Medicine- Biostatistics and Epidemiology

Biases
 Selection bias: occurs when there are unintended differences in the patient populations for a study
 Lead time bias: occurs when a diagnostic test detects a disease earlier, leading to an apparent increase in length of survival when in
reality the difference is only due to earlier detection.
 Measurement bias: when the results are improperly measured.
 Confounding: Occurs when a variable correlates with both dependent and independent variables and can serve to alter the results of
a study if it is not controlled for (i.e. with a multivariate logistic regression model).
 i.e Patients with aortic sclerosis are more likely to have other atherosclerotic RFs, and thereby are at higher risk of
adverse events even if the aortic sclerosis has no direct impact.
 Effect modification: occurs when the risk of a certain condition is only present within a certain subgroup of the population being
studied.

Study types
 A cohort study follows a group of patients who are similar except for a single variable are over time (prospectively). After a certain
amount of time, the incidence of a chosen end point is compared between groups to compute RR.
 A correlational study uses a large sample population in an attempt to correlate a disease with a certain variable, often on a
geographic basis.
 A cross-sectional study is an observational study in which a group of patients with a disease is questioned about the presence of
certain RFs. A weakness of this study is that cause and effect cannot be established with certainty
 A Case-Control study is when a certain number of patients with a disease are retrospectively compared to a control group to
determine if there is a higher prevalence of particular RFs in patients with the disease. (i.e. investigate an acute infectious didase
outbreak as it explores the association between exposure and disease. Data is used to calculate Odds ration.

 Relative Risk (RR) = Incidence (exposed) / Incidence (unexposed)

 Attributable Risk (AR)= Incidence (exposed)- Incidence (unexposed)
 Number Needed to Harm (NNH)=1/ (Incidence (exp)-Incidence (unexp) = 1/AR

Medicine- Cardiovascular system

Activity following MI
 Patients with recent uncomplicated MI (no recurrent angina, arrhythmia, or heart failure) and successful revascularization are at a low
risk of recurrent cardiac events and can resume regular activity (work, sex) 2 weeks after initial event.
 Patients with intermediate risk (stable angina, incomplete revascularization, LVEF <40%) need further evaluation with stress test for
risk stratification.
 Patients with high risk (unstable angina, CHG, ventricular arrhythmia, severe valvular disorder) should be evaluated and stabilized
prior to resuming normal work activity.

Indications for surgical repair of MVR

 Primary MR (intrinsic defect in MV apparatus)
o LVEF 30-60% (regardless of symptoms)
o Only if successful valve repair is highly likely
 Symptomatic patients w/LVEF <30%: Due to life-limiting permanent systolic dysfunction,
 Asymptomatic pts w/ LVEF >60% (surgery is preemptive).
 Secondary MR- from other cardiac disease (myocardia ischemia, dilated cardiomyopathy)
o Medical management, valve surgery is rarely indicated
 A-fib is due to LAE and anticoagulation is indicated to reduce risk for embolic stroke. However, surgery may correct a-fib and
eliminate need for anti-coagulation (although mitral valve replacement (less preferred than repair) with a mechanical MV would
warrant long-term anti-coagulation with Warfarin).
 In severe MR, a large portion of LVEF flows back into LA, so the effective LVEF is much lower than estimated by ECHO

Indications for implantable cardioverter-defibrillator (ICD) placement

 Primary prevention
o Prior myocardial infarction & LVEF ≤30%
o NYHA class II or III symptoms & LVEF ≤35%
 Secondary prevention
o prior VF or unstable VT without reversible cause
o Prior sustained VT with underlying cardiomyopathy

Indications for Cardiac Re-Synchronization Therapy (with biventricular pacemaker)

 LVEF ≤35 & and sinus rhythm with 1 of the following
o QRS >150msec and NYHA class III or IV symptoms on optimal medical therapy
o QRS between 120-150 and NYHA class III or IV symptoms on optimal medical therapy
  NYHA class I or II symptoms on optimal medical therapy undergoing pacemaker or ICD implantation with anticipated frequent
ventricular pacing
 LVEF ≤ 30%, QRS >150msec with LBBB, & NYHA class I or II symptoms on optimal medical therapy.

Hypoplastic left heart syndrome (HLHS)

 mild cyanosis at birth and rapid clinical deterioration with closure of ductus arteriosus, resulting in rapidly developed shock and
acidosis due to reduced systemic perfusion.
 ECHO is diagnostic and shows a small aorta and LV with stenotic or atretic mitral and aortic valves.
 Treatment is PGE1 (alprostadil) to maintain patency of DA
 TGA causes cyanosis without respiratory distress. Survival depends on mixing of bloods between systemic and pulmonary circuits via
ASD or patent DA

AAA repair indications:

 presence of symptoms (severe abdominal or back pain), regardless of size
 aneryusm size (=5.5 cm)
 expansion rate >0.5cm/6 months

Atheroembolism
 seen in patients who have undergone arterial intravascular intervention, but can also be 2/2 trauma or vascular surgery.
 an uncommon complication of cardiac catheterization in which atherosclerotic fragments are dislodged from the aortic wall and
released into circulation. The fragments then embolize to distal sites, classically resulting in either livedo reticularis or "blue toe"
syndrome. Other sites prone to atheroembolization are the kidneys, retina, cerebrum, and GI tract.
 After cardiac catherization, both aortic atheroembolism and contrast-induced nephropathy can lead to acute renal failure.
o Aortic atheroembolism is more likely the causative agent in patients who have atherosclerosis, skin changes in the lower
extremities, and elevated serum and urine eosinophils.

 ACEi initiated within 24hr to 16 days of acute MI have been shown to improve LVEF, prevent ventricular remodeling, and improve
mortality.

Sick Sinus Syndrome (bradycardia-tachycardia syndrome)

 Due to chronic SA node dysfunction.
o Characterized by rapidly alternating supraventricular tachycardia (MC a-fib) and bradycardia (sinus bradycardia, sinus
pause/arrest, or SA nodal exit block).
o Most common symptoms are lightheadedness, presyncope (DOE and angina are also reported), and patients are old with
multiple comorbid medical conditions.
 Treatment: symptomatic sinus bradycardia is treated with pacemaker placement. After pacemaker is placed, tachycardia can be
controlled with rate control medications.

Regardless of baseline LDL levels, all patients age =75 with established cardiovascular disease should be treated with high-intensity statin therapy
to reduce risk fo cardiovascular events. High-intensity statin therapy is provided only by daily use of atorvastatin 40-80mg or rosuvastatin 20-
40mg. Lower doses of these 2 drugs and all doses of other statin agents constitute low-or moderate-intensity statin therapy.

Bacterial endocarditis prophylaxis

 recommended for dental procedures in patients with cardiac conditions that are associated with the highest risk of adverse outcomes
from ID.
o Prosthetic cardiac valves
o previous IE
o valvulopathy in recipients of cardiac transplant.
o Congenital heart diseases (unrepaired cyanotic CHD, repaired CHD with prosthetic material during the first 6mos following
procedure, or repaired CHD with residual defects)
 MVP is MC underlying condition that raises the relative risk of developing IE; however, the absolute risk of developing IE in patients
with MVP (w/ or w/o MR) is low.

Indicated procedure and appropriate coverage:

 gingival manupularion or respiratory tract incision: Viridians strep coverage (amoxicillin)
 GU or GI procedure in setting of active infection
o enterococcus coverage (ampicillin)
 Surgery on infected skin or muscle
o S. aureus coverage (ie vancomycin)
 Surgical placement of prosthetic cardiac material
o S. aureus coverage (vanc)
Prolonged QTc: >450 msec in men, >470msec in women.
 Long QT syndrome (LQTS) can be acquired or congenital.
 Acquired LQTS: Electrolyte abnormalities (↓Mg, ↓K) and drug therapy (fluoroquinolones, antipsychotics).
 LQTS is associated with ↑risk TdP (polymorphic VT).
o Episodes can terminate spontaneously or deteriorate to VF. Symptoms include palpitations, presyncope or syncope, seizure,
and SCD.
 If patients are not in TdP, Prolonged QTC can be asymptomatic.

Cardiac tamponade can cause syncope

 previous radiation therapy (ie. lymphoma treatment) can lead to chronic pericarditis and associated pericardial effusion. Excessive
accumulation of pericardial fluid leads to increase in intrapericardial hydrostatic pressure and compression of Right sided heart
chambers. VR to RA (occurs primarily during ventricular systole and early diastole), is severely compromised by the resultant increase
in RA and RV pressures. Hypotension and syncope can result due to decreased CO.
 Subacute cardiac tamponade: progressive fatigue or dyspnea, classic triad of hypotension, distant heart sounds, and JVD.
 Electrical alternans are due to changes in ventricular axis as heart moves within excessive fluid in pericardial space.
o poor sensitivity, high specificity for cardiac tamponade.

White coat hypertension is managed by ambulatory BP monitoring. Situational hypertension may not be totally benign and can have increased
cardiovascular risks.

HTN with no evidence of target organ damage

 Lifestyle modification and monitoring for up to 1 year.
 If BP increases or does not normalize, or evidence of target organ damage occurs or with high risk comorbidity, start
antihypertensives.

Management of STEMI- SOAPBAN

 S: Statin ASAP
 O: Oxygen for SaO2 >90%
 A: antiplatlet (ASA + clopidogrel/prasugrel/ticagrelor
 P: PCI promptly (within 90 mins)
 B: Betablockers- CI in heart failure, ? risk of cardiogenic shock, bradycardia
 A: Anticoagulation (Unfractionated heparin, LMWH, or bivalirudin
 N: Nitrates (caution with hypotension, RV infarction, or severe AS)

Atrial Flutter
 irregular rhythm (appears regular at high ventricular rates).
 Atrial rate 300/min w/ ventricular rates of 150/100/75 (2:1/3:1/4:).
 Treatment: Cardioversion (pharmacologic or electrical), or cardiac ablation.
 Risk of systemic thromboembolism is similar to that of a-fib, and acutely increases with delivery of therapy. If new a-flut (duration
unknown or >48h) need >3 weeks of anti-coagulation prior to cardioversion or ablation. Can use warfarin, oral factor Xa inhibitors
(apixaban, rivaroxaban), or oral direct thrombin inhibitor (dabigatran)
 IV Ibutilide (class III antiarrhythmic) is approved for chemical cardioversion of a-fib/flut, requires inpatient monitoring 2/2
prolongation of QTc/ risk of Tdp.
 Amiodarone can be used for rhythm control in a-fib/flutter patients but can also trigger cardioversion and so cant be used w/o 3wks
Anti-coag.
 Syncronized electrical cardioversion can be done w/o anti-coag in pts with low thromboelbolic risk AND <48h A-flut

Kawasaki Disease- vasculitis of medium arteries
 Diagnostic criteria: Fever for >5 day & 4 or more:
 Conjunctivitis: b/l, nonexudative
 Mucositis: infected/ fissured lips/ pharynx, strawberry tongue
 Cervical LND: at least 1 LN >1.5cm in diameter
 Rash: Erytheramatous, polymorphous, generalized; preineal erythema & desqumation; morbilliform (trunk, extremities)
 Erythema & edema of hands/ feet
 Tx; ASA + IVIG, Echocardiography
 Complications: coronary artery aneurysms, Myocardial infarction/ ischemia
 Some patients (especially infants less than 6mos) have incomplete (atypical) KD. They fulfill 3 or less criteria but have elevated
inflammatory markers (ESR, CRP) and other supporting laboratory criteria (leukocytosis, thrombocytosis, anemia, hypoalbuminemia,
elevated LFTs, bilirubin, sterile pyuria) reflecting multisystem inflammation. management does not change.

Medicine- Dermatology
Furuncles and Carbuncles
 subcutaneous abscesses involving hair follicles. MCC by S. aureus (MRSA, even in thouse with no hx of healthcare-related exposures).
 If no systemic signs (more common with carbulcles), start MRSA Abx (clindamycin, Bactrim, Doxycycline) and I&D at this time.

Erythema multiforme:
 multitude of symmetric targetoid skin lesion on extensor surfaces of extremities, palms, sole.
 MCC 1-HSV, 2-Medications

Herpes Zoster
 Dissemination of herpes zoster only happens in setting of immunocompromise.
 VZV vaccine is effective in preventing herpes zoster in patients 60 & older.
Post herpetic neuralgia
 Most common complication; persistent pain in distribution of vesicular eruption that lasts 3 or 4 months or more following resolution
of rash.
 Increased risk in older patients who experience severe pain during the prodrome or active phase or the
 eruptions.
 Treatment:
 Should be initiated within 2 hours of rash onset with goal to decrease risk of post herpetic neuralgia and
 promote more rapid healing of vesicular eruption.
 Has not been shown to prevent recurrent episodes.

 Administration of glucocorticoids along with early antiviral therapy may decrease acute pain of herpes zoster but has no effect on
severity or duration of post herpetic neuralgia.
 Immunocompromised state increase risk of recurrence.

Acne Vulgaris
 Comedonal acne: closed or open comedones on forehead, nose & chin that may progress to inflammatory pustules or nodules.
o Treat with topical retinoids (salicylic, azelaic, or gylcolic acid
 Inflammatory acne: inflamed papules(<5mm) & pustules, erythema.
o Mild: topical retinoids + benzuol peroxicide
o Moderate: Add topical Abx
o Severe: Add oral Abx
 Nodular (cystic) acne: large( >5mm) nodules that can appear cystic. noduels can merge to form sinus tracts with possible scarring.
o Moderate; topical retinoid + benxoyl perozide + topical Abx Severe: add oral Abx
o Unresponsive severe: Oral isotretinonin (reduces sebum excretion)
 Oral Abx are also considered when acne is widespread topical abx are impractical.
 Common Abx options include Tetracyclines (tetracycline, doxycycline, minocycline), macrolides, and bactrim.
 Spironolactone can be useful or women with acne related to meustral cycle or associated with hirsutism. Not recommended in men
due to anti-androgeniceffects

Lichen Planus
 well defined lesions usually on flexor surgaces of extremities, mucous membranes, and genetials.
 4Ps: pruritic, planar, polygonal, purple.
 Tx with topical corticosteroids. Antihistamines help control the severe itching.

 Scabies- intensely itchy rash in characteristic distribution (including web-spaces of hands).

o Treatment consists of one topical application of permethrin cream from neck to the soles of the feet, which is washed off
after 8-14 hours.

Medicine- Endocrine, Diabetes, & Metabolism

Myopathies and ESR/CK
 Normal ESR, Normal CK
o Glucocortocoid induced myopathy: progressive proximal muscle weakness & atrophy NO pain or tenderness
 ↑ESR, Normal CK
o Polymyalgia rheumatica: muscle pain & stiffness in shoulder and pevic girdle. + tenderness w/ ?ROM at shoulder, neck, hip.
Responds rapidly to glucocorticoids
 ↑ESR, ↑CK
o Inflammatory mypoathies: puscle pain, tenderness, & proximal muscle weakness. Skin rash and inflammaotyr arthritis may be
present.
 Normal ESR, ↑ CK
o Statin-induced: muscle tenderness/pain. Rare rhabdo
o Hypothyroid myopathy: delayed DTS, myoedema, occasional rhabdo, present featuresof hypothyroidism
Thyroiditis:
 Chronic autoimmune (hashimoto's) thyroiditis: predominantly hypothyroid features, with a diffuse goiter.
o dx: positive TPO Ab, variable RAIU uptake.
 Painless (silent) thyroiditis- Mild, brief hyperthyroid phase,
o Variant of Hashimoto's.
o Small, non-tender goiter, Spontaneous recovery
o dx: positive TPO Ab, low RAIU
 Subacute (de Quervain) thyroiditis- prominent fever and hyperthyroid symptoms
o likely post-viral inflammatory process, painful/tender goiter
o dx: elevated ESR & CRP, low RAIU
o tx: NSAIDs, +glucocortocoids for persistent sx
 Anti-thyroid drugs (methimazole) inhibit synthesis of thyroid hormone and are not effective in thyroiditis, which causes release of
preformed hormone. They can be used with Graves (typically associated with ophthalmopathy and positive thyrotropin Ab), and
nodular thyroid disease.

 Postpartum thyroiditis-
 Autoimmune inflammation of thyroid follicles and preformed thyroid hormone (similar to silent thyroiditis but by definition occurs
within 1 year of pregnancy. Both are variants of Hashimoto's (classic chronic lymphocytic) thyroiditis
 MC in women with preexisting autoimmune thyroid d/o or other autoimmune endocrinopathies, and may recur with subsequent
pregnancy.
 It follows a tri-phasic course.
o hyperthyroid phase (1-3 mos)
o hypothyroidsm (4-6 mos)->
o euthyroid state (within 1 year)
 20-40% of patients (w/ a more severe initial hypothyroid phase or a high titer anti-TPO Abs) may develop persistent or recurrent
hypothyroidism with a palpable goiter similar to Hashimoto. Counsel pts with PT about hypothyroid sxs. Consider annual TSH level.
 Beta blockers are excreted in breast milk in small amounts; however, can be given to manage sxs of hyperthroidism with close
monitoring of baby.

Adrenal Adenomas
 the majority are nonfunctional (incidentaloma)
 the finding of an adrenal mass, decreased ACTH, and elevated cortisol suggests a functional adrenal adenoma (~15%). MC are cortisol
secreting, and result in features of Cusing's syndrome).
 In the presence of the hyperfunctioning adenoma, the CRH and ACTH levels are supresed (negative feedback inhibition). the rest of
the adrenal cortex (responsible for cortisol production) atrophies due to not being stimulated by trophic hormones. Because of this,
these patients need stress-dose corticosteroids in order to prevent and treat adrenal crisis.
 Slight elevations in plasma fractioned metanephrines measurements are not reliable unless the clinical suspicion of
pheochromocytomais high)
 Pts with pituitary apoplexy can have adrenal crisis but also c/o headache and visual chagnges.

In episodes of recurrent Bedtime hyperglycemia, Increase predinner insulin lispro dose. Because of its rapid onset and short half-life, it won’t
cause nocturnal hypoglycemia.

Primary Hyperparythyroidism (PHPT)

 dx: hypercalcemia with elevated PTH

 Etiology: parathyroid adenoma (MC), hyperplasia, carcinoma. Increased risk in MEN 1 & 2A

 Sxs: Asymptomatic (MC)/ nonspecific symtoms (fatigue and constipation). Stones, moans, psychriatic moans
 Indications for parathyroidectomy:

o Age less than 50- likely to develope complications later in life, symptomatic hypercalcemia (stones)
o Complications: osteoporosis with T-score <-2.5, fragility fracture, nephrolithiasis/calcinosis, CKD (GFR <60ml/min

 Elevated risk for complications: Calcium >1g/dl above ULN, urinary calcium excretion >400mg/day

 In patients older than 50 with asymptomatic hypercalcemia and no complication of PHPT, regular follow-up with serum calcium, Cr,
and DXA (PHPT affects cortical bone and DXA of the radius should be included)

 Foot ulcers: Common in diabetics due to diabetic neuropathy and peripheral arterial disease. Neuropathy-related ulcers tend to affect
pressure points. Arterial insufficiency ulcers tend to affect the distal extremities. Tight glycemic control is the best method in
preventing foot ulcers in diabetics

 Menopausal hormone therapy (MHT) is most effective treatment for menustral hot flashes.

 Effects of combination ER/PR MHT

o Beneficial:

 Menopausal symptoms, bone mass/ fractures, colon cancer, T2DM, All-cause mortality (Age <60)
o Detrimental

 VTE, Coronary heart disease (age >60), Sgroke, gallbladder disease

o Neutral:

 cognition/dementia, endometrial cancer (increased with unopposed ER, ovarian cnacer, allcause mortality (age =60)

 MHT can be safely used for a short period of time (3-5 years) in younger, low risk women
 CI include established coronary heart disease, active liver disease, Hx breast cancer, VTE, or stroke.

 Initial assessment of obesity

 History: Back pain, OA, ASCVD, OSA?

 Biometrics: HR, BP, Weight, Waist circumference

 Labs: Glucose (or A1c), TSH, lipids, Hepatic enzymes


 Management of obesity
 Lifestyle
o physical activity =20-30mins/day, 5-7 days/week, diet low in calories (1500/day, and fat (33g/day), decreased food portion
size.
 If lifestyle changes result in failure to lose weight AND BMI =30 or =27-29 + comorbidity, go to pharmacologic management

 Drug treatment options:

o Orlistat: 1st-line. inhibits pancreatic lipase ? decreased fat absorption. Assn w/ GI effects.

o Phentermine- sympathomometic that provides rapid, short-term weight loss. Monotherapy is associated with significant re-
gain and little long-term benefity, so is given with topirimate as phenylteramine/topiramate
o Lorcaserin: reduces appetite by activating 5-HT2C receptor in hypothalms

o Buproprion/naltrexone
o Liraglutide
 Failure to lose weight AND BMI =40 (or =35 + comorbidity), consider bariatric surgery

 In men, prolactinomas can cause impotence, ED, galactorrhea, and bitemporal Hemianopsia. Diagnosis is confirmed with an elevated
prolactin level and MRI brain revealing a pituitary mass. Initial treatment consists of a dopamine agonist such as bromocriptine or
carbegoline, regardless of tumor size or severity of neurologic symptoms. In over 90% of patients, pharmacologic management
decreases prolactin secretion and reduces the size of the mass. Surgery should be reserved for patients
 Patient with irregular menses: Pelvic US to evaluate for endometrial thickness, myometrial abnormalities, and ovarian
structure/development.
 PCOS: 2 of 3: Oligomenorrhea, hyperandrogenism, polycystic ovaries on US.
 Other findings (acanthosis nigrans, b/l enlarged ovaries). Hyperandrogenism (2/2 steroid overproduction) can be diagnosed clinically
(hirsutism, acne) or biochemically with elevated T levels.
o Pelvic US shows multiple peripheral follicles in ovary with increased ovarian volume (pearl string). Anovulation is due to
imbalanced FSH/LH ratio; however, levels are typically normal and nondiagnostic.
 Comorbidites: Metabolic syndrome, OSA, NASH, Endometrial hyperplasia/ cancer
 Treatment: Weight loss (1st line)/ OCPS (menstrual regulation, reduce signs of hyperandrogenism) / Clomiphene citrate (induce
ovulation).
 Ovarian failure (menopause, primary ovarian insufficiency): presents with secondary amenorrhea, hypoestronism (vaginal atrophy),
not irregular menses. FSH is elevated.


 Abnormal Uterine Bleeding
  Uterine fibroids cause heavy, regular bleeding. Irregular or intermenstrual bleeding suggests other pathology.
 Endometrial hyperplasia/ cancer: Rfs include obesity, chronic anovulation/ PCOS, nulliparity, early meanrche/late menopause,
Tamoxifen use.

 Present as heavy, prolonged intermenstrual &/or postmenopausal bleeding.

 Dx with Endometrial Bx (gold standard). Pelvic US for postmenopausal women


 Inflamaotry breast cancer:

 Diagnosis requires a core biopsy and histopathologic demonstration of tumor invasion of the dermal lymphatics.

 axillary adenopathy, pea d'orange, and nipple involvement (eryhema, crusting, retraction)

 Vulvovaginal atrophy

 Presentation: MCC Menopause/postpartum (2/2 breastfeeding- suppresses ovulation resulting in low ER levels, but breastfeeding
should NOT be discontinued)

 Symptoms: dryness/ irritation/pruritis, dyspareunia, vaginal bleeding, urinary incontinence, recurrent UTIs, pelvic pressure

 Physical Exam: Narrowed introitus, pale mucosa, Decreased elasticity and rugae, petechiae, fissures, loss of labial volume, decreased
pubic hair, elevated pH (>5) of vaginal discharge.

 Treatment: 1st-line: Vaginal moisturizer and lube. If no improvement, topical vaginal estrogen

 Bacterial Vaginosis: pH >4.5

 Vaginal candidiasis; Normal pH (4-4.5)


 PCOS: increased risk of T2DM. Screening with OGTT is recommended.

 Serum DHEA- produced in adrenal glands. Elevated levels (i.e. adrenal tumor) results in frank virilization rather an hyperandrogenism.

 Elevated 17-hydroxyprogesterone is characteristic of late-onset non-classical Congenital Adrenal Hyperplasia (CAH), which can present
with oligomennorhea. Virilization is seen

 Virilization: deepening of voice, clitoromegaly, male pattern baldness

 Hyperandrogenism: hirsutism, acne.

 Low dose Dexamethasone suppression test: Screen for Cushing’s syndrome, which can present with obesity and menstural
irregularities. However, patients have additional features (plethora, round face, ecchymoses, abdominal striae)

 Plasma aldosterone-renin ratio: evaluate primary hyperaldosteronism (HTN, hypokalemia, metabolic alkalosis)

 Palpable breast mass
 Age >/=30: Initial exam is diagnostic Mammography.

o If mammography reveals a benign or intermediate lesion, US is performed to further characterize mass to determine whether
bx is indicated

o If mammography shows lesion concerning for malignancy (spiculations, calcifications), US is not required
 by core needle bx is immediately performed.
 Age <30: US +/- mammography
o Simple cyst -> needle aspiration (if patient desires)
o Complex cyst/ mass (solid mass) -> Image-guided core bx
 An excisional bx is indicated when a core needle bx cannot be performed, a cyst does not resolve with FNA, or when a core needle bx
reveals indeterminate or atypical results (LCIS, atypical hyperplasia)

Gastrointestinal and Nutrition
 Anticoagulated patents that develop serious bleeding require promote and rapid reversal of the anticoagulation.
 If taking warfarin, d/c warfarin and give 10mg Vitamin K via slow IV infusion. 2 to 3 units of FFP can be given at set intervals if clinically
indicated.

 INR should be closely monitored, additional Vitamin K or FFP can be given if it remains elevated.

 PO vitamin K can be given if elevated INR but no active severe bleed.


 Femoral Hernia- Pass inferior to inguinal ligament and lie MEDIAL to femoral N, A, V.

o MC in elderly women. Higher risk of strangulation and incarceration (as compared to inguinal hernias).
 Inguinal hernias- pass above inguinal ligament

o Indirect Inguinal hernia- pass into inguinal ring and can descend into scrotum
 Obturator hernia- pass through obturator foramen

 Hereditary Hemochromatosis- AR, Fe deposition into tissue leading to multisystem organ damage.
o Skin: hyperpigmentation
o MSK: arthralgia, arthropathy and chondrocalcinosis
o GI: ↑LFTs w/ hepat& ?omegaly ? cirrhosis and ?risk HCC
o Endo: DM, Secondary hypogonadism & hypothyroidism
o Cardiac: Restrictive or dilated cardiomyopathy & conduction abnromalities
o ID: ↑ susceptibility to Listeria, Vibrio vulnificus, Yersinia
o Manifests clinicaly in 4th to 6th decade of life
o Initial Eval: Fe studeis (↑Fe, ferritin, transferrin saturation.

o Confirm dx by genetic testing for hemochromatosis associated mutations (I.E> HFE). Liver bx can be useful to stage the extent
of liver involvement.


 Anal cancer associated with HIV infection, and is due to HPV. High risk of anal cancer in MSM, genital warts, hx receptive anal
intercourse

 Intussusception: intermittent bouts of severe abdominal pain with inconsolable crying, ± vomiting with normal behavior in between
episodes. Dark stools suggest bowel ischemia.
 Dx and Rx is air or saline contrast enema under imaging after vitals are stabilized.

 Medication induced esophagitis

 Doxycycline, NSAIDS< KCL< Bisphosphonates get stuck in esophagus and cause localized chemical burn to esophageal mucosa (Most
commonly at level of aortic arch due to esophageal comprssion by the aorta.

 Doxycycline causes injury by becoming highly acidic (pH <3) in the presence of water.

 Chest pain w. odynophagia leading to dysphagia.

 discontinue culprit drug.


 Hematochezia- due to LGIB or brisk UGIB. Findings suggestive of UGIB are hemodynamic compromise, orthostasis, and Bun:Cr >20:1. If
bleeding source is unclear, NG lavage with aspiration of bile and absence of blood increases the likelihood of LGIB (but does not exclude
distal UGIB)

 If LGIB is suspected for hematochezia: need to do bowel prep for colonoscopy. If normal c-scope, do EGD.

 If EGD is normal, evaluation for obscure sources of GI bleeding should be considered.

 Hemodynamically stable patient with normal C-scope, normal EGD: videocapsue endoscopy

 Hemodynamically unstable patient with normal C-scope and EGD->angiography or nuclear medicine test (tagged RBC) with radioactive
tracer is considered, but require active blood loss for visualization of bleeding sites.

 Foreign body ingestion

 2-view neck and CXR (PA and lateral) confirms location and distinguishes between coin (MC, homegenous object with sharp. crisp
edge), and battery (double ring sign)
 can be asymptomatic or have dysphagia/ odynophagia/ gagging/ vomiting/ drooling/ chest pain.
 Management:
o Ingestion time <24h AND asymptomatic: observe, repeat xray in 12-24h to ensure passage beyond pylorus.
o Ingestion time >24h/unknown duration OR symptomatic: Endoscopic coin removal

 Complications: Esophageal erosion, perforation, stricture, fistula

 Emergent bronchoscopy is appropriate for airway foriegn body causing respiratory compromise (stridor, wheezing, respiratory
distress.

 An esophageal coin appears liner on lateral X-ray. A tracheal coin appears linear in PA view

 Acute Pancreatitis:

 Oral nutrition should be initiated as soon as patient have. Otherwise, in severe cases, enteral nutrition support should be pursued via
a NJ or NG feeding tube within 72 hrs of hospitalization.

 Benefits of oral/enteral feeding are reduced mortality, organ failure, infection rate, and need for surgery. Mechanism involves
improved intestinal barrier due to stimulation of gut immune system and reduced bacterial translocation (and consequently, reduced
bacterial infection of the inflamed pancreas). It also reduces need for placement of CVCs and associated complications

 A liver mass in patient with HepB and evidence of chronic liver disease is highly concerning for HCC, a tumor that originates from
hepatocytes (liver parenchyma). AFP can be elevated or normal in 40% of cases.


 Chonal atresia

 unilateral is MC. chronic nasal discharge in childhood.

 Bilateral: noisy breathing (stertor), cyanosis that worsens with feeding, improves with crying

 if suspected an attempt should be made to pass a small catheters via each nostril into pharynx. Failure to pass is highly suggestive and
requires a CT scan for confirmation.
 Tx: oral airway, surgical repair

 Tracheoesophageal fistula (TEF)

 increased secretions or coughing, choking, and respiratory distress after feeding.

 if suspected, attempted insertion of a gastric catheter followed by CXR is first step in determining whether esophageus is patent. If it
ends in the esophageal pouch  esophgeal atresia.

 H-type TEF (fully developed treache and esophagus with distal connection) is diagnosed with upper GI series.

 Primary Sclerosing Cholangitis is a common condition seen in patients with UC, and causes a cholestatic pattern of laboratory
abnormalities, including elevated bilirubin and ALP.

 Dx is confirmed with ERCP showing multifocal strictures and dilatations of the intra- and extrahepatic bile ducts.

 Initially, patients are usually asymptomatic, and disease is often detected initially by lab abnormalities. If symptoms do occur, fatigue
and pruritis are most common

 Liver bx is no good; can’t distinguish between PSC and PHC, for example.

 Chron’s disease
 Fistulas (communications b/w 2 epithelial lined organs) can develop when transmural inflammation penetrates through the serosal
layer of the bowel wall.

 Enterovesial fistula: recurrent UTI due to gut pathogens or


 In children, inguinal hernias present with an asymptomatic, reducible groin mass that is more pronounced with maneuvers increasing
intra-abdominal pressure. Prompt surgical correction is required in all children with inguinal hernias to avoid potential serious
complications like strangulation and incarceration.

 In children with an undescended testicle, wait until 6 months of age before definitive treatment because the affected testicle may
descend spontaneously.

 Hernias (i.e. incarcerated) are second MCC SBO. Surgical intervention is required due to risk of strangulation


 the single greatest RF for development of pancreatic adenocarcinoma is cigarette smoking. Cessation dramatically reduces risk of
pancreatic cancer.


 Hirschsprung:

 Diagnose with rectal suction biopsy, demonstrating absence of ganglion cells from affected segment and nerve fiber hypertrophy.


 A retroperitoneal hemorrhage is a rare, potentially life-threatening condition associated with the use if anticoagulation, and patients
on Warfarin are at risk even if their INR is within the therapeutic range. If suspected  CT abdomen.
 patients c/o LUQ pain or back pain.
o (+)Psoas sign- pain that worsens with active flexion fo the thigh at the hip.


 Umbilical hernia:

 common congenital defect due to incomplete closure of the abdominal wall at birth, resulting in a gap at the umbilical fascial ring. It
typically closes spontaneously during first few years of life, but may take longer to close if the budge is >1.5cm, or if the patient is African
American.

 If the hernia is reducible, asymptomatic, and not enlarging, surgical correction can be deferred until age 5. As the size of the
abdominal wall defect is relatively large, the risk of bowel incarceration or strangulation is low.

 Though they are usually isolated findings, they can also occur with patients with underlying medical conditions such as hypothyroidism
(lethargy, poor feeding, dry skin), and beckwith-Wieldemann syndrome (hypoglycemia, macrosomia, macroglossia, hemihyperplasia).

 Emergent surgery if evidence of incarceration (irreducible hernia), or strangulation (ischemia from incarcerated bowel).


 Hematology and Oncology
 If AAA is secondary to atherosclerosis, smoking cessation is important as it decreases rate of aneurysmal growth.
 For aneurysms 3.0-4.0 cm, annual screening every 2-3 years is recommended.

 AAA typically don’t rupture unless >5cm diameter


 Unprovoked DVT young patient: consider inherited hypercoagulable condition.

o MCC inherited thrombophilia is Factor V Leiden, the presence of which results in resistance to the antithrombic effects of
protein C.
o Prothrombin gene mutation (G20210A) is a common cause of inherited thrombophilia, but does not result in increased levels
of thrombin,
o Protein S deficiency and Antithrombin III deficiency are rare causes of inherited thrombophilia.

 Microcytic Anemias
 Iron deficiency: ↓Fe, Ferritin, ↑TIBC
 Thalassemias:

 Defective production of alpha or beta hemoglobin chains. Severity depends on proportion of normal to abnormal alleles and
symptoms range from fetal demise to asymptomatic disease diagnosed incidentally in adulthood.
 Mild cases (beta-thalassemia minor and alpha-thalassemia trait) display hypochromic microcytic anemia with normal RBC count and
RDW. Marked hypochromia of RBCs is out of proportion to mild anemia. PBS shows target cells and nucleated RBCs. Iron studies show
normal/ ↑ Fe and ferritin (2/2 RBC turnover)
 a-thalassemia minor- normal Hgb electrophoresis

 ß-thalassemia minor- ↑Hgb A2 on electrophoresis


 Multiple Myeloma

 normocytic normochromic anemia, hypercalcemia, mild renal insufficiency, and chronic low backpain.
 pneumonia occurs at increased frequency in patients with MM secondary to impaired lymphocyte function and
hypogammaglobulinemia.
 neoplastic proliferation of plamsa cells in the bone marrow cause only destruction and pathologuc fractures that cause back pain,
which can manifest as chronic back pain.

 Diagnosis is confirmed by finding monoclonal protein in serum and/or urine (usually measured by either a serum or 24-hr urine
protein electrophoresis.

 Coagulation Cascade- Intrinsic pathway disorders

 (normal PT, prolonged aPTT) seen in:

o Hemophilia A, B
o von Willebrand disease: vWF is synthesized in endothelial cells and dysfunction of endothelial cells leads to von Willebrand
disease.
o Acquired coagulation factor inhibitors-(Antiphospholipid Abs [cause thrombosis], and inhibitors of factors VIII, IX, and XI)
 "acquired hemophilia"-(Ab to Factor VIII) can occur independently or in association with malignancy, pregnancy, lymphoproliferative
disorders, or rheumatic disease.
o In a patient with an increased aPTT who develop severe bleeding episode with no prior history o f bleeding, a factory VIII
inhibitor ('acquired hemophilia') is the most likely diagnosis.


 Polycythemia Vera (PV)

 a chronic myelodysplastic disorder characterized by elevated RBC mass.

 Majority of pts w/ PV have elevations of all 3 major cell lines.
 Consider if pt presents w/ abnormal thrombotic event and splenomegaly in the presence of elevated RBC mass
 Dx with genetic mutation analysis demonstrating JAK2 mutation.
o Historic criteria are LAP score and elevated serum B12 binding capacity,but are nor sensitive or specific.

 Secondary Polycythemia needs to be ruled out.

o O2 sat% is normal, EPO is low in PV.

o O2 sat% is decreased, EPO is high in secondary polycythemia.

 Lysosomal storage diseases

 Gaucher disease: Most common. AR, deficiency of glucocerebrosidase resulting in accumulation of glycolipid within lysosome.

 Clinical findings: HSMG, anemia, thrombocytopenia, osteopenia, bone pain, and pathologic fractures (2/2 minor trauma).

 Dx by mutation analysis or demonstrating decreased glucocerebrosidase levels in leukocytes.

 Glycogen storage disease: abnormal glycogen metabolism resulting in hypoglycemia, hepatic dysfunction, and skeletal muscle
disorders.
  Amino acid disorders: affected become acutely ill after protein feeding in early childhood or demonstrated developmental delay or
regression later in childhood. I.E. Maple syrup urine disease, phenylketonuria).

 Nucleotide metabolism disorders: Lesych-Nyhan, gout, Adenosime deaminase deficiency


Infectious Diseass
 Enterohemorrhagic E. coli (EHEC) infection
 bloody diarrhea, abdominal pain/tenderness, hyperactive bowel sounds, NO fever.

 exposure to animals (farms, petting zoos) or ingestion of undercooked beef (ingestion of very few organisms can cause disease).

 Variable inoculation, symptoms can occur up to 10 days after exposure.

 Dx made either by stool culture using sorbitol-MacConkey agar or by finding Shiga toxins in stool using DNA probes.

 Management is supportive with spontaneous resolution in 7-10 days after disease onset in absence of HUS
 Avoid Abx as they increase risk of HUS (ARF, MAHA, thrombocytopenia)

 Norovirus- viral gastroenteritis in school aged kids or cruise ships. Emesis with watery (non-bloody) diarrhea 1-2 days after an infected
contact.

 S. aureus: rapid onset (horrs rather than days), prominent emesis, profuse watery (non-bloody) diarrhea.

 Shigella- bloody diarrhea, +FEVER, cramps. contracted via contaminated food or water

 ICU patients with indwelling Foley or recent Abx treatments have high risk for candiduric. Most cases are due to colonization rather
than active infection, but infection should be suspected if:
o Patient complains of urinary symptoms
o neutropenia on labs
o systemic signs of infection

o if =1 of these findings, will need Fluconazole or Amphotericin B.

o Caspofungin is reserved for invasive, severe, or fluconazole resistant candida infections.

 If zero findings, pts should undergo measures to reduce risk of candida infection, such as removal and replacement of bladder
catheters (to eliminate colonization) or limiting Abx treatments.

 Pretussis: Gram-(-) bacillus transmitted by respiratory droplets.

 3 stages
o Catarrhal (1-2wks): mild cough, rhinitis
o Paroxysomal (2-6wks): cough with inspiratory "whoop", posttussive emesis after paroxysms

o Convalescent (wks to months): gradual resolution of sxs

 Dx: Pretussis culture or PCR, lymphocyte predominant leukocytosis
 Treatment:
o Macrolide for patient and macrolide prophylaxis for all close contacts regardless of vaccination status.
o Close contacts should receive th prtusis vaccination according to the recommended schedule fi they are not already fully
immunized.

o Treatment during catarrhal stage may help shorten disease duration. After catarrhal stage, helps decrease transmission but
will nnot decrease duration.

 Pneumocystis jirovecii is a common cause of PNA in HIV patients with CD4 <200. Indolent onset of fever, dry cough, dyspnea, weight
loss.
 CXR shows diffuse interstitial or alveolar infiltrates.

 First line diagnostic test is sputum induction (with hypertonic saline)- Sensitivity (50-90%) If induced sputum is inconclusive, do
fiberoptic bronchoscopy with BAL (sensitivity 90-100%)


 Vertebral Osteomyelitis
 o S. aureus bacteremia, fever, back pain, inflammatory markers, imaging evidence of contiguous vertebral body destruction
o Pts undergoing HD. catheter are >10x more likely to develop bacteremia than those with AV fistulas.
 MC causes are coagulase negative staph and S. aureus. Both are Gram(+) cocci in clusters, S. aureus is far more likley to cause
vertebral osteomyelitis.
 Pts with radiographic findings c/w vertebral osteomyelitis (contiguous vertebral body destruction with diskitis), and positive blood
cultures with likley pathogen usually do not require CT guided needle biopsy of affected bone for diagnosis.
 However, they do require evaluation for ID with TEE or TTE (esp. if they have hx valvular dz)

 Acute otitis media- bulging and erythematous tympanic membrane, fever.

 MC diagnosed bacterial infection in children.

o Recurrence is common can, (esp in hx of multiple previous AOM episodes, attend day-care, ore exposed to second hand
smoke.
o Recurs in upto 25% of cases.
 If recurrence within 2 weeks, same causative agent. if recurrence occurs after 2 weeks, different bacteria.
 Extension to the mastoids to cause mastoiditis is rare

 if hearing loss happens, it is conductive in nature and due to presence of fluid in the middle ear cavity or due to disruptions in
tympanic membranes.

 Cholestoma: collection of epithelial cells and debris. May form due to injury to TM or inflammation in the setting of chronic suppurative
otitis media or tympanic membrane perforation. Incidence in AOM is very low.


 a protozoa transmitted via ingestion of contaminated food or water.

 Amebic liver abscess is MC manifestation of extra-intestinal disease.

o Risk is greatest in men in 40s/50s with underlying cirrhosis or alcoholic hepatitis.
o Manifestations begin 8-20weeks after inoculation, and include fever, RUQ pain, and nonspecific symptoms.
 Imaging reveals a round, well-defined hypoechoic mass in the right hepatic lobe.

 Diagnosis:
o blood serology and antigen detection.
 Aspiration is not required by is often performed if cyst is large (rupture risk), or if alternate diagnosis requires exclusion. Aspirate
resembles "anchovy paste", is aseptic with negative gram stain.
 Treatment: metronidazole and intraluminal Abx (paromycin)

 Hydatid cysts are caused by the tapeworm Echinococcus granulosus. Cysts grow slowly over years and remain symptomatic until
>10cm. Fever is rare without cyst rupture.


 Candida vulvovaginitis
 not associated with adverse outcomes if it occurs in pregnancy.

 thick, yellow, clumpy, no malodorous discharge and normal vaginal pH (4.0-4.5), with vulvovaginal pruritis.
 Treatment is indicated for symptomatic relief
o 1st line treatments include clotrimazole, miconazole, and nystatin (all safe throughout pregnancy).
 Oral fluconazole use in 1st trimester is associated with risk of spontaneous abortions, congeital defects (cleft palate, femoral bowing,
congenital heart disease) and is ised to treat nonpregnant patietns with candida vulvuvaginitis, and is not pregos.

 Trichomonosiasis: thin, yellow, smelly, basic dischage with vaginal inflammation. treat patient and sexual partner

 Bacterial vaginosis: thin, off-white, fishy, basic discharge iwith no inflammation, and positive whiff test (amine odor with KOH). Tx is
metronidazoleor clindamycin.

 Physiologic leukorrhea- ? Estrogen in pregnancy ? thin, whitem mildly smelly discharge. No pruritis, no treatment needed.

 Patients with moderate to severe PJP infections are at risk for respiratory decompression after initiation of treatment due to rapid
lysis of organisms with rsultant inflammatory response.
 Pts with confirmed PCP who have respiratory distress, tachypnea, and/or hypoxia requrie ABGs.
 o Concomitant corticosteroids are used in pts who meet certain hypoxemic requirements:
 (A-a gradient >35mHg on room air -OR-
 partial pressure O2 <70mmHg.
 In current clinical practice, SpO2 <92% on RA is used to determine need for steroids, but ABG remains standard of
care.


 Diagnostic test of choice for CDI is bacterial toxin detection, typically with PCR. PCR has high sensitivity, and negative PCR is usually not
repeated and indicates no CDI.

 C. diff infection (CDI) can range from mild watery diarrhea to fulminant colitis with toxic megacolon. Mild colitis presents as watery
diarrhea (sometimes up to 10-15x/day), low grade fever, abdominal pain, leukocytosis.

 Severe CDI may not have profuse diarrhea but will have signs fo systemic toxicity such as high fever, WBC >15,000, and serum Cr >1.5x
baseline.


 human bite wounds should never be sutured close and IV Abx are required if frank infection is present.
o Treatment of choice is Augmentin
 Normal human mouth flora:

o Aerobes (staph, strep, Eikenella)

o Anaerobes (prevotella, fusobacterium)


 Disseminated Gonococcal Infection (DGI)
 presents as either purulent monoarthritis or a triad of:

o Tenosynovitis: typically involving distal extremities

o Dermatitis: isolated pustules/ papules (on hands and feet)

o Polyarthralgia: asymmetric, migratory joint pain

 primary infection is in GU, pharyngeal, or rectal mucosa, but is usually silent and follow by acute fevers, chills, and malaise.
 RFs include recent menses, pregnancy or postpartum state, complement deficiency, and SLE

 If DGI is suspected: Nucleic acid amplificaiton test of urine and suspected primary infection sites (vagina, pharynx), synovial fluid
analysis, blood cultures.

 Treatment:
o IV Ceftriaxone q24h + 1 dose of azithromycin (to cover possible Abx resistant gonococacal strains and possible co-infection
with Chlamydia)
 Anti-Streptococcal (i.e. anti-streptolysin O) titers are used in the evaluation of acute rheumatic fever.

 TNFi are used to treat inflammatory disorders such as RA, psoriasis, Chron’s disease. Patients on TNFis are at serious risk of infection.
Prior to TNFi initiation, they need to be screened for TB.
 Risks of TNFi are: injection site/ infusion reaction, Neutropenia, serious infections, demyelinating diseases, Heart failure, cutaneous
reactions, malignancy, Autoimmune reactions.
 S. aureus can cause a necrotizing pneumonia.

 Recurrent cellulitis is typically associated with dermatophyte infections, lymphedema, or chronic venous insufficiency.

 Dermatophyte infections are more common in those with previous saphenous venectomy (i.e. Hx CABG).

 Tenia pedis: scaling, fissuring between toes. Tinea unguium (thickened, yellow nail)

 Daily suppressive Abx are sometimes given to patients with recurrent cellulitis due to recalcitrant underlying conditions (lymphedema
or severe venous insufficiency)


 Zoster Vaccination (Live, attenuated Vaccine)
  Indication: Adults >60 (ACIP), Adults >50 (FDA)
 Contraindications:
o Congenital or acquired immunodeficiency
o HIV/AIDS w/ CD4 <200
o Immunosuppressive or immunomodulating therapy -(prednisone, infliximab)
o Cancer treatment with radiation or chemotherapy
 History of solid organ transplant

 Women who are or may be pregnant

 PPSV23; Adults younger than 65 who have chronic heart, lung, or liver disease, diabetics, or those who currently smoke or abuse
alcohol.

 At 65yo, they should get 13-valent pneumococcal congujated vaccine, f/b revaccination with PPSV23

 Meningococcal Vaccination: age 11-12 with a booster at age 16-21. Primary vaccination can also be given at any age to adults at
increased risk for meningococcal disease (i.e. asplenia, travel to endemic environments)

 HepB: Pts with chronic liver dz, and adults in certain high-risk groups (MSM, IVDU, health care workers)

 HiB: age <5 (begining at 2mos)


Male Reproductive System
 Men with a history of prostate cancer treated with prostatectomy typically undergo surveillance with serial PSA measurements as
there is evidence that early detection of recurrence of prostate cancer improves survival, with androgen ablation therapies used for
systemic recurrence and adjunctive radiotherapy for local recurrences.
 PSA should be close to 0 following prostatectomy. Increases are abnormal. If a rise is detected, imaging studies such as US, bone scan,
MRI, or CT can be used to detect the site of recurrence.

 Patients with prostate cancer require risk stratification with DRE, PSA level, and prostate bx with Gleason score to help determine
appropriate treatment.

 Very low risk (and many low risk) prostate cancer should receive initial treatment with active surveillance rather than definitive
therapy (eg radical prostatectomy, radiotherapy).

 Active surveillance includes monitoring serum PSA every 3-6 months, having a DRE yearly, and having repeat prostate biopsy at the end
of year 1 to ensure that high grade disease was not missed on the original biopsy.

 Acute urinary retention can be caused by sympathomimetic and anticholinergic medications in post-op patients and in those with
bladder outlet obstruction (BPH). Treat with prompt bladder decompresion (with urethral or suprapubic catheter) and remove offending
medications.


 Varicocele- tortuous dilation in pampiniform plexus surrounding spermatic cord and testes. Soft irregular mass that ↑ in size w/
standing & Valsalva. Can cause ↑scrotal temp, increasing risk for infertility and testicular atrophy.
 confirm dx w/ US: retrograde venous flow and dilation of pampiniform plexus.

 MC on left side (Left spermatic v. drains into L renal v. which then passes between SMA and Aorta. Compression beneath SMA
("nutcracker effect") can lead to increased pressure in spermatic vein and venous dilation.

 R sided varicocele can be sign of malignant compression (RCC) and warrants CT imagining.

 Hydrocele: collection of peritoneal fluid b/w layers of tunica vaginalis and presents as a cystic scrotal mass.


 Most young and middle aged men with acute UTI symptoms have acute prostatitis rather than a UTI with cystitis. Dx with DRE
demonstrating a warm, edematous and very tender prostate. Empiric Abx with either Bactrim or fluoroquinolones for 6 weeks.


  PEG tubes for enteral feedings has not demonstrated any survival benefit in patients with "advanced dementia" when compared to
patients with similar degree of dementia who were not tube fed.
 Appropriate goals of PEG tube in patients with advanced dementia are to provide comfort through hydration, nutrition, and access for
medication delivery.
 PEG tubes may lower risk of aspiration than enteral feedings but do not necessarily prevent aspiration PNA.
 PEG tubes have no significant affect in management of pressure ulcers.
 Liquid diet carries high risk of aspiration in patients with severe dyusphagia
Nervous System
 Prior history of cerebral vascular accident is most significant RF for development of recurrent stroke

 Stroke RFs (CHADS2VASc)

o Sex (Men +1)_

o CHF hx (+1)
o History of Stroke/TIA/Thromboembolism hx (+2)
o HTN (+1) Age <65 (0), 65-74 (+1), >74 (+2)
o Diabetes (+1)
o VAScular disease (+1)

 Parkinson Disease:

 A clinical diagnosis requires presence of bradykinesia in addition to either tremor or rigidity. Unilateral onset, persistent asymmetry of
symptoms. A clear response to dopaminergic therapy (levodopa/carvidopa, pramipexole) is supportive of diagnosis.

 Postural instability is a late complication resulting in frequent falls and is not required for diagnosis.

 Parkinson-Plus Syndromes:

 can also present with bradykinesia and rigidity; however, distinguishing features include rapid progression, symmetric motor signs, lack
of tremor, falls early in course of disease, dysautonomia, and poor response to dopaminergic therapy.

o Progressive supranuclear palsy- PPS with vertical gaze palsy and falls 2/2 postural instability. No resting tremor.

o Multisystem Atrophy- more likely presents with orthostatic hypotension than PD


 Focal (partial) Seizure- originate from one cerebral hemisphere, may be 2/2 an underlying structural abnormality (i.e. brain tumor).
 Presentation involves u/l convulsing, writhing, or stiffening. Automatisms (i.e. blinking) and vocalizations (i.e. moaning) can also occur.
o If simple partial, awareness remains intact.
o If complex partial, impaired cognition.
o Aura (unusual taste, smell or sound) can occur and may help determine location of origin Post-ictal period of tiredness often
follows. can have secondary generalization if cross ver to other cerebral hemisphere.

 Neuro exam can have local fundings but a normal neuro exam neither excludes structural abnormality or alerts management.
 MRI is 1st diagnostic step and most sensitive method to eval tumor, structural abnormality, or ischemia. seizures 2/2 brian tumors ahve
high rate of recurrence so antiepileptic therapy is recommended. If MRI normal, consider LP to eval for metabolic or genetic condition.
 Dx w/ MRI, EEG


 Migrans: u/l, throbbing with phonophobia, photophobia, nausea, vomiting. resolve within hours but can last fora day or more.

 Prophylactic medications are recommended for patients with >2 migraine headache days a month to decrease frequency, duration
and intensity.
 MC first line preventative therapies are ß-blockers (metoprolol), TCAs (amitriptyline), and anticonvulsants (Valproate). they are started
at low dose as and slowly titrated up over months


 Guillain-Barre Syndrome
 acute, Immune mediated polyneuropathy 2/2 cross-reacting Abs against peripheral nerve components; often preceded by GI
(campylobacter) or respiratory infection Presentation:
  symmetric muscle weakness (begins in legs), depressed or absent DTRs autonomic dysfunction (arrhythmia, ileus), respiratory
compromise, paresthesias, oropharyngeal, facial, or respiratory muscle weakness.
 Diagnosis:

o largely clinical. CSF with elevated protein & normal leukocyte count, electrodiagnostic findings (EMG)
 Treatment:

o IVIG or plasmapheresis, monitor autonomic and respiratory function

 A sensory level typically indicated a spinal cord lesion (i.e. transverse myelitiits). Pts with spinal lesions often ahve symmetric, b/l
motor weakness and autonomic dysfunction.

 BPPV

 displacement of otoliths in posterior semicircular canals resulting in short episodes of vertigo (under 1 min) after certain head
movements (such as rolling over in bed orlooking up while standing).
 Treatment consists of head positioning exerises, such as the Epley maneuver.


Ophthalmology
 Keratoconjunctivitis sicca (dry eyes)

 C/o dry, gritty eyes, additional symptoms include eye irritation, photophobia, blurry vision (worse at end of day).
 Assn w/ connective tissue diseases (MC Sjogren’s syndrome, or RA, SLE; normal lab values suggest against connective tissue diseases ,
absence of mouth dryness is pertinent negative finding making Sjorgen's syndrome less likely)

 Treatment: 1st like: artificial tears (methylcellulose drops)

 Can consider topical cyclosporine or topical corticosteroids for resistant cases.

 Conjunctivitis

 Allergic:
o always b/l, duration <30mins to perenial, watery discharge, assn w/ ocular pruritis.
o Itching is hallmark.
o Seen in pts with other atopic diseases (asthma, allergic rhinitis- pale nasal mucosa, clear rhinnorhea).
o PEx can show infraorbital darkening dye to vasodilation from sinus congestion.
o Can be acute (new pet), seasonal (pollen) or year round (dust, mold).
o Tx is allergen avoidance and topical therapies (antihistamine, mass cell inhibitors)
 Bacterial:
o u/l or b/l, Duration 1-2 weeks, purulent discharge, assn w/ unremitting ocular discharge
 Viral:
o u/l or b/l. Duration 1-2 weeks. Watery/mucoid discharge. assn w/ viral prodrome.


Poisoning and environmental Exposure

 Lead intoxication

 Severe (>70 mcg/dl): treat with IV dimercaprol and EDTA

 Moderate (45-69 mcg/dl): Treat with oral DMSA (succimer)
 Mild (<44 mcg/dl): no benefit from chelating agents. Educate, notify public health people to further evaluate the environment and
home.
o Blood lead level should be repeated in 1 month.

 Acute Acetaminophen toxicity

 4 stages
o 0-24h- asymptomatic or nonspecific complaints
 o 24-72h- hepatotoxicity
o 72-96h- peak of LFT abnormalities
o 4-14d- recovery period.
 If presentation is within 4hrs of ingestion, activated charcoal is given for gastric decontamination and serum acetaminophen levels are
measured 4 hours after, levels are correlated with time since ingestion on Rumack-Matthwe nomogram to determine if NAC is
required. levels are not drawn before 4 hours after ingestion because are unreliable and poor predictors of toxicity.

 if presentation is 4-24h after ingestion, serum levels are immediately measured and empiric NAC is given while awaiting results.
Prompt administration of NAC is recommended (even in asymptomatic patients, ideally before onset of liver injury, as NAC is highly
effective in preventing hepatotoxicity.

 AST, ALT, BUN, Serum Cr are measured to asses hepatic injury and hepato-renal syndrome.

Pregnancy, Childbirth and Puerperium

 Initial prenatal visit:

 H&P, US (gestational age)

 Rh Type and Ab screen. Rh type determines who will require RhoD Ig at 28 wks gestation and postpartum to prevent
alloimmunization. An Ab screen (coombs test) identifies alloimmunized pts who may be at risk of hemolytic disease of fetus and/or
newborn. These pts may require future monitoring with Ab titers and Serial US.
 Hb/Hct, MCV
 UA and UCx

 serological tests of syphillis, HIV, HepB, rubella, varicella -Nucleic acid amp. test for chlamydia, -Guideline based Pap test
 A baseline 24h urine total protein for pts who are either at risk of developing preeclampsia (renal dz, chronic HTN), or who have >2+
proteinuria.
o This tests establishes a baseline assessment of renal function. -24h urine for total protein is repeated if pt develops HTN.

 If gestational HTN, (no change). If preeclampsia (inc. protein)

 OGCT-24-28wks. If Rfs for undiagnosed T2DM (BMI >30, hx GDM), initial visit.

 An RhD-negative patient with rising anti-RhD titers has already undergone alloimmunization, the development of anti-D antibodies.

 Alloimmunization occurs when an RHD-neg mother had an RhD-Pos fetus and is exposed to RhD antigen on fetal RBCs, eliciting an
immune response.

 The goal of administirng anti-D Ig is to prevenet alloimmunization in the mother by binding of the exposed RhD antigen sites.

 A mother sensitized to the D antigen will have a positive Ab test and positive indirect Coombs test (to determine Ab titer levels), which
screen of hemolytic diseases and fetal anemia
 If pt is already sensitized (positive titer), anti-D Ig will not be effective in preventing alloimmunization.
 More than a 4x rise in Ab titers is concerning for significant risk of hemolytic disease and should prompt fetal evaluation of anemia and
hydrops fetalis.


 Fertility

o Fecundity: ability to become pregnant

o Fecundability: Probability of pregnancy per menstrual cycle; 15-30% in healthy couples.

 Infertility:
o Age less than 35: no pregnancy in >12mos.
o Age 35 or older: no pregnancy in >6mos (as opposed to 2 mos due to decreased ovarian reserve and decreased fecundability)
 Semen analysis is initial laboratory test for infertile couple (noninvasive, male factor infertility is common etiology)
 Ovarian reserve is assessed with 3 day FSH level, and ovulation is confirmed by a day 21 progesterone level.
 Hysterosalpingography: an invasive imaging study used to diagnose anatomic causes of infertility. Can be performed to evaluate for
tubal patency in patients with possible tubal scarring form prior PID or ectopic pregnancy.


  ParvoB19 infection in adults presents as a flulike illness, occasionaly accompanied by a rash and arthralgias.
 Pregnant patients require special consideration given associated risk of complications, including fetal anemia, hydrops fetalis, and
fetal demise. They require serial ultrasound assessment for anemia and hydrops fetalis.
o Anemia is diagnosed via middle cerebral artery doppler. Hydrops fetalis diagnosed by abnormal fluid collection in at least 2
body compartments (i.e ascites, pleural effusions).
 Anemia is transient and requires treatment with intrauterine fetal blood transfusions only when severe.
 Correction of severe anemia improves with severity of hydrops fetalis and survival rate.

 Diagnosis of B19 in pregnant Patients:

 Acute infection: B19 IgM Abs in immunocompetent. NAAT for B19 DNA in immunocompromised.
 Previous infection: B19 IgG Abs

 Fetus: PCR analysis o amniotic fluid for B19 DNA


 Diabetes and pregnancy

 Patients with medication-controlled diabetes during pregnancy are delivered at 39 weeks gestation. Expectant management of pts
with medication controlled diabetes past 39 weeks is associated with increased risk of IUFD, fetal macrosomia, shoulder dystocia.

 Fetal
 postpartum hemorrhage:
 loss of =500ml blood after vaginal delivery, or =1000ml after C/S, is an obstetric emergency and leading cause of maternal mortality.
Rfs are prolonged labor, chorioaminitis, uterine overdistention

 A retained placenta occurs when placenta is not delivered within 30 mins of fetal delivery and is associated with previous uterine surgery
( C/S), Tx is manual extraction, which an be incomplete  retained POC which can cause inadequate uterine contractions after delivery
(uterine atony) and PPH.
 Idiopathic uterine atony can be treated with uterine massage and uterotonic medications (oxytocin).

 Uterine atony and PPH 2/2 retained POC do not and management is supportive care and removal of POC.

Psychiatric/ Behavior & Substance abuse

 High dose prednisone can increase risk of developing psychiatric symptoms. Longer duration increases risk, and can start at any time
when on steroids. Psychosis and anxiety also occur.

 Major Depressive Episode:

 5/9 symptoms: Sleep disturbances, appetite change, low energy, psychomotor changes, low mood, anhedonia, guilt,
focus/concentration difficulty, SI
o Low mood or must be present
 may occur in response to variety of stressors (including loss of loved one)
 Duration >2 weeks
 Social & occupational dysfunction
 SI related to hopelessness and worthlessness

 Grief reaction (bereavement)

 normal reaction to loss.

 Feelings of loss and emptiness

 Symptoms and sad feelings revolve around loss of deceased -Functional decline less severe
 Worthlessness, self-loathing, guilt & SI less common
 Thoughts of dying involve joining the deceased
 Intensity decreases over time (weeks to months)
 Management of acute grief includes expressing empathy, education about range of typical grief symptoms, and monitoring.

 Patients without mental disorders should be reassured that transient hallucinations are also consistent with acute grief and are not
psychotic.

 Inhalant abuse:

 glue, toluene, NO, amyl nitrate, spray paints

 transient euphoria, lethargy, poor coordination, LOC. Immediate effects last 15-45 mins.
 Hypoxia, cardiac dysrhythmia, slurred speech, disorientation, careless or dangerous behavior, and seizures.
 A rash around mouth or nostrils can be seen due to drying effects of inhalants in the skin.
 Rapidly eliminated

 Bulimia Nervosa: pharyngeal erythema without exudates, parotid gland enlargements.

 Bulemia Nervosa

 1st line tx is CBT. SSRIs (esp Fluoxetine) are also component of treatment. Bupropion is contraindicated as it can cause seizuresin
patients with active symptoms of BN.


 Second generation antipsychotics are used to augment antidepressants in treatment-resistant depression  Metabolic effects, new
onset diabetes

 Delusional disorder: fixed delusions without other symptoms of psychosis and intact functioning (apart from the impact of the
delusion)
 Somatic symptom disorder: excessive anxiety about multiple physical symptoms but are not delusional
 Illness anxiety disorder: Fear of having a serious undiagnosed medical condition but do not have a rigidly fixed delusion that they have
a disease. They can acknowledge the possibility that they don’t have a feared illness and are treated with psychotherapy rather than
pharmacotherapy.
 Body dysmorphic disorder: OCD-related disorder that involves preocupation with previved decectes in appearance butnot delusional
 Insomnia

 Alcohol reduces sleep onset latency, as BAC drops, causes disruption in sleep archictecture., causing restless sleep and increaed
nighttime awakenings. Avoid alcoholic beverages in the evening.


 Bipolar disorder must be ruled out before initiating antidepressant therapy for major depression (screen for history of manic or
hypomanic episodes).
 Monotherapy
 TCAs: still used in treatment-resistant depression and chronic pain syndromes.

 Multiple MOA:
o inhibit reuptake of NE & 5-HT, Antihistamines (sedation), a-antagonists (hypotension), cardiac Na channel blockers (conduction
delay), and anticholinergics (dry mucous membranes, pupillary dilation).

 TCA Toxicity:
o vital sign abnls, mental status changes, seizures, anticholinergic toxicity. Cardiac conduction abnormalities are common and
can degenerate into VT and VF.

 Treatment of choice for QRS prolongation is NaHCO3, which increases TCA protein binding and reduces affinity of TCA in the Na
channel and be given to all patients with TCA overdose with ARS widening >100msec or evidence of ventricular arrhythmias.
 Avoid Class 1A and 1C antiarrhythmics and Physostagmine

o Class 1C also block cardiac fast Na channels and wosens cardiac effects of TCA
o Physostagmine us used to treated isolated anticholinergic toxicity but has been associated with cardiac arresest in TCA
overdose

 Depression

 comorbid in patients with dementia and recent CVAs.

 can present as neurovegetative or "agitated depression" with anxiety and restlessness.

 Citalopram is used to treat depression in patients with dimentia and stroke and there is benefit in nonaggressive behavioral agitation.
o There is a dose-dependent QT prolongation, doses above 20mg should not be used in patients >60.
  Antipsychotics may be used to treat severe behavioral disturbances in dementia However, due to their association with increased
cardiac mortality in patients with demeita, their use is typically reserved for patients exhibiting behavioral aggression.

Pulmonary & Critical Care

 Acute Exacerbation of COPD

 Cardinal symptoms:
o increased dyspnea.
o increased cough (more frequent or severe).
o sputum production (change in color or volume)
 Diagnostic findings: CXR with hyperinflation. ABG with hypoxia, CO2 retention (chronic &/or acute)
 Management:
o O2 (target 88-92%.

o Inhaled bronchodilator
o Systemic glucocorticoids
o Antibiotics (if >1cardinal symptoms)
o Oseltamivir if evidence of influenzae
o NPPV (with BiPAP) if signs of ventilatory failure (tachypnea, accessory muscle use, acidic pH)
 Predictors for successful NPPV include youth, good neurologic status, and moderate hypercarbia (pCO2 < 92).
 Contraindications include respiratory arrest, severe encelopathy, inability to cooperate, and inability to clear
secretions or mucosa.

 Other predictors of NPPV failure are tachypnea = 30.min or initial pH <7.25.

 in NPPV failure or contraindication, endotracheal intubation is performed.

 Deconditioning in hospitalized patients is very common, and typically occurs in patients with severe illnesses that result in prolonged
bedrest and immobility. Other Rfs for deconditioning include preexisting disability and coexisting chronic medical conditions.
Management consists of a multi-faceted team approach to restore the patient's pre-morbid functional status.


 The presence of a malignant pleural effusion in patients with lung cancer is poor prognostic sign regardless of tumor cell type.

 Pts with NSCLC (including adenocarcinoma) with a malignant pleural or pericardial effusion are classified as stage IV (advanced,
incurable disease). Management is palliative.

 Although many patients with malignant pleural effusions may remain asymptomatic and do not need to be treated, many develop
symptoms associated with the effusion (i.e. SOB). Initial management is large-volume thoracentesis. If effusion reaccumulates and the
patient has a very short expected survival, repeat thoracentesis can be performed once symptoms recur. More aggressive intervention
is required for patients in whom the effusion reaccumulates rapidly (in <1month) or in those with longer expected survival. In these
cases, chemical pleurodessis is most appropriate, and consists of oblitering the pleural space by inducing pleural inflammation and
fibrosis using a sclerosing agent (i.e. talc)


 Pulmonary Embolism

 Pulmonary infarction is a potential complication of acute PE and typically appears on CT scan as a peripherally located, hemispherical
consolidation abitting the pleura
 Hypotension after initiation of PEEP is due to an acute increase in intra-thoracic pressure, which in patients with intravascular volume
depletion, can cause a marked decrease in VR and CO. Hypotension is best treated with a bolus of IVf, and by lowering PEEP if possible
 Tension PTX

o air passes into pleural space during inspiration. Defect closes during expiration  ↑ in pleural space air volume & pressure
 mediastinum shifted away. Vena cava compressed by accumulating air pressure  decreased Venous return to RA
hypotension.
 Other symptoms include tachycardia, tachypnea, reduced breath sounds on affected side, JVD.
o CXR confirms dx: demonstrates pleural line with peripherial radiolucency devoid of lung markings, ipsilateral depressed
hemidiagraphm, and widened rib spacing, and mediastinal shifting to contralateral side.
o Tx: emergent decompression via needle insertion at midclavicular line of 2nd ICS, and/or chest tube placement..

 Suspect in acutely hypotensive pt on mechanical ventilation or recent history of chest trauma or thoracic procedure (CVC placement)
  Tension PTX can lead to cardiac arrest.

 Pulmonary Arterial Hypertension

 Primary elevation in pulmonary arterial pressure due to thickening of pulmonary artery smooth muscle and fibrosis of pulmonary
arterioles.

 Hypoxemia (significantly exacerbated by exercise) occurs due to combination of reduced blood delivery to pulmonary capillaries and
impaired gas exchange.
 PEX: clear lungs, may reveal signs of RHF (JVD, LE Edema)
 CXR: enlargement of pulmonary arteries in absence of evidence of lung pathology.
 Management: Initial: TTE (estimates PA pressures)
 Diagnostic confirmation with Right heart catherization.

 Patients with history of Hodgkin lymphoma have high risk of secondary malignancies (most common lung, breast, thyroid, bone, and
GI.
 Smoking in combination with prior radiotherapy or chemo greatly increases risk for lung cancer.

 OSA
 STOP BANG Survey
 Snoring
 Tiredness
 Observed apnea or choking/gasping
 Pressure (HTN)
 BMI >35
 Age >40
 Neck size: M >1in (43.2cm), W: >16in (41cm).
 O]0-2= low risk, 3-4 = intermediate risk, >4= high risk
 ARDS and Mechanical Ventilation

 Decrease incidence of ventilator-associated lung injury with low TV ventilation (6-8ml/kg predicted body weight)
o lower TV decreases risk of alveolar over-distention and provoking barotrauma.
o lower TVs are generally well tolerated with the main adverse effect being development of hypercapnic respiratory acidosis,
which can be partially managed by increasing the RR.
 FiO2 should be adjusted along with the PEEP to maintain oxygenation within acceptable range. A persistently high FiO2 (>60%) can
result in oxygen toxicity. To maintain oxygenation, ↑PEEP so FiO2 levels are not in the O2 toxicity inducing range.
 Minute Ventilation (TV x RR) should be set according to each patient's metabolic requirements. High MV can result in respiratory
alkalosis.

Renal, Urinary Systems, and Electrolytes
 Patients receiving immunosuppressive agents after a kidney transplant are at risk of developing nephritis as a result of infection with
BK virus, a polyomavirus.
 BK-induced nephritis is characterized by fever, worsening renal function, UA c/w interstitial nephritis, and bx findings of renal tubular
damage and prominent basophilic intranuclear inclusions.

 Confirm dx with allograft bx. Treatment is deceasing immunosuppression and in some cases antiviral therapy.

 Glucosuria in asymptomatic child  ask questions about diabetes symptoms first.

 Patients with severe nephrotic syndrome are predisposed to thrombotic events. possibly due to loss of natural anticoagulants in the
urine. Thrombosis most commonly occurs in renal veins and deep veins of the LE.

 Chronic renal vein thrombi are usually asymptomatic. Acute renal vein thrombi often lead to renal infarct but are not seen in
nephrotic syndrome.
 Increased risk of venous clots in cerebral veins and arterial clots in the cerebral or lower limb vasculature.
 Highest risk in patients with membranous glomerulonepropathy.
 Nephrotic patients also have an increased risk of infection, but infections are usually caused by typical organisms such as
pneumococcus, and not due to OIs.

 Urinary Incontinence
 Stress: leaking with cough, lifting, sneeze

o Due to decreased urethral sphincter tone or urethral hypermobility -seen in men with previous prostate surgery aor
multiparous women.
 Urge: sudden, overwhelming urge to urinate

o Due to Detrusor hyperactivity

 Overflow: incomplete emptying & persistent
o Due to Impaired detrusor contractility or bladder outlet obstruction as in BPH
o

 autonomic parasympathetic innervation controls contraction of detrusor during urination.

 Diabetic autonomic neuropathy [DAN] (or other autonomic nerve injury such as MS, spinal cord trauma) results in impaired detrusor
contractility  urinary retention  elevated intra-vesicular pressure, and eventually OUI
o Orthostatic hypotension is seen in DAN


 HyperKalemia in EKG:

 progressive changes of peaked T wave, shortened QT interval, lengthening of PR interval and QRS duration, and eventually formation
of a "sine wave".
 Most commonly due to worsening renal failure and can be precipitated by certain medications including ACEi, ARBs, or K-sparing
diuretics.


 Metabolic Alkalosis and hypokalemia
 Causes:
o Vomiting
o diuretic use
o abnormal renal Na handling (Bartter’s and Gittleman’s)
 Urine Cl

o GI losses: Cl is reabsorbed from urine due to volume depletion and hypochloremia  ↓Urine Cl
o Diuretic use or B/Gs: Unable to reabsorb Cl  inappropriate loss of Cl- in urine  ↑ Urine Cl
 Low urine Na is not seen in patients with volume depletion & metabolic alkalosis because kidneys need to dump Na to excrete excess
bicarb despite underlying volume depletion.
 Urine K
o is ↑ in metabolic alkalosis with hypoKalemia of any etiology. GI losses  hypoK 2/2 increased solute delivery to the distal
tubule and hyperaldosteronism, which cause increased urinary losses of K.
o Urine K is also ? in diuretic use and B/G's.
 Urine pH is high (>.70) in all cases of metabolic Alk w/ hypoK due to increased urinary excretion of bicarbonate.
 Volume depletion is present in all potential etiologies of metabolic alkalosis, w/ hypoK, so urine osm should be high in all cases to
compensate.

 Hypertension and Gout:

 Diuretics decrease functional excretion of urate and should be avoided when possible (even if uric acid level is normal, diuretics can
increase it.

 Losartan has a mild uricosuric effect and is an effective 1st-line tx for hypertension in patients with gout.


 Hyponatremia

 Hypovol HypoNa- low [Na] w/ findings of dehydration on exam & labs

 Pathophys:
o Prerenal azotemia (Bun;Cr >20:1).
o Low [Hco3] = metabolic acidosis (2/2 decreased tissue perf -> ADH release -> water retention, HypoNa
 Treatment
 o fluid resuscitation with isotonic fluids (to suppress further ADH and allows for appropriate excretion of excess water,
correcting [Na].

 Hypertonic saline:

 only for severe Hyponatremia ([Na] <120mEq) AND w/ associated symptoms (seizure, obtundation, coma, respiratory arrest).

 Water restriction:

 tx for HypoNa 2/2 chronic fluid overload (heart/ renal failure), SIADH, or primary polydypsia

 Vasopression antagonists:

 Renal Cell Carcinoma

 triad of manifestation

o Hematuria (which can result in anemia), Flank pain, and Flank or abdominal mass.
o Mass is non-tender, moves with respiration.
o +/- B symptoms and paraneoplastic syndrome (erythrocytosis) -Dx with CT scan of abdomen.

 Nephrectomy can be curative in pts with localized disease. Overall 5-yr survival >70%.

 Polycystic Kidney disease: can result in flank pain and hematuria (due to renal hemorrhage). ALso causes moderate to severe
hypertension, is usually b/l, and + Family history (most cases are AD)

 Pyonephrosis- pus withinthe kidney ususally doe to urinary tract onbstruction. Patients are acutely ill (fever, malaise(, and can
decompensate quickly.

 Ovarian masses orcolon cancers have masses taht do not move with respiration.

 CKD patients with GFR <30 should receive education in renal replacement therapy

o Kindney transplant: [early prep to treat comorbidities] superior outcomes compared to dialysis.
 Patients with certain comorbidites are ineligible (malignancy, substance abuse. coronary artery disease)
o Hemodialysis: via primary AV fistula, synthetic AV fistula, or a double-lumen, cuffed tunneled catheter. Grafts take weeks to
months to mature.
o Peritoneal dialysis: require least time for prep as patients can receive dialysis through a peritoneal catheter immediately after
insertion (although 10-14 days of lead time is associated with lower leak rates)

 Hypercalcemia in malignancy:

 Causes:
o PTHrP secretion(MC): squamous cell, renal/bladder, Gyn/breast malignancies
o 1,25(OH)Vitamin D: Lymphomas

o Bone mets: breast, multiple myeloma, lymphoma.

 Clinical features

o Mild to moderate: Nausea, fatigue, constipation, ileu

o Severe: Confusion, weakness, delerium, coma. Impaired renal urinary concentration resulting in polyuria with dilute
urine(nephrogenic diabeties insipidis), which can manifest as urinary incontinence and lead to .hypovomemia. QT is shortened.
 Humoral hypercalcemia of malignancy (HHM). PTHrP causes increased bone turnover and reabsorption of calcium from distal tubules.
Hypercalcemia is usually severe (>14mg/dl) and rapid-onset.

o management is with aggressive hydration with isotonic saline and discontinuation of medications that increase [Ca] such as
thiazides
 Acute hypocalcemia: ?QT interval, neuromuscular instabilitt and/or tetany (paresthesias, muscle cramps, perioral numbness)
Rheumatology/Orthopedics and Sports
 child with nonaccidental trauma

 Skeletal survey, CT head, fundoscopic exam


 Statin induced myositis (SIM)

 wide spectrum of myopathic syndromes associated with statins, ranging from symple myalgias to severe rhabdomyolysis.

 CK elevations to >10x ULN is diagnostic. AST is most commonly associated with liver pathology, it is also released from damaged
msucle cells of pts with myositis.

 SIM can occur at any time during course of tx with statins but is most commonly seen in the first few months of therapy. However,
patients who are concurrently taking medications that inhibit CYP3A4 are more susceptible to muscular damage, as blocking
metabolism of statins through this pathway results in higher serum statin levels.

 CYP3A4 inhibiting medications include: Cyclosporine, HIV protease inhibitors, gemfibrozil, and macrolide inhibitors.

 Interstitial pulmonary fibrosis and esophageal hypomotility are seen in scleroderma. Heart failure can occur as a primary abnormality
or secondary to lung disease. Patients with scleroderma may have limited skin involvement without the classic skin sclerosis; these are
said to have limited cutaneous scleroderma and are frequently positive for anti-centromere Ab.
 Sevre GERD is due to esophageal hypomotility and incompetence of the LES

 Rheumatoid Arthritis

o symmetric joint symptoms, worse in morning

o Radiographs show periarticular osteopenia, joint effusions, symmetric joint space narrowing. Marginal erosions are seen in
more advanced disease.

 Wrists and knees re commonly involved. inflammatory markers are elevated. Anemia of chronic disease is common.

 DMARDs are only drugs that can alter long-term course of the disease and prevent disability.

 DMARDS are cytotoxic agents and include nonbiologic agents (hydroxychloroquine and MTX), as well as biologic agents (i.e. TNF-a
inhibitors, rituximab).

 RA involves small joints, such as those in the hands and tends to be symmetric. Unilateral large joint arthritis would be unusual for RA.
OA and RA can COEXIST in the same patient.

 Synovial fluid analysis:

o non-inflammatory (OA): <2,000 WBC/ml

o inflammatory (RA/ Gouty Arthritis): 2,000-75,000 WBC/ml

o infectious arthritis: >75,000 WBCs, & >75% neutrophils

 Reactive arthritis: Hx STI, concurrent GI Sxs, dysuria, or vision problems. Inflammatory synovial aspirate)

 Osteonecrosis most commonly affects femoral head but can also involve distal femur and proximal tibia.

 Corticosteroid use increases risk. Synovial fluid is non-inflammatory.


 Hip pain due to OA presents with pain in the groin exacerbated with movement.

 All patients with severe or persistent hip pain despite a trial of conservative treatment should undergo a through physical exam as as
well as initial diagnostic imaging with plain radiographs.

 MRI of hip indicated to identify osteonecrosis, tumors, fractures not identified on plain radiographs, and infections, but is not an
appropriate initial imaging modality..

 Degenerative changes of lumbar spine

 seen in middle aged adults engaging in regular heavy lifting

 Lumbar X-ray findings of disc space narrowing, traction osteophytes, and end-plate sclerosis are classic for degenerative disc disease.
 Management of LBP 2/2 DDD with no red flags is NSAIDS and f/u in 4-6 weeks.
o Red flags: hx cancer, weight loss, pain at night, urinary sxs, fever.
o MRI is indicated with persistent neurological deficits, suspicion for infection or cancer, pain persisting for >12weeks.

 Silicosis- multiple, bilateral, small (<1cm) round nodules in the upper lobes on chest imaging.

 Sarcoidosis: Parenchymal lung disease affects predominantly the upper lobes. CXR is first line and can detect interstitial lung disease
and hilar LND before symptoms arise. High-res CT is more sensitive and common findings (in addition to adenopathy) include ground-
glass opacities, bronchovascular irregularities, fibrosis.
o confirm dx with transbroncial biospy demonstrating noncaseating granulomas

 Usual interstitial PNA is pathologic manifestation of idiopathic pulmonary fibrosis (but also seen with end-stage finding with chronic
hypersensitivity pneumonitis, drug toxicity, and rarely sarcoidosis. Consists of primarily peripheral and basal reticular opacities.

 Granulomatosis with polyangiitis (Wegner's) is a systemic vasculitis primarily affecting the upper and lower respiratory tracts and the
kidneys.
 A major cause of death in these patients is diffuse alveolar hemorrhage, marked by dyspnea, hypoxemia, hemoptysis, and diffuse
alveolar opacities on CXR. Require ventilatory support and high mortality rate.


 Ruptured biceps tendon

 anterior shoulder pain, hearing a "pop" bruising after weight lifting

 surgical rpair fro athletes, young, activepatients. Less active patients or elderly can be managed conservatively.


 Management of Gout

 can be precepted by acute medical illness or excess alcohol intake.

 Treatment options are NSAIDS, colchicine, and systemic or intra-articular glucocorticoids.
 Once acute symptoms resolve, a urate-lowering medication is indicated in pts with frequent gouty attacks, chronic gouty arthropathy,
gouty tophi, recurrent uric acid kidney stones, or renal insufficiency.
 Allopurinol can lower uric acid levels; however, change in uric acid levels during initiation can trigger an acute gouty flare. Therefore,
pts should also receive additional prophylactic therapy during initiation and titration of urate-lowering drugs.
o Colchicine can be used (even in mild-to-moderate renal impairment.
 Diet restriction includes plant and low-fat dairy with reduction in fish, red meat, and organ meats (liver), overall protein restriction is
not recommended.

 Patellofemoral pain syndrome:
 poorly localized anterior knee pain in young athletes (women) due to chronic overuse or malalignment (angular deformities, weak hip
abductors). Can also acutely after trauma.
 Patellofemoral compression test: reproduction of pain when quadriceps is contracted while the patella is compressed into the
trochlear groove
 Management: Activity modification, short course NSAIDS. Stretching and strengthening exercises with emphasis on quadriceps and hip
abductors.
 Tibial stress fractures: localized pain and point tenderness

 Anserine bursitis: localized pain and tenderness at medial aspect of kne joint distal to the joint line. Symptoms are
episodic/acute (not chronic), and is not felt at anterior knee
 Patellar tendonitis: tenderness at inferior margin of patella MC in jumping spors. Episodice pain localized to inferior
patella and patellar tendon.
 Prepatellar bursitis: anterior knee pain that is acute and highly localized (unlike PFPS) with visible swelling anterior to
patella.
o Can be complicated by secondary infection to S aureus

 Polymyalgia rheumatica
 proximal muscle ache and stiffness, typically in shoulder and hips, that is worse in the morning. (hard to get dressed in morning)

 High association with GCA; need to ask about headaches, jaw pain, and vision problems. In the absence of findings suggestive of GCA,
treatment consists of glucocorticoids for symptomatic relief of pain.
  Nearly

 Patients who have ankle pain following inversion injury may have either a simple sprain or a fracture of the distal fibula and/or tibia.
 The Ottawa Ankle Rules state that the patients who have pain near the malleoli and either an inability to bear weight or bony
tenderness at the malleoli should nave plain films taken (generally 3-view x-ray series)

Social Sciences (Ethics/Legal/professionl)
 ADHD is considered a disability under the Individuals with Disabilities Education Act (IDEA). A PCP should advocate for child's rights
and educational needs at school.

 Intellectual disability or cognitive impairment does not automatically imply the lack of decision-making capacity. Patients may have
this capacity provided that they can communicate rationally and demonstrated comprehension of the proposed treatment,
alternatives, and the consequences of their decision.

 IFUD (stillbirth)

 after delivery, refer to the baby by name, encourage parents to see and hold baby (grief management, decreased risk for depression,
PTSD, anxiety compared to parents who decline contact). Give them as much time as they want, let them decide when to separate
from baby. Moments such s footprints and photographs should be provided to the parents. Don’t’ talk about next pregnancy as that
can be perceived as being dismissive of the current pregnancy.

 An oral advanced directive can be honored if a pathet is diagnosied with a aterminal or irreversible condition and the patients wish are
declared to the physician in the presence if two witnesses.


 Medicaid

 Children compromise ~50% of medicaid enrolees but reporesent only 15% or Medicaid expenditures. The elderly and disabled
compromise a much smaller percenetage of enrolees, but consume a disproprtinately larger protion of medicald dollras due to their
greater health problems and need for speicalzed care.


 The Requestor is a role reserved for trained Organ Procurement Organization (OPO) staff member, but can also be done by a physician
who has undergone specialized training. If physician is not requestor, can play important role in explaining the meaning of brain death
and in being present and supporting the OPO staff when the option of organ donation is presented.

 An untrained physician cannot unilaterally decide whether a family should be approached regarding organ donation.
 It is not unethical unless a conflict of interest exists
 It is appropriate to initiate discussion ofrgan donation with family when the patient is brain dead but still on hemodynamic and
respiratory life support. Optimally, brain death should be discussed seperately from the request fororgan donation (increased family
satisfication and consent rate)

 Acute Coronary Syndrome: includes UA and NSTEMI
 Dual antiplatet therapy (ASA, P2Y12 receptor blocker such as clopidogrel, prasugrel or ticagrelor), Beta-blocker, Statin, and
Anticoagulation therapy (unfrax Heparin, LWMH, bivaluridin, and foldoparinux)
 Cardiac catherization is For STEMI only; not UA or NSTEMI

 IV adenosine isused fro acute treatment of SVT

 Delayed puberty in males: no testicular enlargement by 14 years of age, or testicles are <2.5cm, or development is delayed for 5 or
moreyears fron the onset ofgenital enlargement.
 Initial evaluation requires bone age determination. If Bone age is older or equal to chronological age, further testing is needed.
 Post exposure prophylaxis for HIV
 Those with the following exposure are at risk: percuatenous injury, mucous membrane (eyes) orn nonintact skin exposure to infected
body fluids.
 High risk fluids are Blood, or fluids contimanited with visible blood, semen, and vagina secretions. Low risk fluis are SSF, synovial,
pleural, pericardial, or amniotic fluids. No risk is seen with urine, fecs, tears, or vomit if there is no visible blood.
 If PEP is required, it is a 3-drug regemine started before laboratory confirmation, with duration for 4 week. Most affective if initiated
within 1-2 hours of exposure.
  Sexual history should be obtained routinely and physicians hsould normalize sexual health concerns and provide patients with the
opportunity to openly discuss these issues.
 Cardiac resynchronization therapy with the Biventricular pacing device is recommended in:
o patients in sinus rhythm with a combination of symptomatic heart failure, left ventricular ejection fraction less than 35%, and
LBBB with QRS >150msec.
 Indications for ICD (to prevent SCD) are:
o Prior MI and LVEF ≤ 30, or NYHA class II or III symptoms & LVEF ≤ 35%.
 Implantable cardioverter-defibrillator and biventricular pacemaker placement can be placed at same time.
 Causes of hand dermatitis include irritant contact, allergic contact, dyshidrotic ezema
 Irritant contact dermatitis
o MCC occupational hand dermatitis. Chronic exposure to mild irritants (solvents and detergents) can lead to pururitis,
erythema, hyperkeratosis, and fissuring of hands.
o Occlusion of irritants under rubber gloves is a typical cause of ICD in health care workers.
 Phototoxic dermatitis
o Can be due to drugs (diuretics, antibiotics, NSAIDs, others). Presents as erythema with or without bulla or vesiculization over
sun-exposed areas such as dorsal hands, forearms, upper chest and face.

 Rapidly progressive weakness of the lower extremities following a URI, accompanied by sensory loss and urinary retention, is
characteristic of transverse myelitis.
o Neuro exam initially shows muscle flaccidity and hyporeflexia, but later shows muscle spas city and hyperreflexia.
o In acute Transverse myelitis – compressive lesions or other causes should be ruled out

 Seborrheic dermatitis: erythematous plaques with loose, greasy-looking scales in the scalp, central face (eyebrows, nasolabial folds),
ears. Malassezia species may place a role in the pathogenesis
 Treatment options:
o include topical antifungal agents (topical ketoconazole, or selenium sulfide),
o Keratolytic agents (sailysilic acid)
o coal tar
o topical glucocorticoids
o topical calcineurin inhibitors (pimecrolimus and tacrlimus).
o If SD resistant, does not resolve with the above, can use oral antifungals..
 SD is a chronic, relapsing condition. Initial treatment provides significant improvement in symptoms but patient usually need
intermittent re-treatment (topical ketoconazole or ciclopirox

 Hepatic encelopathy
o due to elevated Ammonia after a precipitating events.
 drugs (sedatives, narcotics)
 hypovolemia (diarrhea, diuretics)
 Hypokalemia,
 ↑ Nitrogen load (GI bleed),
 Infection (PNA, UTI, or SBP)
 portosystemic shunting (TIPS).
 Cirrhotic patients taking diuretics (for volume overload) can present with HE, which is likely due to: hypovolemia (dry mucous
membranes, high BUN), Hypokalemia (Acidosis facilitates conversion of NH4+ (ammonium) to NH3 (ammonia), and metabolic
alkalosis (results in decreased urinary loss of ammonia).
 HE presents as sleep pattern changes, AMS, ataxia, asterixis
 Treatment includes correcting precipitating factors (Fluids, Abx), and ↓ blood ammonia concentrations (lactulose, rifaximin). Hold
diuretics and repeat volume.
 Ammonium (NH4+) does not cross BBB Ammomia (NH3) is predominant at low pH.
 UGIB is a common instigator for UGIB and can be diagnosed with NG lavage

Temporality of different study designs
 Past
o Retrospective cohort: reviews past records to compare disease incidence in those with Risk factors and those without Risk
factor
o Case-control: Compares risk factor frequency amongst diseased cases and non-diseased controls
 most appropriate study design to investigate an outbreak of an acute infectious disease. Allows for quick localization
and outbreak source
 Present
o Cross-sectional: begin with risk factor or exposure status and compare disease prevalence to provide a snapshot.
 not used to investigate outbreaks or etiologies
 Present  Future
 o Prospective cohorts: compare disease incidence in those with risk factors and those without.
o Clinical trial: compare for outcome of interest
 Correlational studies attempt to measure associations between multiple variables and are generally conducted by natural observation,
surveying, or archival research. Help develop, but not test the hypothesis.

 Untreated acromegaly:
 ↑ mortality mainly due to cardiovascular disease (Htn, LV dysfunction, asymmetrical septal hypertrophy, conduction
defects, coronary atherosclerosis, myocardial fibrosis.
o Early cardiovascular disease is reversible my treatment.
 Also have higher risk of colon cancer and incidence of polyps. Screening should be done every 3-5 years.

Bicuspid Aortic Valve

 Etiology:
o MCC CHD. Can occur as an isolated lesion or with other CHDs ( Coarctation of Aorta, sib-or supra-valvular aortic
stenosis, VSD, and sinus of Valsalva aneurysm.
o Predominant in Males
o Present in 30% of patients with Turner
o Autosomal dominant with incomplete penetrance, or sporadic
 Diagnosis: Screening echocardiogram for patient and first degree relative
 Complications
o Can lead to progressive aortic dilation(which can occur in aortic sinuses, aortic root, or ascending aorta) 
thoracic aortic aneurysm formation with risk for aortic dissection.
 Dissection is at aortic root or ascending aorta.
o Severe regurgitation or stenosis
o Infective endocarditis
 Management
o Follow up echocardiogram every 1-2 years.
 Balloon valvuloplasty or surgery (valve and ascending aorta replacement
 Bullous pemphigoid: (TENSE, ITCHY)
 Autoimmune disorder characterized by prodromal symptoms of itching and urticaria follow by tense bullae with
erythematous urticarial lesions. Oral lesions can occur but are transient
 Diagnosis is based on skin biopsy (from edge of intact blister) and serum analysis for basement membrane antibodies.
 Management of mild cases can be with topical high-potency steroids, but more severe cases require oral steroids.
 Steroid-sparing drugs for patients with prolonged symptoms include Azathioprine, MTX, oar a combination of antibiotic
(tetracycline) with nicotinamide. Low- or High potency topical steroids should not be used form more than 3 months. The
risk of tinea infections is reduced by adding topical antifungal agent.
o Side effects of steroids: Skin atrophy (incidence reduced with concurrent use of topical tretinoin), and Rosacea
(esp. when facial rash is treated with steroid).
 Steroid induced rosacea occurs when a facial rash is treated with low-potency topical steroids that produce resolution of
the lesion, and the symptoms recur but require a higher potency steroid (the rosacea may be refractory to further
treatment). This making it necessary to discontinue the steroid which may then induce rebound erythema and pustule
outbreak which can be treated with a course of tetracycline (250mg Qid) or erythromycin (250mg Qid)
 Pemphigus Vulgaris- Flaccid bullae, Oral lesions, skin sloughing
 Dermatitis herpetiformis: Itching. Crusttingand vesicels of elbow, knees, buttocks. Celiac disease.
 Linear IgA bullous dermatosis: Grouped lesions that follow a linear or annular path

 SSRI-associated Sexual dysfunction- MC long term side effect of SSRI and common cause of nonadherence
 Management
o r/o other causes of sexual dysfunction
o Switch to non-SSRI antidepressant: Bupropion or Mirtazapine
o If patient is SSRI-responder, Adjunctive therapy with sildenafil or Bupropion
o Dose reduction for patients on high-dose SSRI (monitor for loss of efficacy)

 Throbotic thrombocytopenic purpura (TTP)- microangiopathic hemolytic anemia, severe thrombocytopenia, normal
coagulation studies
 Acquired syndrome due to formation of autoantibodies to ADAMTS13 (a plasma metalloprotease responsible for cleaving
of ultra-long strings of vWF off the endothelia wall. When levels of ADAMTS13 becomes severely deficient, uncleaved
strings of vWF trap and activate platelets, resulting in microvascular thrombi, causing the following:
o Platelet consumption  severe thrombocytopenia (↑ bleeding time, normal PT/PTT
o Intravascular RBC shearing, leading to signs of MAHA (schistocytes, ↑ indirect bilirubin, LDH, &
aminotransferases.
 Require Emergent plasma exchange to remove autoantibodies against ADAMTS13. Platelet transfusion is not
recommended unless severe bleeding occurs additional platelets can actually worsen ongoing intravascular thrombosis.

 Cat-scratch disease- presents with a cutaneous lesion and regional lymphadenopathy following a cat scratch or bite
 Azithromycin is 1st line antibiotic.
 Confirmatory tests include serology for B. henselae Antibodies. Lymph node biopsy is reserved with diagnosis is uncertain
and demonstrates noncaseating granulomas and positive Warthin-stain (silver stain) for B. Henslea.
 Complications include suppuration of adenopathy (most common), visual loss due to neuroretinitis, encephalopathy,
fever of unknown origen (fever ≥ 14 days) and HSMG
 Acute lymphadenitis: MCC are strep and staph. Emperic Abx is Clinda.

 Patients with a fracture flowing minor trauma (ground-level fall) should be tested for osteoporosis using Dual-energy x-ray
absorptiometry (DEXA scan). Bome marrow density scan of central bone should be done
 osteoporosis can be diagnosed with DEXA based on T-score (number of standard deviations above [+] or below [-] the
mean for a healthy 30-year old of the same gender and ethnicity.
o Normal: T score -1 and above
o Osteopenia (low bone mass): T-score -1 to -2.5
o Osteoporosis: T score -2.5 or below
o Severe or established osteoporosis: T-score -2.5 or lower with ≥ fragility fracture
 Indications for pharmacological therapy of low bone density
o Post-menopausal women with T-score ≤ 2.5 or those with a history of low trauma hip or vertebral fracture
regardless of T score.
o Presence of osteopenia with an elevated 10-year fracture risk based on the Fracture Risk Assesment Tool (FRAX),
wich predicts risk based on clinical factors as well as BMD at femoral neck.
 Pharmacological therapy is recommended with the 10-ur calculated probability by FRAX is >20% for major
osteoporotic fractures or >3% of hip fracture
o Bisphosphonates (Alendronate) are first line for post-menopausal osteoporosis. Total intake of elemental calcium
is 1200mg/day and Vitamin D (800IU).
o Teripartide (PTH 1-34, a Parathyroid hormone fragment) is expensive and used as a second line agent in pathetns
who have failed bisphosphante therapy.
o HRT is not recommended as 1st line because of elevatred risk of MI, stroke, DVT, PE, Breast cancer

 Carotid artery dissection- an important cause of Horner’s syndrome
 Unilateral head ache with ipsilateral Horners signs (meiosis, ptosis, ± anhydrosis (partial Horner’s).
o Horner syndrome results from the disruption of symphatetic nerves innervating the face and eyes, and travel
along the carotid artery.
o Anhydrosis may be absent in internal carotid artery dissection (partial Horner’s syndrome) because sweat nerve
fibers travel along with the carotid artery.
 Seen with trauma, connective tissue disease, smoking, neck manipulation, hypertension, or a 3-point restraint seatbelt in
MVAs
 Imaging of head and neck vasculature is required. CT-Angiography is good first step, but it results are negative and
dissection is still suspected, can do a catheter angiography (gold standard) or magnetic resonance angiography.
 Management consists of antithrombotic therapy (antiplatelet agents ro anticoagulation
 Stroke is a potential complication

 Diaper dermatitis
 Contact
o spares creases and skinfolds (not typically exposed to contributing factor
o can happen after diarrhea
o Treat with topical barrier ointment or paste Zinc Oxide, Petrolatum).
  Keep area dry, frequent diaper changes, exposure of skin to air, avoidance of excessively tight diapers,
and application of barrier creams (as above).
 Gentle cleaning with wipe and water or alcohol- & fragrance-free wipes.
 Low potency steroid ointment can be considered if it persists. Never use a high-potency corticosteroids in
the diaper area due to risk of systemic absorption nad adrenal suppression.
o Can have bacterial superinfection (presents with pustular drainage or honey-crusted lesions- topical Abx
(bacitracin, mupirocin) are first line
 Candida
o 2nd MCC diaper dermatitis
o Beefy-red rash involving skinfolds with satellite lesions
o Topical antifungals are treatment

 Evaluation of Gross (visible) hematuria
 Hx Trauma or suspected stone?
o Yes Imaging (CT/US)
o No  obtain UA and UCx (UA confirms presence of hematuriand can differentte b/w infections, and Glomerular
or extraglomerular causes
 Evidence of infection & +urine cx or symptomatic(dysuria, ↑frequency, urgency)  Antibiotics
 New proteinuria and RBC casts  Evaluate for glomerular causes renal US, 24-h urine stidues,
serological studies, and eventual renal biopsy)
 Unclear Etiology and those with risk factors for urologic malignancies (age >35, smoking, chronic analgesic
abuse, pelvic irradiation hx, chemical exposure) Urology referral for Imaging, Cystoscopy, Urine
cytology

 Classification of Angina
o Classic
 Typical location (substernal), quality and duration
 Provoked by exercise or emotional stress
 Relieved by rest or nitroglycerine
o Atypical
 2 of 3
o Non-anginal
 Less than 2 of 3
 Suspected ACS (typical chest pain, RFs for CAD, non-specific EKG changes) should be given 325 ASA, sublingual
Nitroglycerine in cases of active pain. Serial EKGs every 30 mins, and at least 2 Troponin I levels, 3 hours apart (keeping in
mind that they may require up to 6-12 hours after onset of symptoms to become detectable.
o Negative troponin levels but ongoing chest pain and/or evolving ischemic changes in ECG Unstable angina
o Significantly Elevated troponin levels = NSTEMI
 Management of UA/NSTEMI
 Risk assessment using TIMI score (thrombolysis in myocardial infarction); 1 point for each
o Age ≥ 65
o ≥3 CAD risk factors
o Known CAD with >50% stenosis
o Use of ASA in the past 7 days
o ≥ 2 anginal episodes within preceding 24 hours
o Elevated serum cardiac biomarkers
o ST-segment deviation >0.5mm on admission ECG
 Low risk (0-2)  stress test; Intermediate (3-4) or high (5-7) risk  Early coronary angiography (within 24 hours)
 Immediate coronary angiography indications:
o Hemodynamic instability
o Heart failure or new MR
o Recurrent chest pain
o Ventricular arrhythmia

 Odds Ratio- measure of association between exposure and an outcome. Statistical association does not imply causation!
o OR < 1: Exposure is associated with lower odds of the outcome
o OR = 1: Exposure is not associated with the outcome
 o OR > 1: Exposure is associated with higher odds of the outcome.

 Bilateral Hilar adenopathy ± paratracheal lymph node enlargement is charasteric in patients with sarcoid. Elevations in
ESR, AVE, and calcium can also be seen in sarcoid, but are nonspecific an d can occur in other medical conditions as well.

 Knee injuries
 Anterior Cruciate Ligament Injury
o 2/2 Rapid deceleration or direction changes or Pivoting on lower extremity with foot planted
o Symptoms
 Popping sensation at time of injury
 Rapid onset pain that may be severe
 Significant swelling (effusion/ hemarthrosis)
 Feeling of Joint instability
o Exam findings: Anterior laxity of the tibia relative to femur (anterior drawer test, Lachman’s test)
o Diagnosis: MRI
o Treatment:: RICE +/- Surgery
 Medial Collateral Ligament injury
o Trauma to lateral side of knee when the foot is planted.
o Tenderness at the medial knee along the joint line (where tibia and femur meet), and there may be laxity when
the lower extremity is gently forced into abduction with the knee stationary (valgus stress test)
o No hemarthrosis unless concurrent ACL injury
 Meniscal tear
o Subacute or chronic locking or catching sensation in the knee.
o Effusions ( when they occur), develop slowly and hemarthrosis is rare

 Primary CNS Lymphoma (PCNSL)
o Degree of immunosuppression is major determinant of survival.
o Initiation of HAART in HIV+ patient is good prognostic sign, and is associated with improved prognosis especially in
patients who demonstrate an improvement in immune system (↑ in CD4# and ↓ in Viral load)

 End of Life care and Medical Futility
 End of life care: d/c therapies and/or shift to palliative therapies. Begins when the curative therapy is likely futile.
o Futility can be physiologic (treatment is extremely unlikely to allow survival) or qualitative (offers minimal benefit
at the cost of significant pain and suffering). When futility is reached, goal of therapy shift toward minimize
discomfort, anxiety, or distress for patient or family.
 AMA approach to medical futility
o Prior deliberation (ie. Advanced directives)
o Family meetings: Joint-decision making with care team based on outcome data
o Palliative care consultation
o Medical ethics committee agree that additional care is futile
 All providers must
o Transfer within intuition
o Transfer to different intuition
o Cease futile interventions

 Reactive Arthritis (ReA)
 Presentation: within 1-4 weeks of inciting infection. New symptoms suggesting ReA in patient with history of chlmycida
infection should prompt repeat testing for the infection even in the absence of obvious symptoms of GU chlamydia.
o NAAT for GU chlymidia is Urine. NAAT for Lymphogranuloma venerum is of the penile lesion.
o (dark-field microscopy is on syphilitic changer before seroconversion)
 MSK: Asymmetric peripheral oligoarthritic, Enthesitis, Dactylitis
 Extraarticular symptoms:
o Ocular: uveitis, conjunctivitis
o Genital: Urethritis, cervicitis, prostatitis
o Dermal: Keratoderma blennorhagicum, circinate balanitis
o Oral ulcers
 Treatment: Treat active chlamydia infection (Abx)as well as symptoms of arthritis (NSAID). If arthritis symptoms persist
despite NSAIDS,  intraarticular steroids  systemic steroids DMARDS (Sulfasalazine, MTx, Hydroxychloroquine) in a
step wise fashion

 Number Needed to Harm is a measure that indicates how many patients need to be exposed to a particular risk factor
over a given period of time before a harmful event occurs in one patient.
o NNH is the inverse of the Absolute risk increase (or the attributabile risk), which is the incidence rate between the
exposed and the non=exposed
 Odds ratio: “pooled” if based on results of multiple trials (Meta-analysis).
o Ratio of Incidenc of a given outcome in one group , compared to the incidence of the same outcome in a different
group

 Vibrio vulnificus- free living, gram negative bacteria found in estuary and marine eniromenents. Infections occur following
ingrestion (oysters) or wound infection. Patient with certain characteristics (liver disease, diabetes) are at high risk of fatal
infection, including rapidly progressive cellulitis, hemorrhagic bullae and septic shock. Diagnosis is made by blood and
wound clutres and treatment with IV antibiotics (IV Ceftriaxone and Doxycycline) should not be dealayed. Mycobacterium
marinarum is found in slt and fresh water and can cause wound infections, but esions are popular and ulcerative (not
nectotic and bullous) and develop within days not hours)

 Sinus bradycardia can be a complication of inferior wall MI as the SA node is supplied by RCA in 60% of people.
o Sinus bradycardia is due to ischemia of the SA node and the RV wall triggering an increase in vagal tone.
o Usually transient if occurring after inferior wall MI. Severe bradycardia can occur, leading to cardiogenic shock
(hypotension, cold extremities, and pulmonary edema).
o Anticholinergic therapy with IV Atropine is initial treatment for patients with hemodynamically significant
bradycardia due to inferior wall MI, and results in increased CO and symptomatic improvement.
o Although patients with Right Ventricular MI are typically preload dependent with clear lungs and should often be
initially managed as if hypovolemic, severe bradycardia can lead to decreased LV CO and cardiogenic shock, the
administration of fluids without increasing HR causes worsening pulmonary edema.
 Dobutamine: B-1 agonist that treats cardiogenic shock primarily by increasing LV contractility (improves Stroke Volume)
 Epinephrine is sometimes used to treat symptomatic bradycard in not responsive to atropine, but because it leads to an
large increase in myocardial O2 demand 2/2 stimulating a-1 and B-1 receptors, and is typically contraindicated in patients
with MI.
 IV Nitroglycerine infusion causes decreased preload due to dilation of venous capacitance vessels, and can be used to
relieve pulmonary edema in some scenarios (such as hypertensive emergency), it is contraindicated in patients with
hypotension and/or preload-dependent RVMI
 MEN 1
 Pituitary adenomas:
o Secretion of prolactin, GH, ACTH, or be nonfunctioning. Mass effects (headache, visual field defects)
 Primary Hyperparathyroidism:
o Indications for parathyroidectomy
 Symptomatic hypercalcemia, or [Ca] > 1mg/dl above ULN
 End organ complications(osteoporosis, CKD, Nephrolithiasis)
 Increased risk of complications (>urinary Calcium >400mg/ day
o Patients <50 are likely to develop complications later in life and should also undergo parathyroidectomy. As
patients with MEN1 present at relatively young age, most should be offered surgery.
o Surgical approach
 MEN1 patients usually have multiple parathyroid adenomas and require subtotal (≥3½ glands) or total
parathyroidectomy with auto transplant into a muscle pocket
 Pancreatic/GI neuroendocrine tumors:
o Gastrinoma- recurrent peptic ulcers
o Insulinoma: hypoglycemia
o VIPoma- Secretory diarrhea, hypokalemia, Hypochlorhydria (decreased production of HCL in stomach)
o Glucagonoma: weight loss, necrolytic migratory erythema, hyperglycemia
 Can also have additional findings (multiple cutaneous lipomas)
