaluate lost function and surgical needs.
In older individuals you may consider Ice, rest, NSAIDs and physical
therapy.
4.4. Radial Head Fracture
4.4.1 Definition:
Common, FOOSH is the usual mechanism of injury.
4.4.2 Symptoms and Examination:
Pain at the radial head, worsen with supination of pronation.
Swelling and bruising of the elbow.
4.4.3 Diagnosis:
Radiographs using Mason classification.
4.4.4 Management:
- Simple non-displaced Immobilization followed by rehabilitation
- >2mm displaced Surgery
4.5. Condylar Fracture
4.5.1 Definition:
Commonly involves the lateral epicondyle in pediatrics.
FOOSH or pulling off are the usual mechanism of injury.
4.5.2 Diagnosis:
on with positive fad pad sign in lateral elbow radiographs.
4.5.3 Management:
Long arm cast for 4-6 weeks.
- >2mm displaced or open fracture Surgery
4.6. Epicondylar Fracture
4.6.1 Definition:
Most common elbow fracture in 5-7 years. Occur after FOOSH.
4.6.2 Examination:
Inspects for any signs for neurovascular compromise.
Page | 628
4.6.3 Diagnosis:
Radiographs based on Gartland classifications.
4.6.4 Management:
Long arm cast in <90 degrees flexion for 3 weeks.
Weekly follow to ensure no interval displacement.
4.7. Elbow Dislocations
4.7.1 Definition:
- Pediatrics Most common
- Adults Second to shoulder dislocations
Axial loading is the main mechanism.
4.7.2 Examination:
Swelling and deformity.
Inspects for any signs for neurovascular compromise.
4.7.3 Diagnosis:
Radiographs.
4.7.4 Management:
Reduction with 5-10 days elbow splint at 90 degrees, and early
rehabilitation.
Surgical consultation for complex reeducation or failed reduction.
Chapter 5: HAND AND WRIST
PATHOLOGIES
5.1. Carpal Tunnel Syndrome
5.1.1 Definition:
 Entrapment neuropathy of the median nerve at the volar wrist region.
 Secondary to repetitive use, anatomic anomalies, or direct trauma.
 Women during pregnancy are also affected.
 Pain and numbness are located over the thumb, index, middle, and
radial half of the ring fingers.
 Thenar muscle atrophy and weakness can be noted at a later stage.
 Tunnel’s and Phalen’s tests both have high false-positive and false-
negative rates.
 A positive flick test has better clinical reliability.
Page | 629
 An EMG/NCV study can show a delay in median nerve conduction
velocity and depict the severity of entrapment.
 Diagnostic ultrasound has been validated for the diagnosis of carpal
tunnel syndrome.
 Activity modifications to optimize ergonomics and the use of a night-
time wrist splint are considered first-line treatments.
 Corticosteroid injection of the carpal tunnel can provide variable
short-term relief.
 Surgical decompression can be considered for recalcitrant symptoms
or in the setting of an acute carpal tunnel syndrome.
5.2. De Quervain’s Tenosynovitis
5.2.1 Definition:
 Inflammation and swelling of the extensor tendon sheath secondary
to overuse.
 Commonly seen with other overuse conditions.
Exam elicits pain with limited ROM and a positive Finkelstein test.
Ensure a negative grind test, as a positive test indicates 1st CMC
arthritis.
Diagnosis is mainly clinical.
Diagnostic ultrasound can concur with the diagnosis.
Page | 630

 Consider activity modification with a thumb spica brace, rest, ice, and
NSAIDs as initial treatment.
 Tendon sheath corticosteroid injection has been proven an effective
treatment modality.
 Surgical decompression may be needed for persistent or recurrent
symptoms despite conservative measures.
5.3. Scapholunate Sprains
5.3.1 Definition:
 Post-traumatic pain in the dorsal wrist region.
 The mechanism of injury often falling onto an outstretched hand
(FOOSH).
 Pain is worsened with gripping or ulnar/radial deviation.
 Tenderness to palpation over the dorsal scapholunate ligament is
present.
 A radiograph can rule out other common injuries after a FOOSH.
 Look for a widening of the scapholunate space >3 mm or a
scapholunate angle >60.
 Managed initially with splinting followed by active ROM as tolerated.
 Consider early referral to hand surgery to avoid advanced
scapholunate collapse.
Page | 631
5.4. Raynaud's Phenomenon

5.4.1 Definition:
 Also referred to as primary or idiopathic Raynaud’s phenomenon.
 It is a transient episodic vasoconstriction response that commonly
affects digits.
 Usually has no underlying pathology and has a low risk of developing
complications compared to Raynaud’s disease.
 A common trigger is a cold weather with a higher prevalence in
females and those under 40 years of age.
 Affected individuals might complain of pain or paresthesia.
 Pathognomic exam findings include clearly demarcated pallor of the
affected digit followed by cyanosis or erythema.
Diagnosis is clinical and may require laboratory testing to rule out
underlying rheumatologic or connective tissue disorders.
 Management includes patient education to avoid triggers such as cold
and smoking cessation if applicable.
 Nifedipine has good evidence for reducing the frequency and severity
of attacks.
5.5. Raynaud's Syndrome
5.5.1 Definition:
 Also referred to as secondary Raynaud’s phenomenon, since it is
secondary to underlying disease.
 It is commonly seen with connective tissue diseases such as
systemic sclerosis, Sjogren’s syndrome, SLE, RA, or polymyositis.
History and exam findings may be more severe compared to primary
Raynaud’s.
Appropriate laboratory evaluation can identify the underlying etiology in
most cases.
Management is geared towards optimizing the underlying causative
disease in addition to symptomatic treatment as indicated in the primary
Raynaud’s phenomenon.
Page | 632
5.6. Chilblains (Pernio)

5.6.1 Definition:
A cold-induced mild injury that causes inflammation of small vessels of
the affected area such as the face, hands, or feet leading to small
patches of inflamed skin.
This is a mild cold injury when compared to frostbite. In frostbite the
affected individual complains of pain, and itching; the exam shows a
shiny red plaque on the skin with no skin disruption or gangrene.
Immediate recognition and rewarming of the affected area is important,
avoid rubbing, apply lotion to help with itching, and protect the affected
area by dressing appropriately for the weather. Symptoms usually get
better within the first 2 weeks.
5.7. Ganglion Cysts
5.7.1 Definition:
These are synovial cysts containing mucinous materials. Commonly
affects the hand and can develop along a tendon or within a joint space.
The dorsal wrist region is the most common location.
A soft palpable mass is noted on the exam and is mostly asymptomatic.
The mass transilluminates with light.
Diagnosis is clinical. Radiographs are often normal and are not indicated.
If obtained, diagnostic ultrasound or MRI can depict the dimensions and
extension of the cyst.
 Observation is recommended as 2 out of 3 ganglion cysts seen in
pediatrics will spontaneously resolve within one year.
 Aspiration or closed rupture can be performed if symptomatic with a
high risk of recurrence.
 Surgical resection might be indicated for persistent cysts.
5.8. Common Finger Ligamentous and Tendon Injuries
5.8.1 Definition:
Injury of the ulnar collateral ligament (UCL) of the thumb with or without a
Stener lesion, in which the torn UCL is displaced and preventing its
likelihood of healing.
Page | 633

 A Stener lesion is one of the surgical indications.
 Other mild injuries can be managed with a thumb spica cast for 4
weeks followed by a rehabilitation program.
5.9. Mallet Finger
5.9.1 Definition:
 Can be uncommonly referred to as a baseball finger.
 Disruption of the extensor mechanism of the affected finger.
 Usually affects the insertion point at the distal phalanx.
 The preferred management is an extension finger splint for 6 weeks.
It should be always worn, splitting compliance is crucial. This is
followed by 4 weeks of nighttime splinting.
 Consider surgery with large bony defects or failure of conservative
measures.
5.10. Jersey finger
5.10.1 Definition:
Avulsion injury to the Flexor Digitorum Profundus tendon at its
attachment at the distal phalanx.
Prompt referral to hand surgery is warranted.
5.11. Boutonnière deformity
5.11.1 Definition:
 Deformity caused by extensor tendon central slip injury at the middle
phalanx.
 Can be due to acute trauma or chronic secondary to arthritis.
 Managed conservatively with extension splint at the PIP while
allowing DIP motion for 6 weeks.
 Consider surgery if large bony defects or if indicated otherwise.
5.12. Stenosing tenosynovitis (trigger finger)
5.12.1 Definition:
Caused by inflammation of the flexor tendon. Can be degenerative or
secondary to external compression at the A-1 Pulley.
Page | 634

Catching is noted during finger extension with pain in the flexor tendon
region.
 Corticosteroid injection to the tendon sheath can be attempted with
caution not to inject the tendon due to the risk of rupture.
 Surgery if injection fails the patient.
5.13. Common Hand and Wrist Fractures
Common radial fractures
5.13.1 Colles fracture
Definition:
 A common distal radius fracture with dorsal tilting of the distal
fragment.
 Secondary to falling onto an outstretched hand (FOOSH).
Management plan:
 Managed with closed reduction and a short arm cast if the fracture is
extra-articular.
 Open reduction is preferred for intra-articular fractures or if indicated
otherwise.
5.13.2 Smith fracture
Definition:
Another FOOSH injury of the distal radius with the wrist flexed leading to
a volar tilting of the distal fragment.
Management plan:
Same management as Colles fracture with less angulation allowed.
Galeazzi fracture
Definition:
Radial diaphyseal fracture with dislocation of the radioulnar joint distally.
Management plan:
Managed with open reduction and internal fixation (ORIF).
5.13.3 Barton fracture
Definition:
 Distal radius intra-articular fracture with radiocarpal joint dislocation in
dorsal or volar direction.
 Mechanism of injury involves high energy forces.
Pain, ecchymosis, and deformity can be seen.
Page | 635
Investigations:
Radiographs should be obtained to confirm the diagnosis.
Management plan:
Initial management measures include ensuring proper neurovascular
exam and intact skin, with immobilization using a splint and urgent
referral to orthopedics.
5.14. Common ulnar fractures
5.14.1 Nightstick fracture
Definition:
Fracture of the ulnar shaft.
Management plan:
 Can be managed non-operatively with cast immobilization if
nondisplaced.
 Requires ORIF for significant displacement or if otherwise indicated.
5.14.2 Monteggia fracture
Definition:
Ulnar proximal diaphyseal fracture with dislocation of the radial head.
Management plan:
ORIF for the ulnar fracture with attempted closed reduction of the radial
head.
5.15. Common carpal fractures
5.15.1 Scaphoid fracture
Definition:
 By far the most commonly fractured carpal bone.
 Mechanism of injury FOOSH.
Pain at the anatomical snuffbox region.
Investigations:
 Radiographs can miss up to 10% of fractures.
 Consider MRI, CT, or bone scan for persistent pain after 2 weeks of
initial management.
Management plan:
 Managed initially with thumb spica brace and repeat radiographs in 2
weeks if they were negative initially.
 Proximal pole fractures are at high risk for nonunion due to the poor
blood supply and would warrant surgical referral.
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 Unstable fractures need urgent orthopedics referral after proper

immobilization.
5.15.2 Triquetral fracture
Definition:
 The second most common carpal bone fracture.
 A FOOSH injury that commonly affects the dorsal aspect of the
triquetrum leading to a chip fracture.
Tenderness to palpation on exam distal to the triangular fibrocartilage
complex (TFCC).
Management plan:
 Management is mostly conservative with volar wrist splint
immobilization for 4–6 weeks followed by rehabilitation.
 Consider referral to orthopedics if wrist instability is reported or if
otherwise indicated.
5.16. Fingertip Injuries
5.16.1 Subungual Hematoma
Definition:
Hematoma accumulation under nail secondary to crush injury.
Pain and bluish discoloration of nail bed noted on exam.
Investigations:
If concerned about a fracture, obtain radiographs, otherwise x-rays are
not indicated for pure subungual hematoma evaluation.
Management plan:
Manage conservatively with drainage via sterile nail perforation or
consider nail removal with debridement if the hematoma is >50% of the
nail bed.
5.16.2 Nail Bed Laceration
Definition:
Laceration can involve both the nail and nail bed.
It will likely cause a significant hematoma.
Management plan:
Consider removal of the affected nail followed by suture repair of the
affected nail bed and consider tetanus vaccine and oral antibiotics if
indicated.
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5.16.3 Nail Avulsion Injury

Definition:
Caused by high-energy trauma.
Investigations:
Consider radiographs for underlining fracture evaluation.
Management plan:
Evaluated nail bed for laceration and repair as indicated.
5.16.4 Amputated Digits
Definition:
 Complete amputation of the digit is usually secondary to traumatic
dissection, avulsion, or crush injury.
 It is a surgical emergency and requires prompt transfer to a
replantation capable facility.
Management plan:
If an amputated digit is present, wrap it in sterile gauze and keep it inside
a biohazard plastic bag on ice water to maintain viability and transfer to
replantation capable facility.
Chapter 6: SPINE PATHOLOGY
6.1. Cervical Radiculopathy
6.1.1 Symptoms and exam
Common in elderly patients with neck pain radiating to the upper
extremity, possibly from chronic nerve compression or cervical disc
disease. Follows dermatome pattern, positive Spurling test with potential
sensory loss and weakened reflexes.
6.1.2 Diagnosis and management
Diagnosis of disc herniation is based on clinical examination.
Radiographs may show chronic degeneration, but MRI is the best
imaging modality if conservative measures fail after 4-6 weeks or if red
flags (high-risk trauma, fever, recent surgery) are present. Initial
treatment includes NSAIDs, physical therapy, stress reduction, and
muscle relaxants for spasms.
6.2. Cervical or Lumbar Strain/Sprain
Poor posture, overuse, or stress causing neck and back pain with limited
ROM, tenderness, and stiffness in affected muscles. Can also affect the
upper shoulder region.
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Diagnosis made with Hx and PE. Treated with heat, NSAIDs, ROM,
massage, and muscle relaxants. Encourage mobility and avoid rest.
Imaging may be necessary if red flags or failed conservative treatment.
6.3. Whiplash Injury
Rapid flexion to hyperextension or vice versa can cause neck injury,
affecting muscles, ligaments, nerves, or bones. Symptoms include pain
in the lower neck and upper shoulder, and severe cases may cause
dysphonia or dysphagia. Ensure no focal neurological deficits are
present.
Diagnosis is through clinical examination. Radiographs may not show
much. Treatment includes NSAIDs, rest, and early ROM exercises.
Usually recovers in a month.
6.4. Cervical Myelopathy
Cervical spinal cord compression causing neurologic problems is often
due to chronic degenerative disc disease. Symptoms include neck pain
with radiating arm pain, and abnormal motor, sensory, or reflex functions
on the exam.
Radiographs and MRI can reveal spinal degeneration and nerve
compression. Treatment varies and may include non-surgical options
such as medication, physical therapy, lifestyle changes, or surgical
intervention if necessary.
6.5. Torticollis
Torticollis is a head tilt caused by the one-sided contraction of the
sternocleidomastoid muscle. It can be congenital or due to injury, virus,
abscess, or tumors. Painful on the touch of the affected muscles.
Diagnosis is based on symptoms, but imaging may be needed if red
flags are present. Management focuses on treating the underlying cause.
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6.6. Spinal Disc Herniation

Herniated disc causes lower back pain with nerve root involvement,
worse with sitting/coughing. Most common at L4-L5 or L5-S1. Positive
straight leg test with or without decreased reflexes. Watch for red flags
such as saddle anesthesia indicating cauda equina syndrome.
Diagnosis is based on symptoms. Treatment typically involves NSAIDs,
physical therapy, weight loss, activity modification, and muscle relaxants.
Corticosteroids may be prescribed for acute flare-ups. If no improvement
after 4-6 weeks or if red flags appear, imaging such as radiographs and
MRI of the lumbar spine is necessary. Surgery may be recommended if
conservative measures fail.
6.7. Degenerative Disc Disease
The disease is often caused by age but can also be present from birth.
Risks include repeated trauma, obesity, infections, smoking, and
genetics. Symptoms include pain and reduced reflexes if nerve roots are
affected.
Radiographs show signs of degeneration such as bone growth and
decreased disc space. Treatment includes NSAIDs, weight control, and
physical therapy for core strengthening. If symptoms persist, MRI and
corticosteroid injections may be needed. Consider referral for surgery in
severe cases.
6.8. Lumbar Spinal Stenosis
Neurogenic claudication is spinal canal narrowing causing pain and
tingling that worsens withstanding and improves with bending. Causes
include degenerative disc disease, herniated discs, and thickened
ligaments. Consider vascular claudication if the pain improves with rest
after exercise.
Diagnose degenerative changes with x-rays. Try NSAIDs, therapy, and
activity changes for 4-6 weeks. If no improvement, consider MRI and
surgery consult.
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6.9. Cauda Equina Syndrome

Cauda equina syndrome is a surgical emergency caused by
compression of the lower spinal nerve roots leading to severe pain,
weakness, and loss of sensation in the legs and lower body. Causes may
include trauma, herniation, stenosis, hemorrhage, infection, or
inflammation. The exam shows sensory and motor deficit, absent
reflexes in the legs, and loss of sensation in the perineal and anal
regions.
MRI is the gold standard imaging method. An early diagnosis and
immediate surgical intervention are essential to decompressing affected
nerve roots.
6.10. Vertebral Compression Fracture
Compression fractures are common in elderly individuals with
osteoporosis, caused by mechanical falls with axial loading. 1 in 2 elderly
individuals over 80 years may experience this fracture. Risk factors
include age, postmenopausal women, previous fractures, metastatic
bone disease, and osteoporosis. Symptoms include midline back pain
and limited range of motion.
Vertebral compression fractures can be diagnosed with X-rays.
Treatment options range from non-surgical (NSAIDs, brace, physical
therapy) to surgical (kyphoplasty, vertebroplasty, decompression) if there
is a risk of nerve damage or other measures fail. High-energy burst
fractures may require emergency surgery due to spinal cord involvement.
6.11. Rib Fractures
Rib fractures are often caused by trauma such as car accidents or falls
and can be single or multiple. Symptoms include worsening pain with
breathing and tenderness upon palpation. Hidden injuries such as lung,
liver, spleen, or kidney may be present. Check for paradoxical breathing,
which indicates a serious flail chest requiring surgery.
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Diagnosis of rib fractures can be made clinically, but chest radiographs
may be taken for confirmation. Treatment includes pain management
with NSAIDs, rest, avoiding triggering activities, and breathing exercises
to prevent atelectasis and pneumonia. In cases of a flail chest, surgical
evaluation is necessary for open reduction and internal fixation.
6.12. Costochondritis
Tietze syndrome is a condition characterized by chest wall pain and
swelling due to inflammation of the joints connecting the ribs to the
sternum. Causes include trauma, coughing, overuse, or infection.
Symptoms may resemble a cardiac problem, so a thorough evaluation is
necessary.
Diagnosis is based on clinical symptoms, but additional tests may be
done to rule out heart or lung issues. Treatment involves using NSAIDs,
rest and stretching.
6.13. Acute Osteomyelitis
Osteomyelitis is an infection in the bone or bone marrow, usually caused
by inflammation. It can be contagious and can become chronic in
individuals with underlying conditions such as surgery, trauma, diabetes,
and IV drug use. The most common pathogen is staph aureus.
Symptoms include pain, fever, swelling, tenderness in the affected area,
and draining wounds that track to the bone.
Get CBC, ESR, CRP, and blood cultures. Consider X-rays or MRI to
assess infection. Bone biopsy and cultures are best for diagnosis. Start
empiric IV antibiotics and adjust based on cultures and response.
Treatment can take 6 weeks and ID consultation is needed. Use CRP to
monitor response. A surgical evaluation may be necessary for
debridement.
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Chapter 7: HIP AND THIGH

PATHOLOGIES
7.1. Hip Osteoarthritis
A degenerative disease of the hip, Pain is often reported anteriorly, the
exam may be positive for limited hip ROM and positive log roll or FADIR
tests.
Hip radiographs often show narrowing of hip joint space, osteophytes.
Management with NSAIDs, weight management, physical therapy, and
patient education. Corticosteroid injections can be considered for acute
flares. Surgical consultation may be needed for persistent symptoms
beyond 4–6 weeks.
7.2. Greater Trochanteric Pain Syndrome
trochanteric bursitis, it is pain due to inflammation of the greater
trochanteric bursa.
Pain is usually localized over the lateral hip.
Diagnosis is clinical. Attempt a trial of conservative measures including
NSAIDs, physical therapy.
7.3. Iliotibial Band (ITB) syndrome
Friction over the lateral femoral condyle with overuse.
Exam demonstrates a positive Ober test and tenderness to palpation
over the lateral femoral condyle.
Diagnosis is clinical, ITB stretching, and foam roller exercises have been
proven effective. You may also consider ice, NSAIDs, and activity
modification.
7.4. Snapping Hip Syndrome
Popping sensation about the hip, Management is symptomatic and
mostly geared towards treating the underlying etiology.
7.5. Sacroiliac Joint Dysfunction
Mainly caused by degenerative changes. Pain is inferior to the posterior
superior iliac spine.
Radiographs are sufficient to make the diagnosis with history and
physical exam.
Management is NSAIDs, physical therapy, weight management, and
pelvic belt.
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7.6. Hip Fractures

Mostly due to trauma or fall leading to a fracture of the femoral neck,
intertrochanteric, or subtrochanteric region.
The exam will likely be limited due to pain mainly with internal rotation.
Radiographs in both AP and lateral views are sufficient to make the
diagnosis.
Surgical management is warranted in most cases.
7.7. Pelvic Ring Fracture
High energy trauma disrupts the pelvic ring which includes the sacrum
posteriorly and innominate bones anteriorly, associated with other
underlying orthopedic, urogenital, or abdominal injuries.
Initial management including hemodynamic resuscitation and monitoring
the airway. Radiographs can assist in fracture classification. A pelvic
binder centered over the greater trochanters is recommended for
stabilization. Once stabilized, transfer to a trauma center.
7.8. Hip Dislocation
Commonly seen with high energy trauma (dashboard injury) causing
posterior dislocation of the femoral head in about 90% of cases. Pain
and inability to bear weight. Deformity, leg length discrepancy, fixed
adducted, and internally rotated hip.
Radiographs. Urgent reduction followed by advanced imaging to
evaluate for subtle fractures, joint loose bodies, or other soft tissue
injuries. Operative management is indicated if reduction fails, with major
concomitant fractures.
7.9. Femoral Shaft Fracture
High energy trauma or gunshot injury in young adults, Falls from ground
level in the elderly.
Pain and inability to bear weight. Radiographs to confirm the diagnosis.
Management is open reduction and internal fixation. However, a long leg
cast or hip spica cast might be sufficient in pediatrics with a nondisplaced
fracture, elderly with unstable comorbidities.
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Chapter 8: KNEE AND TIBIAL

PATHOLOGIES
8.1. Knee Osteoarthritis (OA)
Knee osteoarthritis results from
degenerative changes to the
hyaline cartilage, bone, and
synovium leading to chronic
diffuse knee pain. It usually
involves the medial joint line and
pain is worse with increased
activity. Even though this is a
highly prevalent condition in
older individuals, make sure you
obtain a good history and
exclude other possible etiology
such as referred pain, infection,
tumors, etc.
Joint line tenderness, effusion, and joint bony enlargement might be
noted on physical exam with decreased ROM
Weight-bearing radiographs can aid in the diagnosis and assist in the
radiological classification of severity using the Kellgren and Lawrence
classification system. A conservative approach is reasonable starting
with patient education, weight management, physical therapy , as
needed oral or topical NSAIDs, and a knee unloader brace. If no
improvement in 4–6 weeks, consider corticosteroid injections for short-
term pain relief but should not exceed 4 injections in a single joint per
year as this might be detrimental to the joint. Hyaluronic acid and
platelet-rich plasma injections have mixed evidence and can be
considered in mild OA. Surgical referral for joint replacement is
reasonable if all measures fail or if indicated otherwise. Take into
consideration both patient symptoms and imaging findings when
managing individuals with OA as people with advanced disease could
have minimal symptoms and vice versa.
Page | 645
8.2. Meniscal Tears

Both medial and lateral knee menisci
are vulnerable, however, medial
meniscus tears are more common.
Pain on either joint line with
mechanical symptoms such as
locking, catching, or popping are the
hallmark. Positive McMurray and
Thessaly tests with tenderness to
palpation at the joint line may also be
present. Effusion may be present
8.2.2 Diagnosis and
management
MRI is the modality of choice.
Orthopedic evaluation and surgery are
indicated when there are mechanical symptoms, root tear, and in most
symptomatic young individuals. Surgical options include meniscectomy,
meniscal repair, or transplantation.
However, in older individuals with degenerative meniscal injury and no
mechanical symptoms, conservative measures can be attempted first.
8.3. Anterior Cruciate Ligament (ACL) Tear
The ACL stabilizes the knee
and prevents anterior
translation of the tibia on the
femur. It is commonly injured
during sports. Most patients
will report feeling a pop
followed by pain and effusion.
Instability might also be
reported. These findings are
not specific, so a proper
physical exam is important.
Positive Lachman and anterior
drawer tests will be present. Effusion can be noted as well.
Page | 646

The clinical exam can be diagnostic. MRI is the gold standard imaging to
evaluate ACL tears and other associated pathologies affecting bone,
meniscus, and other ligamentous structures as seen in the unhappy triad
(injury to ACL, MCL, and meniscus).
Management is individualized based on the affected individual’s age,
associated injuries, current symptoms, and activity level. This can range
from physical therapy to build muscular strength to compensate for the
deficient ACL in older individuals to surgery in younger active individuals
or if otherwise indicated.
8.4. Collateral Ligament Injuries
Both medial and lateral collateral
ligaments (MCL/LCL) can be
affected. However medial
collateral ligaments are affected
more commonly. Tenderness to
palpation along the collateral
ligament and positive valgus or
varus laxity stress testing will likely
be noted on the physical exam.
Ensure no other accompanied
pathologies when evaluating LCL such as those seen with posterolateral
corner injuries.
The physical exam is sufficient to make the diagnosis. Radiographs can
be obtained for osseous pathology evaluation. Treatment is mostly
conservative with a hinged knee brace for protection and early ROM
rehabilitation for 6–8 weeks to prevent stiffness. Surgery might be
indicated if other pathologies are present.
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8.5. Patellofemoral Pain Syndrome (PFPS)

PFPS is a common cause of
anterior knee pain. Pain is typically
worse with walking upstairs or
prolonged sitting which loads the
patellofemoral joint. Females can
be affected due to increased Q
angle, the elderly can be affected
due to arthritic changes. The exam
might demonstrate tenderness to palpation around the patella with
manual muscle testing indicating weak quadriceps leading to increased
lateral patellar mobility. Consider patellar instability if positive patellar
apprehension test and ensure no history of patellar dislocation.
Radiographs with emphasis on sunrise views can show malalignment
with lateral patellar tilting but are not necessary to make the diagnosis.
Arthritic changes might be noted in the elderly indicating patellofemoral
osteoarthritis. An exercise program focused on quadriceps strengthening
and hamstring stretching with NSAIDs as needed for pain is the main
management approach. Consider knee brace with patellar cutout and
foot orthotics if indicated.
8.6. Bursitis
Bursitis and inflammation of an
affected bursa around the knee
including but not limited to
prepatellar, infrapatellar, pes
anserine, and ITB bursae. Pain
occurs in the affected bursa with a
history of frequent kneeling,
recent trauma, or overuse. Can be
infectious so check for
constitutional symptoms.
Tenderness to palpation with
swelling and redness can be
noted on exam.
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Diagnosis is clinical and management includes activity modification, ice,
compression, and NSAIDs. If concerned about infectious etiology,
aspirate and send for synovial analysis and consider a 10 day course of
oral antibiotics. consider corticosteroid injection. Surgical resection is
rarely indicated.
8.7. Quadriceps and Patellar Tendon Injuries
Injuries can include tendinopathy and partial or full-thickness tears.
Anterior knee pain with acute trauma and feeling a pop should raise your
suspicion of possible tearing. Chronic aching with overuse might indicate
tendinopathy. Failed extension mechanism at the knee on exam
indicates full-thickness tearing or patellar fracture.
Obtain radiographs to evaluate for bony pathologies. Evaluate patellar
positioning and whether patella alta (proximal displacement), patella baja
(distal displacement), or fracture is noted. Full-thickness tearing with
impaired extensor mechanism warrants surgical evaluation. For partial
tears, consider immobilization in full extension for 4–6 weeks followed by
rehabilitation. Tendinopathy can be treated based on stage but will likely
improve with supportive care and physical therapy. Disruption of the
extensor mechanism warrants surgical evaluation.
8.8. Medial Tibial Stress Syndrome (MTSS) and Tibial
Stress Fracture
MTSS is commonly referred to as
shin splints. Both conditions
present with anteromedial tibial
pain that worsens with high-impact
activities.
Symptoms are relieved with rest.
Ensure there are no red flags such
as nocturnal pain with
constitutional symptoms that might
indicate neoplasm or infection. If
exertional musculature pain is
present, consider exertional compartment syndrome. Tenderness to
Page | 649
palpation along the anteromedial tibia and a positive hop test are noted
on the physical exam.
Radiographs can show oblique cortical breaks or periosteal reactions but
are not always present. MRI or triple phase bone scan can distinguish
both conditions. Management is conservative with patient education,
NSAIDs, ice, and physical therapy with emphasis on cross-training in
MTSS. If a stress fracture is present, relative rest and avoiding heavy
impact on the affected leg for 4–8 weeks until the pain is resolved.
8.9. Compartment Syndrome
A clinical condition in which osteofascial intracompartmental pressure is
elevated enough to cause symptoms due to mechanical compression.
This can be divided into acute or chronic exertional compartment
syndrome. Legs are commonly affected . Etiology varies depending on
the clinical context. Fracture commonly causes an acute pressure
elevation leading to pain out of proportion with passive stretching of the
affected compartment, paresthesias, pallor, diminished pulses distally,
paralysis, and swelling. Inappropriate tight cast placement after fracture
without allowing time for swelling to reduce is another major risk factor. In
chronic exertional compartment syndrome, the symptoms are similar but
less severe and usually brought up by intense workouts and relieved by
rest.
Early recognition is critical in acute compartment syndrome as this is a
surgical emergency that requires immediate evaluation. Diagnosis can
be clinical in emergent situations, time is tissue when evaluating an
acute compartment syndrome. Management will include mechanical
optimization with removing a tight cast if present, fasciotomy within 6
hours of symptoms start, fracture management, and other measures as
indicated. Compartment pressure measurement can be appropriate in
non-specific, less acute, non-emergent situations, or in chronic exertional
compartment syndrome. Compartment-diastolic pressure can be
measured and interpreted by orthopedics. If a difference (delta P) of >30
mm Hg, then management can be non-operative. Laboratory testing is
not used to make the diagnosis.
Page | 650
8.9.3 Nocturnal Leg Cramps

Severe nocturnal muscle cramping that affects the calf muscles
commonly. The etiology remains unknown, however, it is thought to be
due to muscle fatigue and nerve excitation. Multiple risk factors have
been reported such as underlying vascular disease, spinal stenosis,
drug-induced, and other medical conditions. Diagnosis is clinical and
laboratory work-up is not required in most cases. Management is mostly
conservative . Some studies have shown the benefit of multivitamin
supplementation in pregnancy, however, more studies are needed.
8.10. Fractures Around the Knee Joint
8.10.1 Distal femur fracture
Symptoms and exam
Fracture commonly seen with high energy forces in young adults or as a
result of mechanical falls in vulnerable older individuals. Can be
classified into supracondylar or intercondylar fractures with or without
articular involvement. Symptoms can range from pain with weight-
bearing in mild injuries to significant swelling and deformity in more
severe cases.
Radiographs can assist in diagnosis .Management depends on clinical
context and is mostly surgical with open reduction and internal fixation,
however, a hinged knee brace might be acceptable in an older
nonambulatory individual with multiple serious comorbidities.
8.10.2 Tibial plateau fracture
Page | 651
Symptoms and exam

A proximal tibial fracture is commonly seen with high energy trauma in
the young or falls in the elderly causing valgus or varus stress with axial
loading at the knee joint. Concomitant meniscal or ACL injury may be
seen. Pain with weight-bearing with or without instability may be noted.
Knee effusion and limited ROM are present on the exam. Assess for
associated injuries.
Radiographs to assist in diagnosis and classification using Schatzker
classification and advanced imaging such as CT may be needed to
identify comminution and articular depression. Orthopedics referral is
recommended as treatment is often surgical fixation. Some individuals
with nondisplaced split fractures with proper alignment, or if indicated
otherwise, might be managed with a hinged knee brace for 8–12 weeks
under orthopedics supervision to allow gradual ROM.
8.11. Tibial eminence fracture
Symptoms and exam
Also commonly referred to as tibial spine fracture, it is an avulsion type
injury affecting the ACL insertion point to the tibia. Commonly seen in the
pediatric population between 8–14 years of age. It is thought to be due to
incomplete ossification of the intercondylar eminence. Mechanism of
injury varies but can involve rapid deceleration or hyperextension and
rotation as seen in sports. Pain and inability to bear weight is common
and physical exam usually illustrates knee effusion.
Radiographs of the knee can demonstrate fracture and MRI may be
indicated to assess other associated injuries such as meniscal, ACL, or
chondral defects. Management includes closed reduction followed by
cast immobilization in full extension for 4 weeks, followed by physical
therapy. Surgical indications include displaced fracture fragments, failed
reduction, or if otherwise indicated.
8.12. Tibial tubercle fracture
Symptoms and exam
Commonly seen in the adolescent male population aged 12–15 years of
age. Can result from forceful contraction of quadriceps seen in sports
such as basketball, American football, sprinting, or jumping. The fracture
can be classified using Ogden classification based on the level of
fracture and displacement of the involved segment.
Page | 652

Radiographs can illustrate the fracture and aid in classification.
Contralateral radiographs are recommended for comparison.
Management can be nonoperative with immobilization in full extension
cast after acceptable closed reduction for 6 weeks . consider
immobilization and referral to orthopedics.
8.13. Patellar fracture
Symptoms and exam
The patella is the largest sesamoid in
our body. Fracture of the patella is
usually a result of direct trauma, fall
into a flexed knee, or sudden vigorous
contraction of the quadriceps
muscles. It can be classified based on
fracture patterns such as vertical,
horizontal, comminuted, patellar
sleeve, etc. Pain and swelling are
common presenting symptoms. The physical exam is extremely
important to assess extensor mechanism integrity. This can be assessed
by asking the patient to perform active leg raise while supine.
Radiographs can assist in confirming the diagnosis and illustrate the
pattern of fracture. Management can be conservative with immobilization
in extension and full weight-bearing if closed, non-displaced, vertical, and
most importantly intact extensor mechanism. Otherwise, refer to
orthopedics for further evaluation and surgical management if indicated.
Chapter 9: FOOT AND ANKLE
PATHOLOGIES
9.1. Ankle Sprains
9.1.1 Definition:
 An injury occurs when the ankle rolls, twists, or turns in an awkward
position.
 Pain with swelling and ecchymosis are the most common presenting
symptoms in the acute setting.
Page | 653
 The exam should be performed while considering the validated

Ottawa ankle rules.
 Other exam findings may include limited ROM and positive anterior
drawer test in anterior talofibular ligament (ATFL) injuries.
 Consider syndesmotic injury (high ankle sprain) if positive squeeze
test, which can be problematic with prolonged recovery.
 Radiographs are indicated if recommended by Ottawa ankle rules.
 Diagnostic ultrasound can help evaluate affected ligaments.
 Initial management should include relative rest, protection, elevation,
ice, and NSAIDs.
 Allow early ROM exercises while swelling decreases.
 Educate affected individuals about sequelae of ankle sprain within the
next 12 months and encourage working with physical therapy on
strengthening and proprioceptive training.
 A functional ankle stabilizer brace may be used while returning to
activity.
 Consider referring high-risk ankle sprains with syndesmotic
involvement to orthopedics or, if otherwise indicated.
9.2. Charcot Foot
9.2.1 Definition:
 An inflammatory neuroarthropathy that affects the foot and ankle.
Major risk factors include but are not limited to:
o A history of peripheral neuropathy.
o Age >40 years.
o Long-term diabetes mellitus.
o Obesity.
 Acute foot swelling with or without recent trauma.
 Erythema.
 Increased warmth.
 Minimal to no pain.
 Unilateral foot edema with decreased sensation on monofilament test
and decreased deep tendon reflexes on physical exam.
 Foot and ankle derangement with deformity and ulceration can be
expected in delayed presentation.
Page | 654

 Bilateral weight-bearing radiographs are recommended.
 Look for soft tissue swelling, subtle subluxation, or ligamentous
avulsions.
 Advanced imaging such as MRI, CT scan, or bone scan can be
considered if radiographs are inconclusive.
 Prompt recognition.
 Patient education.
 Immediate immobilization may last 3–12 months until clinical and
radiographic improvement is evident.
 Surgery is indicated for severe dislocation or instability.
 The role of bisphosphonates, calcitonin, and denosumab in managing
Charcot neuroarthropathy remains uncertain. These agents might be
beneficial in a selected group of patients.
 Consider referral to foot and ankle surgery if the presentation is
delayed, in cases of instability, or otherwise indicated.
9.3. Achilles Tendon Rupture
9.3.1 Definition:
 It is a complete or partial tear that occurs when the achilles tendon is
stretched beyond its capacity, resulting in an inability to plantarflex. It
commonly feels like a painful pop or hit on the back of the ankle,
concurrent with a quick stop-and-go movement.
 Deformity.
 Swelling.
 A positive Thompson test can be evident on the exam.
 Diagnosis can be made clinically.
 Radiographs can be obtained to exclude bony avulsion.
 Diagnostic ultrasound has been validated in the evaluation of Achilles
tendon pathologies.
 MRI may be helpful for preoperative planning.
Depending on the clinical context and orthopedics consultation is
recommended=>Management may be nonoperative with progressive
immobilization starting in hyperflexion or operative repair.
Page | 655
Section 12: Urgent Care

Chapter 1: TRAUMA
1.1. Assessment:
 Primary survey (aim to perform a sequential primary assessment and
treat life-threatening conditions.):(ABCDE)
Prerequisites: gloved, gowned, and protected.The primary survey
encompasses the ABCDEs of trauma care and identifies life-threatening
conditions by adhering to this sequence (in a 10-second assessment):
1. Airway maintenance with restriction of cervical spine
motion
)If the patient is talking then this means their airway is patent).
 Assess, clear, and protect airway: jaw thrust/chin lift, suctioning if
airway is not patent.
 Perform oropharyngeal airway or endotracheal intubation with in-line
stabilization for a patient with a depressed level of consciousness or
inability to protect the airway. (Do not use nasopharyngeal airway if
basal skull fracture is suspected)
 Create a surgical airway if there is significant bleeding or obstruction
or laryngoscopy cannot be performed.
 Reinstate immobilization of the c-spine with appropriate devices like
hard cervical collars or hard blocks with strapping once an airway is
established.(Don’t mobilize the neck until cervical spine injury is ruled
out- stabilize neck: By holding the patient’s face on each side to keep
the head still. Apply a cervical collar when available.)
 If the patient is not breathing, start basic life support and alert the
cardiac arrest team.
2. Breathing and ventilation
 Ventilate with 100% oxygen use a bag-valve-mask device, monitor
oxygen saturation.
 Auscultate for breath sounds.
 Inspect thorax and neck for deviated trachea, open chest wounds,
abnormal chest wall motion, and crepitus at neck or chest.
 Consider immediate needle thoracostomy for suspected tension
pneumothorax (large bore cannula into the 2nd intercostal space at
the midclavicular line).
 Consider tube thoracostomy for suspected hemopneumothorax.
Page | 656
3. Circulation with hemorrhage control

 Assess for blood volume status: skin color, capillary refill,
radial/femoral/carotid pulse, and blood pressure.
 Place two large-bore peripheral IV cannulas, obtain blood (CBC,
renal, toxic screen, glucose) at same time save and crossmatch 4
units of RBCs.
 Begin rapid infusion of a warm crystalloid solution, if indicated.
 Apply direct pressure to sites of brisk external bleeding.
 Consider central venous or intraosseous access if peripheral sites are
unavailable.
 Consider pericardiocentesis for suspected pericardial tamponade.
 Place patient in the left lateral decubitus position in late-trimester
pregnancy.
4. Disability (assessment of neurologic status)
 Perform screening neurologic and mental status examination,
assessing:
o Pupil size and reactivity
o Limb strength and movement, grip strength
o Orientation
o Glasgow coma scale score
 Consider measurement of capillary blood glucose level in patients
with altered mental status
5. Exposure/environmental control
 Completely disrobe the patient (avoid hypothermia), and inspect for
burns and toxic exposures.
 Logroll patient, maintain a neutral position and in-line neck
stabilization.
 Inspect and palpate the thoracic spine, flank, back, and buttocks (look
at the patients face for any signs of pain).
 If there are any bandages on the patient’s limb(s) remove them and
look for any injuries.
 Assess if need for x-ray (c-spine/chest/pelvis)
Page | 657
 Secondary survey (Rapid head to toe examination):

Take (AMPLE) history of Allergy/ Medications currently used/Past illness,
Pregnancy/Last meal/ Events related to injury.
1. Head examination
 Identify and control scalp wound bleeding with direct pressure,
sutures, or surgical clips.
 identify facial or airway instability.
 Identify hemotympanum.
 Identify epistaxis or septal hematoma; consider tamponade or airway
control if bleeding is profuse.
 Identify avulsed teeth or jaw instability.
2. Neck examination
 Cervical immobilization should be continued until all aspects of c-
spine injury have been ruled out.
 Check for c-spine tenderness, subcutaneous emphysema, tracheal
deviation or laryngeal fracture.
 Check for any evidence of penetrating neck injury.
3. Chest examination
 Look- symmetry of chest wall, check open wounds.
 Listen- air entry on each side, areas of reduced air entry, crepitations
or rhonchi.
 Feel- palpable rib fracture, reduced chest movements, dullness on
percussion.
4. Abdominal examination
 Inspection- any obvious lump or fullness/ laceration/ contusion.
 Palpation- superficial and deep tenderness, guarding, rigidity, liver or
spleen enlargement/ penile and perineum examination/ assess pelvic
stability.
 Percussion- check for diffuse dullness if hemoperitoneum or ascites,
tympanic sounds over acute gastric dilatation.
 Auscultation- bowel sounds.
5. Musculoskeletal examination
 Look- bony deformity, bruises, subluxation or dislocation at the joints
in upper and lower limb.
 Feel- soft tissue tenderness, any joint laxity and palpable bony
deformity, press on each side of the pelvis checking the patients face
for any signs of pain. If there is any deformity, splint the fracture to
reduce deformity.
Page | 658
 Move- move different joints and look for any laxity or abnormal
motion.
6. Neurological examination
 Examine GCS, cranial nerves, sensory and motor examination.
 Back and spine examination.
 Log roll the patient and examine the spine for any palpable
tenderness, step or penetrating injury.
 Palpate the spinous processes for tenderness.
 Perform a rectal examination to check the anal tone.
Page | 659
Page | 660
Chapter 2: STATUS EPILEPTICUS

2.1. Definition:
Status epilepticus is a neurologic emergency when a single seizure
lasts more than or equal to 5 minutes or two or more seizures without
recovery of consciousness between seizures.
2.2. Management of Status Epilepticus:
 Focused history and physical examination toward causes and
subsequent injuries.
 Examination; identification of causes; checking airway, breathing, and
circulation; begin treatment simultaneously.
 Goal: seizure control as soon as possible and within 30 minutes of
presentation.
 Airway: keep airway open using NGT, consider

intubation in established status epilepticus
 Breathing: Place on oxygen
 Circulation: Insert a large-bore IV access and obtain
bedside glucose level. Administer normal saline
 Monitoring: keep on cardiac monitor, pulse oximeter,
and end-tidal capnography.
 Place urinary catheter to monitor urine output.
 Monitor temperature continuously and treat
hyperthermia with passive cooling.
 laboratory evaluation: Blood glucose, metabolic
panel(include ca & mg), lactate, and if appropriate,
pregnancy test, toxicology screen, and
anticonvulsant levels.
 Radiographic studies, such as CT scan, need to be
delayed until seizures are controlled.
Page | 661
 If hypoglycemia suspected administer IV glucose

 If toxic ingestion suspected place GI decompression
 If bacterial meningitis or encephalitis is suspected
administer empiric antibiotics or antivirals (Do not attempt
lumbar puncture during status epilepticus.)
 Status Epilepticus Treatment: goal (5-10 min)

 IV Lorazepam: 2 mg up to 0.1 mg/kg
 OR IV diazepam: 10-20 mg
 Plus one of the following:
 IV fosphenytoin: 20 PE/kg at 150 mg/min
 IV phenytoin: 20 mg/kg at 50 mg/min
 IV levetiracetam: 2000-4000 mg
2.3. Refractory status epilepticus

2.3.1 Definition
 Status epilepticus is a neurologic emergency when a single seizure
lasts more than or equal to 5 minutes Or two or more seizures without
recovery of consciousness between seizures.
 Treatment: Goal ( <30 min)

 IV Midazolam: Load with 0.3 mg/kg then infusion 0.05-
2 mg/kg/hr
 OR IV propofol: 1 mg/kg IV, then 1-10 mg/kg/hr; or
ketamine 5 mg/kg/hr
 OR IV phenobarbital: 20 mg/kg at 50-75 mg/min
 Intubate patient, Neuro ICU admission, Continuous
EEG monitoring
Page | 662
Chapter 3: HTN EMERGENCY

3.1. Definition:
 Hypertensive emergency:
o Acute elevation of blood pressure (≥180/120 mm Hg) with end-
organ damage, E.g., brain, heart, aorta, kidneys, or eyes.
 Hypertensive urgency (Severe Asymptomatic Hypertension):
o Profound elevation in BP (≥180/120 mm Hg) without acute
target organ dysfunction.
3.2.1 History:
 Severe BP elevation may cause mild symptoms (e.g., headache,
lightheadedness, nausea, SOB, palpitations, epistaxis, and anxiety)
without acute target organ injury.
 Targeted symptom history to identify a potential hypertensive
emergency:
o Previous hypertension history, medical history ( CAD, CHF, CVA,
CKD, PVD, DM, sleep apnea), family history of risk factors,
Secondary causes ( family or personal history of kidney disease,
medications and illicit drug use, clinical features of metabolic
disorders (e.g., thyroid disease, pheochromocytoma,
hyperaldosteronism))
Target organ injury:
Neurologic: (headache, vision changes, vomiting, seizure, neurologic
deficits),
Cardiovascular (chest pain, SOB, syncope, history of palpitations or
arrhythmias, back pain), Renal (oliguria, anuria)
Peripheral arteries (claudication, cold extremities, weak distal pulses)
Pulmonary (sleep apnea, chronic lung disease)
 Often normal in patients with severe asymptomatic hypertension
 Signs of target organ injury:
o Neurologic: (change in mental status, motor or sensory deficits)
o Ophthalmologic: (arteriolar narrowing, hemorrhage,
papilledema)
o Cardiovascular: (arrhythmia, murmur, displaced point of
maximal impulse, third heart sound gallop, peripheral edema)
o Pulmonary (rales, hypoxia, tachypnea E.g., pulmonary edema)
Page | 663
o Vascular (diminished/absent peripheral pulses, abdominal bruits,

unequal pulses or BP, raised JVP).
 Hypertension urgency  Investigation is not required
 Hypertension emergency:
o Diagnostic testing based on symptoms
 The most ordered tests:
o Complete metabolic panel
o ECG
o Cardiac enzymes
o CBC
o Urinalysis
o Chest x ray
o CT head.
The goal: minimize end-organ damage by initial BP reduction while
avoiding hypoperfusion of cerebral, coronary, and renovascular beds
except acute aortic dissection because of high risk of inadequate BP
control.
Hypertensive emergency:
Intensive monitoring is needed, BP control should be achieved within 1-2
hours. Hospitalization is required with IV treatment using
antihypertensive agents such as GTN, Sodium Nitroprusside, Labetalol,
Nicardipine.
Hypertensive urgency:
 30 minutes of rest in a quiet room produce a fall in blood pressure
≥20/10 mmHg.
 Blood pressure should be reduced over hours to days depending on
patient factors.
 Blood pressure should be lowered gradually to <160/100 mm Hg.
MAP should not be lowered by more than 25 to 30% over the first
several hours. When this goal is achieved, antihypertensive
intensification is recommended every 2-4 weeks to achieve BP goals.
Patients who have not been compliant often can safely resume their
outpatient medications.
 Standard short-acting antihypertensive agents used in severe
asymptomatic hypertension include:
o Oral Clonidine (but not intended as long-term therapy) at a dose
of 0.1 to 0.2 mg
Page | 664
o Oral Captopril (if the patient is not volume overloaded) at a dose

of 6.25 or 12.5 mg
Page | 665
Page | 666
Chapter 4: TOXICOLOGY
4.1. Clinical Features
 A detailed history is paramount for proper management.
 Ascertain the type(s), amount, timing, and route of exposure(s), as
well as the number of persons involved.
 Physical examination: assess mental status, pupil size and reactivity,
skin temperature, presence or absence of sweat, muscular tone,
gastrointestinal motility and mucous membrane moisture.
4.2. Diagnosis and Differentials
 Recognition of a toxidrome narrow the differential diagnosis in an
unknown or suspected poisoning.
 Acetaminophen and aspirin are common and treatable coingestants.
They should be screened for any suspected poisoning, or patients
with altered mental status of unknown etiology.
4.3. General Approach
 Begins with assessment and stabilization of ABC rather than
administering a specific antidote.
 For externally contaminated: removing clothing and copious irrigation
of the skin is a priority as soon as possible. Rescue and hospital
personnel should wear personal protective gear, including gowns, eye
protection, and masks.
 Patients presenting with sedation, obtundation, or coma and
overdose of opioid is a possibility should receive empiric treatment
with naloxone (0.2-2.0 mg IV every 2-3 min to maximum of 10mg in
adults and 10microgram/kg for child), check BM if low give glucose
(50-250ml 10% glucose IV IN 50ML), For alcohol withdrawal or
malnourished individual Give thiamine (100 mg tds ), generally
accepted as safe but the use of parenteral thiamine should be done
with resus facilities at hand.
 Empiric use of flumazenil if a benzodiazepine overdose is likely.
 Hypotension is managed with fluid resuscitation; vasopressors should
be considered only when blood pressure is refractory to fluid
administration. Ventricular dysrhythmias are treated according to
standard ACLS measures unless treatment of a specific toxin dictates
alternative therapy.
 Benzodiazepines are first-line therapy for seizures following exposure
to most toxins.
Page | 667
 All patients with intentional poisoning: referred for psychiatric

evaluation once medically stable. Pediatric may require social worker
evaluation.
Remember the general approach by the Mnemonic Resus-RSI-DEAD
Resus: Resuscitation
 Airway, Breathing, Circulation, Seizure control, Correct hypoglycemia
&hyperthermia, Resuscitation antidotes
R: Risk assessment
 Agent(s), Dose(s), Time since ingestion, Current clinical status
&Patient factors
S: Supportive care and monitoring
I: Investigations
 Serum glucose, ABG, Serum electrolytes, CBC, LFT, Pregnancy
screening, Blood ethanol concentration, Screening (e.g., paracetamol
concentration levels), ECG
D: Decontamination
 GI Decontamination, Activated Charcoal, Gastric Lavage & Syrup of
ipecac (not recommended)
Charcoal (best option):
 If given < 30 min, decreases absorption by 70%, If 30-60 min,
decreases absorption by 30%
 Dose: 1-2 g/kg (max 100 g)
 Contraindications: The ingested substance is not to bind to the
charcoal, If the airway is not protected, If the patient is actively
vomiting
Gastric lavage (36-40 Fr tube):
 Helpful if used within 60 min, Reserved for lethal poisonings, Risk for
iatrogenic injury (aspiration, esophagus)
E: Enhanced elimination
A: Antidotes (Table 4.1)
D: Disposition
Page | 668
Table 4.1 – Different agents and their antidotes

Agent Antidote
Acetaminophen N-Acetylcysteine (NAC)
Arsenic BAL, DMS
Aspirin Alkaline diuresis, hemodialysis
Beta-blocker Glucagon, intralipids
Barbiturate Alkaline diuresis, hemodialysis
Calcium channel blocker Calcium, glucagon,
glucose/insulin, intralipids
Carbamate Atropine
Carbon monoxide 100% O 2, hyperbaric O 2
Warfarin FFP / Vit K / PCCs
Cyanide Sodium nitrite, sodium
thiosulfate, hydroxocobalamin
Digitalis Digibind (fab antibodies)
Ethylene glycol Bicarbonate, ethanol, dialysis, 4-
MP
TCA Sodium bicarbonate, intralipids
Heparin Protamine
Hydrofluoric acid Calcium, magnesium
Iron Deferoxamine
Isoniazid (INH) Pyridoxine (Vit B-6)
Lead BAL, DMS, EDTA
Mercury BAL, DMS
Methemoglobin Methylene blue
Methanol Bicarbonate, ethanol, dialysis, 4-
MP
Nitrites Methylene blue
Opiates Naloxone
Organophosphates Atropine, 2-PAM
Oral hypoglycemic Glucose, glucagon, octreotide
agents
4.4. Definition:
 Overdose: > 75mg/kg in any 24-hour period, serious toxicity:>
150mg/kg.
 Threshold for paracetamol-induced hepatic injury in adults:>10 g or
>200 mg/kg (whichever is less) in 24 hours. So, 10 g is the toxic dose
for all those heavier than 50 kg.
Page | 669

4.5.1 Clinical phases of paracetamol toxicity
 Phase 1 (0-24 hours): asymptomatic, GI symptoms: nausea and
vomiting.
 Phase 2 (18-72 hours): RUQ and pain, N/V, rising LFTs.
 Phase 3 (72-96 hours): abdominal pain, N/V, peak LFTs, jaundice,
encephalopathy, renal failure, death.
 Phase 4 (4 -14 days): resolution.
 All patients: Serum paracetamol concentration & LFTs
 Patients with acute liver injury:: VBG – pH and lactate, electrolytes,
urea and creatinine , Glucose, Coagulation profile, Ca, Mg and Ph
Figure 4.1 –Nomogram for paracetamol toxicity

Limitations of nomogram
 Not validated before 4 hours or after 16 hours
 Each country has different nomograms and units
 Screening and Testing for paracetamol in the first 24 hours are
necessary as patients are asymptomatic with toxic doses. Beyond 24
hours, symptoms should be evident (nausea, vomiting, abdominal
pain, or encephalopathy). Equally, do not discharge symptomatic
patients.
4.5.4 Decontamination
 Immediate-release 50 g of activated charcoal within 2 hours (up to 4
hours if >30 g of paracetamol).
 Modified-release 50 g of activated charcoal within 4 hours
Page | 670
 Activated charcoal dose in children is 1 g/kg – max 50 g.

4.5.5 Antidote
 Intravenous NAC (N-Acetylcysteine).
 Wait until 4-hours post ingestion before taking urgent samples for
paracetamol levels. If the patient presents at 4–8 hours post
ingestion, take samples as soon as possible.
 If the levels are above the treatment line give the acetylcysteine
regimen. Do not delay acetylcysteine beyond 8 hours post ingestion.
 IV infusion can be stopped if the levels come back as below treatment
line.
 Anaphylactoid reactions occur anywhere: stop the infusion, loratadine
PO or promethazine IV, salbutamol nebulizer if bronchospasm occurs.
4.5.6 Disposition
 The majority of paracetamol ingestions can be managed in the ward.
 In all patients who receive 20 hours of acetylcysteine, 2 hours before
completing the infusion, check ALT/AST and paracetamol
concentration to determine the need for ongoing acetylcysteine.
 Patients with hepatotoxicity (AST/ALT >1000 IU/L) and rising INR will
require discussion with a clinical toxicology service.
Chapter 5: DKA
5.1. Definition:
Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of
diabetes mellitus.Occurs predominantly in patients with type 1 (insulin-
dependent) diabetes mellitus, and 10% to 30% of cases occur in newly
diagnosed type 2 (non–insulin-dependent) diabetes mellitus.DKA is the
leading cause of death in persons younger than 24 years with diabetes,
most often because of cerebral edema.
The clinical manifestations of DKA are related directly to hyperglycemia,
volume depletion, and acidosis.
Symptoms:
 polyuria and polydipsia
 hyperventilation
 nausea, vomiting, and abdominal pain.
 Impaired mental status
Page | 671
 Features of precipitating factor: omission or reduced daily insulin

injections, dislodgement/occlusion of insulin pump catheter, Infection,
Pregnancy, Hyperthyroidism, pheochromocytoma, Cushing’s
syndrome, Substance abuse, Medications (steroids, thiazides,
antipsychotics, sympathomimetics), Heat-related illness,
Cerebrovascular accident, GI hemorrhage, Myocardial infarction,
Pulmonary embolism, Pancreatitis, Major trauma, Surgery.
Sign:
 Tachycardia, orthostasis or hypotension, poor skin turgor, and dry
mucous membranes
 Kussmaul respirations
 fruity odor on the breath found in some patients.
 The absence of fever does not exclude infection,
 Hypothermia is present occasionally because of peripheral
vasodilation.
 Abdominal pain and tenderness
A blood glucose level >250 milligrams/dL (13.8 mmol/L), an anion gap
>10 mEq/L (>10 mmol/L), a bicarbonate level <15 mEq/L (15 mmol/L)
and pH <7.3 with moderate ketonuria or ketonemia constitute the
diagnosis of DKA
Check blood ketones (β-Hydroxybutyric acid βHB and Acetoacetate
AcAc), venous blood gas, bicarbonate levels, and anion gap, to avoid
missing euglycemic DKA because the degree of hyperglycemia may not
be significant.
Obtain a rapid bedside glucose level, a urine test strip, and an ECG to
check for hyperkalemia
Obtain a CBC, serum electrolytes, BUN and creatinine, urinalysis and
phosphate/magnesium/calcium level.
Arterial blood gas: venous pH has replaced ABG, but may be required in
critically ill patients
Obtain Blood cultures and other laboratory tests or imagining as clinically
indicated.
Page | 672
Table 5.1 – Diagnostic criteria for diabetic Ketoacidosis

Moderate Severe
Mild(serum (serum (serum
glucose>250
glucose > glucose >
mg Per dL
[13.88 mmol 250 mg per 250 mg per
Criterion per L ]) dL) dL)
Anion gap >10mEq > 12 mEq > 12 mEq
perL(10 per L (12 per L (12
mmol per L) mmol per L) mmol per L)
Arterial pH 7.24 to 7.30 7.00 to < < 7.00
7.24
Mental Alert Alert/drows Stupor/com
status y a
Serum 15 to 18 10 to < 15 < 10 mEq
bicarbonate mEq per L mEq per L per L (10
(15 to 18 (10 to < 15 mmol per L)
mmol per L) mmol per L)
Serum Positive Positive Positive
ketone
Urine Positive Positive Positive
ketone
The goals of therapy are:
 Volume repletion
 Reversal of the metabolic consequences of insulin insufficiency
 Correction of electrolyte and acid-base imbalances
 Recognition and treatment of precipitating causes
 Avoidance of complications.
Page | 673
Table 5.2 – Treatment pathway for DKA

Treatment Time Comments
Brief history/examination 0–2 If glucose > 250,

Monitor, glucose, ECG, hours urine + ketones,
urine/serum ketones. IV: assume DKA, search
1) NS 15-20 mL/kg/hr for for percipient,
the first hour infection, check ECG
2) 0.2 NS TKO for hyperkalemia,
Send electrolytes, CBC, infarction
phosphate, calcium,
magnesium, VBG, Begin flow sheet for
consider blood/urine vital signs, mental
culture status, BS, lytes, AG,
venous pH, I/Os
Perform detailed
history and exam
If initial K+ >5.2 initiate IV 2–3 Initial electrolytes:

infusion of regular insulin at hours check osmolarity, AG,
0.1-0.14 unit/kg/hr. Repeat BS, corrected sodium
K+ STAT in 2 hours.If initial and potassium
K+ >3.3 and <5.2 and urine
output add 20-30 mEq of K+ Initial K determines
to each liter of fluid and further therapy
insulin drip as aboveIf initial Adequate urine output
K+ is < 3.3 hold insulin drip is essential before
and give K+ at 20 to 30 mEq initiating K therapy
per hour until K+ is > 3.3
then initiate insulin drip as
above Repeat glucose,
electrolytes, AGIf AG
>25 or glucose >800 or
significant comorbidity,
consider ICU
disposition
After NS bolus: generally 3–4 If AG <25 or glucose

for eunatremia or <800 or significant
comorbidity, consider
Page | 674
hypernatremia give 0.45 hours floor or diabetic unit

NS at 250-500 mL/hr with disposition
K+ supplement as above
For hyponatremia continue Rate of hydration is
NS at 250-500 mL/hr dependent on
If pH less than 6.9 may hemodynamics,
give 100 mmol of hydration status, urine
NaHCO 3 in 400 mL of output
water with 20 meq KCL at
200 mL/hr.
Repeat every 2 hrs until Patient pH > 6.9 do
pH > 7.0, check K+ every 2 not require NaHCO 3
hours.
Active goals: Adequate fluid 4 – 12 Recheck glucose,

infusionInsulin infusion hours lytes, AG, VBG, mental
Maintain potassium 3.3 to status, I/Os, check
5.2Lower glucose by 75 results of initial
mg/dL/hr Maintain adequate phosphate,
electrolytes When glucose magnesium, calcium.
approaches 200 change IV Check lytes every 2
to D5 0.5 NS with 20 to 40 hours initially in the
mEq KCL/L and/or decrease ED. Check glucose
insulin rate to 0.02-0.05 hourly.
units/kg/hr
If blood glucose does
not decrease by 10%
after 1 hour of
therapy, give 0.14
units/kg bolus then
resume previous rate
If blood glucose
decreasing faster than
50-75 mg/dL/hr,
decrease insulin
drip.🡪🡪Check glucose
hourly.
Page | 675
Correct estimated fluid 12 – 48 If young and new-

deficit in the first 24 to 36 hours onset diabetes avoid
hours excess free water,
monitor carefully for
Maintain serum glucose development of
180 to 200 and continue cerebral edema, and
insulin drip for at least 12 have mannitol
hours or until DKA bedside.
resolves: glucose < 200
and AG normal, pH > 7.3 Recheck lytes, glucose
and HCO3 > 15 and AG: repeat in 4
hours If taking PO,
Patient able to eat: give consider oral K, Phos,
SC short and long acting Mg, replacement as
insulin, feed patient, needed
discontinue IV insulin 1-2
hours after SC insulin
Late complications
Refractory acidosis
Cerebral edema
Vascular thrombosis
ARDS
Mucormycosis
Disposition and follow up: The majority of patients require

hospitalization. Patients presenting early in the course of their illness
who can tolerate oral liquids may be managed safely in the ED or
observation unit and discharged after 6 to 12 hours of therapy.
Chapter 6: Obstetric emergency
Emergencies Before 20 Weeks of Gestation
6.1. Miscarriage:
6.1.1 Background
Miscarriage, also called spontaneous abortion, or early pregnancy loss is
a non-viable intrauterine pregnancy before the 13th week of gestation
6.1.2 Classification of Miscarriage:
 Anembryonic pregnancy or blighted ovum: gestational sac develops
without any embryonic structures.
 Embryonic/fetal demise or missed miscarriage: pregnancy loss after
embryonic development, with closed cervical os and no bleeding.
Page | 676
 Threatened miscarriage: bleeding before 20 weeks of gestation, with

closed cervical os and viable fetus.
 Inevitable miscarriage: open cervical os, without passage of the
products of conception; typically presents with bleeding
 Incomplete miscarriage: some, but not all, products of conception
have passed, with an open cervical os
 Septic miscarriage: incomplete miscarriage associated with infection.
 Complete miscarriage: all products of conception have passed, with a
closed cervical os
6.1.3 Symptoms & signs:
Symptoms of miscarriage include vaginal bleeding and uterine cramping.
D/D: ectopic pregnancy and normal pregnancy
 Laboratory evaluation: should include a CBC, quantitative B-HCG
level, blood type, and Rh
 Radiographic evaluation: transvaginal U/S should be performed in
any woman presenting with pain and/or bleeding in the first-trimester.
 Hemodynamically stable patient: can be managed expectantly,
medically with misoprostol with or without mifepristone or surgically
with vacuum or manual curettage
 Hemodynamically unstable patients: require urgent Gynecology
consultation and surgical intervention.
 Rh(D) immunoglobulin should be considered in Rh-negative patients
with miscarriage.
Emergencies After 20 Weeks of Gestation
6.2. Placenta Previa:
6.2.1 Background:
Placenta previa occurs when placental tissue extends over the internal
cervical os. The differential diagnosis for bleeding occurring at >20
weeks includes:
 Normal labor with bloody show
 Placental abruption
 Vasa previa
 Uterine rupture
 Vaginal or cervical trauma
Page | 677

A pregnant woman in the late second or early third-trimester with vaginal
bleeding and no abdominal pain, occurring after sexual intercourse.
When placenta previa is known or suspected, do not perform a speculum
exam or digital exam because they can precipitate additional
hemorrhage.
 Radiographic Evaluation: Transabdominal U/S is the initial imaging
modality of choice and should be adequate to make or exclude the
diagnosis. Most cases of placenta previa are diagnosed antenatally
with U/S during routine second-trimester anatomic survey.
 Stable patients presenting with bleeding placenta previa are admitted
to the obstetric service for monitoring.
 Patients with bleeding placenta previa should be stabilized with
crystalloid resuscitation and blood products transfusion as needed.
 Administer antenatal corticosteroids if the bleeding episode occurs
between 23+0 and 36+6 weeks.
 Consider a course of magnesium for neuroprotection if the bleeding
episode occurs between 23+0 and 31+6 weeks
 Administer a dose of anti-D immune globulin (RhoGAM) to Rh-
negative women who have bleeding from placenta previa.
 Delivery will also often be performed if there is significant bleeding
close to term (approximately 34 to 36 weeks and onward).
 Cesarean delivery becomes urgent if the patient with placenta previa
is in active labor or has ongoing maternal or fetal instability that is not
responsive to resuscitation.
Page | 678
Complicated Delivery and Postpartum Complications

6.3. Breech Delivery:
6.3.1 Background:
Breech presentation is the presentation of the fetal feet or buttocks. Has
higher morbidity rate for the mother and fetus than a normal cephalic
presentation.
6.3.2 Risk Factors
 Preterm gestation.
 Multiple gestations.
 Intrauterine growth restriction (IUGR).
 Previous breech presentation.
 Uterine abnormalities (bicornuate uterus, septate uterus, fibroids).
 Placental abnormalities.
 Multiparity.
 Abnormal fetal cephalic anatomy.
Symptoms: feeling fetal movement or kicking in the lower abdomen or
near the rectum, vagina, or bladder and subcostal discomfort from the
fetal head..
On physical examination, the clinician may be able to palpate the hard
fetal head in the uterine fundus or feel the soft buttocks in the lower
uterine segment.
 Radiographic Evaluation U/S is the most important tool and
radiographic test to diagnose breech presentation.
 Laboratory Evaluation: Lab tests do not play a role in the diagnosis or
management of breech delivery.
 Breech delivery is best managed by allowing spontaneous delivery
with no assistance until the fetal umbilicus is visualized.
 In the event of vaginal breech delivery, the delivering physician
should maintain hands off the breach as much as possible and never
pull on the breech from below.
 Complications of vaginal breech delivery include cord prolapse, head
entrapment, and birth trauma. If at all possible, the patient should be
transferred to Labor & Delivery for a cesarean section.
Page | 679
The End
Page | 680
Page | 681

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Family Medicine Guide: The Handbook

Handbook Founders and Editors In-Chief

Scientific Committee of The Family Medicine Guide: The

Authors of The Family Medicine Guide :The Handbook:

Dr. Ghadah Al-Ghamdi Dr. Norah Alenezi

Designing and Editing Committee for family medicine Guide :

Dr. Adel Yasky

SECTION 1: FAMILY MEDICINE ................................................................. 9

CHAPTER 23: NEPHROLOGY ........................................................................... 233

CHAPTER 1: PALLIATIVE CARE ......................................................................... 445

SECTION 11: ORTHOPEDICS ................................................................ 618

Section 1: Family Medicine

Other tests for secondary causes of dyslipidemias and they

 Low risk group: if 10-year risk score is <5%, focus on lifestyle

2.6. Adverse effects of statins:

2.9. Bile acid sequestrants:

2.10. PCSK9 monoclonal antibodies:

Gestational diabetes (GDM)

Screening for GDM: performed at 24–28 weeks of gestation in pregnant

3.2. Screening for diabetes:

Table 3.3 – Risk based screening for DM2 or prediabetes in

3.5. Prevention of DM2:

Table 3.6 – Approach to individualization of glycemic targets

Long Life expectancy Short

Absent Important Severe

3.7.2 Combination therapy:

Continuous subcutaneous insulin infusion or ‘insulin pump’ therapy is

3.9.1 Blood pressure management:

3.9.2 Lipid management:

3.10.2 Diabetic retinopathy:

Table 3.12 – Treatment options of diabetic retinopathy according to

o Skin atrophy can indicate ischemia

o Observe the patient walking for:

 Wash in lukewarm water, dry thoroughly (including between the toes),

 Repeat their capillary blood glucose 10 to 15 minutes later. If it is still

3.12.4 Follow up:

o use of rapid-acting insulin analogs to reduce risk of hypoglycemia

If last systolic blood pressure (SBP) 120–139 mmHg or last diastolic

 Tobacco use: All adults

4.2. Premarital counselling and testing:

Have 1 or more CVD risk factors (dyslipidemia, diabetes, hypertension,

4.4. 6 to 17 years of age:

5.1.6 Adult management:

Red flags (ER referral): muffled voice, drooling, stridor, Respiratory

5.2.3 Diagnosis/Clinical tool:

Table 5.2 Centor criteria strep pharyngitis

Importance of distinguishing bacterial from viral pharyngitis

Azithromycin: Clarithromycin: Clindamycin:

 ABG: respiratory acidosis

5.4.3 Physical examination:

Table 6.1 Causes of cough

In the case of a coughing patient, to make a diagnosis a combination of a

o respiratory rate, accessory muscle use, retractions, lung sounds.

Chronic cough (>8 weeks):

Allergic UACS The: treated

Dry cough, begin within Stopping ACE inhibitor, cough

Reversible airflow Regular use of inhaled

system, Painkiller (analgesic) overuse (e.g., medication overuse

 In adults with suspected subarachnoid hemorrhage, it is crucial to

Table 7.1.Medication options for treatment of primary type headache

Table 7.1.Medication options for treatment of primary type headache

 fatty liver disease

9.3. Morphologic approach: