ADDISON’S DISEASE

INTRODUCTION

Adrenal insufficiency may be primary due to an intrinsic inability of the adrenals to elaborate enough
hormones (e.g., in Addison’s disease) or secondary due to inadequate ACTH formation or release.
For primary failure aldosterone is lost as well and ACTH levels are usually elevated, resulting in salt
wasting, hyperkalaemia, hypotension and hypovolemia, and hyperpigmentation.
For secondary failure, aldosterone is intact and potassium and volume status is usually normal. There is
also no associated hyperpigmentation.

CLINICAL PRESENTATION

History: fatigue, weakness, apathy, anorexia, nausea, vomiting, weight loss, Skin pigmentation,
dizziness, syncope, abdominal pain & depression.
Physical examination: examine the following for hyperpigmentation: the hand creases, the mouth,
and lips, uncovered areas, the nipples, areas irritated by belts or rings. Examine for vitiligo, sparse
axillary, and pubic hair. Examine the abdomen for adrenal scar (if the scar is pigmented, think of
Nelson's syndrome-due to pituitary macroadenoma- and examine field defects). Blood pressure to R/O
postural hypotension. Tell the examiner that you would like to do a short (1-24) ACTH test (Synacthen
test).

INVESTIGATIONS

 FBC (lymphocytosis, eosinophilia).

 Electrolytes (hyponatraemia, hyperkalaemia, hyperchloremic acidosis, hypercalcemia).
 Blood glucose, (hypoglycaemia).
 Short ACTH (1-24) (Synacthen) test; if positive, follow up with a prolonged ACTH stimulation
test.
 ACTH and cortisol levels.
 Adrenal autoantibodies.
 CXR for tuberculosis.
 Plain radiograph of the abdomen for adrenal calcification.
 CT scan of the adrenals.

TREATMENT

 Lifelong Hormone Replacement Therapy- both the glucocorticoid & mineralocorticoid portions
should be replaced
 Glucocorticoid: Hydrocortisone 20-30 mg/d (taken with meals). ⅔rd. taken in the morning & ⅓rd.
in the late afternoon. Dose reduction in hypertensives, diabetics, & those with S/E of the drug
(insomnia, irritability, & mental excitement).
 Mineralocorticoid: Fludrocortisone 0.05-0.1mg/d. Adjust dose depending on postural
hypotension.
 Follow up every 6 months.
 Note: In Addisonian crisis, intravenous fluids and hydrocortisone should be administered (after
drawing a blood sample for cortisol determination).
 ANAEMIA

INTRODUCTION: Anaemia is defined as a haemoglobin concentration less than the lower limit
of normal for the patient’s age and sex. It is not a diagnosis but a clinical sign or symptom.

HISTORY
BIODATA:
 Age: elderly- anaemia of chronic diseases e.g., TB, chronic kidney
disease (CKD), and malignancy; in the young, sickle cell disease,
 Sex: female>male (pregnancy and menses)
 Occupation: farmers, herdsmen (prone to parasitic infestation)
 Religion/tribe: vegetarians like Hindus (prone to B12 deficiency)

PRESENTING COMPLAINT(S): most are non-specific symptoms. They include:

 Tiredness, headache, weakness, dizziness, light headedness (due to low level of
oxygen in CNS)

 Tinnitus (can be the only presenting symptom)

 Claudication (due to hypoxia in calf muscles)

 Chest pain (exacerbation of stable angina due to myocardial hypoxia)

 Palpitation (compensatory increase in heart rate to meet body oxygen requirement)

 Other symptoms may suggest the etiology e.g., bleeding diathesis may suggest
leukaemia or lymphomas, hematemesis- PUD, CLD etc.

HISTORY OF PRESENTING COMPLAINT(S)

 Course:? onset of symptom
? progression of symptom
? limitation of activities,? Extent of limitation.
? hx of cravings for dirt, paint (pica), ice (pagophagia)-suggests Fe
deficiency
 Causes:
 ? hx of diagnosis of HIV or hx suggestive of HIV (anaemia due to HIV)
 Upper GI bleeding associated with long standing hx of epigastric pain
radiating to the back associated with meals (PUD).
 Upper GI bleeding +jaundice +right hypochondriac pain (CLD)
 
? hiccups, body itching, decreased urine production or absent urine
production, haematuria, polyuria, nocturia. (Chronic kidney disease,
CKD)
 ? paroxysmal cough, blood-stained sputum, wheeze, body itching,
loose stools (gastrointestinal helminthic infestation).
 ? recurrent infections
 ? recurrent bleeding from minor trauma,? exposure to radiation or
anticancer (cytotoxic) drugs. (Bone marrow aplasia)
 ? long standing fever, cough, weight loss or contact with chronically
coughing adult. (TB)
 Hx of blood donation
 ? frank blood per rectum or blood-stained stool (haematochezia)
(lower GI bleeding)
 Complications:
 ? dyspnoea on exertion (mild, moderate, or severe exertion),
orthopnoea, paroxysmal nocturnal dyspnoea (PND) and/or ankle
swelling. (Heart failure)
 ? confusion, delirium, altered level of consciousness. (Shock, if acute
haemorrhage is the cause)
 ? difficulty in swallowing (dysphagia secondary to long-standing Fe-
deficiency anaemia, also known as Paterson-Brown-Kelly or
Plummer-Vinson syndrome).
PAST MEDICAL HISTORY:
 ? past admission, reason for the admission.
 ? past surgery (e.g., gastrectomy or tumour excision).
 ? recurrent blood transfusion.

DRUG HISTORY:
 ? anticoagulant (bleeding)
 ? aspirin or other NSAIDs (Upper Gastrointestinal bleeding)
 ? anticonvulsants e.g., phenytoin (B12 deficiency)

 ? anticancer drugs, chloramphenicol (bone marrow suppression)

FAMILY HISTORY:
 ? of similar condition, the affected family member
 ? of any other disease condition.
SOCIAL HISTORY:
  ? alcohol (excessive chronic ingestion is associated with poor
nutrition and decrease dietary intake).
 ? smoking (chronic smoking is associated with many cancers which
can cause anaemia of malignancy or chronic disease).
 ? consumption of clay or laundry starch- Iron is rendered less
absorbable.

EXAMINATION
General examination:
 Respiratory distress, cardiac position (? presence of heart failure as a
complication)
 Fever: infection, haemolysis, or malignancy
 Pallor: check the conjunctiva, tongue, palms (especially the creases), and
soles of feet.
 Jaundice (? haemolysis or hepatic disease)
 Mouth: angular cheilosis and smooth beefy tongue (Fe deficiency)
 Petechiae (thrombocytopenia 20 bone marrow aplasia)
 Lymphadenopathy: Infections and malignancies
 Hand: koilonychias (spoon shaped nail secondary to long-standing Fe
deficiency. anaemia).
 Pedal/ankle oedema (? heart failure as a complication).

Systemic examination:
 Cardiovascular system: Pulse (tachycardia, low volume pulse, bounding
pulse), BP is reduced, displaced cardiac apex (? Heart failure) usually from
uncompensated anaemia
 Abdomen: splenomegaly, hepatomegaly, or any other palpable mass.
 Respiratory system: tachypnoea,
 GCS: if low, may be due to decreased perfusion to the brain

INVESTIGATIONS
 Full blood count:
 Low Hb (normal: male=13.5-17.5g/dl, female=11.5-15.5g/dl).
 Low packed cell volume (PCV) or Haematocrit (HCT): normal male
=40-50%, female=35-45%
 Low RBC count: normal male=4.3-6.0x106/μL, female=3.5-5.0x106/μL
  Mean corpuscular haemoglobin (MCV): normal MCV=80-95fL
Low MCV denotes microcytic anaemia (Fe def. anaemia, chronic
disease anaemia, thalassemia etc.).
Normal MCV denotes normocytic anaemia (acute blood loss, renal
failure).
High MCV denotes macrocytic anaemia (folate, Vit. B 12 def., others:
alcohol, liver disease)
 Mean corpuscular haemoglobin (MCH): normal MCH=30-35g/dL
Low MCH denotes hypochromic anaemia (Fe def. anaemia, chronic
disease anaemia)
Normal MCH denotes normochromic anaemia (anaemia of acute
blood loss, anaemia secondary to renal failure).
 Reticulocyte count:
Low reticulocyte count denotes decreased RBC production e.g., bone
marrow suppression, folate or B12 def.
High reticulocyte count denotes increased RBC production e.g.,
haemolytic anaemia
 Laboratory investigation of iron deficiency anaemia: this check for serum
Fe level, total iron binding capacity (TIBC), and serum ferritin level. Some
possible results are summarized below.
Parameter Result Differential Diagnosis
Serum Fe level Low Fe deficiency, anaemia of
chronic diseases
TIBC Raised Fe deficiency

Normal/low Anaemia of chronic disease

Serum ferritin level Low Fe deficiency

Normal or high Anaemia of chronic disease

 Blood film examination:

This is carried out to look at the red call morphology.
 Red cells with normal appearance are seen in anaemia due to acute
haemorrhage.
 Abnormally large red cells may be seen which suggests
megaloblastic anaemia.
  Abnormally small red cells with faint colour and associated pencil-
shaped red cells may be seen in Fe def. anaemia or chronic disease
anaemia.
 Red cells with abnormal morphology (e.g., sickled, spherocytes,
elliptocytes or poikilocyte) are seen in haemolytic anaemia since they
are easily destroyed in the spleen. In addition, red cell fragments
might be seen, which also suggests an ongoing intravascular
haemolysis due to DIC (disseminated intravascular coagulation),
microangiopathy, burns, HUS (haemolytic uremic syndrome, etc.).
 Microscopy: stool, urine, or sputum for microscopic blood loss that can lead
to iron deficiency over time.
Stool microscopy for the ova of hookworm.

 Chest x-ray: this can be done when there are features of heart failure.
Cardiomegaly, prominent pulmonary vascular markings, pleural effusion, or
other incidental findings.
 Other investigations:
 Clotting profile if abnormal bleeding is present.
 Upper/lower gastrointestinal endoscopy.
 Bone marrow examination.

TREATMENT
Treatment depends on the onset of the anaemia (sudden or gradual), severity (mild,
moderate, severe) and etiology.
Severe Anaemia <7 g/dl
Moderate Anaemia 7 – 9 g/dl
Mild Anaemia 10 – 12 g/dl
 Based on the onset:
 Acute anaemia: treat the underlying cause. If mild or moderate, give hematinic.
If severe, offer whole blood transfusion and treat the cause.
 Chronic anaemia: In chronic anaemia, adaptation has occurred by increasing
fluid reabsorption and consequent intravascular volume expansion.
Treat the underlying cause. If mild or moderate, administer hematinic.
If severe, treat the underlying cause and offer packed cell transfusion. In the
absence of packed cells, sedimented red cells or whole blood can be given,
however a diuretic must be added to avoid volume overload and impending
heart failure.
 Based on severity:
 Moderate to severe anaemia is treated by nutritional supplementation and
treatment of the underlying cause.
 Severe anaemia is treated by blood transfusion. Whole blood is transfused when
the anaemia is acute in onset. However, packed cell transfusion is preferred if
the onset of the anaemia is insidious.

 Based on etiology:
 Fe deficiency anaemia is treated with iron supplementation and treatment of
the underlying cause. Oral iron supplementation (ferrous sulphate) is
administered in mild to moderate Fe deficiency anaemia. Severe iron deficiency
anaemia is treated using parenteral iron supplementation (e.g., iron sorbitol,
iron dextran).
 Megaloblastic anaemia is treated using folate or B12 supplementation.
 Chronic disease anaemia: treat/manage the disease. Specific treatment
may be required under some conditions e.g., erythropoietin in CKD.
 BRONCHOGENIC CARCINOMA

INTRODUCTION

Is a malignant primary tumour of the lungs from the bronchial epithelium lining. Responsible for
95% of primary lung tumours. They are classified into small cell lung carcinoma (SCLC) and Non-
small cell lung carcinoma (NSCLC).

HISTORY

BIODATA

 Age
 Sex: Male > Female

PRESENTING COMPLAINT

 Cough
 Haemoptysis
 Symptoms of bronchial obstruction: breathlessness
Noisy breathing (whistling sound)
Note: disease has a silent and insidious progression, thus some patient present with symptoms
of complications.

 Chest pain
 Pain in shoulder and inner aspect of the arm
 Neck swelling

HISTORY OF PRESENTING COMPLAINT

 Course:
Symptoms may be due to:
1) Local tumour growth: cough, haemoptysis, wheeze and stridor, dyspnoea, pleuritic
chest pain,
(2) Invasion or obstruction of adjacent structures: SVC obstruction, hoarseness
(recurrent laryngeal nerve palsy), dysphagia (esophageal compression), stridor (airway
obstruction), hemidiaphragm paralysis (phrenic nerve compression)
(3) Growth in regional nodes through lymphatic spread:
(4) Growth in distant metastatic sites (brain, bones, liver, adrenals, bone marrow)
(5) Remote effects of tumour products (Para neoplastic syndromes)
They often present in that sequence
  Risk factors

 ? smoking, COPD, exposure to radiations

 R/O differentials
? chest pain, orthopnoea, Paroxysmal Nocturnal Dyspnoea (R/o Congestive Cardiac
Failure)
? Fever, night sweats, > 2 weeks, contact with a coughing adult (R/o Tuberculosis)
? burning epigastric pain, worst while lying down, exacerbated by hunger and relieved
by meal with associated brown coloured blood (R/o Acid Peptic Disease)
? allergy (R/o Chronic asthma)
? fever, flu-like symptoms (R/o Infectious mononucleosis)
 Complications
weight loss (duration)
Metastasis: Brain- headache, loss of consciousness, early morning vomit, convulsion
Liver- yellow discoloration of the eye, anorexia,
Bone pain
Skin swellings
Dysphagia
Change in voice (Left recurrent Laryngeal nerve affectation)
NOTE: the following are notable complications which should be ruled out
Horner’s syndrome: resulting from carcinoma in the lung apex affecting the sympathetic
chain at or above the stellate ganglion. (Ipsilateral ptosis, enophthalmos, miosis,
anhidrosis of the face)
Pancoast’s syndrome: pain in the shoulder and inner aspect of the arm with muscle
wasting in the hand due to malignant destruction of T1 and C8 roots in lower part of the
brachial plexus by an apical lung tumour
 Care
What type of care offered and its significance on condition?

PAST MEDICAL HISTORY

? known diabetic or hypertensive

? epileptic disorder

? retroviral status

SOCIAL AND FAMILY HISTORY

*Cigarette smoking (calculate pack years), duration, if patient has stopped, enquire when.

Occupation: coal miners

EXAMINATION

 General physical examination

Chronically ill-looking (+/- respiratory distress), wasted. Hyperpigmented
(paraneoplastic syndrome).
+/- jaundice
+/- pallor
+/- significant peripheral lymphadenopathy
Digital clubbing +/- hypertrophic osteoarthropathy
+/- pedal swelling (cor pulmonale

Others: features of Superior vena cava obstruction- suffusion, neck swelling, facial
swelling conjunctiva oedema, dilated veins on the chest wall
 Respiratory system
Respiratory rate increased
+/- stridor
Trachea may be central or deviated to collapsed side (due to complete/ partial bronchial
obstruction which causes atelectasis of lobe or whole lung)
Chest symmetry and expansion may/ may not affected
Chest wall tenderness (dermatomal pain)
Dull percussion node on collapsed lobe or lung
Reduced breath sounds
+/- Monophonic wheeze
+/- Crepitations, bronchial breath sounds (pneumonia)
 Other systems
Cardiovascular: increased pulse rate, hypertension, raised Jugular venous pressure,
murmur, distanced heart sounds (due to pericardial effusion), pericardial rub, pedal
oedema
Gastrointestinal: tender hepatomegaly +/- ascites
Central Nervous: cranial nerve palsy, hemiplegia/ hemiparesis, urine/ faecal
incontinence

NOTE: Paraneoplastic syndrome

Bronchogenic cancer is associated with paraneoplastic syndrome (check definition in text book).
Notable peptides include; Adrenocorticotropic hormone, antidiuretic hormone, gastrin-
releasing peptide, calcitonin, parathyroid hormone-related peptide. Thus, features of SIADH,
hypercalcemia, should be looked for.

Note Addison’s crisis may result due to adrenal gland infiltration.

INVESTIGATIONS

 Chest radiograph
Tumour sites: Central (Hilar) unilateral enlargement
Peripheral pulmonary opacity- irregular well circumscribed lesion
Apical (Pancoast tumour)
Complications: Lung abscess- well circumscribed radio-opaque lesion +/- air-fluid level
Pleural effusion- Homogenous opacity obliterating costophrenic angle
Broadening of mediastinum (hilar lymphadenopathy)
Enlarged cardiac shadow
Rib destruction (commonly 1st and 2nd ribs)
Computed Tomography (CT) or Magnetic Resonance Imaging (MRI) of the chest can be
done if available and affordable.
 Bronchoscopy and biopsy- to confirm diagnosis and stage the tumour
 Sputum cytology
 Pleural fluid cytology
 CT of the chest and upper abdomen (liver and adrenals)
 Others:
Full blood count
Clotting profile
Liver function test
Renal function test + Urea, Electrolyte and Creatinine
Hormonal assay: Cortisol, Adrenocorticotrophic hormone
Brain CT/ MRI

MANAGEMENT

 Surgical: treatment option for NSCLC

 Radiotherapy: palliative for end stage disease
Used in conjunction with chemotherapy for treatment of SCLC

 Chemotherapy: for SCLC

  Laser therapy and stenting
 Psychotherapy

PROGNOSIS

Overall prognosis is very poor with around 70% of patients dying within one year of diagnosis
and only 6-8% surviving 5 years after diagnosis.
 CEREBROVASCULAR DISEASE

INTRODUCTION

It is one of the neurological emergencies because " time is neurone". The ischaemic or
infarctive is the commonest (80-90%) while haemorrhagic constitutes 10- 20%.

HISTORY

BIODATA

 Age:
>50years in males
>60years in females
<40 - 45 years in both sex (stroke in the young)
 Sex M: F is 2:1
NB; ask whether the patient is right-handed or left?

PRESENTING COMPLAINT: usually sudden/gradual onset of

 Inability to use/weakness of one side of the body(R/L)

 Facial weakness of one side
 Inability to talk/speak

HISTORY OF PRESENTING COMPLAINTS

 Course
 symptoms lasting more than 24Hrs - If less than 24 hours then it’s a Transient
ischaemic attack.
 ? Onset, duration, progression of symptoms and the last activity before the
symptoms:
 Sudden onset of symptoms in the absence of activity (ischaemic which could be
thrombotic or embolic)
Gradual and progressive weakness (likely thrombotic).
Weakness maximum at onset but improves with time (likely embolic)
Sudden onset of symptoms at peak of activity (likely haemorrhagic)
? Headache, dizziness, slurring of speech, visual disturbances nausea and vomiting
? Urine or faecal incontinence
? history of similar attack in the past
? who noticed the illness and the time it lasted
? any loss of consciousness or convulsions
 Risk factors:
DM, HTN, obesity, smoking, alcoholism, history of past TIA, use of OCPs, family
history of stroke
R/O other differentials
I. History of head trauma - intracranial bleeds
II. Febrile followed by slow onset of presenting symptoms (r/o encephalitis, brain
abscess)
III. Any history of preceding convulsion (r/o Todd’s paralysis)
IV. History of last feed (r/o hypoglycaemia)
V. R/O focal migraine
VI. Known Hbss? especially in stroke in the young
VII. Insidious onset of symptoms - brain tumours
VIII. Insidious onset of symptoms in a patient suspected to have tuberculosis -
Tuberculoma
Complications
-History of sores on the waist or lower extremities (bedsores)
-Leg swelling with associated pain (DVT)
-Pain on micturition (UTI)
-Features of raised intracranial pressure (ICP) such as headache, blurring of vision
(herniation) and projectile vomiting
-History of depression
-Features of hyperglycaemia i.e., polyuria and polydipsia
-Features of hypoglycaemia
-Features of pneumonia such as cough fever (orthostatic pneumonia)
Care
What was done to the patient from the onset of symptoms at home, in transit and
while on admission in the hospital?

PAST MEDICAL AND SURGICAL HISTORY

Inquire about past hospital admission and reason, any cardiovascular surgery or vascular
catheterization?

FAMILY/SOCIAL HISTORY

-Inquire about family history of risk factors

-Ask about physical inactivity/sedentary lifestyle.
-Ask about social habit of cigarette smoking, drug abuse, alcohol, or other intoxicants
ingestion
  Systemic review

EXAMINATION

General Physical Examination

Comment on the general appearance of the patient, take note of the posture, pressure
areas, running IV fluid, NG tube, urethral catheter, and urine bag,

Neurological Examination

1. higher centre functions: GCS, speech, judgement, memory etc.

2. motor “BTPR” (always compare findings in the opposite side): features are
usually that of upper motor neuron lesion except for the first week of stroke
where they may have indeterminate features due to spinal shock.
3. sensory examination
4. cerebellar examination

Systemic Examination

Particular attention to CVS (for etiology) and Respiratory system (for complications).

INVESTIGATIONS

 To confirm diagnosis
-Brain CT scan: it differentiates ischemic from haemorrhagic stroke. In ischaemic
stroke earliest CT scan changes are visible within a few hours after the event but
may be delayed for a few days or more. (Read CT features of stroke)
-magnetic resonance imaging (MRI)
- Random blood sugar (r/o hypoglycaemic coma and hypoglycaemia is a
complication and poor prognostic factor of stroke)
-Electrocardiography
 Others
a) Full blood count, platelets, and ESR
b) Chest X-ray
c) Lumbar puncture
d) Lipid profile
e) Urea electrolyte and creatinine

MANAGEMENT

 ABC of resuscitation: maintain airway, ensure patient is breathing and give I.V fluid
(normal saline)
 Urgent RBS Must be done: hypoglycaemia is a differential and both
hyperglycaemia and hypoglycaemia are poor prognostic factors. Commence
soluble insulin when RBS > 14mmol/l even if the patient is not diabetic.
 If patient is unconscious pass NGT and catheter. Patient should remain NPO for 1st
48 hrs.
 Careful monitoring of blood pressure: Control blood pressure only if;
a- Persistent absolute systolic b.p > 220mmHg
b- Persistent absolute diastolic b.p > 120mmHg
c- Stroke co-existing with any of the hypertensive emergencies (e.g., hypertensive
encephalopathy, acute left ventricular failure. acute MI, dissecting aortic aneurysm,
ARF, malignant hypertension etc.
d- When the Mean arterial b.p > 145mmHg. [MABP= Diastolic B.P + 1/3 (pulse
pressure). Pulse pressure= Systolic B.p - Diastolic B.p]
NB: REDUCE B.P CAUTIOUSLY PREFERABLY THROUGH ORAL OR NGT
 If there are features of raised ICP:
-Nurse at 300 head up tilt
-Avoid noxious stimuli
-Give 20% mannitol at 0.5 to 1g/kg over 30 mins and repeat every 8 hrs for 24 hrs
- frusemide I.V 40mg daily or b.d for 5 days.
- intubation and hyperventilation
 Control temperature if pyrexic: Fever is a poor prognostic factor.
 If there are signs of aspiration pneumonia, give IV antibiotics.
 Use of thrombolytics in ischemic stokes- however benefit obtained if given within 3
hrs of onset of stroke otherwise it’s not beneficial. e.g., of thrombolytics-
streptokinase, recombinant tissue plasminogen activator.
 Antiplatelet agents after haemorrhagic stroke was ruled out- aspirin 300mg start
oral or PR then 75 mg maintenance.
 DVT prophylaxis: Refer to paraplegia
 Early physiotherapy.
NOTE: Haemorrhagic stroke should be managed in an ICU. Patient should be
planned for neurosurgical review and possible interventions.

SECONDARY PREVENTION
a- Bp control
 Routine antihypertensive therapy should be introduced 2 weeks following stroke
 If BP remains elevated – target blood pressure is: Diabetics:<130 / <80mmHg,
Non-Diabetics <140/85mmHg
  Suggested therapy is: ACE INHIBITOR (Ramipril, Perindopril) PLUS Thiazide
Diuretic (Bendrofluazide, Indapamide). Combination therapy is the most effective
 Lifestyle advice should be given (to lose weight, reduce alcohol consumption,
avoid adding salt to food and increase exercise). Patients should be educated about
hypertension, the need for life long treatment & regular monitoring of their blood
pressure. They should be informed of their BP readings & given a diary to record
future measurements.

b-Lipid lowering
 Lipid lowering treatment with a Statin has been shown to be beneficial to ALL
patients with ischaemic stroke.
 ALL patients following ischaemic stroke or TIA should be commenced on a high
dose if: TOTAL CHOLESTEROL is > 3.5mmol/L, unless known to be intolerant of
statins. Suggested therapy is: SIMAVASTATIN 40mg or PRAVASTATIN 40mg
(especially if on Warfarin – no drug interactions)
 Liver function tests & CK should be checked after 4-6 weeks of treatment
 Additional dietary advice should be given on a lipid-lowering diet.

NB: Causes of stroke in the young

1. Mitral valve prolapse

2. Patent foramen ovale
3. Sickle cell anaemia
4. Fibromuscular dysplasia
5. Migraine
6. Cocaine / oral contraceptives
7. Congenital AV malformation
8. Antiphospholipid syndrome
9. Atrial fibrillation
 CHRONIC KIDNEY DISEASE (CKD)

INTRODUCTION:

CKD is a Kidney damage for ≥3 months and/or a ↓ GFR <60ml/min/1.73m2 for ≥3 months
with or without kidney damage.
Kidney damage refers to structural or functional abnormalities of the kidney (from
abnormal urinalysis, imaging studies or histology). With time many patients with CKD
progress to ESRD.
End-stage renal disease (ESRD) = decreasing GFR < 15ml/min/1.73m 2 accompanied by signs
and symptoms of kidney failure that necessitate RRT.

HISTORY

PRESENTING COMPLAINTS

 Uremic symptoms
 Anorexia, nausea, vomiting, diarrhoea, hiccup, pruritus
 Fatigue, lethargy (anaemia)
 Change in behaviour, increase daytime somnolence (encephalopathy)
 Epistaxis, bleeding gums, hematemesis, melena (platelet dysfunction)
 Kidney symptoms
 Polyuria
 Nocturia
 Oliguria

HISTORY OF PRESENTING COMPLAINTS

Course: duration of illness >3 months

Cause:

 Hypertension: pt. is a known hypertensive; for how long; is pt. on medications; regular? if not
why; is patient on follow up? is it regular?
 Diabetes: is patient a known diabetic or with symptoms of polyuria, polyphagia, & polydipsia;
clerk as HTN above
 CGN: previous hx of sore throat or skin lesion
 Drug induce: hx of prolong intake of traditional concoction, NSAIDs, or antibiotics (specify)
 HIVAN: known RVD; hx of symptoms; hx of risk factors
 Family hx of kidney disease: polycystic kidney disease, reflux nephropathy
 Heavy metal nephropathy: long term use of mercury containing soap (e.g., Tura) or cream (e.g.,
Hg containing skin lightening creams)
 Sickle cell nephropathy: known HbSS; hx of symptoms
R/O differentials

 CCF: body swelling, dyspnoea, fatigue

 CLD: hx of jaundice, steatorrhea, & risk factors
 Nephrotic syndrome: hx of body swelling, frothiness of urine
 Diabetic mellitus: polyuria, polydipsia, polyphagia, numbness

Complications

 Anaemia: easy fatigability, dyspnoea

 Coagulopathy: easy bruising, bleeding from orifices
 Encephalopathy: confusion, drowsiness, coma
 Neuropathy: numbness, paraesthesia
 Endocrinopathy: menstrual irregularity, ↓libido
 GIT: features of acute pancreatitis, PUD
 Renal osteodystrophy: fracture
 Gout: painful toe

Care

 Drugs taken; any hx of dialysis? how frequent, has pt. had an A-V shunt, any complication?
 Outcome of care

SOCIAL HX:

 Is there any interference of life by symptoms or by treatment e.g., dialysis?

EXAMINATION

Pertinent findings are those of anasarca with facial puffiness, altered sensorium, asterixis, raised blood
pressure, respiratory distress, sensory polyneuropathy, pericardial friction rub.

INVESTIGATIONS

To confirm diagnosis

 Urinalysis: proteinuria, haematuria, and glycosuria

 Urine M/C/S: RBC cast, WBC cast, CGN cast (waxy, broad), granular cast, eosinopyluria
 U/E/Cr: ↑Urea, ↑Cr, ↑K, ↓Ca, ↓HCO3, ↑Uric acid, ↔ or ↓Na, ↑PO4.
24hr urine clearance/ spot mid-stream urine analysis is done for estimation of GFR
o Creatinine clearance= (140-age) x lean body weight (kg) (x 0.85 in female)
In mL/min plasma Cr (mg/dL) x 72
 USS: shrunken kidneys (<9cm). Normal is 14cm. NB: kidneys are of normal size in polycystic
kidney disease, carcinoma, HIVAN, amyloidosis, sarcoidosis.
 Notes on urinalysis
 Proteinuria is seen when:
o ↑serum proteins (e.g., Bence john proteins)
o ↑tubular secretion
o ↓reabsorbsion of N filtered proteins
o ↑protein filtration
normal protein excretion is <150mg; normal Pr/Cr ratio is <0.1, in heavy proteinuria, the
ratio is ≥3; microalbuminuria approximates to 20-300mg/min.
 Haematuria
o Microscopic- red cells detected on microscopy
o Macroscopic- gross redness or coca cola urine
 Urine pH
o Normal: 4.3-8.0 using dipstick
o Acid urine is seen in infections by E. coli
o Alkaline urine is seen in infections by Pseudomonas and Proteus

Notes on urine microscopy

 Pyuria: high levels of WBC in urine.

o For uncentrifuged urine:<3WBC/mm3-normal; 3-10 is doubtful and >10 is significant
(Pyuria)
o For centrifuged urine: <5/HPF is normal; >5/HPF is significant(pyuria)
 Bacteriuria: urine sample containing >105bacteria/mm3
Pyuria without Bacteriuria is seen in:
i. Current antibiotic use
ii. AGN
iii. Urinary TB
iv. Renal or bladder calculi
v. Analgesic nephropathy
vi. Contamination of specimen
vii. Partially treated UTI
viii. Steroid therapy
ix. Chemical cystitis
x. Bladder tumour/use of cytotoxics
 Casts: Types and significance
i. Hyaline cast: seen in normal urine but increased in concentrated urine or with use of a
loop diuretic
ii. Granular cast: seen in chronic proliferative or membranous glomerulonephritis, DM
nephropathy, amyloidosis, or proteinuria
iii. Fatty cast: nephrotic syndrome, early HTN
iv. RBC cast: seen in acute nephritis, proliferative GN, malignant HTN
 v. WBC cast: presence indicate interstitial disease as in proliferative GN and
pyelonephritis
vi. Broad waxy cast: seen in CKD
vii. Bacterial cast: bacterial pyelonephritis

Investigations to know the extent of the disease

1. FBC:
o ↓Hb from: ↓erythropoiesis, nutritional deficiency, ↓lifespan of RBC, depressed bone
marrow, mucocutaneous bleed, haemodialysis, bone marrow fibrosis from ↑PO4
o WBC
o Platelet
2. PT/PTTK/INR: R/O bleeding diathesis
3. CXR, ECG, ECHO for features of heart failure
4. Serum alkaline phosphatase- renal osteodystrophy

To rule out differentials

 RBC
 LFT, HBsAg, HCAb, and HIV screening
 Lipid profile
 X-ray of hip, head, and spine
 Serum complement levels - May be depressed with some GNs
 Autoantibody assay: ANA, Anti-sm, Anti-Rho, Anti-La, etc. (Lupus nephritis)
 C-ANCA and P-ANCA levels - Helpful if positive in diagnosis of Wegener granulomatosis and
polyarteritis nodosa or microscopic polyangiitis, respectively
 Anti–glomerular basement membrane (anti-GBM) antibodies - Highly suggestive of underlying
Goodpasture syndrome

Establish Diagnosis

In clinical practice, the diagnosis is on serum creatinine >177mmol/L or creatinine clearance of

<50ml/min in the presence of one of the following:

 Long standing hx of symptoms >3months

 Documented evidence of impaired renal function of (3-6months)
 Presence of sonologic evidence of CKD such as shrunken kidneys (bipolar diameter <9cm)
bilaterally or grade iii nephritis on USS
 Radiologic evidence of renal osteodystrophy
 Histologic evidence of CKD
 Coexistence of a disease known to cause CRF in the absence of any obvious cause of ARF
 Low serum Ca2+ and high PO4
 High ALP in renal osteodystrophy
TREATMENT

Treatment options include:

1. Conservative treatment –for earlier stages of CKD.

2. Renal replacement therapy (RRT)- for stage 5 CKD or where conservative treatment fails

1) Conservative Management
 Patients that benefit include:

1. Earlier stages of CKD.

2. Those who refuse RRT.

3. Those in whom life expectancy is very short.

4. Those who cannot afford Rx.

 Goals of Conservative Management

1. Delaying or halting the progression of chronic kidney disease.
2. Treating the manifestations of chronic kidney disease.
3. Timely planning for chronic renal replacement therapy

 Delaying or halting the progression of chronic kidney disease by:

1. Treatment of the underlying condition if possible.
2. Avoidance of nephrotoxins such as IV radiocontrast, nonsteroidal anti-inflammatory agents,
aminoglycosides
3. Encourage smoking cessation, as smokers tend to reach ESRD earlier than non-smokers.
4. Monitoring and prompt treatment of infections.
5. Protein restriction?
6. Increase water intake to ≈3L/day to enable the kidneys excrete urea and other toxic substances
7. Salt restriction
8. Restrict potassium intake

 Treating the manifestations of chronic kidney disease.

1. Anaemia: with recombinant human erythropoietin in the setting of adequate iron store; if not
available or response is poor, blood transfusion is resorted to. Anaemia may respond to iron
supplements alone.
2. Hyperphosphatemia with dietary phosphate binders and dietary phosphate restriction
3. Hypocalcaemia with calcium supplements with or without calcitriol
4. Hyperparathyroidism with calcitriol or vitamin D analogs
5. Volume overload with loop diuretics.
6. Metabolic acidosis with oral alkali supplementation.
7. Hypertension: use combinations with ACE inhibitors or ARBs as tolerated, with close
monitoring for renal deterioration and for hyperkalaemia. Target BP is 130/85
8. Oedema: loop diuretics
9. Renal osteodystrophy: give vitamin D supplement, ↓ dietary phosphate and/or use phosphate
binders (calcium carbonate, calcium lactate)
10. Hyperuricemia- allopurinol
11. Hyperlipidaemia-dietary modifications, statins.

 Timely planning for chronic renal replacement therapy

1. Early education regarding natural disease progression, different dialytic modalities, renal
transplantation, patient option to refuse or discontinue chronic dialysis, FINANCE!
2. Timely placement of permanent vascular access (arrange for surgical creation of primary
arteriovenous fistula, if possible, and preferably at least 6 months in advance of anticipated
date of dialysis)
3. Timely elective peritoneal dialysis catheter insertion
4. Timely referral for renal transplantation

2) Renal replacement therapy (RRT)

o Dialysis
o Renal transplant

Indications for dialysis

Clinical:

o Encephalopathy
o Uremic pericarditis
o Pulmonary oedema
o Persistent uremic symptoms
o Restless leg syndrome

Biochemical

o Cr ≥300mmol/L in wasted elderly patient or ≥600 in young patient or 100mmol/L rise

per day
o Urea ≥30mmol/L or 10mmol/L rise per day
o K ≥6.5mmol/L or 1mmol/L rise per day
o HCO3 <10mmol/L
o GFR <15ml/min

Forms of dialysis

o Peritoneal dialysis
o Haemodialysis
Peritoneal dialysis

In form of either continuous ambulatory or manual automated.

Advantages Disadvantages

1. Immediate initiation 1. Bacterial/chemical peritonitis

2. Less complicated 2. Protein loss
3. Portable (CAPD) 3. Hyperglycaemia
4. Fewer dietary restrictions 4. Multiple abdominal surgery
5. Short training time
6. Less cardio stress
7. Choice for diabetics

Haemodialysis

Advantages Disadvantages

1. Rapid fluid removal 1. Vascular access problems

2. Rapid removal of urea & creatinine 2. Dietary & fluid restrictions
3. Effective K+ removal 3. Extensive equipment
4. Less protein loss 4. Hypotension
5. Lower triglycerides 5. Added blood loss
6. Home dialysis possible 5. Trained specialist required
7. Temporary access at the bedside

Complications of dialysis

1. Thrombosis, infection, and haemorrhage at the vascular access

2. Fever: from bacteraemia, pyogens, or overheated dialysate
3. Anaphylaxis
4. Hypotension
5. Cardiac arrhythmias
6. Air embolism
7. Pericardial tamponade
8. Haemorrhage from anticoagulant into GIT, brain etc
9. Electrolyte imbalance ↓↑Na, ↑↓K
10. Fits from disequilibrium (Kenedy) syndrome
11. Mechanical complications, blockade of tubes by clots, omentum or fibrous encasement
12. Hypoglycaemia, Hypoalbuminemia
13. Small bowel obstruction from peritoneal sclerosis
14. Abdominal and inguinal hernia
 15. Atelectasis, pneumonia, pleural effusion

Contraindications to dialysis

Peritoneal-infection at the site

Haemodialysis- hypotension, active bleeding

Management of patients on chronic dialysis

 Adequate protein intake (1-1.2g/kg)

 Fluid intake limited between 500-1000ml
 Na and K intake limited to 2g each
 Vitamin B, C, and folic acid supplement because they are dialyzable
 Iron supplement PRN
 Anabolic steroid (e.g., testosterone) may also be given to stimulate erythropoiesis
 Phosphorus intake restricted and administering phosphorus binders to maintain the
predialysis level
 Modification of dosages of drugs excreted by the kidneys

Renal transplant

 From cadavers, siblings, or parents

 ABO and HLA compatibility
 Drugs used to prevent rejection includes
o Cyclosporine
o Prednisolone and azathioprine
o Antilymphocyte globulin
 CHRONIC LIVER DISEASE (CLD)

DEFINITION

Is defined as clinical or pathological spectrum of liver disease of varying etiology lasting for more than
six months and characterized by hepatic necrosis, inflammation with or without fibrosis or neoplastic
transformation

HISTORY

BIODATA

Occupation: health worker

PRESENTING COMPLAINTS (symptoms usually >6months)

 Abdominal swelling/distension
 Yellowish coloration of eyes
 Pruritus
 Amenorrhea
 Abnormal hair distribution(F)
 Hyperpigmentation

It is worthy of note that presenting symptoms are many and non-specific. Careful and detail history is the
key to diagnosis

HISTORY OF PRESENTING COMPLAINTS

 Character: abdominal swelling- onset; progression; ever regressed? Spontaneous or with

medications; painful or not; no. of episodes; swellings elsewhere;
 Course
 When and how the symptoms starts, associations, worsening episodes and
improvement. Clark all symptoms thoroughly.
 Slow onset of symptoms and rapid development/deterioration
 Cause
 Fever, recurrent intermittent jaundice, recurrent malaise, anorexia, nausea, vomiting
upper abdominal discomfort and weight loss; patient is a known IVDU, hx of needle
stick injuries, multiple sexual partners, hx of blood transfusion, hx of surgery,
scarification marks, etc. (? hepatitis B or C)
 A young/perimenopausal woman, with amenorrhea, acne, arthralgia + features of c.
hepatitis (autoimmune hepatitis)
 History of ingestion of poorly stored grains (? Aflatoxin)
  Living in riverine areas and history of childhood haematuria (? schistosomiasis)
 Family history of liver disease (? α1 antitrypsin deficiency) and neurologic/dystonic
symptoms (? Wilson’s disease)
 Nonspecific symptoms with hematemesis, jaundice right hypochondriac pain,
abdominal distension in a chronic male alcoholic. Here ask for the type, quantity,
duration of use, and the CAGE questions (? alcoholic liver disease)
 Chronic use of traditional concoctions. (Unknown toxins)
 Chronic use of drugs such as methyl dopa(antihypertensive), amiodarone
(anitarrhymic), nitrofurantoin (antibiotic) (? drug induced hepatitis)
 Known or newly diagnosed diabetic with brownish/bronze skin discoloration and joint
pains (Hemochromatosis)
 Inquire about other features suggestive of primary biliary cirrhosis, cardiac cirrhosis
and primary sclerosing cholangitis
 R/O differentials: (refer to the corresponding sections)
 CCF:
 CKD:
 Abdominal TB:
 Nephrotic syndrome
 Complications. Clerk around;
-Synthetic functions impairment
-portal hypertension
-Hepato-renal syndrome
-hepatic encephalopathy (RISC- Reversal of sleep pattern, Increase somnolence, Semi
coma, Coma)
-hepatocellular carcinoma (Rt hypochondrial pain in a patient with initial ascites)
Care
Ask about what was done to the patient right from the onset of symptoms. These
include past and present traditional medication, religious incantations/food restrictions,
and hospital admissions.

SOCIAL HISTORY

Cigarette smoking, alcohol (including locally produced ones) ingestion (? amount) and
indiscriminate use of drugs

FAMILY HISTORY

Family history of autoimmune disorders in a female with stigmata of CLD

OCCUPATIONAL HISTORY

Health workers (Hbv), workers in heavy chemical industries

PAST MEDICAL AND SURGICAL HISTORY

 Hx of Hospital admissions?

SYSTEMIC REVIEW

There are often multisystemic effects of chronic liver disease; therefore, all systems must be
thoroughly reviewed.

EXAMINATION FINDINGS

Most of the findings are non-specific but may give a clue to a particular etiologic agent and many are
due to complications of the disease, referred to the peripheral stigmata of CLD.

 Signs associated with etiology;

Alcohol: parotid swelling, dupyuteren’s contracture, peripheral neuropathy, cerebellar signs,

hepatomegaly.

Wilson’s disease: cerebellar signs, Keiser-Fleisher ring, sun flower cataract

Hepatitis C: scarification marks, tattoos

 Signs of decongestion:

Encephalopathy: drowsiness, asterixis, exaggerated deep tendon reflex

Coagulopathy: bruising

Hypoalbuminemia: ascites, leukonychia, peripheral oedema

Portal hypertension: ascites, upper GI bleeding, caput medusa and rectal bleeding

NB: gynecomastia, testicular atrophy, and female pattern hair distribution are due to aromatization
of peripheral androgens.

INVESTIGATIONS

 To confirm diagnosis
i. LFT: bilirubin ↔ or ↑, albumin↓, ALT and AST ↑, ALT: AST ≥2 in alcoholic liver disease,
prolonged PT, ALP↑ in cirrhosis and PLCC
ii. Abdominal ultrasound scan: Hepatomegaly, splenomegaly shrunken or nodular liver,
reverse flow in the portal vein, ascites.
iii. Liver biopsy
o Criterion to fulfil for safe liver biopsy
1. Cooperative patient
2. PT < 4 seconds prolonged
3. Pt > 100×109 /L
 4. Exclude: bile duct obstruction, localized skin infection, advanced COPD, and
severe anaemia.
iv. Endoscopic retrograde cholangio-pancreatography (ERCP)
v. Ascites fluid analysis (both gross and microscopic)
 To determine etiology
I. Serology: HBV, HBC, HBsAg, and HCAb- viral hepatitis
II. Serum ferritin/Fe binding capacity – hemochromatosis
III. Autoantibodies; ANA, AMA and SMA – autoimmune hepatitis
IV. Serum ceruloplasmin – Wilson’s disease
V. α1-antitrypsin deficiency
VI. α- Fetoprotein – PLCC
 To determine the extent (complications) of the disease

a) PCV: May be high secondary to high erythropoietin as in PLCC as a paraneoplastic

syndrome, but may occasionally be low due to bleeding and bone marrow suppression from
infections
b) WBC: ↓(cirrhosis) or ↑ (hepatitis)
c) Clotting profile: ↑PT and INR
d) RBS/FBS: ↓
e) U/E/Cr: ↓urea

TREATMENT

 General measures
 Good nutrition,
 Avoid high protein diet (impaired ammonia metabolism) low salt diet if + ascites
 Avoid NSAIDS, sedatives, opioids, and alcohol
 Give cholestyramine for pruritus

 Treatment of complications
 Bleeding: Identify source of bleeding; give vitamin K 10mg x 3/7; give platelets
concentrates, FFP or blood as required; banding for bleeding esophageal varices.
 Infections (e.g., SBP): Cefuroxime and metronidazole
 Ascites: Bed rest, fluid restriction, low salt diet, diuretics (spironolactone, furosemide);
daily weight monitoring (target ↓½kg/day); therapeutic paracentesis and salt free
albumin for refractory ascites.
 Treat hypoglycemia when RBS is <2.2mmol/L
 Encephalopathy: Bed head tilt to 20® and 20% mannitol or acetazolamide as
decongestants; lactulose and neomycin to reduce NH3 production
 Albumin IV and/or hemodialysis - Hepato-renal syndrome

 Specific treatments
o Viral hepatitis: Interferon α, lamivudine and ribavirin
o Alcoholic hepatitis: Complete abstinence from alcohol, steroids, pentoxifylline (anti
TNF) and participation in alcohol counseling programs
o Autoimmune hepatitis: Azathioprine and prednisolone
 o Drug induced liver disease: Withdraw the offending drug
o Wilson’s disease: Penicillamine
o Hemochromatosis: Deferoxamine and bloodletting
o Liver transplant is the only definitive treatment for patient with chronic liver cirrhosis

NB: Precipitants of hepatic encephalopathy

1. Constipation
2. High protein diet
3. GI bleeding
4. Infection
5. Medications-opiates, benzodiazepines, antidepressants, antipsychotics
6. Diuretic therapy
7. Renal failure
 CHRONIC MYELOGENOUS LEUKAEMIA (CML)

INTRODUCTION

Chronic myelogenous leukaemia is a myeloproliferative disorder characterized by increased

proliferation of the granulocytic cell line without the loss of their capacity to differentiate. More than
90% of cases results from a cytogenetic aberration known as the Philadelphia chromosome. It
progresses through 3 phases: chronic, accelerated and blast.

HISTORY

BIODATA;

 AGE; It peaks at 40-60 years [quite rare in children]

 Sex; slightly higher in males

PRESENTING COMPLAINT

 Abdominal swelling/discomfort, diaphoresis, weight loss, fatigue, exercise intolerance

(chronic phase)
 Bleeding, ecchymosis, petechiae (accelerated phase)
 Fever, bone pain (blast phase)

HISTORY OF PRESENTING COMPLAINT

 COURSE:
 It progresses slowly, usually presenting with features of the phases in chronology.
There may be skips and overlaps however
 RISK FACTORS
 Exposure to ionizing radiation
 Exposure to benzene (from
 R/O DIFFERENTIALS
 Myelodysplastic syndrome (difficult to differentiate)
 Myeloproliferative disease (less of abdominal discomforts + hx of gouty arthritis-due
to hyperuricemia; tinnitus, priapism, or stupor-due to leukostasis)
 infectious mononucleosis (hx of close contact with patient with pharyngitis + hx of
sore throat, fatigue, and prolong malaise about 3 years ago)
 COMPLICATIONS; Look for complications of anaemia and bleeding + visual complications,
bone tenderness or features of secondary infections
 CARE; ask for the care sought, where was it sought? Any improvement? If yes, what are the
markers of improvement

EXAMINATION FINDINGS

 General Physical Examination may reveal the following:

  Chronically ill looking evidence by wasting
 Pale and febrile
 Bruises or ecchymoses
 Lymph node enlargement
 Abdomen; splenomegaly [in 80% of Pts, mostly massive] and hepatomegaly [with soft
edge]
 Eye/fundoscopy; retinal haemorrhage
 Musculoskeletal System; Bone tenderness and oedema

INVESTIGATIONS;

 Full Blood Count

 Hb: mild to moderate anaemia
 WBC: ↑↑ (20000-60000/uL) with predominant neutrophils and mild elevation of
basophils and eosinophils.
 PLATELET: increased, decreased, or normal.
 BLOOD FILM; Neutrophilia with whole spectrum of myeloid cells including blasts
 BONE MARROW ASPIRATION;
 Hypercellular with expansion of the myeloid cell line and its progenitor cells.
 Megakaryocytes are prominent and may be increased
 CYTOGENETICS; t (9,22) or the Philadelphia chromosome
 X-RAY; Lytic lesion

TREATMENT

Goals

 Haematologic remission (normal FBC count, physical examination i.e., no organomegaly)

 Cytogenetic remission (normal chromosome returns with 0% Ph-positive cells)
 Molecular remission (negative PCR result for the mutational BCR/ABL m-RNA)

Options of treatment/Medications

1. Imatinib
 A tyrosine kinase inhibitor
 Initial dose of 400mg, but may be increased to 800mg in sub-optimal responders
 Could be used for all the 3 phases
2. Alpha interpheron
3. Hydroxyurea
 Good in debulking and controlling the blood count but does not alter the natural history
4. For patients with myeloid blast crisis, AML induction chemotherapy could be used in addition to
a tyrosine kinase inhibitor
5. Stem cell transplantation (SCT)
 CHRONIC OBSTRUCIVE PULMONARY DISEASE (COPD)

INTRODUCTION

Chronic Obstructive Pulmonary Disease (COPD) is a group of obstructive lung diseases primarily
characterized by irreversible limitation of airflow usually resulting from an increase in resistance caused
by partial or complete obstruction at any level. Two disease entity fall into this group namely:
Emphysema and Chronic bronchitis

HISTORY

BIODATA

Age: > 40 years

Race: prevalence now on the increase in Asia and Africa (related to increase in cigarette smoking)

PRESENTING COMPLAINTS

NB: Both forms co-exist, rarely do they present as separate entity

 Breathlessness
 Cough
 Exercise intolerance

HISTORY OF PRESENTING COMPLAINTS

 Course:
Onset, duration
Note: Chronic bronchitis is diagnosed clinically as a persistent productive cough in most days of
the week for at least 3 consecutive months in at least 2 simultaneous years.
Symptoms aggravated by exercise at the initial stage and later present even at rest.
Cough productive of sputum (may be purulent) seen in chronic bronchitis or in emphysema with
chronic bronchitis
Exacerbating factors:
? upper respiratory tract infection
? Changes in weather i.e., temperature changes

? Non-compliance with (or under dosing of) medications

? Cardiac arrhythmias
? Environmental exposure to pollens, fumes, allergens, or other irritants
? Left ventricular dysfunction
? Drugs e.g., beta blockers

 R/O differentials:
 ? Fever, Cough, weight loss and night sweats > 2 weeks (R/o Tuberculosis)
? Known asthmatic or hx suggestive of attacks when exposed trigger factors (R/o chronic asthma)
? Chest pain, Orthopnoea, Paroxysmal nocturnal dyspnoea, leg swelling (R/o Congestive Cardiac
Failure)
Note: Cor Pulmonale is a complication of COPD
? Copious, purulent mucoid sputum more in the morning (R/o Bronchiectasis)
? Haemoptysis (R/o Lung Cancer)
? Fever, cough (R/o Pneumonia)
 Complications:
Headaches (due to hypercapnia)
Leg swelling (due to hypoxic kidneys or cor pulmonale)
Weight loss (if emphysema only)
Bluish discoloration of mucosae
Haemoptysis
 Care:
What medical care received and if there was significant improvement?

PAST MEDICAL HISTORY

Known asthmatic

Known diabetic or hypertensive

Retroviral status

SOCIAL AND FAMILY HISTORY

*Cigarette smoking (recognized causative agent) calculate pack years. Duration and whether patient has
stopped smoking (when)

Use of biomass fuels (for cooking especially in this environment)

Occupational hazard (coal miner)

EXAMINATION

 General Physical examination

Acute on chronically ill-looking patient [(evidenced by respiratory distress with respiratory effort
on a wasted individual) or obese in case of chronic bronchitis]
+/- dehydrated
+/- pallor
 +/- cyanosed (marked in patients with chronic bronchitis, later stages of emphysema and in
patient with both- due to hypercapnia)- “blue bloaters”
+/- plethora- “pink puffers” – in emphysema resulting from hyperventilation in its early stage
NO digital clubbing
+/- pedal oedema
 Respiratory system
Increase in respiratory rate
“Barrel shaped” chest- increased antero-Posterior and transverse diameter
Trachea is central
Normal chest expansion
Resonant percussion node
Quiet breath sounds, crackles may accompany infections
 Other systems
Cardiovascular: (complication-cor pulmonale) Increased Pulse rate, Hypertension, Raised JVP,
normal or displaced apex, murmurs, tender hepatomegaly, ascites, and pedal oedema

INVESTIGATIONS

 Chest radiograph: no specific findings however help to rule out other differentials or presence of
complications like bullae, subcutaneous emphysema
 Spirometry: to assess lung function (aids in the classification of COPD into mild moderate and
severe which is crucial in the management)
Forced Expiratory Volume (FEV1) is reduced < 80%
FEV1/ FVC <70% (FVC: Forced Vital Capacity)
 Full blood count: polycythaemia (secondary to hypercapnia)
 Pulse oximetry (< 93%)
 PaCO2 increased and PaO2 reduced
 Others:
Sputum Acid Fast Bacilli
Mantoux test
Blood sugar
Retroviral screening
Electrocardiography and Echocardiography

MANAGEMENT

Management based on severity of disease

 S/ Severity PBD FEV1% of Treatment
No FEV1/F predicted
VC

1 At risk >0.7 ≥80 Behavioural modification and monitoring

2 Mild ≤0.7 ≥80 Short-acting bronchodilator as needed

3 Moderate ≤0.7 50-80 -Short-acting bronchodilator as needed

-Regular treatment with one or more long-acting

bronchodilators

-Rehabilitation

4 Severe ≤0.7 30-50 -Short-acting bronchodilator as needed

-Regular treatment with one or more long-acting

bronchodilators

-Inhaled glucocorticosteroids if repeated exacerbations

-Rehabilitation

5 Very severe ≤0.7 <30 -Short-acting bronchodilator as needed

-Regular treatment with one or more long-acting

bronchodilators

-Inhaled Glucocorticosteroids if repeated exacerbations

- Treat complications

- Rehabilitation

- Long-term oxygen therapy if in respiratory failure

- Consider surgical options

NB: at risk-patients who smoke or have exposure to pollutants, have cough, sputum, or dyspnoea
 MANAGEMENT OF ACUTE EXCERCEBATION
 Oxygen: O2 (24 – 28%) via face mask (aim PaO2>8.0Kpa
 Nebulised bronchodilators: Salbutamol 5mg/4hr and ipratropium 500mg/6hr
 Steroids: I.V hydrocortisone 200mg stat and prednisolone 30 – 40mg/day for 1-2 weeks
 Antibiotics: if sputum purulent, pyrexial, new changes on CXR, give Amoxil/Ceftriaxone +
macrolide (azithromycin, clarithromycin, or erythromycin)

 If no response with above, repeat nebulized bronchodilators and consider I.V

Aminophylline; give loading dose of 250mg over 20 min (if not on maintenance methylxanthines)
and maintain infusion at rate of 500ug/kg/hr. ECG monitoring is required if given >24 hrs.
 Consider intubation and mechanical ventilation if PH < 7.26, PaO2 < 8.0KPa and PaCo2 is rising.
 Consider a respiratory stimulant e.g., Doxapram 1.5- 4mg/min I.V for patients unsuitable for
mechanical ventilation.
 I.V.F replacement, if patient is dehydrated. Avoid I.V fluids in established Cor Pulmonale.

NB: Life style modifications

Avoid smoking
Cooking resources: avoid biomass fuel
Occupational change
Nutrition
Psychotherapy
 CUSHING SYNDROME

INTRODUCTION

Cushing syndrome is a systemic disease that results from chronic glucocorticoid excess (endogenous or
exogenous sources). Endogenous Cushing’s syndrome is due to increased cortisol production by the
adrenal gland.

HISTORY/EXAMINATION

General

• Truncal (centripetal) obesity, thin extremities, supraclavicular fat pads, posterior cervical fat
(“buffalo hump”), “moon facies”
• Hypertension

Skin

• Thin skin, facial plethora, hirsutism in women, wide purple striae, acne, easy bruising, and poor wound
healing, mucocutaneous candidiasis

Musculoskeletal

• Osteoporosis, pathologic fractures, avascular necrosis (AVN)

• Proximal myopathy (more prominent in lower limbs)

Neuropsychiatric

• Emotional lability, depression, euphoria, frank psychosis, gonadal dysfunction

• Oligomenorrhea / amenorrhea in women, decreased libido / impotence in men

Metabolic

• Glucose intolerance (frank diabetes less common), hyperlipidaemia, polyuria, nephrocalcinosis

ectopic ACTH production

• Hyperpigmentation, hypertension, hypokalemic metabolic alkalosis, weight loss, weakness (typical

features of Cushing’s syndrome usually absent)

Note: Hirsutism is not common in Cushing's syndrome caused by exogenous steroids because they
suppress adrenal androgen secretion
INVESTIGATIONS

Screening tests

1. 24-hour Urinary free cortisol (UFC)- >140 nmol/day suggests Cushing syndrome
2. Overnight Dexamethasone stimulation test (DST): it requires administration of 1 mg of
dexamethasone at 11 PM with subsequent measurement of cortisol level at 8 am. A value of
less than 1.8 mcg/dL (50 nmol/L) excludes Cushing syndrome.
3. Others: Midnight serum cortisol >7.5 micrograms, midnight saliva cortisol >550 ng/dL

Confirmatory test

 Low dose dexamethasone suppression test

o Dexamethasone 0.5 mg q 6 x 48 hours
o Measure urine cortisol during the last 24 hours (urine free cortisol >20 micrograms/dL
or urine 17-hydroxycorticosteroid >4.5 mg/d) Or
o plasma cortisol (failure to fall to <5 micrograms/dL)

Tests to determine site of hormone secretion

 ACTH levels may distinguish ACTH independent (adrenal or exogenous glucocorticoids)-lower

levels- from ACTH dependent (pituitary, ectopic ACTH)-elevated- causes.
 Corticotrophin-releasing hormone (CRH) test (helpful in distinguishing pituitary-led Cushing's
disease from ectopic corticotrophin secretion).
 Inferior petrosal sinus sampling is used to distinguish primary and ectopic sources of ACTH.
 Others: CXR for carcinoma of the bronchus, plain radiograph of the abdomen for adrenal
calcification, USS of the abdomen for adrenal tumours.

TREATMENT

• Cushing’s Disease: Transsphenoidal resection of pituitary adenoma

• Adrenal neoplasms: resection

• Ectopic ACTH: resection if possible

• Bilateral adrenal hyperplasia: may need adrenalectomies (lifelong glucocorticoid and

mineralocorticoid replacement)

• Medical adrenalectomy

 Medications that inhibit steroidogenesis such as: Ketoconazole, Metyrapone, Mitotane,

Aminoglutethimide or Octreotide
Notes

 Cushing's disease is increased production by the adrenals secondary to excess pituitary

ACTH, whereas Cushing's syndrome is caused by excess steroid from any cause.
 Pseudo-Cushing syndrome: is a medical condition in which patient displays the signs,
symptoms, and abnormal hormone levels seen in Cushing syndrome, however there is no
problem in the hypothalamo-pituitary-adrenal axis. Seen in chronic alcoholics and
depressed patients. Normal features restore with discontinuation of alcohol or
improvement of emotional status.
 DIABETIC EMERGENCIES

These are spectrum of life-threatening events that may occur in either type 1 or type 2 diabetic
patients. They are;

1. Diabetic ketoacidosis (DKA)

2. Hyperosmolar hyperglycaemic state (HHS)
3. Hypoglycaemia

Both DKA and HHS are characterized by very high blood glucose levels resulting from severe lack of
insulin.

DKA:

Is an acute complication of diabetes mellitus characterized by a triad of hyperglycaemia, ketosis,

and metabolic acidosis. It mainly complicates type 1 diabetes, where it may be the first
manifestation of the disease and rarely people with type 2 diabetes.

HHS:

It mainly occurs in older people with type 2 diabetes, in about one third of the cases of HHS, it is the
first manifestation of type 2 diabetes. The blood glucose rises to very high levels but acidosis does
not develop, the residual insulin is sufficient to prevent ketogenesis. Elevated blood glucose leads
to increased serum osmolality, this results in dieresis and fluid shift, increased urination causes
body wide depletion of water and electrolytes causing extreme dehydration.

Both have the same principles of management with little differences.

Management includes;

History

Physical examination

Investigations

Definitive treatment

HISTORY: it should be short and precise

BIODATA;

PRESENTING COMPLAINT(S): polyuria, polydipsia, nausea, vomiting, abdominal pain, altered

level of consciousness, change in breathing pattern.

Ask for history of diabetes, if yes, ask for duration, type of treatment the patient is on (injection or
tablets), is the patient drug compliant? And if regular on follow up.
History of precipitating factors; newly diagnosed diabetic, infection (ask for fever) the commonest
is UTI and URTI. So, ask for history of cough, pleuritic chest pain, painful micturition, and
suprapubic pain (note that a diabetic can have an infection without any fever due to relative
immunosuppression).

Ask for features of myocardial infarction; chest pain, excessive sweating, epigastric pain. It must
always be ruled out in any diabetic presenting with DKA/HHS. Remember diabetics are at risk of
silent MI (MI without any pain).

Ask for missed dose of insulin, or insulin administration while fasting or taking oral
hypoglycaemics without eating.

PHYSICAL EXAMINATION;

parameters of interest are level of consciousness (delirium, drowsiness, and lethargy, atimes
comatose), hydration status, acetone breath, pyrexia, kussmaul’s breathing (rapid shallow
breathing), tachycardia, normal or low blood pressure, increased capillary refill time.

INVESTIGATIONS;

 Urgent random blood sugar

 Urgent urinalysis: for ketonuria, glycosuria, with or without proteinuria (onset of diabetic
nephropathy) and nitrates(infection).
 Urgent serum urea, electrolytes, and creatinine: ideally this should be done every 1hr, but
can be done 8hrly for the first 24hrs daily subsequently until the patient is stabilized.
Abnormalities seen include; elevated serum urea due to dehydration or background renal
impairment, raised creatinine (cross reaction with ketones), serum potassium may be high,
normal, or low (in DKA/HHS, serum potassium is high or normal but there is severe
depletion of total body potassium).
 Urgent arterial blood gases; for blood pH.
 ECG to rule out MI
 FBC and ESR (for evidence of infection)-they tend to have leucocytosis, if >25,000 is
suggestive of infection.

DIAGNOSTIC CRITERIA FOR DKA/HHS

Criteria DKA HHS

RBS (mmol/L) 14-33 or 35 >/=33.5 or 35
Blood pH <7.35 >7.35
Serum HCO3(mmol/L) <18 >18
Ketonuria 2+ or more or ketonemia Nil or trace
Plasma osmolality(mosm/L) 290-319 >/= 320
Anion gap(mmol/L) >15 <12
DEFINITIVE TREATMENT:

Principles of management of hyperglycaemic crises;

1. Correction of fluid and electrolyte deficit

2. Correction of hyperglycaemia
3. Correction of acidosis when indicated
4. Treatment of precipitating factor(s)
5. Prevention of complications

Correction of fluid and electrolyte deficit;

Fluid of choice is normal saline, administer 1L over 30 mins, then 1L over the next 1hr, then 1L over
the next 2hrs, and 1L 4hrly subsequently until RBS becomes </= 14 mmol/L.

Note; if a patient has background heart or kidney disease, modify the fluid therapy to avoid
circulatory overload.

Correction of hyperglycaemia:

This involves the use of soluble insulin; it should be started after administering 2-3L of IV fluid to
avoid circulatory collapse.

The loading dose is 10 IU IV and 10 IU IM stat doses. Followed by 6IU IV hourly in DKA and 3IU IV
hourly in HHS, with hourly RBS check before giving the next insulin dose.

This is continued until RBS </= 14 mmol/L, the rate of reduction in blood sugar should be 3-4
mmol/L/hr. if it is more than that, adjust the hourly dose of the insulin to achieve so and vice versa.

Correction of acidosis:

This is usually not corrected actively because with adequate fluid and insulin therapy acidosis
corrects itself. However, if HCO3- is <10 mmol/L is an indication for correction of acidosis with 50ml
of NaHCO3 in 500mls of normal saline. also, when K+ is >/= 6.5 mmol/L or Ph of < 7.0 are indications
for correction of acidosis.

Treatment of precipitating factor(s):

The commonest precipitating factor here is infection, so administer broad spectrum antibiotic e.g.,
cephalosporins. If precipitant is MI, it should be managed accordingly.

As RBS becomes </= 14 mmol/L, patient should be fully reassessed. Of interest is the hydration
status, level of consciousness, and vital signs. At this point, the management should be changed to
the following;
1. Change normal saline to 5% dextrose.
2. If patient still has altered consciousness and cannot take orally, continue insulin to 6IU 2 hrly or
12IU 4hrly intravenously. If he is still dehydrated, you may continue with IVF N/S or 5% dextrose
saline until he becomes conscious, well hydrated and can take orally, then change to
subcutaneous insulin 8hrly 30 mins before meals.
3. If patient can take orally and is well hydrated, then you can change to subcutaneous soluble
insulin 8hrly 30 mins before meals.

Correction of electrolyte imbalance:

Most important is potassium replacement, is administered as follows;
Serum K+(mmol/L) Amount of KCL to give in IVF
>/= 5.5 Don’t give KCL observe
4.5-5.4 13mmol/L
3.4-4.4 26mmol/L
<3.5 39mmol/L

PREVENTION OF COMPLICATIONS;
Patients with HHS are at risk of thromboembolism, administer subcutaneous heparin 5000 U
12hrly to prevent this.
Other complications include;
i) Complications of the disease; hypotension, ARF, coma, aspiration
pneumonia, orthostatic hypotension, cerebral oedema, DVT,
hypothermia, ARDS.
ii) Complications of treatment; hypoglycaemia, hypokalaemia,
pulmonary oedema, cerebral oedema.

HYPOGLYCEMIA:
Is RBS </= 2.5 mmol/L, it can cause irreversible brain damage.
PRESENTING COMPLAINTS; feeling of faintness, dizziness/light-headedness, sweating,
confusion, restlessness, irrational behaviour. They may convulse or even be found in coma.
The precipitating factors are mainly insulin overdose or administration without food or taking
OHA without eating (esp. sulphonylureas).
MANAGEMENT:
Urgent random blood sugar must be done. Secure an intravenous assess with a cannula
(preferably)
Give 50% glucose 50-100ml bolus IV in double dilution using a large peripheral vein.
Maintain on 10% dextrose water IV 1Liter 6hourly until patient can take orally.
Monitor hourly blood sugar until stable
Withhold all anti-diabetic medications including insulin until patient is stable.
If glucose infusion is not immediately available, give a bottle of soft drink (Coca-Cola, Fanta) or
place a cube of sugar in patient’s mouth if he/she can take orally.
In the absence of a glucometer, in any person with diabetes if found to have sudden onset of
sweating, tremors, confusion and altered consciousness, draw blood, and send to the
laboratory for urgent RBS. Then GIVE IV 50% dextrose 50ml bolus and maintain on 10%
dextrose until result of RBS is available.

Once patient is stable, before discharge, counsel the patient on warning signs of
hypoglycaemia i.e., tremors, sweating, irritability, headache, etc.
 HEART FAILURE (CCF)

INTRODUCTION:
Congestive cardiac failure is a condition in which there is inadequate cardiac output for body’s needs.
it is characterized by:
-Left ventricular dysfunction.
-Exercise intolerance.
-Breathlessness.
-Fluid retention &
-Decreased longevity.

BIODATA:
 Age: commoner in elderly (It increases with age, affecting 6–10% of people > 65, reaching 30%
in those aged over 80years).
 Sex: males>females.
 Race: commoner among blacks.

PRESENTING COMPLAINT(S)
Presentation depends on the type of heart failure (i.e., whether it is right, left, or congestive cardiac
failure).
A. For LHF, cough, breathlessness, tiredness, & exercise intolerance.
B. For RHF, generalized/ankle swelling, right upper abdominal pain/heaviness, abdominal
swelling.
C. For CCF, there is a combination (to a variable extent) of signs of LHF & RHF with marked severe
wasting (cardiac cachexia).
NB.: Cachexia is due to a combination of anorexia, impaired absorption due to low cardiac output
skeletal muscle atrophy due to immobility & increased levels of circulating cytokines.

HISTORY OF PRESENTING COMPLAINT

I. Course: onset, duration & progression of the symptoms one after another.
Associated symptoms like orthopnoea, PND, production of frothy sputum, haemoptysis, oliguria (other
LHF symptoms); or loss of appetite, nausea, early satiety, neck engorgement and pulsation (other RHF
symptoms).

II. Cause(s):
 Hypertension- history of HTN, when & where diagnosed, on any anti-HTNsives or not, regular
on HTN clinic or not, family hx of HTN, hx of diagnosed renal disease or not.
 Rheumatic valvular heart dx- history of fever with sore-throat (GABHS)/skin rashes in the
past; history of previous cardiac surgery for valve repair.
 Anaemia (anaemic HF)- history of easy fatigability, palpitation, dizziness.
 Dilated cardiomyopathy and/or peri-partum CM- history of child birth within the last few
months, history of hot-water birth, ingestion of potash pap.
 Ischemic heart disease- preceding history of central/precordial chest pain, aching/burning,
precipitated by exertion, relieved by rest or nitro-glycerine.
  Infective endocarditis- haematuria, tiny blood spots in the finger nails (splinter haemorrhage),
abnormally curved nails (finger clubbing).
 Cor Pulmonale: previous hx suggestive of COPD or other long standing lung disease.
 Diabetes: hx of polyuria, polydipsia, polyphagia, and weight gain

NB: history of precipitants of heart failure is ESSENTIAL in patients with acute on chronic heart failure.
Precipitants are listed below

Rule out differentials

 For the cough
-Bronchial asthma: is pt. a known asthmatic? any history of allergy? any family history of asthma in 1st
degree?
-COPD: history of long-term tobacco smoking, exposure to air pollutants such as NO 2, thick yellowish-
green or white-yellow sputum.
 For the body swelling and pedal oedema
CLD: history of childhood jaundice associated with fever, history of alcohol ingestion.
CKD: history of oliguria &/or anuria, history of diagnosed DM, renal disease in the past, chronic
ingestion of NSAIDs.
Nephrotic syndrome: frothy urine, early morning facial puffiness later involving whole body.

III. Complications
 Uraemia: history of itching, muscle cramps, vomiting, altered consciousness (uremic
encephalopathy).
 Thrombo-embolism: history of leg pain with redness/erythema (DVT), history of weakness or
inability to move any part of the body (stroke).
 Impaired liver function: current history of yellowish discoloration of the eye/ mucosa, delayed
clotting.
 Hypokalaemia: weakness, lassitude, constipation (maybe from k + loosing diuretics or
hyperaldosteronism from activation of rennin angiotensin system).
 Hyperkalaemia: hx of weakness, fatigue, or muscle paralysis (not specific)
 Hyponatremia: history of thirst, dizziness, confusion.
 Arrythmia: (high index of suspicion is required as it may be asymptomatic or present with non-
specific symptoms of palpitation, dizziness, syncope, fatigue etc.)

IV. Care
 Where patient went to after the symptoms first appeared, what was done (drugs,
investigation & results if known).
 Why patient moved to this hospital (self-referral, formal referral from the previous hospital)
 What was done to the patient in this hospital, what he/she is on and if patient has improved
during the care.

PAST MEDICAL HISTORY

History of hospital admission, surgery, blood transfusion in the past? If yes, state reasons.

DRUG HISTORY
Hx of ingestion of recreational drugs like alcohol or cocaine.
EXAMINATION

General physical examination:

 Patient lying on cardiac position.
 Acutely ill-looking (respiratory distress, pains)
 Chronically ill-looking (wasting [temporal recession, prominent zygomas,])
 Pallor (due to haemodilution): Conjunctival pallor, pale mucous membrane.
 Clubbing: Infective endocarditis, congenital heart disease
 Pedal oedema: Right heart failure.
 02 concentration insitu (respiratory distress)
 Urinalysis if patient is bloated to R/O nephrotic syndrome, CKD.
 Weight of patient & compare with that prior to illness if he/she knows.

Cardiovascular system:
 Tachycardia.
 Locomotor brachialis (hypertensive heart disease).
 Normal or low blood pressure
 JVP usually raised (Right heart failure).
 Apex: may be displaced/heaving (hypertension, aortic stenosis); thrusting/diffuse (dilated
cardiomyopathy, mitral regurgitation); dyskinetic (left ventricular dysfunction)
 Heart sound: S3± gallop rhythm.

Gastro intestinal system:

 Abdominal distension with visible distended veins
 Right hypochondrial tenderness.
 Tender smooth hepatomegaly ± splenomegaly.
 Ascites demonstrable by shifting dullness or fluid thrill.

Respiratory system:
 Dyspnoea ±features of pleural effusion.
 Tachypnoea.
 Bilateral fine crepitations ± wheeze.

Central nervous system:

 Asterixis (flapping tremor).

INVESTIGATIONS
A. Specific (to confirm the diagnosis)
Chest X-Ray: (ABCDE)
Alveolar oedema.
B Kerley lines.
Cardiomegaly.
Diversion of upper lobe (bat wing).
Effusion (pleural).
ECG:
 Low voltages-myocyte necrosis/pericardial effusion.
 Features of atrial fibrillation: normal but irregular QRS complex, no P waves, irregular waves at
baseline.
 ±Tachycardia.
 Features of ventricular hypertrophy/ischemia: ST segment depression, ± wave inversion.
 Chamber engorgement.
Echo:
 Identify the underlying pathology/cause: cardiomyopathy, valvular heart disease,
endomyocardial fibrosis
 Reduced ejection fraction
 Increased ejection systolic volume

B. To investigate for complication

U/E/Cr:
 Dilutional hyponatremia
 Hypo/hyper kalemia
 Hypocalcaemia
 Increased urea

Full blood count:

 Low haematocrit (dilutional anaemia)

Liver function test:

 Increased bilirubin (direct and indirect)
 Raised liver enzymes (20 to hepatic congestion and hepato cellular hypoxia and
associated central lobular atrophy).

Fasting blood sugar: reactive hyperglycaemia

Lipid profile: Cardiovascular risk (ischemic heart disease, coronary heart disease)

MAKING THE DIAGNOSIS

The diagnosis of CCF is based on the Framingham’s criteria.

MAJOR CRITERIA MINOR CRITERIA

- PND - Peripheral oedema
- Orthopnoea - Nocturnal cough
- Raised JVP - Dyspnoea on exertion
- Pulmonary rales - Hepatomegaly
- S3 heart sound - Pleural effusion
- Cardiomegaly - Tachycardia >120 BPM
- Pulmonary oedema - Weight loss >4.5 kg within 5
days of treatment onset
TREATMENT (PRINCIPLE OF MANAGEMENT)
i. Treat the underlying cause.
ii. Identify and avert the precipitating factor
iii. Treat the cardiac failure

Treatment of the underlying cause.

This depends on the findings from the history, examination and most importantly (specific)
investigations.
- Valve repair/replacement (in valvular heart disease).
- Cardiomyoplasty (in cardiomyopathy).
- Ventricular assisted device (in ventricular dysfunction).
- Artificial heart.
- Cardiac transplant.

Treatment of the precipitant(s) [NB.: precipitants are simply “THIMPARD”]

T-Thyrotoxicosis.
H-Hypertension.
I-Infection e.g., chest infection, UTI.
M-Myocardial infarction.
P-Pregnancy.
A- Anaemia
R- Rhythm disorders e.g., atrial fibrillation
D- Drugs e.g., NSAIDs- (cause fluid retention), verapamil- (negative inotrope)

Treatment of the heart failure. This includes:

- General measures.
-Drug treatment: Reduction of preload.
Reduction of after load.
Improvement of cardiac contractility.

General measures: These include:

-Educate & explain to the patients & their relatives about the nature of the disease, treatment options
and self-help strategies.
- Bed/emotional rest.
- Diet Good general nutrition should be provided, weight reduction especially for obese.
Avoidance of high salt/fatty foods.
Alcohol consumption, if at all, should be moderate. (NB. Alcohol induced cardiomyopathy requires
abstinence).
- Smoking: giving up
-Exercise: regular moderate exercise within the limits of symptoms.
-Vaccination: influenza, pneumococcal vaccine

Drug treatment: These include:

 Reduction of preload
The mainstay here is the use of diuretics.
-Loop diuretics (furosemide, bumetanide, etacrynic acid):
MOA: Inhibits reabsorption from ascending loop of Henle.
S/E: Hypokalaemia, hyponatremia, hypomagnesemia, hypocalcaemia; hyperchloremic alkalosis;
hypotension; hyperglycaemia, hyperuricemia with gout & myalgia.

- Thiazide diuretics (bendrofluazide, hydrochlorothiazide):

MOA: Inhibits reabsorption at the beginning of the DCT
S/E: Like loop diuretics except that it causes hypercalcemia

 Reduction of afterload
Use of ACE inhibitors and ARBs:
-they decrease the vasoconstriction hence ↓ afterload. Also ↓ Na and water retention so ↓ preload
-ACEI should be avoided in hypotensive patients (SBP<90mmHg), in patients with hyperkalaemia and
bilateral renal artery stenosis, pregnant women and lactating mothers, and extreme caution in patients
with valvular stenosis

 Inotropes
-Digoxin: consider this in patients with LV systolic dysfunction, atrial fibrillation, or those with
thyrotoxicosis. Start with 0.25mg OD PO, but reduce the dose in patients with renal impairment and
the very elderly
-
-Dobutamine
-Dopamine: but note that: The vascular and myocardial receptor effects of dopamine, are dose
dependent. Low dosages of 0.5-5 mcg/kg/min stimulate dopaminergic receptors in the renal and
splanchnic vascular beds, causing vasodilation and diuresis; Moderate dosages of 5-10 mcg/kg/min
stimulate beta-receptors in the myocardium, increasing cardiac contractility and heart rate; High
dosages of 15-20 mcg/kg/min stimulate alpha-receptors, resulting in peripheral vasoconstriction
(increased afterload), increased BP, and no further improvement in cardiac output.

Prognosis: 50% die within 5 years of diagnosis.

 HUMAN IMMUNE DEFICIENCY VIRUS (HIV)

HISTORY:

 BIODATA:
 Age: younger population (<25-30yrs, previously); older population (recently, use of
antiretroviral drugs results in HIV patients living longer)
 Occupation: commercial sex workers, long distance travellers/drivers, health workers
 Marital status: singles

 PRESENTING COMPLAINT(S):
 Acute HIV syndrome: occurs in about 2/3 of individuals with HIV within 3-6 weeks after
primary infection. It is due to rapid replication of the virus. Common symptoms include:
Fever
Headache
Malaise
Lymphadenopathy
Joint pain (arthralgia)/muscle pain (myalgia)
Weight loss
Anorexia
Nausea/vomiting/diarrhoea (especially chronic)
Sore throat
Erythematous maculopapular rash
Meningism
Night sweat
 Clinical latency (asymptomatic stage): persists for an average of 10yrs before the
development of symptomatic disease. It is due to decrease viral load and rise in CD4
lymphocytes. And 1/3 of patients may develop Persistent Generalized
Lymphadenopathy (PGL). PGL is defined as the presence of an enlarged node >1cm, in
2 or more extra-inguinal sites, lasting 3months or longer.
 AIDS-related complex (ARC): it occurs before the onset of AIDS & thus regarded as a
prodrome to AIDS & characterized with following constellation of symptoms and signs:
Fever
Night sweats
Diarrhoea
Weight loss
± Opportunistic infections e.g., oral candidiasis, oral hairy leucoplakia, herpes zoster,
recurrent herpes simplex, seborrheic dermatitis, tinea infections.
 Acquired Immune Deficiency Syndrome (AIDS): occurs after an average period of 10yrs,
although it can occur at any time during the course (progression) of the disease. It
depicts severe depletion of CD4 count (<200cells/μL) with subsequent development of
all sorts of opportunistic infections.
 HISTORY OF PRESENTING COMPLAINT(S):
 ? details of the symptoms related to the above complaints in order to get a collection of
symptoms attributable to a particular disease entity or its complication.
 ? the following as it relates to each major complaint:
-on set
-progression
-development of other symptoms
-regression of other symptoms
-limitation of activities
-care sought (may be in the form of drugs or any other form of intervention)

 PAST MEDICAL HISTORY:

 ? History of blood transfusion, frequency, place & time of the transfusion (blood
transfusion exposes patients contracting HIV. However, it depends on the transfusion
frequency & facilities at the centre where it is done. For symptoms to be attributed to a
transfusion, time span must be significant enough to allow for development of
symptoms.)
 ? Other transfusion-dependent medical conditions like chronic kidney disease (CKD),
bone marrow malignancies (e.g., leukaemia) etc.
 ? History of sexually transmitted infections (STIs): unhealthy sexual practices that lead
to the acquisition of STIs also predispose to the risk of HIV; STIs also cause breach of
epithelial linings which increases the risk of HIV acquisition than intact epithelium.
 ? Past surgery (risk of blood transfusion; organ transplant may transmit HIV)
 ? Past hospital admission, reason & duration

 DRUG HISTORY:
 ? If patient is currently on any drug. Ask about name/description, dosage & for how long
has the drug been taken. This will give an idea whether the patient is on ant-retroviral
therapy (ART). And whether the drugs taken have a possible interaction or cross
toxicity with the drugs to be prescribed. And whether some of the presenting
symptoms are side effects of the drugs the patient is taking. Thus, this emphasis the
need for continuous update of knowledge about drugs, about their action, reaction,
interaction & toxicities.
Examples:
-Cytotoxic chemotherapy (anticancer agents) or immunosuppressive therapy (for transplant
patients) may lead to severe immunosuppression that may lead to the development of
opportunistic infections which can mimic AIDS.
-Chloramphenicol and Zidovudine can have a combined suppressive effect on bone marrow.
-Rifampicin (anti TB) may reduce the serum levels of some anti-retroviral drugs (ARVs).
 -HIV can affect renal function and cause CKD (HIV associated nephropathy, HIVAN). So, when
nephrotoxic drugs are used in HIV management (e.g., streptomycin & amphotericin B) there is a
combined effect on the kidney. Thus, there is need for continuous monitoring of renal function.
 ? History of drug allergy; ask about the name of the drug or its description.

 FAMILY HISTORY:
 ? Of a similar condition (especially in spouse).
 ? Monogamous or polygamous family setting, if married.
 ? Spouse(s) or co-wives in first or second order of marriage (first order marriage=first
marriage in life time; second order marriage=marriage to a different person after a
previous one; and so on).
 ? History of STDs in spouse(s) or co-wives.
 ? Death of spouse(s); ask if cause of the death was diagnosed or not.
 ? Any other family disease e.g., Diabetes mellitus, hypertension, allergy etc.

 SOCIAL HISTORY:
 ? Extramarital relationship; ask if multiple; ask about history of STDs in sexual
partner(s); ask about death of a sexual partner; ask if cause of the death was diagnosed
or not.
 ? Long distance travel; frequency of the travel; duration of stay before returning home.
 ? Illicit drugs use (esp. intravenous drugs).
 ? Sharing of sharps
 ? Smoking or alcohol ingestion.

 SYSTEMIC REVIEW:
 ? Symptoms that have not been asked in all the systems: (CNS, CARDIOVASCULAR,
RESPIRATORY, GASTROINTESTINAL, GENITOURINARY & MUSCULOSKELETAL
SYSTEMS).

 SUMMARY:
This should include all important positive and negative findings in the history.

PHYSICAL EXAMINATION:

 GENERAL PHYSICAL EXAMINATION:

 Condition/mood (depression due to chronic infection or awareness of their diagnosis)
 Acutely, chronically, or acute-on-chronically ill looking.
-Acute ill-looking is evidence by painful distress, respiratory distress, exhaustion etc.
 -Chronic ill-looking is evidenced by wasting of temporal field, prominent facial bones,
intercostal wasting etc. These are consequences of prolonged poor appetite, overwhelming
infection, and hypercatabolism associated with chronic inflammatory processes.
-Acute-on-chronic ill-looking is evidenced by combination of acute & chronic diseases.
 Respiratory distress: evidenced by
-Recession (in-drawing of intercostal spaces, suprasternal or subcostal areas) i.e.,
intercostal recession, subcostal, or suprasternal recession.
-Effortful respiration (use of respiratory accessory muscles), noisy respiration (e.g.,
grunting) etc.
Respiratory distress may occur due to chest infection or CNS infection.
 Eye: conjunctival pallor, scleral jaundice, conjunctivitis.
 Oral cavity: Mucosal dryness, pallor, erythematous areas, ulcers, oral thrush (white curdy
patches which can be removed leaving bare areas), oral hairy leucoplakia (persistent
white hairy patches on the sides of the tongue). Others include: oral warts, gingivitis, oral
Kaposi’s sarcoma, oral lymphoma etc.
 Neck: lymph node enlargement of the main groups i.e., sub-mental, sub-mandibular, pre-
auricular, post-auricular, superficial/deep cervical, & supra-clavicular.
Lymphadenopathy may be associated with Persistent generalized Lymphadenopathy
(PGL), TB adenitis or malignancy (e.g., lymphoma)
PGL is defined as the presence of enlarged lymph node greater than 1cm in 2 or more
extra-inguinal sites lasting for more than 3months in the absence of other causes than
HIV.
 Axilla: lymph nodes
 Elbow: epitrochlear & cubital lymph node
 Groin: inguinal lymph node
 Hand: finger clubbing, palmar erythema, pallor, jaundice
 Popliteal lymph node
 Foot: toe clubbing, erythema, pallor

 SYSTEMIC EXAMINATION: HIV is a multi-systemic disease. So, detailed examination of each

system is necessary. Start from the system that is most affected from history.
 Respiratory:
-Respiratory distress (effortful respiration with intercostal or subcostal recession);
respiratory rate; respiratory pattern (regular or irregular); shape of the chest (e.g.,
barrel).
-Tracheal centrality; chest expansion (symmetrical or asymmetrical); percussion; tactile
vocal fremitus.
-Respiratory sounds; vocal resonance.
 Abdomen:
-Shape (distended, flat, scaphoid); umbilicus (everted, flat, inverted or “smiling”);
moves with respiration or not; scarification marks (surgical e.g., McBurney’s or
traditional scars).
 -Area of tenderness (localized, state exact location, or generalized); enlarged organ(s);
any other mass; check for ascites (shifting dullness, fluid thrill etc.)
-Bowel sounds (diaphragm of stethoscope placed at McBurney’s point, the
approximate location of ileo-caecal valve from surface).
McBurney’s point is at the junction of medial 2/3 and lateral 1/3 of an imaginary line that
extends from the umbilicus to the right ASIS (anterior superior iliac spine)
 Genitourinary: genital ulcers, discharges, genital warts
 Musculo-skeletal:
-Joint enlargement or limitation of movement
-Bulk, tone, power, reflexes
 CNS:
-level of consciousness using Glasgow Coma Scale (GCS), if patient is not fully
conscious.
-Signs of meningeal irritation (neck stiffness, Kerning’s sign, Brudzinski’s sign)
 Skin: rashes, ulcers, erythematous changes, patches, Kaposi’s sarcoma, nodules,
vesicles, drug injection sites etc.

INVESTIGATIONS:

Investigations to be done depend on findings from history and examination.

 To confirm the diagnosis:

 Serum (or salivary) HIV-antibody can be detected using ELISA or with the rapid test kit,
and usually confirmed using Western blot test. (In case of recent infection, HIV antibody
might be negative if within the window period, usually 1-3 weeks after exposure. In such
case, repeat at 6 weeks & 3 months).
 Other tests to establish the diagnosis includes:
o Viral culture
o Core p24 antigen
o Reverse transcriptase PCR (RT-PCR)
o Nucleic acid sequence-based amplification (NASBA)
 BASE LINE:
 Haematology: FBC, differential and film.
 Biochemistry: serum, liver, and renal function; Fasting serum lipid profile; Fasting blood
glucose
 Immunology: lymphocytes subsets, CD4 count
 Virology: HIV viral load, HIV genotype, Hepatitis serology (A, B & C), cytomegalovirus (CMV)
antibody.
 Microbiology: TB (sputum AFB, Mantoux), syphilis serology, screen for STIs.
 Others: chest X-ray, Brain CT, Abdominal ultrasound scans.
TREATMENT:

 Aims of HIV treatment:

 Reduce the viral load to an undetected level (<50copies/ml)
 Improve CD4 count >200cells/mm3
 Increase the quantity and improve the quality of life without unacceptable drug related
side effects or lifestyle alteration
 Reduce transmission (mother-to-child or person-to-person)

 ANTIRETROVIRAL THERAPY (ARV):

 Indications for initiating ARV:
- If CD4 available:
• All patients with WHO stage 4 disease and/or
• All patients with CD4 < 200 /mm3 and/or
• WHO stage 3 and CD4 < 350
If no CD4 available:
• All patients with WHO stage 3 and 4
• Patients with WHO stage 2 and TLC < 1200/mm3
Others regardless of CD4 count:
• Pregnant women
• Patients with HIV associated nephropathy (HIVAN)
• Patients co-infected with hepatitis B

Contraindications to initiating any ARV

• Liver function tests > 5x upper limits of normal
• Creatinine > 3x upper limit of normal

 ARV agents:
1. Nucleoside reverse transcriptase inhibitors (NsRTI)
o Zidovudine (AZT)
o Lamivudine (3TC)
o Abacavir (ABC)
o Didanosin (ddI)
o Stavudine (d4T)
o Emtricitabine (FTC)
 Class specific side effects
o Mitochondrial toxicity
o Lactic acidosis
o Pancreatitis
o Peripheral neuropathy
  Drug specific side effects
o Zidovudine-anaemia, nail pigmentation, bone marrow suppression
o Abacavir-hypersensitivity
o Stavudine-lipodystrophy

2. Non-Nucleoside reverse transcriptase inhibitors

o Nevirapine (NVP)
o Efavirenz (EFV)
 Ineffective against HIV-2
 Class specific side effects
o Body rash
o Elevated liver enzymes
 Drug specific
o Nevirapine-severe hepatitis
o Efavirenz-teratogenicity

3. Nucleotide reverse transcriptase inhibitors (NRTI)

o Tenofovir (TDF)-renal toxicity

4. Protease inhibitors
o Ritonavir (RTV)
o Lopinavir (LPV)
o Sequinavir (SQV)
o Indinavir
 Class specific side effects
o Lipodystrophy
o Bleeding in hemophilias
 Drug specific
o Indinavir-nephrolithiasis, hyperglycaemia
o Nelphinavir, ritonavir, Lopinavir- diarrhoea
o Ampinavir-rash

5. Entry Inhibitors
o Enfuvirtide
o Maraviroc
 6. Integrase Inhibitor
o Raltegravir

First line therapy regimen

For ART-naïve adult patients starting ART at this site, the most common first-line regimen consists of
2NsRTIs and 1NNRTI. Most common regimen is:

Zidovudine + Lamivudine + Nevirapine

Unless:

- The patient is severely anaemic

- The patient is taking rifampin

- The patient has abnormal liver function tests

- The patient has a history of medication allergy to or intolerance of one of the first line drugs

- The patient has taken ART (triple therapy) before

Other 1st line regimens include:

– D4T + 3TC + NVP

– Combivir (AZT + 3TC) + Efavirenz (EFV)

– Tenofovir (TDF) + 3TC + either NVP or EFV

– Abacavir (ABC) + 3TC + either NVP or EFV

Second line therapy

Reasons to change to 2nd line regimen include:

1. Treatment failure, by:
• Clinical failure to improve or worsening (change in WHO stage) after 3 months on
ART

• CD4 failure to improve (by ≈50 cells/mm3) or worsening at 6 months.

• A subsequent fall in CD4 count of 30 percent or more from the peak value or a return
to or below the pre-therapy baseline
2. Drug toxicity
3. Pregnancy
4. Infections e.g., TB/HIV
Second line regimen

A combination of a PI (especially Lopinavir or Ritonavir) and 2 other drugs which the patient was
not taking before is used. Example: Tenofovir + Lamivudine + Lopinavir.
NB: 3TC is combined with TDF because it makes the virus more sensitive to TDF.

Opportunistic infections

1. TB/HIV infection (see TB section)

2. Pneumocystic carinii infection:
Presentation: dry cough, exertional dyspnoea and bilateral crepitations. CXR may be normal
or show bilateral peri-hilar interstitial shadowing.
Diagnosis is established by visualization of the organism in induced sputum, bronchoalveolar
lavage or lung biopsy.
Treatment: high dose co-trimoxazole 120mg/kg/day IV infusion in 3-4divided doses for 14
days. SE- nausea, vomiting, fever, rash, and myelosuppression. Or, pentamidine isothionate
14mg/kg/d IV infusion for 14-21 days. SE- hypotension, hepatitis, myelosuppression, and
arrhythmias.
Prophylaxis is given when CD4 count <200/mm3. Secondary prophylaxis is given after first
attack with co-trimoxazole 480mg in 24hr os until CD4 count >200/mm 3.
3. Candidiasis (oral and esophageal)
Presentation: Oral pain, dysphagia ±retrosternal discomfort
Treatment: Oral-oral nystatin suspension or amphotericin lozenges. Esophageal- fluconazole.
4. Toxoplasmosis (Chief CNS pathogen in AIDS).
Presents with focal signs and symptoms.
Diagnosis: CT or MRI shows ring shaped contrast enhancing lesions
Treatment: pyrimethamine + sulphadiazine or clindamycin for 6 months.
Prophylaxis (with cotrimoxazole) is indicated in patients with serum antitoxoplasma IgG and
CD4 count <100/ml.
5. Cryptococcal meningitis:
Presentation: presents as an insidious meningitis often without neck stiffness.
Diagnosis: Indian ink staining and culture of CSF, detection of Cryptococcal antigen in blood
or CSF.
Treatment: amphotericin B + flucytosine IV for 4 months or until clinically stable, or
fluconazole 200mg/d PO.
Secondary prophylaxis is indicated with fluconazole until CD4 count is >150/ml with negative
Cryptococcal antigens.
6. Mycobacterium avium intracellulare
Presentation: fever, night sweats, malaise, anorexia, weight loss, abdominal Pin, diarrhoea,
hepatomegaly, and anaemia.
Diagnosis: blood culture and biopsy
Treatment: with Azithromycin 1200 mg weekly PO (CD4+ T cell count <50/ml) or
Clarithromycin + Ethambutol +/– Rifabutin (Prior documented disseminated disease)
 INFECTIVE ENDOCARDITIS (IE)

INTRODUCTION: IE is defined as an infection of the endocardial surface of the heart. Types includes
native valve IE (NIE)-which could be acute and subacute; prosthetic valve IE, and IV drug abuse IE.
Acute NIE frequently involves normal valves while subacute IE typically affects abnormal valves.

BIODATA

Sex: Male>female

Age: Adult>children

PRESENTING COMPLAINTS

 Fever, malaise, fatigue, (97% of cases)

 Weight loss, cough, chest pain, anorexia, night sweat, joint pains (35% of cases)
 Symptoms of CCF
 Stroke or gangrene of the gingiva (vascular phenomenon)

HISTORY OF PRESENTING COMPLAINTS

Course:

 Subacute IE- usually has an indolent course of symptoms and less commonly develops CCF and
CVD,
 Acute IE: presents with a more aggressive disease and has a rapid progression to CCF

Cause

 Intravenous drug use (usually presenting with dyspnoea, cough, and chest pain)
 Dental procedure
 History of dysuria, frequency, urgency, nocturia (UTI)
 Hx of immunodeficiency (DM, RVD, malignancy)
 Hx of alcohol abuse

Complication

 History of coca cola coloured urine and facial puffiness (glomerulonephritis)

 Hx of sudden loss of consciousness or inability to move any part of the body (stroke)
 Hx of darkening, loss of sensation and function of the fingers (gangrene)
 Hx of painful subcutaneous lesions in the fingers (Osler nodes)
 Hypotension, metabolic acidosis, fever, leucocytosis, and MOF (sepsis syndrome)

Care

 What has been done so far

PAST MEDICAL HX

 Hx of diagnosis of congenital heart disease

 Hx of valve repair or replacement
  Hx of any open-heart surgery

EXAMINATION

General physical examination

 Delirium, pallor,
 Roth spots (retinal haemorrhage with small clear centre)
 Petechiae (common but not specific)
 Splinter haemorrhage
 Janeway lesions (non-tender macules o palm and sole)
 Osler nodes (painful subcutaneous lesions on the distal fingers)

CVS

 Irregular pulse rate

 Gallops
 Changing heart murmurs
 Pericardial rub

GIT

 Splenomegaly

Respiratory system

 Rales
 Pleural friction rub

INVESTIGATIONS

 FBC
 Anaemia (> in subacute IE)
 Leucocytosis (> in acute IE)
 ↓C3 and C4
 + rheumatoid factor (≈50% of cases)
 ESR Elevated (>90% cases)
 Urinalysis: Proteinuria and microscopic haematuria
 Echocardiography: shows intracardiac vegetations and defects
 2 dimensional cardiac Doppler USS
 Blood cultures: about 3-5 sets of blood cultures are taken in 24 hours (for subacute IE). In acute
IE, 3 sets may be drawn over 30 minutes (with separate venepuncture) to help document a
continuous bacteraemia. If patient is on antibiotics, blood cultures are taken at least 48 hours
after it has been stopped. If results are negative, samples are retaken 7 days later.
 Ventilation perfusion scanning: useful in right sided endocarditis
DUKE’S DIAGNOSTIC CRITERIA

Diagnosis is based on the presence of either 2 major criteria or 1 major and 2 minor criterions.

Major criteria
 Positive blood culture for infective endocarditis
1. Expected microorganisms for infective endocarditis from two separate blood cultures
(Viridans streptococci, HACEK groups, Streptococcus bovis, or community-acquired
Staphylococcus aureus or enterococci, without known primary focus)
2. Persistently positive blood culture: defined as identification of a microorganism consistent
with IE originating from:
 blood cultures that are obtained more than 12 hours apart, or
 All of three or a majority of four or more separate blood cultures, with first and last
drawn at least 1 h apart
3. Single positive culture of Coxiella Burnetii

 Evidence of endocardial involvement supporting the diagnosis of IE

1. Echocardiogram findings of:

(a) Oscillating intracardiac mass present:

(b) Abscess, or
(c) Newly identified partial dehiscence of prosthetic valve, or

2. New valvular regurgitation (increase or change in pre-existing murmur does not count as a
criterion)

Minor criteria

 Fever: = or > 38°C (100.4°F)

 Predisposition to IE: heart condition predisposing to IE, or intravenous drug abuse (IVDA)
 Echocardiogram: findings may be consistent with IE, but major criteria as stated above are not
met
 Immunological phenomena present: Roth spots, Osler's nodes, glomerulonephritis, rheumatoid
factor via laboratory analysis
 Microbiological evidence of IE: blood cultures are positive but major criteria are not met as
previously described, ‡ or serological studies support an infection that is consistent with the
diagnosis of IE
 Vascular phenomena present: major arterial emboli, mycotic aneurysm, septic pulmonary
infarcts, conjunctival haemorrhages, intracranial haemorrhage, Janeway lesions
TREATMENT

Medical therapy

In subacute endocarditis where patients are hemodynamically stable, antibiotic treatment can be
delayed until the causative organism is identified while in acute cases or symptomatic patients,
antibiotics are commenced (usually vancomycin or ceftriaxone) until microbial identification.

1. Penicillin G 2–3 MU/day IV in 6 divided doses × 4/52 or vancomycin 15-30 mg/kg IV q12h × 4/52
in penicillin resistance or allergy
2. Ceftriaxone 2 g/d IV as a single dose for 4 weeks
3. Penicillin G + gentamicin 3 mg/kg qd IV or IM as a single dose or divided into equal doses q8h for
2 weeks

Indications for surgery

1. Congestive cardiac failure

2. prosthetic valve endocarditis (valve replacement is usually required)
3. Persistent sepsis 72 hours after initiation of appropriate antibiotic
4. Recurrent septic emboli 2/52 after initiation of antibiotics
5. Rupture of Valsalva aneurysm
6. Acute aortic regurgitation plus preclosure of mitral valve
7. Fungal endocarditis

Antibiotic prophylaxis

Patients undergoing a dental procedure with one or more of the following cardiac lesions have
indication for a prophylaxis

1. Prosthetic heart valves

2. Prior endocarditis
3. Unrepaired cyanotic congenital heart disease, including palliative shunts or conduits
4. Completely repaired congenital heart defects during the 6 months after repair
5. Incompletely repaired congenital heart disease with residual defects adjacent to prosthetic
material
6. Valvulopathy developing after cardiac transplantation

The following antibiotic regimens are recommended by the American Heart Association for antibiotic
prophylaxis

 Oral Amoxicillin 2.0g

 IV or IM Ampicillin 2.0g
 Azithromycin/clarithromycin 500mg PO
 Oral cephalexin 2.0g
 Clindamycin 600mg PO

Any of these can be given 1 hour before any surgical procedure or dental manipulation
 LYMPHOMAS (excluding Burkitt’s lymphoma)

BIODATA

 Caucasians] African
 Age: bimodal peak of HL: 15-34years and >55 years. NHL>50 years
 Sex: male>female

PRESENTING COMPLAINTS

 Cervical lymphadenopathy-multiple neck swellings

 Weight loss, fever, night sweating
 Abdominal swelling-from hepatosplenomegaly in NHL

HISTORY OF PRESENTING COMPLAINTS

Course:

 ? neck swellings that are painless

 ? presence of such pain or precipitated by alcohol (HL)
 ? presence of Pel-Ebstein fever (high fever for 1-2 weeks followed by an afebrile period of 1-2
weeks)
 ? hx of testicular enlargement, eczematous skin lesions (T-cell mycosis fungoides), seizures or
focal neurologic deficit (CNS lymphoma)-NHL
 ? anorexia

Risk factors:

 ? hx of exposure to pesticides, preservatives, chemotherapy, or radiation

 ? hx of close contact with patient with pharyngitis + hx of sore throat, fatigue, and prolong
malaise about 3 years ago (R/O infectious mononucleosis as a precursor to lymphomas)
 ? hx of diagnosis of HIV or prolong hx of diarrhoea, fever, and weight loss
 ? family hx of similar illness (R/O genetic cause)

R/O differentials

 ? hx of long-standing cough, fever, weight loss, cervical adenopathy, haemoptysis, + prolong

contact with a coughing adult (R/O TB)
 ? hx of painless cervical adenopathy, close contact with a cat ± eye discharge or decrease vision
(R/O toxoplasmosis)
 Abdominal swelling, fatigue, bleeding or petechial rashes, fever, and weight loss (R/O
leukaemia)
 ? hx of administration of an antitoxin, antivenom or any drug + fever, arthralgia, body rashes,
and GI symptoms (R/O serum sickness)
Complications

 Cytopenia due to marrow infiltration:? fatigue, malaise, easy fatigability, bleeding from orifices
 SVC syndrome: ?dyspnoea, facial swelling, head fullness, arm swelling, cough, and chest pain
 Pericardial effusion: ?hx of pericardial pain that is relieved by sitting up and leaning forward and
is intensified by lying supine; palpitation; light headedness and syncope

Care

 What has been done so far

EXAMINATION

On general physical examination

 Patient looks chronically ill looking, may be pale, icteric, febrile, with significant peripheral
lymphadenopathy. Lymph nodes are usually non tender, and rubbery involving mainly the
cervical and axillary groups
(NB: significant peripheral lymphadenopathy refers to presence of at least 2 enlarged nodes
each of at least 2cm in at least 2 non-contiguous extra inguinal sites)

On systemic examination

 GIT: hepatosplenomegaly ± ascites (NHL)

 CVS: pericardial effusion: ↑JVP, muffled heart sounds and hypotension
 Respiratory: pleural effusion

INVESTIGATIONS

 To confirm the diagnosis

o Lymph node biopsy and histology
o Fine needle aspiration cytology
o Bone marrow biopsy

 Others (to know the extent and to prepare patient for treatment)
o FBC: normocytic normochromic anaemia, leucocytosis (HL), eosinophilia (HL),
pancytopenia in advanced stage
o Biochemistry: ↑uric acid, ↑LDL (in NHL)-indicator of rapidly progressing disease, a poor
prognostic factor
o LFT: to R/O liver involvement
o RFT: to asses renal extraction of chemotherapy drugs
 o ESR: monitor disease progression
o Ca++, ALP, phosphate for bone metastasis
o CXR+ CT- R/O thoracic involvement
o CT abdomen
o Immunophenotyping
o Stool microscopy

TREATMENT

Treatment depends on the type of lymphoma (H or NH)

Ann Arbor staging of lymphomas is essential in the management

ANN ARBOR STAGING

Stage 1: involving a single node or group of contiguous nodes on the same side of the diaphragm or a
single extranodal site (1E)

Stage 2: 2 or more lymph node groups on the same side of the diaphragm or limited contiguous
extranodal involvement (2 E)

Stage 3: lymph node groups on both sides of the diaphragm may include the spleen (3S) or limited
extranodal involvement (3E)

Stage 4: multiple or disseminated foci involving 1 or more extra nodal sites

Designations applicable to all stages

A-no symptoms

B-presence of fever, night sweat, and/or weight loss

X- Bulky disease (widening of the mediastinum greater than 1/3 rd or a nodal mass greater than 10 cm)

MANAGEMENT OF HL

Radiotherapy:

 stage 1 and 2

Chemotherapy

 stage 3 and 4;
 stage 1 and 2 with relapse, bulky or B symptoms
Combination

 e.g., stage 1 and 2 – 3 cycles of chemotherapy + involved field radiation

 all stages with B symptoms: chemotherapy (6-8 cycles) + radiotherapy when bulky disease

Bone marrow transplant (autologous or allogenic)

(Agents used: ABVD/MOPP- Adriamycin, Bleomycin, Vinblastin, and Dacarbazine)

Adverse prognostic factors of HL

1. age >= 45 years

2. male
3. stage 4
4. Hb <10.5 g/dl or WBC >15*10^9 with lymphocyte < 8%
5. Mediastinal mass ratio > 0.35
6. >= 4 separate LN region

MANAGEMENT OF NHL

 NHL are classified into indolent and aggressive lymphomas based on their progression
 Histopathologically, indolent NHL comprises mainly of follicular lymphomas and small
lymphocyte lymphomas while aggressive NHL comprises mainly of diffuse large B cell
lymphomas and mature T cell lymphoma

Treatment of indolent NHL

 Localized-involved field radiotherapy

 Advanced
o Watch and wait
o Conventional therapy-cyclophosphamide+ prednisolone (28 days)
o High grade regimen-CHOP (21 days)

Treatment of aggressive NHL

 Stage 1 and non-bulky stage 2- 3 cycles of CHOP+I involved field radiotherapy

 In other more advanced stages: R-CHOP, EPOCH-ICE, ESHAP etc.
 Adverse prognostic factors of NHL

1. Age>60
2. ↑LDL
3. Presence of B symptoms
4. Poor performance status
5. T-cell phenotype
6. CNS/BM involvement
7. Stage3/4
8. Bulky tumour

Notes

Difference between HL and NHL

S/No Parameters HL NHL

1 Cell type B-cell Mainly B-cell
2 Nodal spread Centripetal contiguous Centrifugal non-
contiguous
3 Extra nodal tumour Unusual Usual
4 Hematologic spread Rare Common
 ACUTE MENINGITIS

INTRODUCTION

An infection of the meningeal covering of the brain & spinal cord, often fatal with significant morbidity
& mortality hence is a medical emergency. Duration of symptoms is usually within hours to days

BIODATA
High in developing countries due to:
 Poor hygiene
 Climate (hot, dry, and dusty) but decreases with onset before rain

PRESENTING COMPLAINTS (PC)

 Fever
 Headache
 Neck stiffness
 Can’t open eyes in light (photophobia)
 Vomiting
 Drowsy or Loss of consciousness
(N/B atypical presentation -lethargy with absence of classical presentation- in elderly &
immunocompromised patient)

HISTORY OF PRESENTING OF COMPLAINTS

Course
? Onset, duration, and course of symptom
? Coma and focal neurological signs (severe bacterial meningitis)
? Purpuric rash and very rapid, abrupt onset of obtundation and circulatory collapse (meningococcal
meningitis with septicaemia)
? unwell for weeks or months with recurrent fever, sweating, joint pain and transient rash (chronic
meningococcaemia)
Cause
Infections
 Exposure to pt. with similar illness- (meningococcal meningitis)
 Hx of URTI, SCD, Splenectomy, Alcoholism--- (S. pneumonia)
 Immunocompromised, Hospital acquired infection, Recent brain surgery or head injury (gram –
ve organism, staph aureus)
 intake of unpasteurized milk, raw vegetables consumption and soft cheese - (L
monocytogenes)
 TB meningitis:? Chronic cough, night sweat and fever. Hx of contact with chronically coughing
adult. Hx of immunosuppression.
 ? ear pain/ discharge (R/O otitis media)
 ? Painful parotid swelling (R/o mumps)
  Painful rash and ulceration of mouth, hands, feet, buttocks, and thighs. (R/o echovirus= hand-
foot-mouth syndrome)
 ? Trauma/ skull fracture, neurosurgical procedure - r/o direct inoculation

Non-infectious
Neoplasm (malignant meningitis) - anorexia, anaemia, and asthenia
? SLE
Complications
a. Shock (oliguria, hyperpyrexia, impaired consciousness, hyperventilation, collapse rapid thread
pulse etc.)
b. Coma
c. Seizures
d. Cerebral abscess
e. Decreased hearing or deafness
f. DIC (bruising and bleeding)
g. Renal failure (oliguria, decrease urine output, hyperkalaemia, and metabolic acidosis)
h. Pericarditis (septic or reactive)
i. Septic arthritis
j. Peripheral gangrene
Care
Care sought including use of traditional medications, investigations, and results, plans and
treatment

PAST MEDICAL AND SURGICAL HISTORY

 Diagnosis of the following conditions; pneumonia, TB, otitis media, DM, HIV, and cancers
 Previous surgery

FAMILY HISTORY AND SOCIAL HISTORY

 Socioeconomic status, environmental hygiene, ventilation, alcohol ingestion and cigarette
smoking
 Hx of similar illness in the family

EXAMINATION
 General
 Temperature
 PR, RR and BP
 Kernig’s sign (extension at the knee with hip joint flexed causes spasm of the hamstrings)
 Brudzinski’s sign (passive flexion of the neck causes flexion of the hips and knees)
 Neck stiffness
 Rashes and Petechial haemorrhages (meningococcal meningitis)
  lymphadenopathy
 CNS
Do a detailed Neurological examination including GCS

Investigations

 Full blood count (anaemia, leucocytosis raised ESR and low platelets especially in long standing
cases)
 Blood culture
 Imaging such as CT and MRI
 Lumbar puncture may show the following depending on the causative agent

Feature Normal Acute bacterial Viral meningitis Tuberculous

parameters meningitis meningitis
1 Colour Clear and Cloudy Clear Clear/cloudy
colourless
2 Pressure 5-18 mmHg Normal/high Normal Normal/high
3 Red blood 0 Normal Normal Normal
cells
4 Leucocytes Total: <10/mm3 Very high (>1000; Slightly high High (<1000; relative
relative (<1000; relative lymphocytosis)
granulocytosis) lymphocytosis)
5 Glucose 2.2-3.9 mmol/L Low (<1/2 of plasma Normal Low (<1/2 of plasma
level) level)
6 Protein 0.15- 0.50 gll Very High (>1.5) Normal/high (<1) Very High (1- 5)
7 Culture Negative Positive for bacteria Negative for Negative/positive for
bacteria MTB

NB:
-CT scan is recommended before a lumbar puncture if there is suspicion for a raised ICP; a concomitant
RBS should be taken right before the LP
-lymphocyte predominance may occur in L. monocytogenes
-Diabetics may have elevated CSF sugar
-Gram stain & culture yield is significantly reduced with prior use of antibiotic
-CSF Ag & Ab assays most helpful in pt. with prior antibiotic use
-polymorphonuclear lymphocytosis may be seen in early TB meningitis

Other CSF investigations include; -

 Lactate dehydrogenase
 Lactic acid concentration
 Bacterial antigen assay
MANAGEMENT
 Admit the patient
 Commence empiric antibiotic within an hour of admission using broad spectrum antibiotics.
 Correct non-neurologic complication e.g., dehydration, electrolyte imbalances
 Define treatment with CSF, blood culture and other results.
 Supportive management may include O2, IVF’s, NG tube feeding, urinary catheterisation, strict
fluid balance, anticonvulsants. Patients may require neuro-monitoring and neuro-nursing-GCS,
pupillary size, regular fundoscopy.
 Monitor complication with serial U/E/Cr (SIADH) & repeat brain CT when necessary (e.g. brain
abscess, cerebral oedema, brain herniation)
 In case of suspected tuberculous commence antituberculosis drugs - Refer to TB section for more
information.

PREVENTION

 General measures: improvement in environmental sanitation, personal hygiene, and health

education
 Chemoprophylaxis: oral rifampin. Others: ciprofloxacin, ceftriaxone or spiromycin to close
contacts of the patients.
 Vaccination: e.g., with polyvalent vaccine A, C, Y and W135 (Menomune).
Indicated for:
 Structural or functional asplenia
 Age>65
 Travellers to hyper endemic and epidemic areas
 Patients with component compliment deficiency
 Individuals with chronic cardiopulmonary illness
 NEPHROTIC SYNDROME

INTRODUCTION

It is a syndrome characterized by heavy proteinuria, hypoalbuminemia, hypercholesterolemia, and

massive generalized oedema

HISTORY

BIODATA;

Address: areas with heavy metal poisoning e.g., Zamfara-Pb poisoning

PC; usually of generalized body swelling

HISTORY OF PRESENTING COMPLAINTS;

Course;

Onset: sudden or insidious

Duration: acute or chronic

When was it first noticed?

From where does it originate (face)

Does it move throughout the course of the day? Is it worse in the morning or at the end of the day?

Is it affected by elevation? (r/o dependent oedema)

Has the urine change in quantity or quality (frothy urine in NS)?

Cause

Hx suggestive of DM, SLE, lymphoma, leukaemia, amyloidosis, sickle cell anaemia (secondary causes of
NS)

Rule out differentials;

Ask hx of shortness of breath, PND, orthopnoea (r/o cardiac cause)

Ask hx of jaundice pruritus abdominal swelling (r/o hepatic cause)

Ask hx of diet (r/o protein energy malnutrition)

Ask hx of Na retaining drugs like NSAID (ibuprofen, naproxen), corticosteroids etc.

Ask hx of cold intolerance (r/o hypothyroidism)

Ask hx of bloody diarrhoea & steatorrhea (r/o protein losing enteropathy)

Complications;

Ask for features of hyperlipidaemia e.g., ischemic chest pain, intermittent claudication.

Ask for features of renal failure e.g., oliguria, anuria

Ask for features of anaemia, immunosuppression.

Care;

What has been done so far?

Is px on diuretics?

How much weight has px lost so far?

PMHx

Hx of DM, HTN (adults), SCD?

Hx of recent infection (r/o post infectious)

DRUGS & ALLERGIES:

Heavy metals e.g., Hg, Pb etc.

Drugs-penicillamine.

FAMILY\SOCIAL HX

PHYSICAL EXAMINATION:

 Generalized pitting oedema(anasarca),

 ± ascites, hypertension, haematuria, and pleural effusion

INVESTIGATIONS:

 Urinalysis- Proteinuria 3+ or 4+
 Urine sediment examination-fatty casts and fat bodies in a “Maltese cross” appearance
 Urinary protein measurement: either spot or 24-hour collection
 Urine electrophoresis- selective proteinuria-to assess degree of glomerular damage
 Serum albumin:<2.5g/dL
 Lipid profile (↑total cholesterol, ↑ LDL-cholesterol, ↑ triglycerides, normal or ↓ HDL)
 Stool: S.mansoni ova
 Serum chemistry: ↓Na, ↓total Ca
 Renal biopsy
TREATMENT:

SUPPORTIVE

 Weigh daily, monitor BP, urinalysis.

 Monitor input/output
 DIURETICS – Mild, not fast acting ones – Thiazides preferred.
 2° hyperaldosteronism - Spironolactone

Diet:

– Protein of high biologic value

- Normal intake if renal function is normal.

-Cholesterol & saturated fatty acids be curtailed

Modest exercise to discourage thromboembolic phenomena

Avoid femoral tap.

ARBs, ACE-inhibitors & NSAIDs to reduce proteinuria

Resistant oedema: Salt poor albumin +furosemide

SPECIFIC RX;

Depend on the cause

NB: prednisolone in minimal change disease

 PARAPLEGIA

INTRODUCTION: Paraplegia refers to the impairment in the motor and sensory functions of the lower
limbs. Causes may be intracranial (e.g., parasagittal falx meningioma), spinal (most common), and due
to peripheral nerve diseases (e.g., Guillain-Barre syndrome). In this environment, Pott’s disease is the
commonest cause.

HISTORY

BIODATA

PRESENTING COMPLAINTS

 Weakness or inability to use both limbs

HISTORY OF PRESENTING COMPLAINTS

Course:

 ? Sphincteric dysfunction sensory lossmotor dysfunction (lesion is from within the spinal
cord)
 ? Motor dysfunction sensory loss sphincteric dysfunction (lesion is from without the spinal
cord)
 ? back pain, which may extend to the flank (radiculitis)

Cause:

 ? long standing history of fever, weight loss and cough or contact with a chronically coughing
adult. Typically presents with evening pyrexia and night cries (R/O Potts disease)
 ? Hx of frequency, urgency, straining, hesitancy, haematuria+-weight loss (metastatic prostatic
cancer)
 ? known RVD or long standing hx of weight loss, diarrhoea, and fever (HIVAM)
 ? an elderly with history of severe back pain (may involve other bone) + symptoms of
hypercalcemia (R/O multiple myeloma)
 ? hx of a respiratory or gastrointestinal infection, followed by within weeks of an acute onset of
symmetrical, ascending, and progressive weakness +_finger dysesthesia (Guillain-Barre
syndrome)
 ? hx of similar weakness but involving a different location that later resolves +-fatigue+-
cognitive dysfunction (multiple sclerosis)
 ? hx of painless ulcer on the genitals or painless non pruritic rashes on the body (R/O Tabes
dorsalis from syphilis)
 ? Pt is a vegan or had a surgery of the stomach/intestine, or long-term anorexic (subacute
combine degeneration of the chord)
 ? hx of RTA (traumatic injury of the spine)
Complications

 ? hx of sores on the waist or extremities

 ? leg swelling associated with pain (R/O DVT)
 ? loss of muscle mass in the lower extremities
 ? pain while passing urine (UTI)

Care

 What was done so far?

 Is patient on wheel chair transfers, walking aids etc.

PAST MEDICAL HX

 Hx of diagnosis of TB &/or HIV; was patient on medication, was he compliant, for how long has
he been taking the medications, any complication from the medications

FAMILY AND SOCIAL HISTORY

 Any family hx of paraplegia (R/O familial spastic paraplegia)

EXAMINATION

Motor: findings are usually that of UMNL including: wasting, no fasciculations, increase tone, increase
power, increase reflexes, ankle clonus.

Sensory: establish a spinal level

NB:

 Examine the spine: in Potts’s disease, there may be a tell-tale kyphus (or gibbus) or reversal of
lumber lordosis
 examine upper limbs
 check for cerebellar signs (multiple sclerosis)
 try to localize the level of lesion using the following:
o spasticity of the lower limb alone lesion of thoracic chord(T2-L1)
o irregular spasticity of lower limbs with flaccid weakness of scattered muscle of lower
limb lesion of lumbosacral region (L2-S2)
INVESTIGATIONS

To confirm

 tuberculin skin test

 microscopic identification of the AFB from samples obtained from sputum, bone, or Para spinal
abscess collected via CT guided percutaneous sampling
 B12 assay
 CSF analysis (+ identification of malignant cells)
 PSA
 Retroviral screening
 Spinal arteriography (R/O spinal artery thrombosis)

Ancillary

 FBC
 Spinal X-ray: lytic destruction of the anterior portion of the vertebral bodies, increased anterior
wedging, collapse of the vertebral bodies, enlarged psoas shadow with or without calcification.
 CT scan
 MRI

TREATMENT

 Multidisciplinary
 Principle of treatment includes:
1. Prevent bed sores
 Regular turning of the patient
 Use of low air loss mattresses, Clinitron bed (fluidized by warm air), Pegasus
bed (alternating pressure) and Nimbus bed (dynamic floatation)
 Padding of pressure areas with specific appliances can prevent sores developing
and progressing. These include heel pads, horseshoe head rings and a variety of
pressure relieving cushions for wheelchairs
2. Prevent contractures
 Commence early physiotherapy (early, regular passive movement of the limbs)
3. Prevent DVT + embolism
 Regular turning of the limbs
 Use of elastic compression stockings
 IVC filters
 Use of anticoagulants
4. Nursing care-bladder and bowel care
5. Specific treatment of the cause
 Pott’s disease: treat with anti-TB (refer to TB section)
 PEPTIC ULCER DISEASE

Peptic Ulcer Disease is generally characterized by burning upper abdominal pain often worsened by
hunger and relieved by meals.

PRESENTING COMPLAINTS: Epigastric pain, nausea, vomiting

HISTORY OF PRESENTING COMPLAINT:

Course

Pain: Often of sudden onset, localised at the epigastrium and may radiate to the back. More severe
early in the morning. Precipitated by NSAIDs, spices, tea, sour drinks, fried oily food etc. More severe
during meals (gastric ulcer) or some 2-3 hrs after meals (duodenal ulcer).

Vomiting: Contains recently ingested food +/- blood.

Cause

? Use of Non-steroidal anti-inflammatory drugs

? Family history of similar illness

? Burns (curling’s ulcer)

? Head injury (Cushing’s ulcer)

? Hx of cigarette smoking

R/O differentials:

Gastritis: Difficult to differentiate unless on endoscopy

Gastroesophageal reflux disease: typical symptoms include heart burn, regurgitation, dysphagia with or
without atypical symptoms (cough, chest pain, wheeze)

Chronic pancreatitis: epigastric pain, radiating to the back that is relieved by leaning forward.

DKA: Known diabetic or history suggestive of diabetes.

Acute MI: sudden stabbing chest pain which may radiate to the left shoulder or left jaw + risk factor of
cardiovascular disease.

Acute cholecystitis: epigastric pain which may radiate to the right scapular + fever

Cholelithiasis: epigastric pain that is colicky, not relieved by antacids, emesis, or flatus may also radiate
to the right scapular +/- jaundice

gastric cancer- long standing hx of epigastric pain, vomiting, anorexia, epigastric mass, and weight loss.
Complications

? History of melaena (passage of black tarry stools)

? Hx of vomiting of blood (NSAID induced ulcers may only present with bleeding)

? Hx of sudden abdominal pain which is severe and pt. may collapse with or without
haematemesis (perforation)

PAST MEDICAL HISTORY: Hx of surgery (gastric ca can mimic PUD)

DRUG HISTORY: NSAIDs, steroids

SOCIAL & FAMILY HX: Hx of smoking, alcohol ingestion

Family hx of PUD or malignancy

EXAMINATION:

Painful distress

Epigastric tenderness

Guarding if peritonitis present

May be pale or in shock if complicated by bleeding

INVESTIGATIONS

 Oesophageogastric endoscopy= picks over 95% of ulcers. Used for diagnosis and exclusion of
malignancy
 13C urease breath test= a quick and reliable test for H. pylori and can be used as screening test
 Stool antigen test= for diagnosis and therapeutic monitoring.
 Barium meal study= picks over 80% of ulcers when double contrast is used
 Serology= IgG for H. pylori
 Chest x- ray: To rule out perforation (free air under the diaphragm)
 FBC
 EU and Cr

TREATMENT

Treatment of PUD depends on the cause. Stopping smoking should be strongly encouraged as it slows
mucosal healing.
  H. pylori associated PUD: (ERADICATION THERAPY)

2 ANTIBIOTICS +ACID SUPPRESSANT

E.g., Omeprazole (20mg) + clarithromycin (500mg)/metronidazole (400mg) + amoxicillin(1g) for 2wks

 NSAIDs INDUCED PUD;

Stop ingestion of NSAIDs

Proton pump inhibitors should be given

H. pylori eradication therapy if test is positive

For pts with arthritis, replace NSAID with COX-2 selective NSAIDs
 PULMONARY EMBOLISM

HISTORY

BIODATA

 Age: >>middle aged to elderly

 Sex: female>male
 Gravidity is a risk factor

PRESENTING COMPLAINT

 Unexplained difficulty in breathing + pleuritic chest pain (main complains)

 Others includes: cough, haemoptysis, fever, palpitation, bluish discoloration of the lips and
mucosa, or collapse
 May present with features of right sided heart failure
 Features of shock (massive PE)

HX OF PRESENTING COMPLAIN

Course

 Symptoms are usually of acute onset in a previously healthy individual or 2-4 weeks post-op

Risk factors

 Hx of pain/cramps and swelling in the calf or thigh (DVT)

 Hx of prolong immobility e.g., air travel, fracture reduction, previous surgery, hospitalization
 Hx suggestive of underlying malignancy (cancer is both a pro-coagulant and the tumour cells
may embolise)
 Hx of use of OCP or hormone replacement therapy
 Hx suggestive of pregnancy, prolong labour, induction of labour (R/O amniotic fluid embolism)
 Previous hx suggestive of DVT or PE (recurrent PE)
 Hx of trauma to the chest (rib fracture) or lower extremity (R/O fat or bone marrow embolism)
 Hx of HTN, PND, orthopnoea (R/O CCFstasisthrombosis)
 Hx of use of warfarin (predisposition to thrombosis in first few days of use)

R/O differentials

 Personal or family hx of asthma, and other allergies (R/O acute asthmatic attack)
 Hx of smoking, chronic cough (R/O COPD)

Complications

 Hx of leg swelling, abdominal distension/pain after initial symptoms, due to cor pulmunale
Care

 What was done to the patient

 What is the current condition of the patient?

PAST MEDICAL/SURGICAL HX

 ? any previous diagnosis/treatment of malignancy

 Hx of previous surgery in the past 2-4 weeks
 Hx of prolong admission prior to the event

FAMILY AND SOCIAL HX

 Hx of IV drug use

EXAMINATION

General physical examination

 Anxious looking patient with central cyanosis, low grade fever, jaundice pedal oedema

CVS

 Tachycardia, ↑JVP, hypotension, load palpable p2

Respiratory system

 Tachypnoea, wheezing, pleural friction rub, chest findings of pleural effusion

Abdomen

 Smooth tender hepatomegaly and ascites may be demonstrable

Note
Well’s score is a clinical predictive tool that suggests a likelihood of PE.

S/No Clinical variables score

1 clinically suspected DVT 3
2 Alternative diagnosis less likely than PE 3
3 Heart rate >100/min 1.5
4 Immobilization >3 days; surgery within 4 weeks 1.5
5 Prior PE or DVT 1.5
6 Haemoptysis 1
7 Cancer 1
 Interpretation: >6=high probability; 2-6=moderate probability; <2=low probability.

INVESTIGATIONS

Non-imaging:

 Blood test: D-dimers, arterial blood gases (low Po2, low Pco2, respiratory alkalosis) FBC, ESR,
clotting profile
 ECG: tachycardia+-RAD
 Hypercoagulation workup (done if no obvious cause for embolic disease is apparent): screen for
antithrombin III deficiency, protein S and C deficiency, lupus anticoagulant, homocystinuria,
connective tissue disorders.

Imaging: may be invasive and non-invasive

Non-invasive:

 CXR: usually normal but may show:

o Peripheral cone shaped opacification above the diaphragm (Hampton’s hump)
o Areas of pulmonary oligemia (Westermark’s sign)
 Chest CT
 CT pulmonary angiography: is the first line investigation if available
 MRI
 Ventilation perfusion scan (lung scan)
 FBC: (WBC may be high)
 Echocardiography

Invasive

 Pulmonary angiography (used to be gold standard but now replaced by CT-pulmonary

angiography
 Contrast phlebography

TREATMENT

Supportive and definitive

Supportive: resuscitation-O2, analgesics, IV fluids

Definitive

 Anticoagulation using LMW heparin + warfarin to in the first few days until an INR of 2.0-3.0
is achieved, then continued warfarin alone (main stay of treatment)
 Thrombolysis/fibrinolysis
 Placement of IVC filters to prevent recurrence
 Pulmonary embolectomy (surgical)
 STEVENS–JOHNSON SYNDROME (SJS) AND TOXIC EPIDERMAL NECROLYSIS (TEN)

INTRODUCTION

These are acute life-threatening dermatoses characterized by extensive epidermal sloughing and
mucositis, usually secondary to drug intake. They represent a single disease with a spectrum of
severity. Skin involvement is up to 10% of body surface area (BSA) in SJS, in SJS-TEN overlap syndrome
the BSA detachment is between 10 and 30% and in TEN the detachment is above 30% of BSA.

IMPLICATED DRUGS

 Antiepileptics (Tegretol, Phenobarbital)

 Antibiotics (Sulphonamides, penicillins, cephalosporins,),
 Antitubercular agents,
 NSAIDS,
 Antihypertensive,
 Antiretroviral agents
 Allopurinol.

CLINICAL FEATURES

 Incubation period is typically a few days to 3 weeks, but less than 48 hours in a patient who has
a history of a similar reaction to that drug.
 Stevens-Johnson syndrome is characterized by skin lesions with involvement of at least two
mucous membranes, and fever.
 Toxic epidermal necrolysis (TEN) it is characterized by confluent bullae and sheet-like
epidermal shedding, fever, and pain. Disease spreads quickly (within 2 to 3 days).
 Other features include: purulent conjunctivitis, photophobia, difficulty swallowing, stomatitis,
dehydration, hepatosplenomegaly, and genital lesions.

DIAGNOSIS:

Clinical

INVESTIGATIONS

complete blood count, serum electrolytes, urinalysis, blood sugar, liver function tests, renal function
tests, chest radiograph, blood culture, skin biopsy (if indicated), and HIV (ELISA).

MANAGEMENT

 Admit patient directly to the burn unit (BU) or an Intensive Care Unit (ICU), where feasible.
Place large-bore intravenous lines in an area of uninvolved skin to ensure adequate intravenous
access. Maintain strict input and output chart.
 Withdrawal of the offending drug and preferably all drugs that are not lifesaving should be
stopped.
 Take swab of body orifices twice weekly to monitor for early infection,
 Fluid replacement: The fluid requirement of TEN patients is usually two-thirds of those of
patients with burns (rule of nine) covering the same area (4 ml/kg body weight x body surface
area involved). Half the calculated fluid is administered in the first 8 hours and the other half in
the next 16 hours. The maintenance regimen should be urine output +500ml/day and the urine
output should be maintained at more than 1000 –1500 ml/day
(NB: total fluids = oral + intravenous fluids)
 Skin care:
o Avoid unnecessary manipulation of skin.
o Adhesive tape should not be applied directly to involved skin when possible.
o Debridement is advised only for sloughed skin or necrotic skin that can no longer serve
as a barrier.
o Eroded skin should be cleaned regularly and covered with topical antimicrobial
ointment or petrolatum impregnated gauze pieces (non-stick dressings).
o Oral and nasal crusts should be removed regularly using normal saline soaks and topical
petrolatum.
o Silver sulfadiazine application should be avoided.
 Nutritional support: After admission, an oral liquid diet via nasogastric tube should be
initiated. If feasible, oral feeding is always preferred. Caloric requirements are calculated as 30-
35Kcal/kg per day. Proteins (approximately 1.5 g/kg per day) are given to avoid a negative
nitrogen balance.
 Temperature regulation: The environmental temperature should be maintained at 30-32°C to
reduce caloric losses through the skin and the resultant shivering and stress.
 Antacids: Antacids reduce the incidence of gastric bleeding. Ranitidine 150 mg twice daily or
Omeprazole 40 mg once daily before breakfast can be infused.
 Analgesics: E.g., pethidine 25-100mg intramuscularly or subcutaneously, or tramadol 50-100
oral or intramuscularly
 Anxiolytics
 Care of the Eyes: Prevention of ocular sequelae requires two hourly instillation of eye drops,
either physiological saline or antibiotics. Ointments can be used at night. An ophthalmologist
should assess ocular involvement.
 Care of the Mouth: Chlorhexidine or hydrogen peroxide rinses help minimize colonization of
the damaged mucous membranes and maintain good oral hygiene. White petrolatum should
be applied to the lips.
 Physiotherapy: Ensure physical therapy daily to preserve limb mobility.
 Prophylactic Antibiotics: Although strictly discourage, this may be given where secondary
infection is highly likely. Empirical coverage should include one antibiotic having anti-
staphylococcal activity and one effective against gram-negative bacteria.
 SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

INTRODUCTION

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect almost any organ
system; thus, its presentation and course are highly variable, ranging from indolent to fulminant.

HISTORY/PHYSICAL FINDINGS

Biodata: SLE mainly affects women aged 14-64 years

The classic presentation of a triad of fever, joint pain, and rash in a woman of childbearing age should
prompt investigation into the diagnosis of SLE.

Patients may present with any of the following manifestations:

Constitutional (e.g., fatigue, fever, arthralgia, weight changes)

Musculoskeletal (e.g., arthralgia, arthropathy, myalgia, frank arthritis, avascular necrosis)

Dermatologic (e.g., malar rash, photosensitivity, discoid lupus)

Renal (e.g., acute, or chronic renal failure, acute nephritic disease)

Neuropsychiatric (e.g., seizure, psychosis)

Pulmonary (e.g., pleurisy, pleural effusion, pneumonitis, pulmonary hypertension, interstitial lung
disease)

Gastrointestinal (e.g., nausea, dyspepsia, abdominal pain)

Cardiac (e.g., pericarditis, myocarditis)

Hematologic (e.g., cytopenias such as leukopenia, lymphopenia, anaemia, or thrombocytopenia)

In patients with suggestive clinical findings, a family history of autoimmune disease should raise further
suspicion of SLE.

DIAGNOSIS

The diagnosis of SLE is based on a combination of clinical findings and laboratory evidence. The
presence of 4 of the 11 American College of Rheumatology (ACR) criteria yields a sensitivity of 85% and
a specificity of 95% for SLE.

ACR mnemonic of SLE diagnostic criteria "SOAP BRAIN MD"

Serositis

Oral ulcers
Arthritis

Photosensitivity

Blood disorders

Renal involvement

Antinuclear antibodies

Immunologic phenomena (e.g., dsDNA; anti-Smith [Sm] antibodies)

Neurologic disorder

Malar rash

Discoid rash

MANAGEMENT

Management of SLE often depends on the individual patient’s disease severity and disease
manifestations.

Pharmacotherapy

Medications used to treat SLE manifestations include the following:

 Biologic DMARDs (disease-modifying anti-rheumatic drugs): Belimumab, rituximab, IV immune

globulin
 Nonbiologic DMARDS: Cyclophosphamide, methotrexate, azathioprine, mycophenolate,
cyclosporine
 Nonsteroidal anti-inflammatory drugs (NSAIDS; e.g., ibuprofen, naproxen, diclofenac)
 Corticosteroids (e.g., methylprednisolone, prednisone)
 Antimalarials (e.g., hydroxychloroquine)

Notes

Pathogenesis of SLE: Gene-environment interactions result in abnormal immune responses that

generate pathogenic autoantibodies and immune complexes that deposit in tissues, activate the
complement system, cause inflammation, and over time lead to irreversible organ damage.

Serology markers may include:

 ANA sensitive but not specific – 95%

 Different staining patterns – Homogeneous, Speckled, Rim, Nucleolar

 Anti-Sm – specific for SLE

 Anti-double stranded DNA – specific but not sensitive

 Single stranded DNA in drug induced SLE

 Extractable Nuclear Antigen (ENA): Anti RNP suggestive of MCTD but present in black SLE

 Anti-Ro/SSA, La/SSB – neonatal lupus and congenital heart block

 Anti-Ribosomal P-lupus- Cerebritis

 ACA/LAC – Anti phospholipid Syndrome/Recurrent Pregnancy Loss

 ESR – markedly elevated (In Nigerian patients. Above 100).

 CRP – usually normal except infections

 TETANUS

INTRODUCTION: Tetanus is a neurologic disorder, characterized by increased muscle tone and

spasms, which is caused by tetanospasmin, a powerful protein toxin elaborated by Clostridium tetani
(know the biology). Tetanus occurs in several clinical forms, including generalized, neonatal, and
localized disease. The median time of onset is 7 days

HISTORY:

BIODATA

 Age: (neonates-neonatal tetanus, elderly: depressed immunity)

 Sex: Male>female (due to occupation)
 Address: rural>urban
 Race: black>Caucasians
 Occupation: >farmers

PRESENTING COMPLAINTS:

 Abnormal body movement in form of spasm, lock-jaw, or convulsion

 Dysphagia
 Neck and back stiffness
 Neck pain
 Grimace facial expression (Risus sardonicus)
 Arching of the back (opisthotonos)
 fever

HX OF PRESENTING COMPLAINTS

 Course:
o there may be a preceding hx of trauma (3-14 days)
o the spasms are painful and do not impair the level of consciousness, they may be
spontaneous or provoked by slight stimulation
 Cause:
o hx of penetrating or burn injury (even a trivial injury is significant)
o hx of otitis media
o hx of an ulcer (sore) on any part of the body
 R/O differentials
o drug hx: especially anticonvulsants (to r/o epilepsy), antiemetic (phenothiazine,
metoclopramide) and strychnine poisoning
o hx of dog bite (r/o rabies)
o hx of fever associated with headache, neck pain and stiffness (r/o encephalitis or
meningitis)
o when pt. had last meal (r/o hypoglycaemia)
 o hx of spider bite (r/o widow spider envenomation)
o hx of injury to the head (r/o SAH)
 Complication
o hx of fracture and additional injuries from violent spasm
o hx of profuse sweating, fever, palpitation (autonomic dysfunction)
o hx of cough and difficulty in breathing (r/o aspiration pneumonia or pulmonary
embolism)
o hx of calf muscle pain/swelling (suggest DVT)
o passage of coca cola coloured urine- rhabdomyolysis which may lead to ARF
o hx of pressure sores
 Care
o what was done to the patient so far both at home and in the hospital and
improvements so far

PAST MEDICAL AND SURGICAL HX

o hx of resent surgical wounds- may give portal of entry

o hx of thyroid surgery- r/o hypocalcaemia which may mimic tetanus
o hx of instrumentation and other procedures
o hx of drug allergy

FAMILY AND SOCIAL HX

o take a good social hx to r/o conversion disorder

EXAMINATION

Patient is usually conscious (GCS 15/15), may be dehydrated. Signs of autonomic dysfunction may be
present such as tachycardia and hypertension.

INVESTIGATIONS

Diagnosis is mainly clinical,

1. WBC may ↑
2. CSF analysis- normal but useful in r/o meningitis
3. Electromyogram- shows continuous discharge of motor units and shortening of silent intervals
4. Muscle enzyme levels may ↑
5. N/B: culture of C. tetany from wound site is of no diagnostic value
6. Spatula test: it is a simple diagnostic bed side that involves touching the oropharynx with a
spatula or tongue blade. In normal circumstances, it elicits a gag reflex, and the patient tries to
expel the spatula (i.e., negative test). If tetanus is present, patient develops a reflex spasm of
the masseters and bites the spatula (i.e., positive test)
TREATMENT

Principle of management

 Resuscitation (ABC of resuscitation)

 Control of spasm using anticonvulsants-Benzodiazepines, barbiturates
 Neutralization of the free tetanus toxins-Human tetanus immune globulin (TIG) at a dose of
3000–6000 units IM, usually in divided doses because the volume is large
 Antibiotics (penicillin and metronidazole) to eliminate the source of the toxins
 Debriding the wound to eradicate spores and alter condition for germination
 Nutritional support (via NG tube or orally)
 Nursing care: cool, quiet, and dark room to minimize disturbance to the barest minimum
preferably in ICU or isolation unit)
 Managing complications

NB:

 Sympathetic over-activity is the main cause of tetanus-related death in the ICU. Treated
with labetalol
 All adults that are partially immunized, unimmunized those recovering from tetanus should
receive vaccine. The primary series for adults consists of three doses: the first and second
doses are given 4–8 weeks apart, and the third dose is given 6–12 months after the second.
A booster dose is required every 10 years and may be given at mid-decade ages—35, 45,
and so on
 Read on NPI for both children and pregnant women.
 THYROID DISEASES

Hypothyroidism: Usually primary but may be secondary to hypothalamic- pituitary disorders. Also
known as myxoedema.

BIODATA:

Sex: F»M

Age: most common in adults aged 30-50 years

Address: Endemic goitre is common in certain places

PRESENTING COMPLAINTS: May complain of any symptom of hypothyroidism. The commonest are
tiredness, weight gain, cold intolerance, and neck swelling (goitre).

HISTORY OF PRESENTING COMPLAINTS

Course

Also ask about other symptoms of hypothyroidism which include:

Hx of Dry, coarse skin

Hx of Impaired memory and cognition, poor concentration

Hx of Swelling of the face and extremities- due to accumulation of hydrophilic mucopolysaccharides in

subcutaneous tissues when hypothyroidism is severe resulting in myxoedema.

Hx of Coarseness of voice and impaired hearing

Hx of Paraesthesia and arthralgias

Hx of Muscle cramps

Constipation

In women hx of infertility and menorrhagia or oligomenorrhea, while there is loss of libido in men.

Cause

Hx of other autoimmune diseases like vitiligo, pernicious anaemia, myasthenia gravis etc. If present
suggest atrophic thyroiditis which is one of the most common cause of hypothyroidism.

R/O Endemic goitre (iodine deficiency) - Enquire if patient is from area known to suffer from endemic
goitre.

Hx of neck radiation for other cause.

Radioactive iodine therapy for hyperthyroidism

Hx of ingestion of large amount of iodine

Hx of subtotal thyroidectomy

Hx of antithyroid medications- e.g., carbimazole, propylthiouracil

Hx of pain in the neck, fever and malaise and initial symptoms of hyperthyroidism is suggestive of
subacute thyroiditis also known as de Quervain's thyroiditis. There may also be history of respiratory
tract infection.

Did symptoms start postpartum? If yes suggestive of postpartum thyroiditis. (Note that postpartum
thyroiditis may be misdiagnosed as postnatal depression).

Hx of postpartum bleeding suggestive of Sheehan syndrome

(NB: Almost all the questions above are directed towards finding a primary aetiology of the disease
which accounts for most cases of the condition. There are however secondary causes of the disease)

Complication

Myxoedema coma - uncommon but high mortality in elderly. Presents with-↓ conscious level, seizures,
hypothermia, hypoglycaemia, severe CCF, hyponatremia, hypoventilation.

Depression-

Anaemia- dizziness, easy fatiguability,

Care: Care received since his symptoms started.

SYSTEMIC REVIEW

This should be exhaustive as hypothyroidism can affect all the systems in the body.

DRUG HISTORY: Ask of hx of ingestion of drugs that may cause hypothyroidism. these include:
amiodarone, lithium, sulfonylureas, antiepileptics (carbamazepine, phenytoin)

FAMILY AND SOCIAL HISTORY

Hx of similar illness in the family- esp. in autoimmune thyroiditis

place of work- r/o radiation exposure

EXAMINATION

General physical examination- pallor, swelling of face and extremities (non pitting), goitre (learn how to
examine a goitre).
CVS- Bradycardia, Hypertension, cold peripheries

CNS-

Neuropsychiatric signs - Dementia, apathy, mental dullness, irritability, sleepiness.

CN deficits, Entrapment neuropathy (e.g., carpal tunnel syndrome)

Cerebellar signs manifesting with ataxia, tremor, and dysmetria

Slowing of voluntary movements and slow relaxing reflexes

MSS: Myotonia, Muscular hypertrophy, proximal myopathy

INVESTIGATION

 Thyroid function test-

 TSH- ↑ in primary hypothyroidism

- slightly ↓ or N in 20 hypothyroidisms due to lack of TSH from the pituitary.

 T4 =↓

(NB -T3 is not reliable in discriminating euthyroid from hypothyroid pts & may not be necessary to
measure.)

- In sick euthyroid syndrome the levels of T3 and or T4 are at unusual levels but the thyroid gland
does not appear to be dysfunctional. it’s often seen in starvation, critical illness, or patients in
intensive care unit

 20 hypo-↓T4, undetected TSH, T3 not indicated

 Thyroid antibodies-TPO, TBG, TSH, T3/T4 Abs

 ↑ chol & TGs

 AST, CK & LDH may be ↑ due to abnormal muscle metabolism

 Anaemia- normocytic/normochromic

-macrocytic-ass pernicious anaemia

-microcytic =Fe def due or menorrhagia

 Other invs depends on clinical situation-CXR, ECG, ECHO

 Thyroid scan- enlarged gland

TREATMENT

 Mainstay of treatment is thyroid hormone replacement

 Dose adjustment required depending on age of pt., cardiovascular status pregnancy, & other
co-morbid states.

 Goal is to have normal TSH, ideally in the lower ½ of reference range.

HYPERTHYROIDISM

BIODATA:

Sex: F»M

Age: most common in adults aged 20-40 years

PRESENTING COMPLAIN: May complain of any symptom of hyperthyroidism. The commonest are
heat intolerance, irritability, difficulty sleeping, muscle weakness and a neck swelling.

HISTORY

Course:

Also ask about other symptoms of hyperthyroidism which include:

weight loss despite good appetite,

Infertility and scarce menstrual flow in women

hair loss

palpitation, tremor of hands and fingers

Frequent bowel movements

Cause:

Most cases are due to primary causes.

Bulging eyes (usually associated with photophobia, eye irritation and/ or diplopia)- graves’ disease

Hx of other autoimmune diseases like vitiligo, pernicious anaemia, myasthenia gravis etc. If present
suggest Graves' disease which is responsible for 60 to 80% of cases.

Hx of neck radiation for other cause.

Hx of pain in the neck, fever and malaise and initial symptoms of hyperthyroidism is suggestive of
subacute thyroiditis also known as de Quervain's thyroiditis. There may also be history of respiratory
tract infection.

If post-partum may be due to postpartum thyroiditis (NB. Thyroid hormones may be elevated during
pregnancy due to effect of HCG and increasing level of oestrogen)

Hx of visual disturbance, headache - Pituitary adenoma

Complication

Hx of progressive weakness and wasting of musculature especially pelvic girdle and thigh muscles -
Chronic thyrotoxic myopathy

Hx of attacks of mild to severe weakness - Thyrotoxic periodic paralysis

Hx suggestive of heart failure or atrial fibrillation

Hx of gynaecomastia

Hx of osteoporosis

DRUG HISTORY: Ask of drugs that could cause hyperthyroidism e.g., amiodarone, thyroid hormone
supplement like levothyroxine (exogenous or occult factitial thyrotoxicosis), exogenous iodine (e.g., in
cough syrup).

FAMILY AND SOCIAL HISTORY:

smoking- ophthalmopathy is more common in smokers

Family History of similar condition

Place of work and residence to rule out exposure to radiation

EXAMINATION

Eye- Proptosis with lid lag and poor convergence

Neck- Goitre (mostly diffuse but may be solitary or multinodular)

Others include pretibial myxoedema, thyroid acropathy (clubbing and swollen fingers), Palmar
erythema, warm sweaty hands, onycholysis, pruritus, diffuse hyperpigmentation, alopecia

CVS - Tachycardia, heart failure (gallop rhythm etc), atrial fibrillation (irregular pulse)
INVESTIGATIONS

 TSH-↓≤ 0.05mU/L

 T4 ↑, free T4 or T3 (T3 is more sensitive as there are occasional cases of isolated 'T 3 toxicosis')

 Abs- TPO, TSH receptors, TSIg, TB- usually present in Graves’ disease

TREATMENT

1. ANTITHYROID DRUGS

 CARBIMAZOLE/METHIMAZOLE

 PROPYLTHIOURACIL-
 Side effects of antithyroid drugs include rash, nausea and vomiting, arthralgia, jaundice, and
agranulocytosis (discontinue treatment if it occurs)
(They are administered by the "gradual dose titration" or by "block and replacement regimen".
Read these)

 PROPRANOLOL- beta blocker needed for symptomatic relief, inhibits peripheral conversion of
T4 →T3, counteracts the excessive sympathetic activity. Avoid in asthmatics, caution in CCF.

2.RADIOACTIVE IODINE- I131 used.

 Accumulates in the gland & gradually destroys the gland by local irradiation.

 Pt must be euthyroid b4 treatment. Stop antithyroid drugs 4/7 before & 3/7 after treatment.

 C/I in pregnancy, breast feeding

 Side Effects- discomfort in the neck, worsening of hyperthyroidism, hypothyroidism,?

carcinogenesis

3.PARTIAL/SUBTOTAL THYROIDECTOMY

 Pt must be euthyroid b4 surgery- stop antithyroid 10-14/7 before operation.

 Give potassium iodide (60mg 3x dly) to ↓ the vascularity of the gland

 Complications- bleeding, Recurrent laryngeal nerve palsy, recurrent hyperthyroidism, transient

hypocalcaemia, hypothyroidism

NB: In Thyroid eye disease collaboration with an ophthalmologist is required

Indications for surgery/radioiodine

 Pt preference
 Persistent S/ Effects

 Poor drug compliance

 Recurrent hyperthyroidism after drugs

 Large goitre which does not remit after antithyroid drugs

(Read Thyroid Storm and Hyperthyroidism in pregnancy)

 TUBERCULOSIS

HISTORY

BIODATA:

Age: elderly

Occupation: health workers

PRESENTING COMPLAINT:

 Cough>3/52, breathlessness, haemoptysis, fever, night sweats, weight loss, chest pain.

HISTORY OF PRESENTING COMPLAINTS:

Course:

 chronic cough productive of mucoid sputum that does not respond to full course of antibiotics
or recurs after a course or courses of antibiotics ± haemoptysis
 chest pain may be pleuritic
 ± wheeze (from compression of the bronchus by enlarged LN)

Cause/risk factors

 Sustained intimate contact with a chronically coughing adult or patient on anti-TB

 Drugs: patients on steroids
 Conditions: DM, CKD, malignancy, HIV, alcoholism, gastric surgery
 Poverty, malnutrition, overcrowding (from social hx)

Complications

 Pleural TB: pleuritic chest pain

 TB adenitis: Hx of neck swelling
 TB spine: Hx of back pain aggravated by straining or cough, band-like sensation followed by
weakness and finally sphincteric disturbance
 Milliary TB: progress hx of fever, malaise, and weight loss
 TB meningitis: headache, vomiting, irritability, depressed consciousness, coma
 Abdominal TB: abdominal pain, distension, diarrhoea/constipation
 TB pericarditis: features of HF, breathlessness, ↑JVP, leg swelling
 GU TB: dysuria, haematuria, flank pain/mass, epididimo orchitis, endometritis
 Skin TB: skin changes include- Lupus vulgaris, Scrofuloderma, Tuberculosis vesicular cutis,
Tuberculous gumma, Tuberculitis, Erythema nodosum
 TB adrenalitis: fatigue, light-headedness upon standing, mood changes, salt craving

Care:
  Investigations and medications so far and outcome

R/O differentials

 Bronchogenic Ca: similar symptoms but with significant smoking

 Bronchiectasis: copious sputum that worsens on sitting up
 Psittacosis: exposure to poultry
 Heart failure: Hx of PND, orthopnoea, production of frothy sputum
 Lung abscess: swinging fever, cough productive of purulent fowl smelling sputum, chest pain
 Occupational lung disease: Hx of exposure
 Pneumocystis carinii: HIV+, dry cough, oral candidiasis,
 Histoplasmosis: closely resembles TB with batwing appearance on CXR in HIV+ pt.
 Kaposi sarcoma: HIV+ pt.; closely resemble TB, skin lesions may be present
 Sarcoidosis: dry cough, external manifestations like hepatosplenomegaly, and
keratoconjunctivitis

PAST MEDICAL HX

 ? previous hx of TB diagnosis
 Previous treatment, compliance, follow ups/DOTs
 RVD, DM, CKD etc

FAMILY AND SOCIAL HX

 Family hx of TB
 Occupation-poverty; quality and quantity of meals-malnutrition; size of room, number of
persons sleeping per room, size, and number of windows-overcrowding.

EXAMINATION

General physical examination

 Chronically ill-looking pt., grossly wasted, icteric, pale, febrile with significant peripheral
adenopathy-commonly cervical-which are initially rubbery and non-tender, later matted and
fluctuant. May be spontaneously discharging through the skin
 ±finger clubbing
 Examine the sputum mug, and the back for gibbus.

Examine other systems as appropriate

INVESTIGATIONS

To confirm diagnosis:

I. Sputum AFB
best collected in the morning
sensitivity= 50-60%
predictors of smear negative AFB: lack of cough, HIV seropositive, CD4<200, age>40, children.
ZN cannot differentiate spp of mycobacterium
read up the procedure
II. Culture
specimens include: sputum, CSF, pleural fluid, ascetic fluid, pericardial fluid, sinus discharge
more sensitive than microscopy
culture media: (I) solid media: Lowenstein Jensen’s medium (2-4 weeks), middle brook medium
(ii) liquid media: Bactec medium (5-7 days), Kirchner medium
III. PCR
IV. Biopsy
V. Tuberculin skin test
VI. New diagnostic tests:
 Light Emitting Diode (LED)
 Loop Mediated Isothermal Amplification (LAMP)
 Nucleic acid amplification
 DNA fingerprinting
 QuantiFERON

Supportive

I. CXR: this may show

 Patchy shadows or nodules especially in the upper lobe
 Consolidation
 Cavitation
 Pleural effusion
 LN enlargement
 Calcification
II. FBC
 Normocytic normochromic anaemia
 ↑WBC
III. ESR ↑
IV. LFT (for commencing anti-TB)
V. U/E/Cr- to know baseline renal function because of excretion of anti-TB drugs and to R/O T
adrenalitis
VI. Other supportive investigations in accordance with extrapulmonary manifestation of TB
DEFINITION OF TERMS

1. New case: a newly diagnosed patient or a patient who has been on anti-TB for <2 months (new
smear positive patient) or was previously declared cured after CAT I treatment
2. Return after default: a patient who commenced anti-TB for 4 weeks, defaults (interrupts
treatment) for a period of 8 weeks, then returns, all the while being smear positive
3. Relapse: a patient found to be sputum positive after previously completing treatment and
being declared cured
4. Cure: a patient who is sputum negative in the last month of treatment and on at least one
previous occasion
5. Treatment completed: a patient who has completed treatment but does not meet the criteria
to be classified as cure or treatment failure
6. Treatment failure: patient is sputum positive at 5 months or later during treatment (i.e.,
persistently remains positive)
7. Died: a patient who died of any reason during treatment
8. PTB suspect: a patient presenting with features that makes the health worker suspect PTB.
9. TB suspect: a patient with symptoms and signs suggestive of TB
10. Others: any patient that does not fit into any of the categories above, but is smear positive

TREATMENT

CAT I:

 new case
 Short term treatment
 2HRZE, 4HR (NTBLP advocates 4RE)

CAT II:

 Previously treated patient who is presently smear positive

 Includes relapse, return after default, and treatment failure
 2HRZE, 1HRZE, 5HRE

MDR-TB:

 Individualized treatment based on sensitivity

Extra PTB:

 Should not be treated for less than for 12 months

ANTI-TB DRUGS

 1st line drugs and their important side effects

1. Rifampicin-hepatitis, vasculitis, thrombocytopenia
2. Isoniazid-peripheral neuropathy, psychosis, optic neuritis; more common in slow
acetylators; Prevented by giving pyridoxine
3. Pyrazinamide-hepatotoxicity, hyperuricemia, hypersensitivity
4. Ethambutol-optic neuritis, ↓colour vision and visual acuity
5. Streptomycin-ototoxicity and nephrotoxicity

NB: all are bactericidal with exception of Ethambutol; rifampicin and isoniazid have high
potency

 2nd line drugs

1. Aminoglycosides: kanamycin, amikacin
2. Polypeptides: capreomycin, viomycin
3. Fluoroquinolones: ciprofloxacin, ofloxacin, moxifloxacin
4. PAS-Paraaminosaliylic acid
5. Cyclocerine
6. Thioamides: ethionamide, prothionamide

ANTI-TB AND CONDITIONS

1. Anti-TB and hepatic dysfunction

 Treatment is ceased when transaminases are:
o 5 times above normal
o 3 times above normal with symptoms
 When restarting treatment, desensitization of patient is done by introducing the less
hepatotoxic drugs before the more hepatotoxic ones i.e., ERHZ

2. Anti-TB and pregnancy/breastfeeding

 Streptomycin is contraindicated (foetal ototoxicity)
 2nd line drugs also contraindicated
 Anti-TB drugs are compatible with breastfeeding

3. Anti-TB and renal failure

 Rifampicin, isoniazid, pyrazinamide can be given in normal doses
 Ethionamide and prothionamide are also safe
 Avoid streptomycin and ethambutol
 Safest regimen to give is 2HRZ/4HR
 4. Anti-TB and liver disease
 Do not give pyrazinamide because it is the most hepatotoxic of anti-TB drugs (P>I>R>E)
 Isoniazid + Rifampicin + 1 or 2 non hepatotoxic drugs (streptomycin & ethambutol)
 Regimen can be used for a total duration of 8 months
 If the patient has severe liver damage, an alternative is SEI in the initial phase, IE in the
continuation phase for a total duration of 12 months (SEI/IE)
 Other recommended regimens are: 2SHRE/6HE or 2SHE/10HE

Indications for steroids

I. TB meningitis
II. TB pericarditis
III. Pleural effusion
IV. TBadrenalitis
V. GU TB
VI. Massive LN enlargement with pressure effect
VII. Severe hypersensitivity reaction to anti-TB drugs

Definition of drug resistances

 Multi-drug resistant TB (MDR-TB): TB whose isolates are resistant in-vitro to at least INH and
Rif (the mainstay of TB treatment)

 Extensive drug resistant TB (XDR-TB): TB whose isolates are resistant to INH and Rif, and AT
LEAST three of the six main classes of Second Line anti-TB drugs

 Pan-resistant TB: TB whose isolates are resistant to all anti-TB drugs

TB/HIV Co-infection

Problems

1. Overlapping side effects of anti TB and ARVs

2. Complex drug-drug interactions
3. Difficulty with adherence to multi-drug therapy
4. Immune reconstitution inflammatory syndrome (paradoxical reaction)

Effects of HIV on PTB

 Weight loss and fever are common in HIV positive patients

 Frequent false negative manteaux test
 On CXR, early HIV shows upper lobe predominance while advanced HIV disease typically show:
lack of cavitation, intrathoracic adenopathy, lower and middle lobe infiltrates, nodular
infiltrates, pleural and pericardial involvement.
  MTB found less often by microscopy
 Destructive forms of TB less common

Strategy for initiating Rx in HIV infected patients with active TB

S/No Criteria Anti TB Rx ARVs

1 Extra PTB irrespective Start immediately Start ARVs as soon as
of CD4 count TB treatment is
tolerated (2 weeks to 2
months)
2 PTB with Start immediately Same as above
CD4<200/mm3
3 PTB with CD4 200- Start immediately Monitor CD4 count.
350/mm3 Start ARVs after
completion of initiation
phase of anti-TB, or
earlier if patient is
severely compromised
4 PTB with Start immediately Monitor CD4 count.
CD4>350/mm3 Consider ARVs if it
drops below 350/mm3

Overlapping side effects of 1st line Anti-TB and ARVs

S/E Anti-TB ARVs

Skin rash PZA,RIF, INH NVP, EFV, ABC
Nausea/vomiting PZA, RIF, RBT, INH ZDV, RTV, AMP, IDV
Hepatitis PZA, RIF, RBT, INH NVP, PI
Leukopenia, anaemia RBT, RIF ZDV

NB

 Do not combine RIF and NVP; instead replace RIF with RBT. RBT is however effective and less
widely available
 Alternatively, replace NVP with EFV
 Rifampicin and PIs are not combined because RIF is an enzyme inducer because it reduces the
bioavailability of PIs thus reducing its effect and promoting resistance.