Basic Concepts

 In USMLE step 2 CK, we get few different kind of questions like which of the fol-
lowing is the best initial test? Which of the following is the most accurate test?
Which of the following is the best initial treatment? Which of the following is the
most accurate treatment? Which of the following is the best next step in the manage-
ment of this patient? Which of the following is the first step in the management of
this patient?
 To give answer to this kind of questions, understand following concepts. Test with
good sensitivity is the best initial test. For example, EKG has good sensitivity to
diagnose and differentiate chest pain so it will be the best initial test for patient with
chest pain. Test with good specificity is the best accurate test. For example, barium
esophagus is the best initial test to diagnose and differentiate dysphagia due to ob-
struction or motility disorder but esophageal manometry is the most accurate test to
diagnose dysphagia due to motility disorder. Other important points in choosing test
are cost effectiveness and safety of test. Same way in the treatment, look at the cost
effectiveness and safety of the treatment. For example, atropine and pace maker,
both are good to start heart in first degree heart block but we use pace maker as a
last resort because atropine is more safe and as effective as pace maker and very
easy to use (just give IV). The most difficult question is the next best step in the
management of this patient. It depends on the condition of the patient when patient
arrives at the hospital / clinic or patient leaving the hospital / clinic [Stable, Un-
stable or discharging time]. For example, patient with chest pain admitted to the
hospital and treated with Aspirin, Clopidogrel, Morphine and Angioplasty, now its
time to discharge, which of the following is the best next step in the management of
this patient? (a) Stress test, (b) Metoprolol, (c) Captopril, (e) Furosemide. Answer is
Metoprolol. Studies have shown that beta blockers have improved mortality rate in
patient with recent MI so adding Metoprolol to patient’s regimen will be the best
next step in the management of this patient. Another example, patient with upper GI
bleed comes to ER, BP – 90/60, which of the following is the best next step in the
management of this patient? (a) Upper GI endoscopy, (b) IV normal saline, (c) fresh
blood (e) Barium Esophagus. Answer is IV normal saline. First we need to stabilize
the patient then we can order imaging studies. Fresh blood comes with its disadvant-
ages like infectious diseases so not a good idea! I hope you’ve got a better idea by
now about how to give an answer to the step 2 CK questions. I have written best ini-
tial test, most accurate test, best initial treatment, most accurate treatment, next best
step and first step in the parenthesis in my notes so it will be easy for you to recog-
nize and remember everything. These notes are for exam purpose only so I have
written them in a way that they ask question on the real exam. In the real life, patient
can present with many different ways and we deal them accordingly but always re-
member standard recommendation and current modification / new in the man-
agement.

Good Luck

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 CARDIOLOGY

 Myocardial Ischemia / Myocardial Infarction: Substernal squeezing chest pain

[pressure / heavy feeling on chest]
 Pericarditis: chest pain relieve by leaning forward
 Costochondritis: chest pain reproduce by palpation
 Dissecting aortic aneurism: tearing chest pain radiate to back
 Pneumonia: pleuritic (increase on inspiration) chest pain
 Pulmonary embolism: pleuritic chest pain, dyspnea, tachypnea
 Esophageal spam (“nut cracker disease”): h/o GERD, gastritis, pain occur after
eating, pain relieved by nitroglycerin or CCB, normal EKG

 Stable angina: chest pain after exertion

 Unstable angina: chest pain at rest [ST Depression] [D → E]
 Myocardial Infarction: chest pain at rest [ST Elevation]
 Prinzmetal angina: chest pain at rest [ST elevation – Transmural Ischemia]
[due to coronary artery spasm. Pain may relieve by little exercise like patient gets
up and walk & pain relieved (Physiology: because exercise causes increase in
Adenosine which is a potent coronary vasodilator)] [Best diagnostic test – An-
giography – shows No atherosclerosis] [Treatment: Ca++ channel blockers
(CCB), Nitrates] [Not Aspirin and β-blockers]

 How will you differentiate between unstable / Prinzmetal angina and MI?
Angina means chest pain comes and goes so even though chest pain occur at rest
in unstable / Prinzmetal angina, you can easily diagnose from the presentation in
the question.

 Best Initial test: EKG; Stress test for Stable angina

 Most accurate diagnostic test: Angiography (Ischemia) / Cardiac Troponin &
CK-MB (Infarction) [Both begin to elevate in 4-6 hrs] [Cardiac Troponin remains
elevated for 1-2 wks] [CK-MB remains elevated for 2-3 days] [best test to check
re-infarction within a week – CK-MB because it disappears in 2-3 days]
 Most accurate treatment for MI / Unstable angina: Angioplasty, Bypass

* Approach to pt present with Chest pain:

 If hx, initial EKG & cardiac biomarkers negative – admit the pt and repeat EKG
and biomarkers in 6-12 h
 If initial EKG & biomarkers are nl, but high suspicion from hx – admit the pt and
r/o CAD with stress test / angiography – if high risk pt [> 65 yr, prior CAD /
ACS] – admit and evaluate for ischemia by stress test or angiography [useful in
further Mx – Angioplasty / Bypass] – if low risk [<65 yrs, no prior CAD / ACS] –
can do out patient stress test within 72 h
 If second EKG & biomarkers are nl and low suspicion from hx – ruled out MI so
start looking for other causes of chest pain
 If initial EKG & biomarkers are positive – admit & start treatment as per below

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  Patient with Stable/Unstable angina and MI should receive Aspirin, Nitrates
and β-blockers (if no contraindications like Asthma, low BP, Heart block etc.)
 Patient should also receive oxygen (if oxygen saturation is low) and morphine (if
patient is still having chest pain; presence of pulmonary edema)
 Stable Angina: once you make diagnosis of stable angina from stress test, do an
angiography followed by angioplasty; if 3 vessels disease or left main coronary
artery disease on angiography, go for bypass [CABG] [CABG has shown reduce
in mortality in pt with 3 vessel disease & left main coronary artery stenosis]
 Unstable Angina (due to vessel blockage by plaque so clot is forming): above 2
steps [Aspirin, Morphine...] + Clopidogrel + Heparin (to prevent further clot-
ting) (not thrombolytics) + Statins [As discussed above, angiography should be
done to guide further management like angioplasty / CABG]
 MI (due to vessel blockage from disrupted plaques so clot is already formed):
above 2 steps [Aspirin, Morphine...] + Clopidogrel + Thrombolytics (to lyse clot
and releive obstruction) (If certain criteria meets) / Angioplasty / CABG [As dis-
cussed above, angiography should be done to guide further management like an-
gioplasty / CABG] + Statins + Low molecular weight Heparin (If not contrain-
dicated) + ACE inhibitors (only If CHF due to acute MI) + Lidocaine (only If
ventricular arrhythmias)
 Angioplasty is superior than thrombolytics for Unstable angina & MI but it is not
readily available all the time [Door-balloon time should be <90 min for maximum
benefit. If delays in angioplasty, give thrombolytics]
 Criteria to use thrombolytics (If it is not contraindicated, if Angioplasty is not
readily available) [C/I: prior ICH, active internal bleeding, etc]
 Within 12 hrs of the onset of MI.
 > 1 mm ST segment elevation in two contiguous EKG.
 New LBBB (Left Bundle Branch Block).

* Stress Test → Indication: to dx CAD (stable angina), to evaluate & risk stratific-
ation in pt with known CAD, ACS, low ejection fraction in asymptomatic patient
→ Contra indications (C/I): acute coronary syndrome (ACS) [Unstable angina
& non-ST elevation MI], acute MI within 48 hours, symptomatic severe aortic
stenosis, uncontrolled arrhythmia, aortic dissection, pulmonary embolism, and
pericarditis → Types: Exercise & Pharmacological → Test Results: HR [must be
achieving >85% of max predicted (220 – age)], BP response, exercise tolerance,
EKG changes [ST depression / elevation] & Imaging [with thallium201 or 99m Tc
or Echocardiography] [abnormal results of imaging – radionuclide defect with
gamma camera or wall motion abnormalities on echocardiography]

* Complication of MI : Ventricular Arrhythmia (MCC of Death)

˗ Rupture (Ant Wall, Papillary muscles, Interventricular Septum) – 3-7 days
˗ Autoimmune Pericarditis (Dressler’s Syndrome) – 6-8 weeks Post–MI – Tx:
NSAIDs
- Sexual activity can be resumed after 2-4 weeks post-MI
- Management of bradycardia following acute MI – IV Atropine. If bradycardia
persist for more than 24-hrs – Transcutaneous pacemaker

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 - Sick sinus syndrome – Alternate tachycardia and bradycardia in a patient who
had MI – Tx: Pacemaker
- Acute right ventricular infarction – IV normal saline bolus (first step); then if
it fails to improve hypotension, give ionotropic agents like dobutamine

at 70% of target rate (after 5-7 days)

• Stress Test Post–MI
at 80% of target rate (after 2-3 weeks)

 EKG changes in Acute MI: Peak tall T-wave → ST elevation → T-wave inversion
→ Q-wave
 Inferior wall MI [RC]: II, III, aVF
 Anterior wall MI [LAD]: V2 – V4
 Anteroseptal [LAD]: V1 – V3
 Lateral wall MI [LAD / Circumflex]: I, aVL, V4 – V6
 Posterior wall MI [Posterior Descending]: V1 – V2

LIPID MANAGEMENT
↓
(<100 mg /dl) < goal > (< 70 mg / dl)
↓ ↓
Coronary artery disease Coronary artery disease
or +
Diabetes, Hypertension, Tobacco Diabetes, HTN, Tobacco

Risk Factors
↑  ↑
One ↓ More than One
 
↓ ↓ ↓ ↓
LDL > 160 mg/dl LDL > 190mg/dl LDL > 130 mg/dl LDL > 160 mg/dl
• Diet • Statins • Diet • Statins

 Statins are best initial drugs for management of high LDL.

 Generalized aches & pain with extremely high CPK in patient taking Statins,
next step?  stop Statins
• Two main factors that reduce risk of CAD – reduce LDL & HTN (in DM patient)

• Discharge Check List:

• Risk stratification: stress test / echocardiogram (to assess EF)
• lower cholesterol [as above]
• lower HTN [<140/90 mmHg and <130/80 mmHg if DM]
• Smoking cessation, Exercise & Wt loss
• ASA (life long), Clopidogrel (9-12 months), Nitrates (prn), β-blockers, ACEI (if
CHF, HTN, DM)

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 Different Clinical Scenario
 Most important is to know when you will do a diagnostic test and when you will
start the treatment for “next best step in Mx” question. For other questions answer
what they've asked [ like best initial choice / most accurate choice]
 If patient comes to the ER with chest pain for last 1-hr and still having pain,
best initial test? – EKG
 If patient comes to the ER with chest pain for last 1-hr and still having pain,
EKG shows ST depression / ST elevation, what will you do now? – Start initial
treatment [Aspirin, Nitrates, β-blockers, Oxygen, Morphine] + pending confirm-
atory tests
 If patient comes to the office with c/o chest pain off & on but no pain at
present, what will you do first? – Stress test (EKG may not show anything cause
no pain now so r/o CAD by stress testing)
 If patient comes to the office with c/o chest pain off & on but no pain at
present, on examination you find 4/6 grade systolic murmur / known case of AS,
what will you do first? - Echocardiogram [Stress test is C/I in symptomatic AS]
 Patient with past medical h/o CAD & other comorbidities (which restrict from
exercise) present with symptoms suggestive of ischemia (i.e. c/o chest discomfort
or feeling heavy in chest for few mins and goes away, etc), next step? –
Pharmacological Stress Testing [eg. Adenosine myocardial perfusing scan] (to
see the progression of ischemia and risk stratification of CAD) [Adenosine and
Dipyridamole scan are C/I in patient with COPD / Asthma. Use Dobutamine in
those patient][Dobutamine may precipitate tachyarrhythmias]
 If above scenario but patient is able to exercise, next step? – exercise stress test
 Different scenario for Stress Testing: Patient present with typical / atypical
intermittent chest pain (exercise stress test); Patient present with typical /
atypical intermittent chest pain with comorbidities which restrict patient from
doing exercise (Adenosine scan); Patient present with typical / atypical
intermittent chest pain with comorbidities which restrict patient from doing
exercise and has Asthma / COPD (Dobutamine scan)
 Patient with previous Unstable angina / MI / bypass present with typical
intermittent chest pain, EKG show changes (depression / elevation) or Stress test
show ST depression / elevation, pt is on initial treatment for chest pain, next step?
Angiography (useful in further Mx – Angioplasty / Bypass)
 Any male patient present with chest pain (usually 2-3 hrs after dinner to confuse
us on the exam), next step? – EKG. If EKG is done & is normal and patient’s pain
relieved by sub-lingual nitroglycerine, next step? – admit the patient and serial
monitoring of cardiac enzymes (always rule out cardiac problem first)
 Any male present with chest pain which didn’t relieve by nitroglycerine & EKG
is non-specific, next step? – admit the patient and serial monitoring of cardiac
enzymes (always try to rule out cardiac cause first)
 Cocaine induced transmural ischemia (ST elevation on EKG), next step? –
initial management of ischemia (Oxygen, Aspirin, Nitroglycerin, Morphine) and
Benzodiazepines; If patient continues to have pain after administration of
benzodiazepines, next step? – Give Phentolamine [alpha1-blocker] [cocaine
causes increase in Norepinephrine which causes HTN by prominent alpha1
action] – If still c/o pain, next step? – Angiography
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 Congestive Heart Failure

↓ ↓
Right Sided Left Sided
• JVD • Pulmonary Edema
• Hepatomegaly • Paroxysmal nocturnal dyspnea (PND)
• Ascites • Orthopnea
• Pedal edema • S3 gallop & murmurs

• Positive Hepato jugular reflex is seen in right side heart failure is helpful in
differentiate cause of lower extremity edema from Heart problem / Liver problem

• Diagnosis :
- History & Physical Examination
- CXR , Echocardiography
- MUGA scan / radionuclide ventriculography for measurement of ejection frac-
tion (most accurate test)
• Treatment :
- Acute CHF (c/o short of breath, etc) – 1st step – give Oxygen – Next step – Diur-
etics (reduce pre-load) [Nitrates, Morphine are helpful too] – If still no improve-
ment – give Dobutamine (ionotropic agent) [Digoxin takes time; Dopamine in-
crease after-load by vasoconstriction]
- After stabilization – ACE inhibitor (reduce after-load) / Angiotensin II receptor
antagonist (those who don’t tolerate ACE inhibitors), β -blockers (Studies have
shown decrease in mortality by beta blockers in patient with CHF)
- Chronic CHF patients should be on Diuretics, ACE inhibitors, β -blockers,
Digoxin
- Spironolactone have been shown to reduce mortality when added with all of the
above chronic CHF drugs

- Asymptomatic patient with low ejection fraction (means heart is failing), next
step? – find out etiology (IHD most common cause so order a stress test)

- Management of acute pulmonary edema due to any cause – Oxygen, Morphine,

Loop Diuretics. If it is due to hypertensive crisis – Give Nitroglycerin or
Nitroprusside. If it is due to acute heart failure – Dobutamine. Next step after
stabilization of patient with acute pulmonary edema of unknown etiology –
echocardiography (to rule out MS or AI)

• Pt on multiple drugs for multiple problems including digoxin, furosemide, next

step?  serum electrolyte measurement (furosemide cause hypokalemia which
may cause digoxin toxicity)

■ Mitral valve Prolapse: Mid-late Systolic Click

- Presentation → Asymptomatic, Palpitation (most common presentation), Chest
pain, Syncope, Sudden death
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 - Marfan Syndrome / Asymptomatic
- Most common cause of mitral regurgitation in U.S.
* Treatment → No specific treatment in most cases
- Endocarditis Prophylaxis → Only If murmur present
- β - blockers → if chest pain occurs, palpitation and autonomic symptoms
- Anti–arrhythmic → if arrhythmia occurs

■ Infective Endocarditis: Splinter hemorrhages , Roth’s spot in eye , Janeway

lesions, Valve regurgitation
- Pathophysiology of Roth’s spot & Osler’s node – immune vasculitis; Janway’s le-
sion – septic emboli
- Strep. Viridians → most common overall cause (previously damage valve )
- Staph. Aureus → IV drug abuse ( Normal / Previously damage valve ) Tricuspid
Valve
- Staph. Epidermidis → Prosthetic devices
- Strep. bovis → ulcerative colitis / colorectal cancer patient

- Conditions that do not require infective Endocarditis Prophylaxis

• pt. with cardiac pacemaker and defibrillation
• Mitral valve prolapsed without regurgitation (without murmur)
• Surgically repaired ASD, VSD, PDA
• h/o Rheumatic fever without valvular dysfunction
• h/o Kawasaki disease without valvular dysfunction
• h/o isolated bypass surgery
• h/o isolated ostium secondum ASD

˗ Prophylaxis of Infective Endocarditis in patient allergic to Penicillin:

Dental, oral, respiratory, esophageal procedure  Clindamycin, Azithromycin
GI & genitourinary  High risk  Vancomycin + Gentamycin
Low risk  Vancomycin
˗ First step – start empiric antibiotics after drawing blood for culture
Next step – Transesophageal echocardiography to see vegetation
˗ Empiric antibiotic for IE in IV drug abuser – Vancomycin + Gentamycin
˗ In general – Nafcillin + Gentamycin

- Loeffler Endocarditis – restricive cardiomyopathy – prominent Eosinophil in-

filtrates leading to the fibrotic thickening of portions of the heart

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 ■ Valvular Heart Disease :

• Stenosis → Problem in opening of valve therefore murmur occurs during opening

of the valve
• Regurgitation → Problem in closing of valve therefore murmur occurs during
closing of the valve

Mitral Stenosis Aortic Mitral Aortic Stenosis

Regurgitation Regurgitation

• Diastolic murmur • Diastolic • Holosystolic • Systolic ejection

decrescendo radiate to the Axilla radiate to carotid
• Opening snap • Austin Flint
murmur
• CXR → double
density Right heart
Border.
•Echocardiography •Echocardiography •Echocardiography •Echocardiography

Treatment Treatment Treatment Treatment

• Diuretics (best • Endocarditis • Digitalis • Endocarditis
initial) Prophylaxis Prophylaxis
• Balloon • Diuretic, ACE • Diuretics , ACE • Surgery if valve
valvuloplasty (if inhibitors inhibitors area < 0.8 cm2
diuretics don’t help) ( Normal 2.5-3 cm2 )
• Valve replacement • Valve replacement • Anticoagulant • Balloon
(If both of above fail ( Presence of Austin valvuloplasty
to relieve Flint murmur
symptoms) indicates the need
for replacement of
the valve )
• Digitalis(if AF) • Valve replacement • Indication for
• Anticoagulant (if surgery – chest pain
AF) / Syncope during
exercise in elders;
Stable angina due to
stenosis next step?
Echocardiography
[not stress test]

• Austin Flint murmur: regurgitant stream from incompetent Aortic valve hits an-
terior mitral valve leaflet producing a diastolic murmur.

• Right sided murmur increase in intensity with Inspiration

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 ∗ Cardiomyopathies ∗

Dilated Hypertrophic Restrictive

• Echocardiography • Echocardiography • Echocardiography

• CHF following • Autosomal Dominant • Catheterization: square
URTI; Anemia, B1 chromosome 14 root sign on tracing
deficiency, etc ventricular pressure
• Treatment • thickening of Interventricular • Mimic Constrictive
septum Pericarditis (see below)
- Diuretics • Mechanism of mitral • Amyloidosis,
regurgitation – systolic anterior • Hemochromatosis
motion of mitral leaflet • Sarcoidosis
- Vasodilators • ejection fraction 80-90 % • Loeffler's syndrome
( Normal 60% ± 5% ) • Scleroderma
- Digoxin • Sudden Death in athletes • EKG – low voltage
• If Arrhythmia Treatment • No good treatment
↓ • β- blockers • Consider Heart transplant
Procainamide / • Ca+ 2 channel blockers
Quinidine
• Anticoagulants • Disopyramide • “speckled pattern” on
echocardiography 
cardiac amyloidosis

• Valsalva / Standing: ↓ Preload→↑ Obstruction

• Squatting / Hand grip: ↑ Preload → ↓ Obstruction
• Increase in Pre-load – decrease murmur in Mitral valve prolapse and Hypertroph-
ic cardiomyopathy.

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 ∗ Pericardial Diseases ∗

Acute Pericarditis Cardiac Temponade Constrictive Pericarditis

• Chest pain • Pulsus paradoxus • Kussmaul’s Sign

↓ ↓ ↓
Relieved by leaning ↓ SBP more than 10 mmHg ↑ jugular venous distension
forward on normal inspiration with inspiration
• Pericardial friction rub • Neck vein distension • Pericardial knock
(Diagnostic) with clear lung
• EKG – diffuse ST • Shock [Beck’s triad – • EKG – low voltage
segment elevation (In MI – Hypotension, JVP, muffled
ST elevation is in different heart sound], next step? →
leads according to Pericardiocentesis. If no
involvement of heart and it blood on pericardiocentesis,
is convex) next? → Thoracotomy
(blood is clotted in
pericardial sac)
• Treatment involves • Echocardiography • Catheterization: square
treating its etiology ↓ root sign
small Heart

• Treatment • D/D: Restrictive

↓ cardiomyopathy
- Pericardiocentesis • CT scan - best choice to
demonstrate thickened
Pericardium
- Subxiphoid Surgical • Treatment
drainage. ↓
- Diuretics
- Pericardiectomy

■ Pericardial Effusion:

• Serosanguineous → TB / neoplasm
• CXR – “water – bottle” configuration of cardiac silhouette
• Echocardiography (Best test)
• Treatment: Fluid Aspiration, Treat etiology

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 ∗ Arrhythmias ∗

Sinus Bradycardia Sinus Tachycardia PSVT

• Rate < 60 / min • Rate > 100 / min • Rate 130-220 / min
• QRS complex – Normal • QRS complex - Normal • Regular rhythm
Treatment Treatment Treatment
• None if asymptomatic • Right carotid sinus • IV Adenosine.
massage

• Atropine (1st choice)

• Pacemaker

∗ Heart Block ∗

1st Degree 2nd Degree 3rd Degree

• PR interval > 0.2 sec. ↓ ↓ • All atrial beasts are

Type – 1 Type -2 blocked.
• usually asymptomatic ↓ ↓ • Ventricles beat by a focus
( Wenckebach ) dropped distal to the site of block.
beat occur (Automaticity of heart)
suddenly
No PR
lengthening
• Tx: usually none. If ↓ ↓ • Tx : Pacemaker
Symptomatic → Progressive Tx:
Atropine. Prolongation of Pace -
PR until a P wave maker
is completely (no resp-
Blocked & onse to
Dropped Atropine)
Beat
↓
• Tx: usually none. If
Symptomatic → give
Atropine.

˗ Premature atrial beats and PVC (premature ventricular contraction)  observe

(never required any treatment)

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 ∗ Atrial Arrhythmias ∗

Multifocal Atrial Atrial Flutter Atrial Fibrillation ( AF )

Tachycardia
• Irregular rhythm • Regular rhythm • Irregular rhythm

• morphology of P wave • 2 : 1 block • 300-500 impulse / min

varies from beat to beat
• Cardioversion if • Tx : cardioversion if Tx : cardioversion if
hemodynamically unstable hemodynamically hemodynamically
unstable unstable or AF is due
to angina / MI
• If hemodynamically • If hemodynamically
stable then give Digitalis / stable then give
Calcium Channel Blockers • Digitalis / β-blockers (IV
(CCB) Metoprolol) / CCB (IV
Diltiazam) to lower the HR
[below 100] and then
elective cardioversion
• Patient with following • If AF for› 48 hrs then
sign / symptoms should give Warfarin 3 weeks
be considered as hemo- before an elective
dynamically unstable: cardioversion and
- Hypotension continue 4 wks after normal
- Chest pain sinus rhythm or do
- Confusion echocardiography to see if
there is any clot or not and
then do cardioversion
• Digoxin – preferred if
poor LV function
• CCB & β-blockers are C/I
in patient with poor LV
function

- DOC for Paroxysmal Atrial fibrillation – Amiodarone

- First step in management (Mx) of stable patient with Multifocal Atrial
Tachycardia – rule out etiology [hypoxia, hypokalamia, hypomagnesemia]

∗ Wolff – Parkinson – White Syndrome ( WPW ):

- Short PR interval followed by a wide QRS complex with a Slurred initial deflec-
tion, or delta wave, that represent early ventricular activation (Pre–excitation Syn-
drome)
- Tx: Cardioversion if hemodynamically unstable
- Procainamide is DOC for WPW
+2
– Digoxin & Ca channel blockers are contraindicated

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∗ Torsade de Pointes:
- Prolong QT interval, wide QRS complex
- Drugs : Quinidine
↓ Procainamide
which Disopyramide
block K+ channel Anti- Psychotics
[Phenothiazine & Thioridazine]
- Tx: Magnesium

- First step in management of unstable patient with Torsade de pointes – immediate

defibrillation. DOC for Tx & prevention in stable pt – IV Mg (give Mg regardless
of patient’s Mg level)
Ventricular Arrhythmias

Ventricular Tachycardia Ventricular Fibrillation

• Rate > 120 beats / min • Significant electrical activity on EKG

with no signs of an organized pattern
• IHD – (most commonly seen)
• QRS complexes are wide and often
bizarre
VT (Pulse) Pulseless VT / VF
 ↓
↓ ↓ Cardioversion
Stable unstable
↓ ↓
IV lidocaine 1 mg/kg cardioversion
or
Amiodarone / Procainamide
(Amiodarone is preferred when poor LV
function)

∗ Asystole : 1mg Epinephrine every 3-5 mins

↓
1 mg Atropine every 3-5 mins
↓
2-5 mg Epinephrine every 3-5 mins

 Patent ostium primum (patent foramen ovale) – failure of septum primum to

fuse with endocardial cushions
 Atrial Septal Defect (ASD) – incomplete adhesion b/w septum primum &
septum secondum – Wide fixed split S2
 VSD – defect in membranous interventricular septum
 PDA – machinery murmur – associated with congenital rubella – PGE2 keep it
open – it shunts pulmonary artery blood to aorta in fetus

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 • Coarctation of Aorta:
˗ Turner’s syndrome
˗ Rib notching on CXR, MRI of chest (best test)
˗ Tx: surgery
˗ Endocarditis prophylaxis required

• Tetralogy of Fallot (TOF):

˗ Pulmonary stenosis, VSD, RVH and Over riding of aorta
˗ Boot shaped hert on CXR
˗ Murmur disappears & cyanosis improves when child squats
˗ Single or soft S2
˗ Tx: Surgery
˗ Endocarditis prophylaxis required

• Transposition of great vessels:

- Cyanosis in first 24-hrs of life, Infants of diabetic mothers
- Give PGE1 to keep open PDA until surgical correction done

■ Acute Rheumatic fever:

- Aschoff bodies (pathognomic) [central area of necrosis surrounded by reactive
Histiocytes (Anitschkow cells)]
- Pericarditis, Polyarthritis, Chorea, Erythema marginatum and subcutaneous
Nodules (Jones criteria)
- Usually occur 1-3 weeks after a preceding Strep. Pyogens pharyngitis
- ↑↑↑ ASO titers
- Treatment of acute infection and monthly Penicillin prophylaxis then after.
- Tx of Sydenham’s Chorea (seen several months after acute attack of Rheumatic
fever; carditis and arthritis manifest within 21 days) – Oral penicillin for 10 days
immediately

• Yong child with Mitral stenosis due to Acute Rheumatic fever without any
symptoms, next step?  Penicillin prophylaxis; If AF develop then consider
anticoagulation

Location of Murmur Conditions

Upper Rt sternal border AS, IHSS
Upper Lt sternal border PS, PDA
Lower Lt sternal border VSD
Apex MVP

 Cardiac Myxoma – left atria – mesenchymal tumor – embolic episode in young

person (next step? Send thrombus for pathologic examination, order echo),
syncopal episode – young adult

 Rhabdomyoma – children – associated with tuberous sclerosis – hemartoma

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  Aortic Dissection → cystic medial degeneration (elastic tissue fragmentation) –
Marfan syndrome & EDS (Ehler-Donlas Syndrome) – usually occurs with in
10cm of the aortic valve – cardiac temponade most common cause of death –
Aortic regurgitation, widening of aortic valve root on Echo – loss of upper
extremity pulse due to compression of subclavian artery
 Best step in management of patient with Acute Aortic Dissection – emergent
surgery. First step – give IV beta blockers [Type A – Ascending aorta (emergent
surgery) Type B – Descending aorta (IV beta blockers)]
 Diagnostic test for Aortic dissection  Transesophageal echocardiography or CT
scan

 Abdominal Aortic Aneurysm → pulsatile abdominal mass, next step? → USG

(first step) / CT scan (before repair) → < 4 cm (observe), > 6 cm (elective repair)
● Tender AAA / Excruciating back pain, fainting episodes, unequal femoral
pulses in patient with known case of AAA → Emergency surgery
[Retroperitoneal bleed causes fainting attacks]
● Complication of AAA repair → Ischemic colitis [30% of cases IMA is the
only artery which supply sigmoid colon and by repairing AAA obstruct IMA
which present as severe abdominal pain, foul smelling diarrhea 2-3 days after
repair, next step? → Sigmoidoscopy followed by exploration]

 Peripheral Arterial Disease (PVD): Intermittent claudication / Rest pain, first

step? → Ankle-Brachial pressure index measurement → Arteriogram (most
accurate test) → stop smoking, stop beta-blockers → start Aspirin, Cilostazol
(Antiplatelet vasodilator) → stent / Bypass (most effective treatment)

 Lerich Syndrome: Aortoillio atherosclerosis – atherosclerosis of hypogastric

artery – c/o impotence and claudication

 Deep vein thrombosis: Duplex USG (Best initial test) → Venography (most
accurate test) → If Duplex USG positive, next step? → LMW Heparin (sc) for 5-7
days followed by Warfarin for 3-6 months (INR 2-3) [only in patient with
metallic heart valve keep INR at 3-4]

• Sign & Symptoms of DVT, next step?  Compression UGS to confirm

diagnosis before anticoagulation treatment (to avoid potentially serious side
effects of anticoagulation therapy in unnecessary pt.)

 Fludrocortisone is the first line medicine for orthostatic hypotension but should
be tried after non-pharmacologic trial fail like discontinue dugs causing
orthostatic hypotension [Nitrates, CCB, TCA, Opiates analgesics]

 Best initial test / next step in management of patient with acute syncope – EKG

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 DERMATOLOGY

■ Urticaria: Type – 1 HS – IgE & mast cell mediated – wheals & hives – Tx:
antihistamines, Desensitization (when trigger cannot be avoided)

■ Morbilliform rashes: rash resembles measles – “typical” type of drug reaction –

lymphocyte mediated – maculopapular eruption that blanches with pressure – Tx:
Antihistamines

■ Erythema multiforme: Mycoplasma / Herpes Simplex – target- like lesions that

occur on the palms & soles – Tx: antihistamines and treat underlying problem
(infection)

■ Stevens – Johnson Syndrome: (Erythema multiforme major) – usually involve

< 10-15 % of the total body surface area – target-like lesions – mucous
membrane involvement oral cavity , conjunctiva , respiratory tract –
Hypersensitivity reaction to drugs

■ Toxic epidermal necrolysis: Cutaneous hypersensitivity reaction to drugs – (+)

Nikolsky sign – skin easily sloughs off – 40-50 % mortality rate – Skin biopsy
(most accurate diagnostic test)

■ Staphylococcal scalded skin syndrome: loss of the superficial layers of the

epidermis – Toxin mediated – (+) Nikolsky sign – Tx: Anti–staphylococcal
antibiotics

■ Fixed drug reaction: localized allergic drug reaction that recurs at precisely the
same anatomic site on the skin with repeated drug exposure – round , sharply
demarcated lesions that leave a hyperpigmented spot at the site after they resolved

■ Erythema nodosum: multiple painful, red, raised nodules on the anterior

surface of the lower extremities – recent streptococcal infection, Celiac Sprue
Initial work up (ASO titer, CXR, PPD) – Tx: treat underlying disease

■ Toxic Shock Syndrome: toxin produced from staphylococcal attached to a

foreign body (tampon use in female during menstruation) – fever , Hypotension ,
desquamating rash , vomiting , involvement of mucous membrane –
Hypocalcemia due to capillary leak leads to ↓ albumin level – Tx: fluid
resuscitation, dopamine (for shock), anti-staphylococcal antibiotics

■ Anthrax: Bacillus Anthracis – infected livestock (occupation hazard of wool

sorters) – black eschar – Diagnosis: gram stain & culture – Tx: ciprofloxacin /
Doxycycline

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  Impetigo: superficial bacterial infection – up to epidermis – honey colored
crusted lesions (Strep Pyogens) & Staph Aureus (bullous impetigo) – Tx:
Mupirocin

■ Erysipeals: both dermis & epidermis involve – shiny red, edematous, tender
lesion, fever, chills, bacteremia – Strep Pyogens – Tx: Systemic antibiotics
(Penicillin G)

■ Folliculitis , Furuncles , Carbuncles: Staphylococcus

- Folliculitis → infection of hair follicle
- Furuncles → collection of infected material around hair follicle
- Carbuncles → several furuncles become confluent in to a single lesion
- Hot tub Folliculitis → Pseudomonas
* Treatment : Folliculitis → mupirocin
- Furuncle & carbuncles → Systemic anti-staphylococcal antibiotics

■ Necrotizing Fasciitis: Very high fever, portal of entry into skin, pain out of
proportion to the superficial appearance, presence of bullae, palpable crepitus –
Group A strep (strep Pyogens) – X-ray (best initial test) will show air in the tissue
– surgical debridement (best initial step, next best step in the management, most
accurate test)

■ Dermatophyte Infection: Microsporum, Trichophyton, Epidermophyton

- Microsporum – Skin , Hair , Nail
- Trichophyton - Hair , Nail
- Epidermophyton – Skin , Nail
- Usually annular lesions expand peripherally and clear centrally
- 10 % KOH preparation ( Best initial test )
- Culture ( most accurate test )
- Bright green fluorescence on Wood’s UV lamp – Microsporum canis
[Easy way to remember – all three affect nail, epidermophyton – skin (epiderm =
skin layer)]
* Treatment: only skin (curis, pedis, corporis) → Topical ( Miconazole ) .
- Hair / Nail ( capitis , unguium ) → Oral Terbinafine / Itraconazole .
- Finger nail → 6 weeks oral Tx . - Toe nail → 12 weeks oral Tx
- Gresiofulvin is used in pediatric population. (Terbinafine is not approved by
FDA in pediatric population)

■ Tinea Versicolor: Malassezia furfur (Pityrosporum orbiculare) – white, scaling

lesions that tend to coalesce – Tx : topical Selenium Sulfide

■ Pityriasis rosea: “herald patch” Christmas tree pattern –self-limited – looks like
secondary syphilis except it spares palm & sole – VDRL / RPR → negative .

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 ■ Pediculosis: lice - Dx → direct examination of hear-bearing area – Tx: Pyrethrins
(OTC – over the counter)

■ Telogen effluvium: loss of hair in response to excessive physiological stress.

■ Scabies: primarily involve web spaces of the hand and feet – burrows and excori-
ation around pruritic lesion – Permethrin (Best initial Tx), Lindane • Nor-
wegian Scabies (in immunocompromised person) → Ivermectin oral

■ Alopecia areata: autoimmune – Tx: localized steroid injection – recurrence of

hair loss can occur after successful treatment

■ Solar lentigo: Freckles – sun exposed area in elderly

■ Seborrheic keratosis: verrucoid lesion with “stuck on appearance” – no

malignant potential – Tx: liquid nitrogen or curettage

■ Actinic keratosis: Precancerous lesion – sun exposed area – can progress to

squamous cell CA – Tx: sunscreen, Topical 5-fluorouracil (5-FU), Tretinoin
(emollient cream) [Tretinoin is also used for wrinkles, hyperpigmentation
(mottled) and rough facial skin]

■ Acanthosis nigricans: Verrucoid pigmented skin lesion usually located in Axilla

– Stomach adenocarcinoma, MEN II b, insulin resistance (DM, Obese)

■ Nevocellular nevus ( Mole ): nevus cells are modified melanocytes

- Junctional nevus → basal cell layer ( childhood )
- Compound nevus → extend into superficial dermis ( adolescents )
- Intradermal nevus → compound nevus loses its junctional component (Adult)
- Dysplastic nevus ( Atypical mole ) → ↑ risk for malignant melanoma – yearly
dermatologic examination require

■ Melanoma: Most common type of malignancy – sun exposed area - ↑ risk in

dysplastic nevus syndrome, xeroderma pigmentosa – asymmetry, borders
irregular, color changes, diameter increased – depth of invasion – best
prognostic factor [< 0.76 mm – do not metastasize, > 1.7 mm – potential for
metastasis] – Tx: Surgical excision – Prevention of malignant melanoma 
Protective clothing

■ Basal cell CA : Most common skin cancer – sun exposed area – upper lip
Raised papule, shiny (or) “Pearly ” appearance – Dx → Punch Biopsy

■ Squamous cell CA : Lower lip – sun exposed area, tobacco use, scar tissue in 3rd
degree burn, Actinic keratosis – ulcerated lesion – Dx → Biopsy

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  Marjolin ulcer → development of squamous cell CA in a chronic leg ulcer →
heaped up tissue growth around the edges → Tx: wide local excision & skin
grafting

■ Pemphigus vulgaris – IgG against desmosomes (intracellular attachment in the

epidermis)
- Suprabasal, (+) Nikolsky sign, Oral lesions
- Acantholysis of karatinocytes in the vesicle fluid

■ Bullous Pemphigoid – IgG against basement membrane [IgG & C3 deposit at

dermal-epidermal junction]
- Subepidermal vesicle, (─) Nikolsky sign
- No Acantholysis of karatinocytes in the vesicle fluid

■ Dermatitis Herpetiformis – IgA-anti-IgA complex deposit at the tips of the

dermal papillae
- Subepidermal vesicle with Neutrophils, microscopic blisters
- Strong association with Celiac disease
- Tx: Dapsone

 Psoriasis – coin-shaped lesions cover with silvery-scale – on extensor surface –

nail pitting – development of lesion in area of trauma (Koebner phenomenon) –
bleeding occur when scale is scraped off (Auspitz sign) – neutrophil collection in
stratum corneum (Munro microabscesses) – Tx: Salicylic acid, Vit-A & Vit-D
derivatives, coal tar, anthralin derivatives, infliximab (immunomodulatory agents)
– mild localize [topical high potency steroids (betamethasone 0.05% cream)] –
Drug causing flare up of psoriasis – Lithium, beta-blockers, ACE inhibitors

 Lichen Planus – shiny, discrete, intensely pruritic, polygonal shaped violaceous

plaques and papules – flexor surface – mucous membranes (mouth and external
genitalia) – association with Hepatitis C (30% of cases)

 Porphyria Cutanea Tarda – Phototoxicity (painless blistering on sun exposed

area), facial hyperpigmentation – Dx: urinary uroporphyrins – Tx: avoid
offending agents (ethanol, estrogen)

 Atopic Dermatitis – extreme pruritus – flexor surface - ↑ IgE – avoid scratching–

Tx: topical steroid, antihistamines, tacrolimus (topical immunosuppressants) –
Type-1 HS
˗ Vesicles over the area of atopic dermatitis – Eczema Herpeticum

 Contact Dermatitis – linear, streaked vesicles (weeping lesion) – Type-4 HS

 Seborrheic Dermatitis (dandruff) – scaly, greasy, flaky skin – pityrosporum

ovale – Tx: Zinc, Selenium shampoo

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  Candadial diaper dermatitis – tomato-red color plaques, satellite papules in
perineal area – Tx: clotrimazole cream

 Stasis Dermatitis – hyperpigmentation built up from hemosiderin in the tissue –

varicose veins for long time.

 Xerosis (Asteotic Dermatitis) – dry skin – elderly (due to decrease in lipid) – Tx:
emollient

 Keratoacanthoma: rapidly growing, benign crateriform tumor with a central

keratin plug – sun exposed area. Regress spontaneously with scarring

 Nummular Dermatitis: coin-shaped lesions (discoid lesions)

 Pompholyx: deep-seated vesicles on the palms, fingers and soles

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 ENDOCRINOLOGY

 Hyperprolactinemia: Excess production (Pituitary adenoma) or

Disinhibition [decrease dopamine – dopamine antagonist (Phenothiazine,
metoclopramide) – dopamine depleting agents (methyldopa, Reserpine) –
primary hypothyroidism (increase TRH-activated dopamine which overcome
the normal dopamine inhibition)] Physiologic [pregnancy, breast feeding, stress]
Other [Sarcoidosis] – Microadenomas (amenorrhea, galactorrhea, decrease libido)
– Macroadenomas (visual field defect – heteronymous hemianopsia) – other
important pathology [hypoestrogenism – osteoporosis]
˗ First step in management of Hyperprolactinemia  rule out Hypothyroidism
(measure THS level)
˗ Diagnosis – Prolactin level › 1000 mIU/L suggest pituitary adenoma.
˗ Tx: Bromocriptine (dopamine agonist), surgery if doesn’t get help with drug.
Stop using dopamine antagonist/deplete drugs.

 Acromegaly: ↑↑ GH (gigantism in children) – pituitary adenoma – b/w 3rd

and 5th decade – c/o unable to wear wedding ring, increase in shoe size –
entrapment neuropathy, osteoarthritis, hypertension, impaired glucose
tolerance, heart failure (late) – symptoms for an average of 9 yrs before
diagnosis – Diagnosis: GH level remains › 1 μg/L after giving 100gm of glucose
orally – Tx: Bromocriptine, Octreotide, surgery

 Laron Dwarfism: congenital absent of GH receptor - ↑ GH, ↓ IGF-1 & un-

detectable GH binding protein in blood

 Hypopituitarism: decrease level of one or more pituitary hormones

(decrease in most pituitary hormones is referred as panhypopituitarism) – FSH &
LH (most common), GH then TSH and lastly ACTH – Causes: Pituitary adenoma
Craniopharyngioma, meningioma, gliomas, Pituitary apoplexy (acute hemorrhage
in preexisting pituitary adenoma - emergency), Sheehan syndrome (postpartum
necrosis of pituitary due to loss of blood intrapartum), Infection, Autoimmune,
Empty sella syndrome – amenorrhea, infertility, decrease libido, fatigue, inability
to lactate (1st sign in Sheehan syndrome) - Tx: replacement of hormones. Cortisol
and Thyroid hormones replacement is most important step in management
during emergency. Treat underlying causes

 CT head – No pituitary + normal hormone level – Empty sella Syndrome

 Very small pituitary tumor on MRI, but no abnormality in hormones and absence
of any symptoms, next step? – repeat MRI after 6-12 months

 Diabetes Insipidus: excessive thirst, polyuria (form dilute urine in the

presence of Hypernatremia) – central (insufficient ADH) & Nephrogenic

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 (unresponsiveness of kidney to ADH) – Diagnosis: (1) increase in Urine Osm
after giving vasopressin – central DI. (2) increase Urine Osm after dehydration
– psychogenic – Tx: central DI – vasopressin (SC) / Desmopressin (intranasally,
SC, orally), Chlorpropamide, Carbamazapine (increase ADH secretion) –
Nephrogenic DI – Amiloride (K+ sparing diuretics) – Mx of Hypotension in pt
with DI – IV normal saline

 SIADH: cancers (small cell CA of lung), Drugs (Chlorpropamide,

carbamazapine) – continuously form concentrated urine in the presence of
hyponatremia – Tx: fluid restriction, Demeclocycline, Lithium.

 * Diabetes Insipidus → elevated Serum Osmolarity

* Primary polydipsia (Psychogenic) → both serum & urine diluted
* SIADH → elevated urine osmolarity

 Conn’s Syndrome: Primary Hyperaldosteronism – adenoma of zona

glomerulosa (adrenal gland) – hypertension (sodium retention), hypokalamia
(muscle weakness) – plasma aldosterone to plasma rennin activity (>30 suggest
diagnosis) (Initial screening test) – Tx: resection [D/D: Renal artery stenosis –
BUN:Cr >20:1, abd bruits, hypokalamia is less severe than Conn’s syndrome; If
Hypokalamia in Conn’s is in 2.something range, hypokalamia in renal artery
stenosis is in 3.something range but less than 3.5; (3.5 – 5.0 normal range)]

• Patient with HTN & hypokalemia, next step? – plasma aldosterone and renin ratio
[Dx: Primary Hyperaldosteronism (Conn’s syndrome)]

 Hyperthyroidism: ↑↑ T3 & T4, ↓↓ TSH – heat intolerance, weight loss,

diarrhea, tremor, arrhythmias; Exophthalmos & dermatopathies(only in
Grave’s disease) – Grave’s disease - ↑ RAIU (radioactive iodine uptake), anti-
TSH receptor antibodies. Toxic nodular goiter (single / multiple) - ↑ RAIU. de
Quarian Thyroiditis – subacute granulomatous, giant cell - ↓ RAIU – painful
(transient hyperthyroidism). Subacute lymphocytic Thyroiditis - ↓ RAIU –
painless (transient hyperthyroidism). Ectopic thyroid tissue – struma ovarii – Tx:
antithyroid drugs (only PTU(propythiouracil) safe in pregnancy), radioactive
iodine, subtotal thyroidectomy (only indicated in pregnancy in 2nd trimester) – Tx:
subacute thyroiditis – NSAIDs & beta-blockers

 Tx of Grave’s disease in USA – radioiodine ablation with concurrent

administration of glucocorticoids to prevent worsening of ophthalmopathy

 Thyroid storm: First step Propranolol (to control symptoms) & PTU and
then radio active iodine or surgery for permanent treatment [Radio active iodine
aggravate hyperthyroidism initially so never give it before giving PTU]

 Tx of hyperthyroidism in pregnancy – PTU; if PTU fails, surgery

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  Hypothyroidism: ↓↓ T3 & T4, ↑↑ TSH (primary) but normal / ↓ TSH
(secondary / tertiary) – cold intolerance, weight gain, amenorrhea, carpal tunnel
syndrome, slow deep tendon reflexes with prolonged relaxation phase,
myxedema (prolonged hypothyroidism) – Hashimoto Thyroiditis: anti-
microsomal antibody, anti-thyroglobulin antibody, lymphocytic infiltration –
associated with lymphoma in thyroid gland – Tx: levothyroxine(T4), in secondary
& tertiary first give hydrocortisone then replace thyroid hormone. – Calcium and
Iron preparation decrease absorption of levothyroxine – Estrogen increase
metabolism of levothyroxine therefore it is important to increase dose of
levothyroxine in patient taking HRT – important side effect: AF and osteoporosis
 Congenital Hypothyroidism: apathy, weakness, hypotonia, large tongue,
abdominal bloating and umbilical hernia – MCC of congenital hypothyroidism
in USA – thyroid dysgenesis – Neonatal screening for Hypothyroidism: total T4
and TSH; If T4 is low and TSH is >20 U/L, next step? – repeat free T4 and TSH
on a regular blood draw to confirm diagnosis
 Asymptomatic Hypothyroidism: look for Anti-thyroid antibodies, abnormal
lipid profile or menstrual abnormality – If any out of three present, start
treatment (levothyroxine)

 Myxedema: results from the accumulation of increased amounts of hyaluronic

acid and chondroitin sulfate in the dermis in both lesional and normal skin – can
be seen in both hypothyroidism and hyperthyroidism – jelly like infiltration in
subcutaneous tissue, eye puffiness, non-pitting edema, drowsiness, lethargy and
coma (in severe cases) – Tx: intravenous steroids, levothyroxine

 Reidle Thyroiditis: intense fibrosis of thyroid gland and surrounding

structure.

 Papillary CA: most common thyroid CA – h/o radiation exposure – Tx:

surgery (small), radiation (large tumor)

 Follicular CA: elderly – spread hematogenously – Tx: near total

Thyroidectomy + post-op- radiation.

 Medullary CA: parafollicular cell of thyroid gland - ↑↑↑ Calcitonin –

association with MEN type-2b – more malignant then follicular – Tx:
Thyroidectomy

 Anaplastic CA: elderly – highly malignant with rapid and painful

enlargement of thyroid gland – poor prognosis

 Patient with Thyroidectomy due to CA should receive thyroxine life long. Check
TSH on follow up visit and it should be below normal (<0.35). If it is greater
than 0.35, increase dose of thyroxine

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  Thyroid nodule: measure TSH (first step); If TSH normal, next step? –
FNAC; If TSH decreased, next step? – Radioisotope scan; If hot nodule (increase
uptake of radioisotope), next step? – Observation

 Most common cause (MCC) of thyroid nodule – benign colloid nodule

 2nd MCC of thyroid nodule – follicular adenoma

 Parathyroid Hormone: It stimulates Osteoclast & 1-α-hydroxylase

(increase production of active form of Vit-D → 1-25-(OH)2-D) – increase Ca+2
level by bone resorption (osteoclast) & by absorption of Ca+2 from gut and
kidney (Vit-D).

 Vit-D: increase absorption of both Ca+2 & Phosphorus (PO4) from intestine +
increase absorption of Ca+2 and decrease absorption of PO4 from kidney.

 Magnesium: cofactor for adenylate cyclase – cAMP is require for PTH

activation – therefore hypomagnesemia can cause hypocalcemia
(hypomagnesemia is the most common pathologic cause of hypocalcemia in the
hospital - Cause of refractory hypokalemia in alcoholics → Hypomegnesemia)

 Calcitonin: inhibit bone resorption

 Primary Hypo- / Hyperparathyroidism: plasma calcium & phosphate

levels are changing in opposite direction EXCEPT CRF which causes
secondary hyperparathyroidism but in CRF there is hypocalcemia &
hyperparathyroidism (moves in opposite direction)

 Pseudohypoparathyroidism – resistance to PTH on its target tissue. High PTH

and High phosphorus [true Hypoparathyroidism has high phosphorus and low
PTH; calcium is low in both]

 Secondary Hyperparathyroidism: Increase PTH, decrease Ca+2 level

& its excretion and decrease PO4 level & normal/increase its excretion

 Secondary Hypoparathyroidism: Decrease PTH, increase Ca+2 level

& its excretion and increase PO4 level & normal/decrease its excretion.

 Hypercalcemia: primary hyperparathyroidism (one gland hyperplasia), PTH-

like substance secretion from CA, Immobilization for prolong time [can cause
excessive bone resorption], Sarcoidosis – Osteitis fibrosa cystica, lytic lesions on
x-rays – serum Ca+2 level more than 10.2 mg/dl – Tx: oral rehydration with 2-3
L/day is very effective in chronic form. Sever Hypercalcemia (›15 mg/dl) is an
emergency – IV normal saline (first step), Loop diuretics, IV Pamidronate.

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  Calcium level above 7 in patient with low albumin level (Normal – 4 g/dl) usually
doesn’t require any intervention

 Hungry bone syndrome: hypocalcemia after surgical removal of a

hyperactive parathyroid gland.

 Hypocalcemia: tetany, muscle cramps / spasm, Chovestic sign (percussion of

Facial N. leads to contraction of facial muscles), Trousseau’s sign (inflation of BP
cuff on the arm of patient above SBP for more than 3 mins leads to flexion of
metacarpophalangeal joints and extension of interphalangeal joint), QT
prolongation on EKG – always check for albumin level (1 gm/dl drop in
albumin → calcium level drop by 0.8 mg/dl) – Tx: for acute condition – IV
calcium gluconate, for chronic condition (low Ca & low PO4 – Vit-D deficiency)
– oral calcium 2-4 gm/day, Vit-D; If associated hyperphosphatemia (eg. CRF) –
dietary phosphate restriction, phosphate binders.

 Pathogenesis of DM: Nonenzymatic glycosylation (glucose + AA) →

↑vessel permeability to protein and ↑athrogenesis; Osmotic damage → Aldolase
reductase (glucose → sorbitol) → sorbitol draws water into tissues causing damage
(eg. retinopathy); Diabetic microangiopathy → ↑synthesis of type-IV collagen in
basement membrane & mesangium
˗ Tight blood sugar control decrease the risk of development of microvascular
complication (retinopathy, nephropathy, neuropathy)
˗ ACE inhibitors has shown to reduce insulin resistance

 Diagnosis of DM: symptomatic patient (polyuria, Ploydipsia, polyphagia)

with random blood glucose level › 200 mg/dl or fasting blood glucose › 126
mg/dl on two occasion or blood glucose › 200 mg/dl at 2 hrs and on at least one
of the earlier samples.

 HbA1c: used to follow compliance of the treatment and glucose control in

patient with diabetes.

 Somogyi effect: rebound hyperglycemia in the morning because of counter

regulatory hormone release after an episode of hypoglycemia in the middle of
night.

 Dawn Phenomenon: early morning rise in plasma glucose requiring

increased amount of insulin to maintain euglycemia. [dawn goes up]

 Insulinoma: increase in both plasma insulin and C peptide

 Exogenous insulin administration: very high insulin level but low C
peptide

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  Sulfonylureas: increase in both plasma insulin and C peptide, plasma/urine
sulfonylurea (+) – Tx of refractory hypoglycemia due to sulfonylureas overdose –
Octreotide

 Management of Diabetic Ketoacidosis:

1. IV Normal saline + IV regular insulin
2. correction of electrolyte imbalance (especially K+)
(D 5% in 0.45% saline with potassium after glucose level reaches 200-250
mg/dl)
3. Treatment of precipitating factor.
˗ Important point to remember in Tx of DKA: Start regular insulin subcutaneously
30-60 mins before stopping IV insulin
˗ Cause of hyperkalemia in DKA – extracellular shift of K+
 Tx of Hyperosmolar Hyperglycemia: Hydration and Insulin. Hydration
[hyponatremia / hypovolemic shock – 0.9% NaCl (Normal saline); Hypernatremia
– 0.45% NaCl (half normal saline)]
 Tx of Alcoholic Ketoacidosis – Hydration (IV fluids containing Dextrose) and
Thiamine

• Type-II Diabetic patient with low bicarbonate, normal blood sugar – order ABG
& lactic acid level – Dx: Metabolic acidosis due to Metformin

 Somatostaninoma – diabetes (inhibits insulin release), gall stones (inhibits gall

bladder motility) and Malabsorption (inhibit release of pancreatic enzymes) – Dx:
measure fasting somatostatin level (>160 pg/ml is very suggestive)

 Best screening and diagnostic test for diabetic neuropathy – nerve conduction
studies (show axonal pattern of nerve damage)

 Primary Hypercortisolism (Adrenal Tumor) - ↑ cortisol, ↓ ACTH

 Pituitary Cushing (Cushing’s disease) - ↑ cortisol, ↑ ACTH. High dose
Dexamethasone test - ↓cortisol, ↓ ACTH by 50%
 Ectopic ACTH secretion - ↑ cortisol, ↑ ACTH. High dose Dexamethasone test –
No suppression of ACTH

 Patient with sign & symptoms of Cushing – low dose overnight

Dexamethasone suppression test (best initial test) – if abnormal then order 24
hrs urine-free cortisol – if abnormal (Cushing Syndrome) – then order high dose
Dexamethasone test – if no suppression of ACTH then order ACTH level – if
high ACTH level (Ectopic ACTH secretion – CT chest will be the next step) – if
low ACTH level (Adrenal neoplasia) – then order Urinary 17KS, DHEA-S &
Abdominal CT – if high level of these hormones and greater than 4 cm mass on
CT (Adrenal CA) – if low level of these hormones and less than 4 cm mass on CT
(Adrenal hyperplasia)

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  If low dose overnight dexamethasone test is normal, Cushing is ruled out
 If 24-hrs urine-free cortisol test is normal, no Cushing

 Young patient with HTN, diabetes, osteoporosis and hypokalamia should screen
for Cushing’s syndrome (order dexamethasone suppression test)
 Patient with central hypothyroidism [low normal TSH and low T4], next step? –
rule out adrenal insufficiency (order cosyntropin stimulation test)
 Tx of acute adrenal insufficiency – IV Dexamethasone (long acting)
 Short-term use of glucocorticoids (less than 3 wks) even in high dose can be
discontinued rapidly without causing significant adrenal insufficiency

• Bitemporal hemianopsia & tanned skin (hyperpigmentation) following

adrenalectomies for Cushing’s disease – Nelson’s syndrome

 17 α Hydroxylase Deficiency: ↓ cortisol and androgen but ↑ 11

deoxycorticosterone (weak mineralocorticoid due to which retention of sodium
occur and hypertension develop)
 21 β Hydroxylase Deficiency: ↓ cortisol and mineralocorticoid but ↑
androgens
 11 β Hydroxylase Deficiency: ↓ cortisol but ↑ androgens and
mineralocorticoid

 Increase ACTH in all of 3 enzymes deficiency (above)

 Male ambiguous genitalia (male pseudohermaphrodite) – 17 α Hydroxylase
 Female ambiguous genitalia (female pseudohermaphrodite) – 21 & 11 β
Hydroxylase
 Female Hypogonadism – 17 α Hydroxylase
 Precocious puberty in male – 21 & 11 β Hydroxylase
 Dx of 21-Hydroxylase deficiency is confirmed by documenting elevated 17-alpha
hydroxyprogesterone (not 17-alpha hydroxypregnenolone)

 MEN 1 (Wermer) – Pancreas (ZE syndrome), Pituitary, Hyperparathyroidism

(3P)
 MEN 2a (Sipple) – Hyperparathyroidism, Pheochromocytoma, Medullary CA
of Thyroid
 MEN 2b (3) – Pheochromocytoma, Medullary CA of Thyroid, mucosal neuroma
(lips/tongue)

 Presence of Y chromosome – germinal tissue differentiate in to Testes.

 hCG + LH → leyding cells → testosterone → wallfian duct (epididymis, ductus
deference, ejaculatory duct) → 5 α reductase convert testosterone in
dihydrotestosteron (DHT) which induce urogenital sinus & genital tubercle to
form penis, prostate & scrotum.
 Sertoli cells → secrete MIF (mullerian inhibiting factor) which inhibit
paramesonephric duct (uterus, uterine tubes, cervix & upper part of vagina)
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  If MIF absent – uterus (paramesonephric duct structure) develop with normal
male structure
 If Testosterone absent – wallfian duct regress (male internal structure not
develop)
 If 5 α reductase absent – DHT not formed. Therefore male external structures
not develop but female external structures develop.
 Absence of Y chromosome – germinal tissue differentiate in to Ovaries. Wallfian
(mesonephric duct) regress and female genitalia develop.
 Testicular Feminization – androgen receptor insensitivity, Mullerian duct
structure develop in the presence of testes. (No effect of testosterone & DHT)

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 GESTROENTEROLOGY

• Choanal atresia – Child become cyanotic when feeds and turn pink when cries

• Gastroschisis → first step? → Sterile wrapping of exposed bowel; next? 

orogasric tube to decompress stomach & IV nutrition

• Omphalocele → shiny, thin, membranous sac at the base of the umbilical cord,
cord goes to the defect, not to the baby → can have multiple defects

• Pyloric Stenosis → Projectile vomiting in infants – hypertrophy of pyloric region

→ Usage of Erythromycin is associated with infantile hypertrophic pyloric
stenosis → Diagnostic test: Abdominal USG → First step in management: IV
fluids & K+ supplement → Tx: Pyloroplasty

• Infant with congenital diaphragmatic hernia, next step?  orogastric tube

placement

* Dysphagia:
 Best Initial Test → barium swallow / barium esophagus
 Dysphagia for solids not liquid → Obstruction – stricture, esophageal CA
Plummer–Vinson Syndrome
• Dysphagia for solids and liquid → Peristalsis problem – Achalasia , Systemic
Sclerosis, CREST, Polymyositis

* Achalasia – Absent myenteric ganglion

• Most accurate test – esophageal manometry [normal amplitude contraction with
high tone of lower sphincter (failure to relax)]
• Best Initial Therapy – pneumatic dilatation

* Esophageal spasm – “corkscrew” pattern on barium study

• Most accurate test – esophageal manometry [high amplitude contraction with
normal relaxation of lower esophageal sphincter]
• Tx: Ca + 2 channel blockers, Nitrates

* Scleroderma [Progressive Systemic Sclerosis (PSS)]

• Most Accurate test – esophageal manometry (absence peristalsis wave with
very low tone of lower esophageal sphincter)
• Tx: Proton-pump inhibitors, Metoclopramide

* Ring & Webs :

• Schatzki’s ring – more distal & located at the squamocolumnar junction
• Plummer-Vinson – more proximal & located in the hypopharynx [iron
deficiency anemia]
• Diagnosis → Barium swallow / Barium esophagus – Tx: Dilatation

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 * Esophageal CA : Tobacco + Alcohol → SCC →Upper 2/3
• GERD & Barrett esophagus → Adenocarcinoma → lower 1/3
• Endoscopy is mandatory. CT chest → to detect degree of spread

* Zenker’s Diverticulum: out pocketing of the posterior pharyngeal Constrictor

muscles at the back of the pharynx
• Bad breath, aspiration pneumonia / lung abscess (anaerobic)
• Diagnosis → Barium study (Esophagography)
• Tx : Surgical resection (Endoscopy & placement of nasogastric tubes are C/I)

• Patient present with aspiration pneumonia due to Zenker’s diverticulum started on

antibiotics (treatment for pneumonia), next step? Esophagography (barium). [Not
scopy]

* Gastroesophageal Reflux Disease ( GERD ):

• Epigastric pain going under sternum , non-productive cough at night (it can cause
worsening of asthma at night by irritating bronchus), bad taste in mouth
• Most Accurate Test → 24-hrs PH monitoring
• Tx: PPIs (best initial), Metoclopramide, H2 – blockers, Nissen fundoplication

• Sliding Hernia of esophagus – GE junction displaced & reach above

• Paraesophageal Hernia – GE junction not displaced

* Barrett Esophagus: Metaplasia (squamous → columnar)

˗ Repeat Endoscopy every 2-3 yrs
˗ Low grade dysplasia → repeat endoscopy in 3-6 months
˗ High grade dysplasia → distal esophagecomy
˗ All patients with Barrett esophagus should be on PPIs

* Mallory Weiss Tear → continuous retching followed by large painless bloody

vomiting (mucosal tear) → Hiatal hernia [predisposing factor] → Endoscopy
(best initial) → Tx: resolve itself

* Boerhaave Syndrome → continuous retching followed by severe chest pain,

Crepitation in the neck, air in mediastinum on CXR [Esophageal rupture – usually
in distal third, posterolateral segment (where there is no serosa) is the most
common site] → Tx: emergency surgical repair

• Esophagitis: Candida Albicans (MCC) typically in HIV patient (CD 4 < 200)
• Next step → Empiric Tx with Fluconazole
• HIV positive → C/O Odenophagia →Already on Anti-fungal → Endoscopy (next
step) Other causes of Esophagitis → HSV, CMV, Aphthus ulcers

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 * Epigastric Pain

↓ ↓
Young Patient without any S/S Patient > 45 yrs. Old
Suggestive of CA with / without S/S suggestive of CA
(Dysphagia, wt. loss)
↓ ↓
Empirical Treatment Endoscopy with biopsy
(PPIs / H2 – blockers)
↓ If no improvement
Endoscopy with biopsy

* Diagnosis of H.pylori:
• Serology (Best initial test), urea breath testing, stool antigen
• Endoscopy with biopsy & histology (Most accurate test)
• CLO test → rapid test on biopsy which check Urease produced by H. pylori
• Breath & Stool Test → Best post-treatment test to check eradication of H. pylori
• Tx: PPI + Clarithromycin + Amoxicillin
• If organism is eradicated & still ulcer persist → check for ZE syndrome

* Zollinger–Ellison Syndrome (ZE syndrome):

• Multiple recurrent ulcers (usually duodenum) , Steatorrhea
• Associated with MEN – I (Parathyroid, Pituitary, Pancreas)
• ↑↑↑ acid production inactivate pancreatic enzymes → malabsorption
• Diagnosis: Elevated gastrin level
• Secretin stimulation test (if gastrin level is non diagnostic in suspected patient)
• Next step after Diagnosis → search for metastasis
↓
Nuclear test (Somatostatin receptor scintigraphy)
• Tx: Localize → Surgical resection, Metastasis → PPIs

* Gastritis:
• Type – A → Atrophic gastritis (Autoimmune) , Vit-B12 deficiency , ↑↑↑ gastrin
• Type – B → NSAID, H. Pylori, Alcohol
• Tx: Vit- B12 replacement, PPIs, H2 – blockers
• Increase chance of gastric CA in patient with Type-A gastritis

* Gastroparesis: weak stomach

• Diabetes neuropathy (MCC)
• C/O early satiety, Postprandial nausea, ↑ Abdominal fullness
• Diagnosis → gastric emptying study
• Tx: Erythromycin / Metoclopramide

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 * Dumping Syndrome:
• 1St → hypertonic chyme release in duodenum → osmotic draw into duodenum
leading to intravascular volume depletion
• 2nd → sudden ↑ in glucose level → ↑ insulin release → Hypoglycemia
• Tx: Eat multiple, small meals

• Protein loosing enteropathy: Enlarge rugal folds – hypertrophy of mucous

cells (Menetrier disease, ZES, lymphoma)

■ Inflammatory Bowel Disease:

* Crohn’s Disease [CD]: Oral / Perianal involvement , palpable Abdominal mass
(granuloma – characteristic of Crohn), Transmural involvement, Skip lesions,
Fistula formation
* Ulcerative colitis: rectum involvement, bloody diarrhea , exclusive mucosal
disease – Patient with ulcerative colitis and pancolitis should begin surveillance
colonoscopy after 8 yrs of having the disease
* Best diagnostic Test → Endoscopy
˗ CD → Anti–Saccharomyces cerevisiae antibodies (ASCA)
˗ UC → ANCA
• CD → Vit–B12, Vit–K, Ca +2, iron deficiency → elevated PT, kidney stones,
Megaloblastic anemia
* Tx: Mesalamine [5-Aminosalicylic acid (5-ASA)] derivatives (best initial)
• Infliximab → CD with fistula formation / refractory to other therapy
• Acute Exacerbation → High dose steroids (Budesonide)

• Young patient with bloody diarrhea, if normal rectosigmoidoscopy – Crohn’s

disease; If rectum if affected – Ulcerative colitis

* Lactose Intolerance: lactase deficiency

• Diarrhea associated with gas & bloating after drinking milk
• Never has blood / WBC in stool
• Diagnosis: stool osmolarity > expected osmolarity, Positive Hydrogen breath test,
positive Clinitest of stool for reducing sugar
• Tx: Remove milk product from diet (symptoms resolve in 24-36 hrs)

* Irritable Bowel Syndrome:

• Abdominal pain relieved by bowel movement
• Diarrhea alternating with constipation
• Tx: High – fiber Diet. Diarrhea predominant → loperamide / diphenoxylate
• Anti–spasmodic agent → dicyclomine / hyoscyamine
• Alosetron → Diarrhea predominant [restricted access in USA]
• Tricyclic Antidepressant → resistant cases

• Tx of chronic constipation in child – dietary modification; If it fails, use laxatives

(milk of magnesia)
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 * Carcinoid Syndrome: tumors of the neuroendocrine syndrome
• Tip of vermiform appendix (most common site) but carcinoid tumors of terminal
ileum most commonly metastasize (liver) and produce carcinoid syndrome
• Diarrhea, Flushing, Tachycardia and Hypotension
• Niacin deficiency (Serotonin & Niacin → Tryptophan)
• Endocardial fibrosis , Tricuspid Regurgitation , Pulmonic stenosis
• Diagnosis : urinary 5 – HIAA ( 5- hydroxyindolacetic acid )
• Tx: Octreotide

* Celiac Disease:
• Anti-gliadin, Anti-endomysial, Anti-transglutaminase antibodies
• Loss of intestinal villi (malabsorption – diarrhea, abd distension, abd pain)
• Celiac disease affect PROXIMAL small bowel
• Function returns if patient is on gluten free diet
• Dermatitis herpetiformis → strong association with celiac disease
• No wheat, rye, oat [contains gluten]

* Whipple’s Disease: Tropheryma whippeli bacilli

• PAS–positive macrophage obstruct lymphatic & reabsorption of chylomicrons
• Chronic diarrhea and weight loss
• Tx: Sulfamehoxazole / trimethoprim or Doxycyclin × 6 months

• Chronic diarrhea, WT loss, generalized lymphadenopathy but no risk factor for

HIV  Whipple diseases  endoscopy with small bowel biopsy (PAS positive
material in lamina propria) [HIV will always there in 5 choices to confuse]

* Diverticulosis:
• Lack of fibers in the diet
• Right sided bleed / Left sided obstruct
• Most common cause of lower GI bleed. (Angiodysplasia – 2nd MCC)
• Most common source of diverticular bleeding – erosion of the artery
• Tx: Increase fibers in diet

• Patient with diverticulosis (showed on colonoscopy) present with active Bleeding

& now stabilized after resuscitation, next step? labeled erythrocyte scintigraphy
(to find source of bleeding)

* Diverticulitis: (left sided appendicitis)

• CT scan (Best test) [Barium study & Endoscopy – contraindicated]
• Tx: Ciprofloxacin and Metronidazole

• Sigmoid colon: most common site for diverticulosis, diverticulitis and polyp
• Rectosigmoid colon: most common site for colon CA

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 • Volvulus of Sigmoid colon → Elderly patient → distended abdomen, similar
episodes in past which resolve itself → Parrot’s beak appearance (coffee bean
sign / omega sign) of large gas shadow on X-ray → Tx : Rigid sigmoidscopy –
Rectal tube → bowel preparation & elective surgery

 Ogilvie Syndrome → Abdominal distension , without tenderness in elderly

sedentary patient after surgery elsewhere in the body (but not Abdominal
surgery) → X-ray : distended colon with cut-off at splenic flexure → Tx :
colonoscopy (both diagnostic & therapeutic); if recur then do colonoscopy one
more time; if still recur then start Neostigmine drip; Cecostomy is the last resort

• Mesenteric Ischemia → Patient with h/o AF / atherosclerotic disease present

with acute abdomen and low bicarbonate (pain out of proportion to physical
findings like absent rebound tenderness, guarding, rigidity, etc) & blood in stool

• Mechanical Intestinal Obstruction → Abdominal pain, constipation, distension

& vomiting (cardinal features of obstruction) → Adhesion / Indirect Inguinal
Hernia
- Fever, leukocytosis, rebound tenderness in patient with indirect inguinal hernia
suggest strangulation

 Paralytic Ileus → post-op-abdominal distension, without tenderness → X-ray →

dilated small bowel, without air fluid level → Absent bowel sound → Tx : NPO
and NG tube suctioning until peristalsis resumes

 Post-op-Intestinal Obstruction: Adhesion → X-ray: multiple air fluid level →

Barium tag: it will “hang” somewhere if there is a mechanical obstruction → Tx:
Reoperation

• Meconium ileus → cystic fibrosis → ground glass appearance on abd x-ray →

Gastrografin enema (both diagnostic & therapeutic)

* Meckle’s Diverticulum → painless large bloody bowel movement in child

(brick red stool) → Technetium scan (99mTc scan) to identify ectopic gastric
mucosa [rule of 2’s – 2 ft from ileocecal valve, 2 inches long, 2 yrs of age, 2% of
population; remnant of Vitelline duct (Omphalomesenteric duct)]

• Hirschsprung Disease (aganglionic megacolon) → Rectal exam may lead to

explosive expulsion of stool & flatus → X-ray: distended proximal colon
(normal) and “normal looking” distal colon (aganglionic).

• Intussception → sausage shaped mass on the right side of the abdomen,

“empty” looking right lower quadrant (Dancing sign), “currant jelly stool”

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 • Acute Abdomen: (rebound tenderness, guarding, rigidity) → Exploratory
laparotomy (1st step in management) [Medical treatment for Any Acute
Abdomen → NPO, NG suction, IV fluids]
 Classic presentation of Acute Appendicitis [pain start in mid epigastric region
and then shifted to RLQ, positive rebound tenderness, Psoas sign, Rovsing’s sign,
etc], next step? → Appendicectomy
 Above presentation, On Abdominal exploration, Appendix is normal but ileum is
inflamed (Crohn’s ileitis), next step? → Proceed with Appendicectomy and close
the abdomen
 Above presentation, On Abdominal exploration, Appendix is normal but ileum &
cecum are inflamed, next step? → Do nothing and close the abdomen [when
cecum is inflamed, Appendicular stump doesn’t heal and it can cause fecal fistula
which leads a hemicolectomy]
 Female patient without classical presentation of appendicitis, next step? → USG
 Classic presentation of appendicitis but 6-7 days old pain, mass on abdominal
palpation, diagnosis? → Appendicular mass, next step? → IV fluid, bowel rest,
IV antibiotics, serial examinations
 If above scenario, 24-hrs after starting treatment, patient is getting worse (spiking
fever, tachycardia, increase in localize tenderness), next step? → CT scan
(Appendicular abscess) → Tx : CT guided drainage

* Gastrointestinal Bleeding:
• First step → Resuscitation / Treatment then find etiology
• FFP → if PT is elevated
• Platelate transfusion → if count < 50,000 / mm3 & Patient is acutely bleeding
• If h/o cirrhosis → Octreotide
* Esophageal Varices → Octreotide during acute episodes
• If still bleeding → emergency endoscopy & place bands around the bleeding
Varices
• If still bleeding → TIPS (complication → worsening of hepatic encephalopathy)
• Propranolol → for prophylaxis of portal HTN
• BUN level is often elevated in patient with upper GI bleed. BUN level >40 in the
presence of normal serum creatinine is very suggestive of upper GI bleed
• Diagnosis of GI bleed:
• Endoscopy (most accurate test)
• Nuclear bleeding scan
• Angiography
• Capsule endoscopy (to visualize small bowel)

• Angiodysplasia (vascular ectasia) – Second most common cause of lower GI

bleeding – Aortic stenosis has been associated with Angiodyplasia

* Colon Cancer: colonoscopy

• Hyperplastic polyp , Juvenile polyp , Peutz –Jeghers → No malignant potential

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 • Tubular polyp (most common neoplastic polyp) , villous polyp , Familial
Polyposis , Turcot syndrome , Gardner syndrome → malignant potential

* Hereditary Non-Polyposis Syndrome (HNPCC) (Lynch Syndrome):

• Mis-match base repair defect
• Colonoscopy every 1-2 yrs start at age of 25 yrs
• Very high incidence of ovarian and endometrial cancer

* Familial Adenomatous Polyposis:

• APC gene confers 100 % penetrance for the development of adenomas by the age
of 35 & colon cancer by the age of 50
• Flexible sigmoidoscopy every 1-2 yrs start at age of 12
• As soon as polyps are found → colectomy.

* Cowden Syndrome:
• Hemartomas, rectal bleeding in a child

* Gardner Syndrome:
• Colon CA + multiple soft – tissue tumors (osteoma, lipoma, fibrosarcoma)

* Turcot Syndrome:
• Colon CA + CNS malignancy

* Peutz – Jeghers Syndrome:

• Hemartomatous polyp + Hyperpigmented spots (lips, buccal mucosa, skin)

• Hemorrhoids / Anal fissure → Proctosigmoidscopy [1st examination then Tx]

[Any anorectal problem (even abscess) → rule out cancer 1st by appropriate
examination and then treatment]

* Acute Pancreatitis:
 Mid epigastric pain classically radiates straight to the back.
 Amylase & lipase (most specific) are extremely elevated
 CT scan (Most accurate test)
 Ranson’s criteria: within first 48-hrs [age(>55yrs), WBCs (>16,000), LDH
(>350 IU/L), Blood sugar (>200 mg/dl), AST (>250 IU/L)] After 48-hrs [Po2
(<60 mmHg), Calcium (<8 mg/dl), BUN increases (>5mg/dl), Hematocrit de-
crease (>10%), Albumin (<3.2 mg/dl), estimated fluid deficit (> 4 L)]
 Billiary & Pancreatic ductal pathology → ERCP (most accurate test)
 Tx: Supportive (NPO, IV fluids, etc). ERCP (sometimes) to remove stone in the
pancreatic duct or to dilate a stricture
 h/o Acute Hemorrhagic pancreatitis + fever & leucocytosis → Pancreatic
Abscess → Tx : Require Drainage
 Pseudopancreatic cyst of less than 6 weeks → observe
 Pseudopancreatic cyst of greater than 6 weeks → intervene

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 * Chronic Pancreatitis:
• Chronic abdominal pain in chronic alcoholics; h/o recurrent acute pancreatitis
• Calcification of pancreas on x-ray / CT scan (initial test)
• Stool elastase; Secretin Test → low trypsin level (most accurate test)
• D-Xylose Test → to differentiate b/w celiac disease / chronic pancreatitis
• If no Absorption of D–Xylose → Celiac Disease
• Tx of Steatorrhea due to chronic pancreatitis – diet modification (low fat diet); If
it fails, give pancreatic enzyme supplements
 Pancreatic head cancer: Palpable gallbladder without significant tenderness

* Billirubin: Senescent RBC → Heme → unconjugated Bilirubin (lipid soluble – can

accumulate in tissue so large amt in blood can cause problem) → bind with
albumin and goes to liver → conjugated in liver [water soluble – easy for our body
to excrete] → secreted in bile → 80% excreted in feces & 20% extrahepatic
circulation [90% liver and 10% renal (in urine)]
* Jaundice: ↑ unconjugated [more hemolysis, liver unable to pick up (Gilbert
syndrome – jaundice with fasting), liver unable to conjugate (Crigler-Najjar
syndrome – deficient enzyme)] ↑ conjugated [liver unable to excrete in bile
(Dubin-Johnson syndrome – black liver) (OCP), ↓ extrahepatic bile flow (gall
stone, CA of head of pancrease)] ↑ Both [liver dysfunction (hepatitis)]
• Pruritus in Billiary disease is due to bile salt which deposits in skin
• For Jaundice, we test billirubin in urine with strip test not urobillinogen (UBG).
UBG is normally present in urine. UBG is absent in obstructive jaundice but
billirubin (conjugated – water soluble) is present in urine in obstructive jaundice

■ Neonatal Jaundice:
- Within first 24-hrs – Pathological [ABO incompatibility (most common cause),
Rh incompatibility, Sepsis, Spherocytosis, G6PD, etc], >13 mg/dl (indirect /
direct hyperbilirubinemia)
- Between 24-36 hrs – Physiological [resolved by 7-10 days, monitor bilirubin
level to prevent Kernicterus (lethargy, irritability, hypotonic seizure) (rare)],
rarely exceed 12.9–15 mg/dl (indirect hyperbilirubinemia)
- After 1 week – Breast milk [diagnosis of exclusion]
- Tx: Phototherapy for indirect hyperbilirubinemia to prevent kernicterus
• Billiary Atresia → Persistent, Progressively increasing jaundice in newborn →
HIDA scan after week of Phenobarbital → If no bile reaches the duodenum after
Phenobarbital stimulation → surgery

* Cirrhosis:
• Best initial test to assess liver cell damage – serum Transaminases
• Liver biopsy (most specific test)
• AST/ALT - >2 is quite specific for alcoholic liver disease. (increase GGT is also
seen in alcoholic liver disease)
• AST - >500 – should suspect viral / toxins / ischemia (AST level in alcoholic liver
problem is usually below 450)

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 • Portal HTN, Esophageal Varices, Ascites, Peripheral edema, elevated PT, low Al-
bumin, spider angioma, palmar erythema, asterixis
• Serum : Ascites albumin gradient ( SAAG ):
SAAG > 1.1 → portal HTN
SAAG < 1.1 → cancer, Infection

• Ascitic patient, already on furosemide, spironolactone, protein & salt restriction

diet, has passed little urine, diagnosis?  Hepato-renal syndrome; next step? 
careful volume loading and stop diuretics
• Respiratory distress due to abdominal distension in cirrhotic patient, next step? 
Paracentesis (diagnostic & therapeutic)

• Management of Ascitic patient:

1. Sodium and water restriction
2. Spironolactone [Anti-androgenic action helps decreasing effect of estrogen]
3. Loop diuretics (furosemide)
4. Frequent abdominal tapping

* Spontaneous Bacterial Peritonitis (SBP):

• Culture of the fluid (most specific test)
• Total WBC > 500 / mm3 / > 250 /mm3 neutrophils → Infection is present
• Cefotaxime / Ceftriaxone (drug of choice)

• Subacute bacterial peritonitis in Ascitic patient, next step?  paracentesis; not

diagnostic peritoneal lavage which is done in blunt abdominal trauma

* Primary Billiary Cirrhosis:

• Anti-mitochondrial antibody
• Granulomatous destruction of bile ducts in portal triad
• Middle – aged women, very less elevation of bilirubin, strong association with
other auto-immune diseases → Sjogren Syndrome, RA, Scleroderma
• Diagnosis: Transaminase are often normal
↑↑ Alkaline Phosphatase & γ - glutamyl transpeptidase
• ↑ risk for hepatocellular carcinoma [HCC]
• Tx: Bile acid sequesters (cholestyramine, Ursodeoxycholic acid), UV light for
Pruritus
• Ursodeoxycholic acid slows the progression of Primary Billiary Cirrhosis (PBC).

* Primary Sclerosing Cholangitis:

• Obliterative fibrosis of intrahepatic & extrahepatic bile ducts
• Strong association with Ulcerative colitis
• Sx – same as primary billiary cirrhosis ( Pruritus; etc)
• Anti-mitochondrial Antibody → negative
• ↑ risk for cholangiocarcinoma (CA of bile duct)

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 * Hemochromatosis:
• Most common inherited genetic disease
• Over absorption of iron [Ferritin (major storage protein) store iron in macrophage
in bone marrow and hepatocytes, circulate in small amt in serum (↓ in iron
deficiency anemia); Hemosiderin degradation product of Ferritin in cell, (doesn’t
circulate) golden brown granules in tissue & blue with Prussian blue]
• Intracellular iron produce hydroxyl ions which damage parenchymal cells
• Cirrhosis, Restrictive cardiomyopathy, Arthralgia, skin hyperpigmentation,
diabetes, Hypogonadism
• ↑ infection with Vibrio vulnificus, Yersinia & L.monocytogens
• Most appropriate treatment of Hemochromatosis – therapeutic phlebotomy

* Wilson Disease:
• Autosomal recessive disease
• ↓ copper transport into bile and ↓ ceruloplasmin synthesis leads to ↓ excretion of
copper from body & ↑ free Cu +2 in the body which deposited in various tissue
and produce damage
• Basal ganglia dysfunction (choreoathetoid movements), Kayser-Fleischer ring
(Slit – lamp Examination), Fanconi Syndrome

• Ruptured Hepatic Adenoma → young woman on birth control pills present

with abdominal pain, low hemoglobin, hypovolemic shock → CT Scan →
Surgical removal

• Amebic liver abscess → h/o Travel to Mexico → jaundice, weight loss, right
upper quadrant pain, diarrhea → Serology for amebic titers → Metronidazole ( if
not cured with Metronidazole → Aspiration )

• Liver Problem → ↑↑↑ transaminase Billiary Problem → ↑↑↑ Alkaline

Phosphatase Alcoholic liver Problem → ↑↑↑ GGT (γ–glutamyl transferase )

* Choledochal cyst – congenital benign dilatation of bile ducts

* Caroli’s Syndrome – congenital cystic dilatation of the intrahepatic biliary tree –
associated with polycystic kidney disease – Cholangitis & Cholangio CA

* Gall stone (Cholelithiasis):

• Cholesterol (80%) (radiolucent) - ↑cholesterol in bile and ↓bile salt & lecithin
• Pigment stone (20%) (radio-opaque) – calcium bilirubinate [Sickle cell anemia]
• Billiary colic → colicky right upper quadrant pain, radiate to the right shoulder,
often aggravated after ingestion of fatty food / Anti-cholinergic drug → USG
[presence of gall stones, no thickening of GB wall]
• Acute Cholecystitis → Female , Forty , Fertile , Fatty → colicky right upper
quadrant pain, radiate to the right shoulder, often aggravated after ingestion of
fatty food → USG [presence of gall stones, thickening of GB wall,
pericholecystic fluid]
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 ˗ Typical acute Cholecystitis presentation but negative USG → HIDA scan
˗ Tx : If patient present within 3 days of onset of pain → Emergent laparoscopic
cholecystectomy; If patient present after 3 days of onset of pain → medical
treatment as of acute abdomen followed by elective cholecystectomy; but if
medical treatment fail → Emergent open laparotomy
˗ Air in GB wall on X-ray → emergent laparotomy
˗ Air in GB, stone in terminal ileum (small bowel obstruction) → GB-enteric fistula
˗ Air within Billiary tree after ERCP → billiary enteric fistula
˗ Any patient with symptomatic gall stones / gall stones complications
(Pancreatitis, Cholangitis, Obstructive jaundice) should not go home without
cholecystectomy
˗ Post-cholecystectomy pain → sphincter of oddi dysfunction, CBD stone or
functional pain

• Obstructive Jaundice → USG (Best next / 1st step in management)

˗ if it is due to gall stone → ERCP (remove gall stone) then laparoscopic
cholecystectomy
˗ If it is due to CA (wt. Loss, Asymptomatic Jaundice) → CT scan → Percutaneous
biopsy → Tx
˗ If it is due to CA (wt. Loss, Asymptomatic Jaundice) → CT scan (negative) →
ERCP → Tx

* Gallbladder adenocarcinoma:
• Risk factors – cholelithiasis, porcelain gallbladder [calcification of GB wall]

 Infant on milk formula – necrotizing enterocolitis – transmural necrosis

 Reye Syndrome:
- Encephalopathy and microvesicular steatosis in Liver
- Recent viral URI, [Varicella, Influenza + Aspirin use].
- Ammonia, Transaminases are markedly elevated
- Liver biopsy → non-inflammatory fatty infiltration, mitochondrial injury

• Hep A vaccine should be given to all unimmunized patient with underlying

chronic liver disease
• Almost all patients with Hep C infection who undergo transplantation have a
documented recurrence of Hep C infection in the transplant liver.
• Tx of acute Hep B (patient already have symptoms) – supportive care
• Tx (prophylaxis) of Hep B exposure (patient has exposed but doesn’t have
symptoms, eg. Needle prick) – Immunoglobulin + Hep B vaccine

S.S.Patel. All rights reserved. Registered with US copy right office 40

 HEMATOLOGY

* Anemia: low Hb (<13 in M & <12 in F) / low hematocrit (<40 in M & <37 in F)
↓
Next step: determine MCV

Microcytic ( MCV < 80 ) Normocytic Macrocytic ( MCV > 96 )

• Iron deficiency • Hemolytic anemia • B12 deficiency

• Thalasemia • ACD • Folate deficiency

• Sideroblastic Next step? – Reticulocyte

count
• Lead poisoning ↑ Reticulocyte count -
Hemolysis
• Anemia of chronic ↓ Reticulocytes – bone
diseases ( ACD ) marrow failure

* MCHC : Mean corpuscular Hb concentration (Avg. Hb concentration in RBC)

↓ MCHC → central area of pallor – Microcytic
↑ MCHC → No central area of pallor – Spherocytosis
N MCHC → Megaloblastic Anemia

• Hb A - α , β Hb F - α ,γ Hb A2 - α , δ
• Daily requirement of Iron – 1 mg/day in M, 2-3 mg/day in F

* Iron Deficiency Anemia:

• Low serum ferritin, serum iron , high TIBC
• Blood loss (menstruation), dietary deficiency
• Most specific test: Bone marrow biopsy

* ACD (Anemia of Chronic Diseases):

• Normal / elevated serum ferritin
• Both serum iron & TIBC → Low
• In treatment of ACD, if erythropoietin level is normal, then periodic blood
transfusion is the best choice to improve anemia

* Sideroblastic Anemia:
• Normal serum ferritin
• Very high transferrin saturation
• High serum iron & Low TIBC
• Most specific test: Prussian Blue stain of RBC in the marrow will show ringed
sideroblast
• Vit-B6 deficiency: ↓ Protoporphyrin & ↓ δ ALA

S.S.Patel. All rights reserved. Registered with US copy right office 41

 • Iron deficiency: ↑ Protoporphyrin & N δ ALA
• Lead poisoning: ↑ Protoporphyrin & ↑ δ ALA

* Thalassemia:
• Underproduction of alpha/beta globin chain
• very low MCV, very low RBC count compare to iron deficiency
• Target cells, Normal serum iron & RDW

Electrophoresis

↓ ↓
Normal Abnormal
↓ ↓
α - Thalassemia trait β - Thalassemia
↓ ↓
All Hb requires α chain for synthesis ↑ Hb A2
So Hb concentration decrease but ↑ Hb F
Relative proportion of the normal
Hb remains the same

- Thalassemia traits of both α & β do not require specific treatment

- Thalassemia major ( β ) requires periodic blood transfusion
- Tx of Iron overload (due to periodic blood transfusion) → Deferoxamine

 “Crew haircut” on skull X-ray is distinctive radiological change seen most often
in patient with Sickle cell anemia & Thalassemia major.

♦ Macrocytic Anemia ♦

↓ ↓
Vit – B12 deficiency Folic acid deficiency

• Peripheral Blood smear: Hypersegmented Neutrophils seen in Both

• How to differentiate: Low B12 level Low RBC folic acid level
↑ Methylmalonic acid
level is seen in only B12

• Schilling Test is occasionally used to determine etiology of B12 def

• Schilling Test: Oral Administration of Radioactive Vit – B12
• Reabsorption → Pure vegan
• B12 + IF → Reabsorption → Pernicious Anemia
• B12 + Antibiotics → Reabsorption → Bacterial over growth
• B12 + Pancreatic extract → Reabsorption → chronic Pancreatitis.

S.S.Patel. All rights reserved. Registered with US copy right office 42

 • Important: Vit-B12 and folic acid require for DNA synthesis in all cells so their
deficiency affect all bone marrow cells, not just RBC.
• Treatment : Vit – B12 IM Folic acid orally

• Diamond-Blackfan Syndrome (congenital hypoplastic anemia) – intrinsic

defect of erythroid progenitor cells which results in increased apoptosis –
megaloblastic anemia without hypersegmented neutrophils [In Vit-B12 and
Folic acid deficiency, megaloblastic anemia with hypersegmented neutrophils]

Hemolytic Anemia
↓
↓ ↓
Extravascular hemolysis Intravascular Hemolysis
- ↑ Unconjugated bilirubin - ↑plasma & urine Hb
- ↑ LDH - Hemoglobinuria
- Spherocytosis - Hemosiderinuria
- Sickle-cell - ↓Serum Haptoglobin
- Immune-hemolytic anemia - ↑ LDH
- PNH (Paroxysmal Nocturnal
Hemoglobinuria)
- G6PD

■ Sickle- cell-Anemia: Autosomal-recessive

- Substitution of Valine for glutamic acid at sixth position on β- globin chain
- Sickle-cell trait → Asymptomatic. Significant manifestation of trait is the renal
concentrating defect
- Screening test: Sickle prep test to diagnose traits
- Most specific test: Hemoglobin electrophoresis
- Treatment: Acute crisis → fluid, Analgesics, O2
- Fever & leucocytosis with/without infection → Antibiotics ⇒ ceftriaxone,
cefotaxime
- Severe (Acute chest syndrome, CNS, priapism) → RBC transfusion
- Hydroxyurea −Prophylaxis − prevent vaso occlusive crisis
- Folic acid supplementation – prevent Aplastic anemia
- Most common complication of Sickle cell disease – splenic sequestration (not
splenic infarction)

• Sudden fall in Hb concentration and virtual absence of reticulocytes on the

peripheral blood smear in sickle cell disease patient – Parvo virus B-19 (slapped
cheek appearance)  Aplastic crisis

■ Hereditary Spherocytosis: Autosomal dominant

- RBC membrane protein defect [spectrin, ankyrin]
- Osmotic Fragility test & ↑ MCHC
- Treatment: Splenectomy

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 ■ Autoimmune Hemolytic Anemia:
- Coomb’s test
- Warm – antibody (IgG), Cold – antibody (IgM)
- Drug – induced → Penicillin, Quinidine, α - Methyldopa

■ Paroxysmal Nocturnal Hemoglobinuria (PNH):

- Loss of anchor for DAF ( Decay Accelerating Factor )
- more complements bind to RBC & intravascular hemolysis occur
- Presentation: Hemoglobinuria in first morning urine
Sign / Symptoms of major venous structure thrombosis
• Treatment: Corticosteroid in severe disease for unclear reason
Anticoagulation for thrombosis

■ G6PD deficiency: ↓ Synthesis of NADPH & GSH (glutathione)

- X-linked recessive
- Hemolysis in the presence of Oxidant Stress
- Oxidant Stress → Infection , fevabeans, Drugs (Sulfa, Dapsone, Primaquine,
Quinidine, Nitrofurantoin, INH)
- Diagnosis → Heinz bodies, bite cells, G6PD level
- Treatment → Avoid oxidant stress

■ Pyruvate kinase deficiency: ↓ Synthesis of ATP

- Autosomal recessive
- PK gives 2 ATPs – its deficiency produce membrane damage – RBC with thorny
projection (echinocytes)

♦ Leukemia ♦

ALL AML CML CLL

• Children • 15-39 yrs • 40-60 yrs • > 60 yrs

( < 14 yrs )
• Thrombocytopenia • Thrombocytopenia • Thrombocytopenia • Thrombocytopenia
Thrombocytosis in
40%
• Pre-B cells - • t (15; 17) in M3 • Philadelphia • CD19 Antigen
CALLA, CD10 & chromosome,
TdT positive t (9 ; 22)
• T cells - CD10 & • DIC in M3 • Bcr-Abl fusion – • Predominantly B
TdT negative ↑Abl kinase activity lymphocytes.
• t (12; 21) – good • Auer rods in M2 & • “Smudge cells”
prognosis M3
• CNS in M4 & M5 • Basophillia • Stages :
CALLA (common M3- Premyelocytic 0 –lymphocytosis
ALL antigen) M4-myelomonocytic 1-lymphadenopathy

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 M5- monocytic 2-spleenomegaly
• Vit–A – useful in 3-Anemia
Premyelocytic ( M3) 4-thrombocytopenia

* Diagnosis: Bone marrow biopsy → > 30 % blast → Acute leukemia

< 30 % blast → Chronic leukemia

Treatment Treatment Treatment Treatment

• Daunorubicin • Cytosine • Imatinib • Stage 0, 1 → No

arabinoside Treatment
• Vincristine • daunorubicin / • if it fails, then • Advanced stage
Idarubicin Bone marrow ↓
Fludarabine
• Prednisone • Vit-A in • Imatinib: • Autoimmune
Premyelocytic (M3) selective inhibitor of hemolysis &
Bcr-Abl tyrosine Thrombocytopenia
kinase ↓
Prednisone
• Asparaginase

• Intrathecal
Methotraxate for
CNS Prophylaxis

* Adult T-cell lymphoma: HTLV-1 [Human T-cell leukemia virus – 1]

- Activation of TAX gene – inhibits TP53 suppressor gene
- ↑ CD4 T-cells
- Skin infiltration and lytic bone lesion [lymphoblast release osteoclast activating
factor] (hypercalcemia)
- Negative TdT

* Hairy cell leukemia: only leukemia without lymphadenopathy

- B-cell leukemia
- Positive TRAP stain (tartrate-resistant acid phosphate)
- Treatment: Pentostatin / 2-Chlorohydroxy adenosine

* Infectious Mononucleosis: EBV – CD21 receptor on B-cells – heterophile

antibody (IgM to sheep’s RBC) – danger of rupture of spleen – When patient
receive ampicillin, Ampicillin-associated maculopapular rash is well known
phenomenon in patient with mononucleosis [Tx: discontinue drug, supportive
treatment and observation]

* Sudden increase in WBC in patient with severe infection or inflammation with

high leukocyte alkaline phosphatase score, diagnosis?  Leukemoid reaction

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 * Myeloid stem cells: RBC, granulocytes, mast cells and platelets – Polycythemia
vera affect myeloid stem cells so increase everything in Polycythemia vera –
myelofibosis (tear drop cells, extramedullary hematopoesis)

* Aplastic Anemia: Pancytopenia [Everything is decreased including RBCs,

Platelets and WBCs]
˗ Bone marrow biopsy – most specific test
˗ Treatment – Allogenic bone marrow transplant (best treatment for < 50 yrs old)
– Antithymocyte globulin, cyclosporine, Prednisone

* Relative Polycythemia – increased RBCs count due to decrease plasma volume

* Appropriate absolute Polycythemia (secondary) – increase RBCs count due to
increase in erythropoietin (EPO) level due to hypoxia [eg. COPD, high altitude];
next step would be measure oxygen saturation (decrease Sao2) in these patients
* Inappropriate absolute Polycythemia (Polycythemia vera and ectopic EPO
secretion) – Polycythemia vera – clonal expansion of the trilineage myeloid stem
cells [increase RBCs, Granulocytes, Mast cells and Platelets]; decrease EPO
(increase Sao2 inhibits EPO secretion) Ectopic EPO secretion – Renal cell CA,
Hepatocellular CA – increase RBCs and increase EPO, normal Sao2 and plasma
volume

* Neonatal Polycythemia – hematocrit >65% - If increase on hematocrit on heel

prick sample, next step? – Recheck sample from peripheral blood (hematocrit 5-
15% lower than heel prick) – If symptomatic (hypoglycemia, hyperbilirrubinemia,
cardiac or respiratory compromise), next step? – hydration and partial exchange
transfusion
♦ Plasma Cell Disorder ♦

Multiple Myeloma Monoclonal Gammopathy of Uncertain

Significance

• Bone pain , Infection, Anemia , • No systemic manifestation like multiple

Renal failure myeloma
• Electrophoresis – IgG monoclonal spike • IgG monoclonal spike on electrophoresis

• X-ray – punched out lytic lesion • No lytic bone lesion on X-ray

(osteoclast activating factor)
• Hypercalcemia • Normal lab test (creatinine, calcium)
• Bence-Jones Protein (Acidification of
urine is required to test BJ protein)
• Bone marrow biopsy (most specific) – • Bone marrow - < 5 % Plasma cells
>10% plasma cells
• First step – serum protein
electrophoresis, plain radiographic skeletal
survey & assessment of renal function

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 • Whole body X-ray should be done once a patient has been diagnosed with
multiple myeloma. Bone scans are not useful for these patients.

■ Treatment - Younger → Bonemarrow transplant

Older → Melphalan & Prednisone
Hypercalcemia → Hydration & loop diuretics and then with
Bisphophonates

* Waldenstrom’s macroglobulinemia (Lymphoplasmatic lymphoma): M spike

with IgM, BJ protein – no lytic lesions like multiple myeloma

 BJ proteins – kappa or lambda light chains

♦ Lymphomas ♦

* Stage of Lymphoma (Hodgkin’s & Non–Hodgkin’s):

˗ A – Constitutional Symptoms Absent

˗ B – Constitutional Symptoms Present (fatigue, Wt .loss, night sweat, etc.)

 Stages: 1-Single lymphnode / single extralymphatic organ one side of

2-Two / more lymphnode / contiguous extralymphatic organ diaphragm

3-Involvement of lymphnode/extralymphatic organ both side of the

4-Multiple disease foci in extralymphatic organ diaphragm
(eg. liver, Bone marrow)

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 Hodgkin Lymphoma Non-Hodgkin Lymphoma
• Reed-Sternberg cells • Reed-Sternberg cell Absent

• Lymphadenopathy is more common • Extralymphatic involvement is more common

(cervical, Supraclavicular, Axillary) (Spleen, liver, stomach)
• B-cells lineage involve • Both B & T cell lineages involve

• Lymphocyte Predominant (Best Prognosis) • HIV, EBV → Burkitt lymphoma, t (8;14 )

• Mixed celluarity • H.pylori → gastric lymphoma (mucosa

associated lymphoid tissues in stomach)
• Nodular Sclerosing (Female) → lacunar cells • CNS involvement is more common in HIV-
positive patient
• Lymphocyte depletion (worst prognosis) • Follicular lymphoma – t (14;18 ), over
expression of BCL2 anti-apoptosis gene
• RS cells – CD15, CD 30 positive • Sjogren syndrome – salivary gland & GI
- B-lymphocyte with somatic hypermutation lymphoma
• Hashimoto’s thyroidits – thyroid malignant
lymphoma
• Diagnosis: Excisional lymphnode biopsy • Diagnosis: Excisional lymphnode biopsy
Next step → determine the extent of disease by Next step → Staging
CXR, Chest CT, Abdominal CT/MRI • Bone marrow biopsy is best initial staging tool
• Staging laparotomy for NHL
• Bone marrow biopsy
• Treatment • Treatment : same as Hodgkin for stages IA ,
 II A, CNS lymphoma
↓ ↓ • B, III , IV → Chemotherapy
I A , II A B , III , IV ↓
↓ ↓ Cyclophophamide
Radiation Chemotherapy Hydroxy – Adriamycin
Adriamycin(doxorubicin) Oncovin [vincristine]
Bleomycin Prednisone
Vinblastine • CD 20 antigen expression →RITUXIMAB
Dacarbazine

 Mycosis fungoides – cutaneous (begins in skin) T-cell lymphoma (not a fungal

infection)
♦ Bleeding Disorders ♦

• Tissue thromboplastin → Factor 7 → Extrinsic Pathway (PT) → Warfarin

• Subendothelial collagen, HMWK → Factor 12 → Intrinsic Pathway (PTT) →
Heparin
• Common final pathway → Factor 10 , 5 , 2 , 1 [ 2-Prothrombin ]
• Heparin → ⊕ AT III → neutralize 9 , 10 , 11 , 12 , Prothrombin & thrombin
S.S.Patel. All rights reserved. Registered with US copy right office 48
 • Thrombin → convert fibrinogen into fibrin monomers [fibrin monomers then
aggregate which are soluble]
• Thrombin → activate fibrin stabilizing factor (13) [once fibrin monomers
aggregate, factor-13 stabilize them by making them insoluble]
• Plasmin → cleaves insoluble fibrin monomers and fibrinogen into fibrin
degradation products [FDP]
• D-Dimers → fragments of cross-linked insoluble fibrin monomers
• Protein C & S ( Vit .K dependent ) → inactivate 5 & 8 → enhance fibrinolysis
• tPA – synthesized by endothelial cell , TxA2 –synthesized by Platelates
n
• VWF – synthesized by endothelial cell & Platelates – Func. → Platelate
Adhesion & Prevent degradation of factor VIII:C
• Platelate Storage → VWF & Fibrinogen (1)
• Platelate receptors → glycoprotein (gp) 1b – VWF ; GP2b:3a – Fibrinogen
• Platelate Factors → PF3 → Prothrombin complex (V, Xa, PF3, Ca+2).
PF4 → Heparin neutralizing factor

■ Hemostasis in small vessel injury: injury → tissue thromboplastin (activates

extrinsic pathway) & exposed collagen (activates intrinsic pathway) →
Endothelial cells synthesize vWF so injury makes it expose to platelets and
platelets start attaching to them and ADP from platelets help aggregating them
(temporary plug) → platelets have fibrinogen at gp2b:3a → activated thrombin
(by intrinsic & extrinsic pathway) convert fibrinogen to fibrin monomers which
aggregate and make soluble plug → thrombin also activate factor-13 which
convert soluble plug into insoluble plug → bleeding stop → tPA activates plasmin
which dissolve fibrin monomer & blood flow reestablish to the tissue

■ Idiopathic Thrombocytopenic Purpura:

- Sign of bleeding from superficial areas of body
- Absent spleenomegaly, Prolong Bleeding time
- Idiopathic Antibody (IgG) Production to the Platelets receptors (gp2b:3a)
- Diagnosis : Anti-platelate Antibody
Bone-marrow → megakaryocytosis – indicate problem with
platelate destruction, not with production
* Treatment: Prednisone (initial therapy)
˗ Corticosteroid should be given if platelets count <30,000/ mm3, otherwise
observe patient
˗ If count fails to raise after Prednisone therapy → IV Immunoglobulin / Rho-
gam
˗ Platelate transfusion (if above fails to raise count)

 Thrombotic Thrombocytopenic Purpura (TTP) – deficiency in vWF cleaving

metalloprotease in endothelial cells leads to ↑↑vWF → more platelets attach to
vWF leads to thrombosis and thrombocytopenia (due to platelet consumption in
thrombosis) – microangiopathic anemia, Renal & CNS involvement – schisto-
cytes (fragmented RBCs), Helmet-shaped cells

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  Hemolytic Uremic Syndrome (HUS) – microangiopathic anemia, thrombocyt-
openia and renal involvement [no CNS involvement]

 Schistocytes – TTP, DIC, Aortic stenosis

■ Giant platelates, greater than expected bleeding for the degree of

thrombocytopenia, Normal vWF level, subnormal ristocetin assay, diagnosis?
 Bernal-Soulier Syndrome; defect?  glycoprotein Ib

■ Von Willebran Disease ( VWD ): Autosomal – Dominant

- Sign of bleeding from superficial areas of body
- Low level of VWF , factor VIII : C
- Ristocetin Platelate Aggregation Test : Abnormal
- Elevated PTT, Normal PT
- Treatment: Desmopressin Acetate, VWF replacement

■ Hemophilia: Autosomal – recessive

- Hemophilia A – factor 8 deficiency, Hemophilia B – factor 9 deficiency
- Sign of deep bleeding → hemarthrosis, hematoma, GI bleeding
- may become apparent at the time of circumcision
- Diagnosis : elevated PTT , Normal PT
- “Mixing Study” : 50 % Patient’s blood + 50 % Normal blood → PTT corrected
→ Hemophilic → If PTT is not corrected → Antibody inhibition of the factor
- Treatment: Desmopressin, Specific factor replacement

■ Vit–K Deficiency: ↓ Production of Factor 2, 7, 9, 10

- Both PT & PTT are elevated
- Diagnosis : correction of PT & PTT after giving Vit-K
- Treatment: Fresh Frozen Plasma in severe bleeding

■ Liver Disease : ↓ Production of All factors except VWF & Factor 8

- Both PT & PTT are elevated
- Diagnosis: H/O liver disease & No correction of PT & PTT after giving Vit-K
- Treatment : Fresh Frozen Plasma

■ DIC (Disseminated Intravascular Coagulation):

- Platelates, ↑↑ PT & PTT, ↑ D- dimmers & FDPS, Low fibrinogen level
schiztocytes on peripheral blood smear
- Treatment: Fresh Frozen Plasma, Platelate transfusion

 SLE:
˗ Anti-phospholipids antibody, false VDRL/RPR positive
˗ Elevated PTT, all other parameters normal, h/o recurrent abortion
˗ Tx: Heparin & Aspirin

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 INFECTIOUS DISEASES

* Best Initial Antibiotics for different Organisms :

 Staph Aureus: Dicloxacillin, Oxacillin [Penicillins] / Cefadroxil, Cefalaxin [1st

generation Cephalosporins]
 If patient is allergic to above groups – Macrolide, newer fluoroquinolone
 If patient has MRSA – Vancomycin / Linezolid
 Streptococcus: Penicillin (if sensitive) / Ceftriaxone / levofloxacin
 Strep Pneumonia: Penicillin G / Ceftriaxone / levofloxacin
 Strep Viridans: Penicillin G / Ceftriaxone
 Strep Pyogens: Ampicillin / Ampicillin + Sulbactam
 Strep Meningitis: Ceftriaxone
 Listeria Monocytogens: Ampicillin
 Legionella Pneumonia: Erythromycin
 Rickettsia in children: Chloramphenicol, Erythromycin
 Rickettsia in adults: Doxycycline
 Lyme disease in children < 9yrs of age: Amoxicillin
 Lyme disease in children >9 yrs of age and adults: Doxycycline
 Lyme disease in Pregnant women: Amoxicillin
 Disseminated Lyme disease [Bell’s palsy, Cardiac involvement, CNS involve-
ment]: Ceftriaxone
 Syphilis: Penicillin G
 Gonococcus: Ceftriaxone
 Chlamydia, Mycoplasma: Macrolides / Doxycycline
 C.Jejunii: Erythromycin
 H Influenzae: 2nd or 3rd generation cephalosporin
 E coli: Ciprofloxacin / Ampicillin
 Pseudomonas: Piperacillin, Ticarcillin [Anti-pseudomonal penicillin]
 Klebsiella: 2nd or 3rd generation cephalosporin
 Cryptococcus: Amphotericin B (severe), Fluconazole (prophylaxis)
 Candida: Fluconazole
 Dermatophytes: Terfinabine (oral) / Meconazole (local)
 PCP: Trimethoprim + Sulfamethoxazole
 Actinomycetes: Penicillin
 Nocardia: Sulfonamides
 Anaerobes: Metronidazole / Clindamycin
 Penicillin and Aminoglycosides have synergistic effects so combination of
both (Penicillin + Aminoglycosides) is used in Enterobacteraceae and
Pseudomonas infections

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  Meningitis: infection of covering of brain – fever, headache, stiff neck and focal
neurologic deficiet
• Causes:
˗ New born (< 1 month ) →Group B Streptococci, E.coli, L. monocytogen
˗ 1 month – 18 yrs Old → N.meningitides
˗ >18 yrs Old → Strep Pneumoniae
˗ Staph Aureus → recent neurosurgery
˗ L.monocytogens → Immunocompromised (Neonates & elderly Patients)
˗ Cryptococcus → HIV positive, CD4+ < 100 cells
˗ RMSF → rash on wrist, ankle → spread towards body
˗ Neisseria → Petechial rash
˗ Cause of viral meningitis in pediatric population in US – Arbovirus and
Enterovirus
˗ CN – 8 deficits is more common long-term neurological deficit

• Sign & Symptoms of meningitis but appear less toxic – Aseptic (Viral) meningitis
[ECHO virus – belongs to enterovirus – Picornavirus family]

• Management:
˗ Lumbar Puncture (Next Best Step / First step in management)
˗ CT scan of the Head (If Papilledema, focal motor deficit, confusion, coma)
then Lumbar puncture (LP)
˗ Culture of the CSF (most accurate test)
˗ Lyme , RMSF , Syphilis → Serologic test
˗ Cryptococcus → India ink test, cryptococcal antigen test
• CSF findings of Bacterial Meningitis – low glucose (<40 mg/dl), increase WBC
count [Neutrophils]
• CSF findings of Viral Meningitis – increase WBC (lymphocytes), normal
glucose
• CSF findings of Cryptococcal Meningitis – low WBC count (<50 cells/L)
(Lymphocytes) , low glucose
• Treatment:
˗ Ceftriaxone (Best initial empiric therapy)
˗ Ceftriaxone + Ampicillin ( if L.monocytogens is suspected)
˗ Amphotericin B (Best initial therapy for Cryptococcus)
˗ RMSF → Chloramphenicol, Erythromycin (children) / Doxycycline (Adults)
˗ Tx of tubercular meningitis – at least 12 months

 Encephalitis: infection of parenchyma of brain – fever, headache, stiff neck and

altered mental status
• Causes:
˗ HSV (temporal lobe) (most common)
• Management:
˗ Lumbar Puncture (Next Best Step / First step in management)
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 ˗ CT scan / MRI of the Head
˗ PCR for HSV
• Treatment:
˗ IV Acyclovir for HSV
˗ Ganciclovir / Foscarnet for CMV

* Brain Abscess:
• Headache, fever, focal neurologic deficit
• CT scan with contrast (Best initial test)
• Biopsy of the lesion + gram stain + culture (most accurate test)
• Treatment: HIV positive → Toxoplasmosis / Lymphoma (90% of cases) →
Pyrimethamine + Sulfadiazine for 14 days followed by CT scan to check lesion
regress or not. If not regress, most probably lymphoma (Tx: radiation)
• Combination of Antibiotics (gram (+), gram(-), Anaerobes)

* Transverse Myelitis – rapidly progressing lower extremity weakness following

URI, accompanied by sensory loss and urinary retention – Dx: MRI
* Epidural abscess – patient with h/o IV drug abuse

* Otitis Media:
• Strep. Pneumoniae (35-40 %) , H. influenzae (25-30%),Moraxella(15-20%)
• Earache, fever, decrease hearing, red, bulging tympanic membrane with loss of
light reflex, immobility of the membrane on insufflations of the ear with air
• Amoxicillin (Best initial therapy) / Amoxicillin + clavulanate (if recent use of
Amoxicillin)
• Azithromycin / newer fluoroquinolone (Alternatives)
• Complications: The most common complication after an episode of otitis media
is another episode of otitis media – Acute mastoditis [pinna displaced inferior &
laterally – X-ray of skull, mastoid – IV antibiotics + surgical debridement
(mastodectomy may require)] Middle ear effusion [A normal appearing tympanic
membrane with decrease movement of pneumatic otoscopy in patient treated for
recent acute otitis media – follow up after 4-6 wks; If not resolved, tympanostomy
may require; referral to ENT]
* Malignant Otitis Externa: Diabetes Mellitus + foul smelling ear discharge &
granulation Pseudomonas Tx: IV Ciprofloxacin

* Sinusitis:
 Headache (worse on leaning forward), facial pain, nasal discharge
 Maxillary sinus x-ray (best initial test)
 Uncomplicated → decongestant , Analgesic
 Complicated (discolored nasal discharge) → Antibiotics

 Pharyngitis:
 Viruses, group A streptococci (15-20%)
 Exudates covering is highly suggestive of Strep.pyogen

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  RM Centor at el criteria for Mx of Pharyngitis – fever, tonsillar exudates, tender
cervical lymphadenopathy and absence of cough – If 1 or 2 present, rapid antigen
test. If test is positive, give antibiotics; If 3 or 4 present, give empiric antibiotics
 Rapid Strep test (Best initial test / next step in management)
 Tx: Penicillin (1st choice), Macrolide / 2nd generation Cephalosporin orally
 Benefit of antibiotic therapy in patient with Strep. Pyogens pharyngitis – it can
prevent Rheumatic fever (not glomerulonephritis)

 Influenza:
 fever, headache, myalgias, fatigue
 Rapid antigen detection method of swab or washing of nasopharyngeal secretion
 Viral culture (most accurate test)
 Oseltamivir / Zanamivir (active against both A & B) → within 48 hrs of onset of
Symptoms
 Vaccination (C/I in patients allergic to eggs)

 Lung Abscess:
˗ chest X-ray (Best initial test)
˗ Biopsy of lesion & culture (most accurate test)
˗ Clindamycin (Best initial Therapy)
˗ Alcoholic, Extremely bad odor ( like decomposing dead animal)

 Pneumonia:
˗ Following flu → Stap. Aureus ( abscess )
˗ HIV positive ( CD4+ < 200 cells ) → PCP
˗ California , desert of Arizona → Coccidiomycosis
˗ Young ( school children ) → Mycoplasma
˗ Alcoholics → Klebsiella
˗ Smoker, COPD → H. influenzae
˗ Elderly pt, CXR – lobar consolidation → Strep. Pneumoniae
˗ Neutropenia, Steroid use, cavitatory lesion, part of the lesion moves on CXR
when patient change position → Aspergilloma (fungus ball)
˗ Exposure to animal at the time of giving birth → Coxiella Burnetti ( Q-fever )
˗ Birds, Triad of pneumonia, spleenomegaly and meningoencephalitis [fever, dry
cough and headache] in immunocompetent host → Chlamydia Psittaci
Pneumonia – Tx: Doxycycline (follow-up on out patient basis)
˗ Old , smoker , Air–conditioning → Legionella
˗ Pneumonia & diarrhea in transplant patient  CMV
˗ Immunocompromised patient, gram (+) branching rods & partially acid-fast 
Nocardia (Trimethoprim-Sulfamethoxazole)
˗ Recurrent pneumonia in chronic smoker, next step?  CT chest to rule out lung
CA which may obstruct bronchus and produce recurrent pneumonia

• Best diagnostic test for patient with recurrent pneumonia [most probable cause

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 will be an endobronchial obstruction] – Flexible bronchoscopy [If question is
“what is the best next step in Mx of patient with recurrent pneumonia?” – order
chest CT scan]

Empiric Therapy

Community – Acquired Community – Acquired Hospital – Acquired

(out-patient) (Inpatient) Pneumonia
Macrolide (1st choice) Hypoxia(<70 PO2) (48-hrs after
Hospitalization)
Newer Fluoroquinolones O2 Saturation ( < 94 % at 3rd generation
room ) Cephalosporin
PR > 24 Carbapenem
Macrolide / Doxycycline + B-lactam / B- lactamase
New fluoroquinolone / 2nd inhibitor combination
generation cephalosporin/
B-lactam + B – lactamase
inhibitor combination

 PPD: PPD is Positive if induration after 48 hrs is

- > 5 mm → HIV Positive , recent exposure to TB , Immunocompromised
- > 10 mm → High risk group ( Health workers , recent immigrant , Homeless)
- > 15 mm → Low risk group
- PPD is Best screening Test (not diagnostic test) to check TB exposure
- PPD positive, CXR negative – INH + Vit-B6 for 9 months; PPD become
positive again on routine test and CXR negative – reassurance and no Tx require
- Prophylaxis for only INH resistant TB – Rifampin for 4-months
- Prophylaxis for both INH and Rifampin resistant TB – Pyrazinamide and
Ethambutol or levofloxacin

 Diarrhea:
˗ Traveler’s diarrhea – E.coli
˗ Undercooked hamburger meat – E.coli 0157 : H7 ( associated with HUS )
˗ Giardia lamblia – camping, contaminated water source
˗ HIV Positive, CD4 < 50 cells, Acid fast oocyst – Cryptosporidium
˗ Ingestion of unrefrigerated meat – Cl. Difficile
˗ Fired rice – Bacillus Cerius
˗ Contaminate Shellfish – V. parahaemolyticus
˗ Severe liver disease patient – V.vulnificus
˗ Diagnosis: Presence of blood in stool by methylene blue test (1st step)
˗ Stool culture (most accurate)
˗ Patient with chronic diarrhea – stool microscopic examination (first step) [not
stool culture]
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 ˗ Treatment: Ciprofloxacin (Best initial empiric therapy)
˗ Cryptosporidiosis → raise CD4+ count
˗ Scombroid → Histamines → Symptoms in few mins → Tx – Anti-Histamines
˗ Salmonella enteritidis diarrhea – supportive care (rarely use antibiotics)
˗ Giardia & Cl. difficile → Metronidazole
˗ For Giardiasis, only symptomatic carries are treated – Asymptomatic carriers are
not treated except for few circumstances like pregnant woman in house,
immunocompromised individual, cystic fibrosis - Tx of Giardiasis in pregnant
women – Paromomycin

 Hepatitis B :
˗ Acute → HBsAg, IgM to HBV
˗ HBsAg → Active disease + Persistent disease
˗ Anti – HBcAb → 1st Ab to appear in Hepatitis B
˗ HBeAg → Active viral production + Infectivity
˗ Anti - HBeAb → Appear after viral no longer detectable
˗ Anti – HBsAg → Protective Ab, Immunization
˗ Window Period ( equivalence zone of Ab production ) → Anti – HBcAb, Anti-
HBeAb
• Treatment : Interferon / Lamivudin (chronic Hep B)
˗ Needle stick injury with HBsAg positive → HB immunoglobulin + HB vaccine
˗ Tx of HBV post-exposure in a patient who already had Hep B vaccine but did
NOT seroconvert after Hep B vaccination – Hep B immunoglobulin

˗ Diagnosis of Acute HAV, HDV, HEV → Presence of IgM antibody

 Hepatitis C:
˗ Blood transfusion
˗ Dx: PCR HCV RNA
• Treatment → Interferon + Ribavirin
˗ Advance stage (cirrhosis) → Liver Transplant

 Pelvic Inflammatory Disease:

˗ Lower Abdominal and pelvic pain, fever, leucocytosis, discharge (vagina)
Cervical motion tenderness
˗ Gram stain & culture of discharge
˗ USG (to exclude ovarian cyst / Tubo-ovarian abscess)
˗ Tx: Single dose Ceftriaxone + Doxycycline for two weeks (out patient)
˗ Inpatient (high grade fever / ↑↑ WBCs) → Doxycycline + IV Cefoxitin
˗ Goal of Tx of severe PID is to obtain high blood concentration of antibiotics as
soon as possible so all therapy should be intravenous. use IV Cefoxitin + Oral
Doxycycline or IV ceftriaxone + oral Doxycycline

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 Fever, urinary frequency, urgency, burning

Purulent Discharge No Discharge

Urethritis (Tx: Ceftriaxone + Azithromycin) Cystitis

Gonococcus Chlamydia - E.coli (>80%)

gram stain Serology Urinary stasis / Foreign
body Predisposes
Culture Ligase chain reaction Suprapubic tenderness

Tx : Ceftriaxone IM Tx Doxycycline(7 days ) Urine Analysis looking for

WBCs ( Best Initial )
Azithromycin Azithromycin(single) Nitrates → Nitrites
(gram(-) organism)
Ciprofloxacin Mucopurulent discharge Urine culture (> 100000
colonies)
Cefixime Dx of Chlamydia is Tx: If uncomplicated,
costlier than Tx so all Trimethoprim /
Purulent discharge patient with gonorrhea Sulfamethoxazole or
receive Azithromycin (1g Quinolones X 3 days
single dose) In DM → 7 days

• Tx Chlamydia infection in pregnancy – Erythromycin 500mg PO four times a day

for 7 days
• Asymptomatic bacteruria is common in elderly, and doesn’t require treatment if
WBC count is less than 20 / HPF. [reassure and repeat urine culture again after 1-
2 months]
• Treatment of UTI /Asymptomatic bacteriuria in pregnancy  Nitrofurantoin
or Ampicillin for 7-10 days
• Uncomplicated UTI can be treated by prescribing TMP-SMX over the phone

♦ Chancre ♦
Painless Painful
10 Syphilis (Treponema Pallidum) Chancroid ( H . ducreyi )
- Dark field exam (best initial for - Genital ulcer, enlarged tender inguinal
primary) lymphnode
- VDRL & RPR (Best initial for 20 & - Gram stain, culture, PCR
tertiary) - Tx: Azithromycin (single dose)
- FTA-ABS, MHA-TP (most specific test) Ceftriaxone 250 mg 1M(single)

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 20 Syphilis
→ Cutaneous rash (symmetrical)
→ Condylomata lata (infectious)

˗ Condylomata Acuminata (HPV): verrucous, papilliform, skin color lesion

˗ Condylomata late (Secondary Syphilis): flat or velvety lesion

* Tertiary Syphilis → gumma, Tabes dorsalis , Argil-Robertson pupils

* Treatment: Penicillin (Benzathin) – 2.4 million units / Week IM for 10 (1 week)

& 20 (3 weeks)
* Tertiary – 10-20 million units / day IV for 10 days
* If Allergic to Penicillin – Doxycycline for 10 & 20
* If Allergic to Penicillin - Desensitization in tertiary & pregnancy.

• No effective prevention is available for Jarisch-Herxheimer reaction (fever, chills)

occur within 24-hrs after starting therapy to syphilis

 Lymphogranuloma Venerum:
- Chlamydia trachomatis (L1,L2,L3)
- Small, transient , non indurated lesion that ulcerates & heals quickly; unilateral
enlargement of inguinal lymphnodes, multiple draining sinuses, buboes
- Diagnosis → serological tests. Isolation of Chlamydia from pus in buboes
- Tx → Doxycycline

■ Granuloma Inguinale :
˗ Donovania granulomatis, calymmatobacterium granulomatis
˗ Painless red nodule that develops into an elevated granulomatous mass
˗ Slow healing & scar formation occur
˗ Giemsa / wright stain , Punch biopsy
˗ Tx → Doxycycline.

 Genital warts:
˗ caused by HPV
˗ Condylomata acuminate
˗ warm , moist surface in the genital areas
˗ Cauliflower appearance
˗ Tx: Imiquimod ( immune stimulant ) , Cryotherapy, Podophyllin ,Laser removal

 Acute Bacterial Pyelonephritis:

- E.coli (MCC) , Proteus , Klebsiella, Enterococcus
- Costovertebral angle tenderness
- Diagnosis : Dysuria, flank pain, urine culture (> 100000 Colonies)
- USG ( to rule out obstruction )
- Tx: Ciprofloxacin for 10-14 days (Any gram (-) Coverage antibiotics)

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  Perinephric Abscess:
- Persistent of pyelonephritis – like symptoms after treatment of pyelonephritis
- Urinanalysis & Urine culture ( best initial test )
- USG (best initial scan)
- Biopsy & culture ( most accurate test for etiology of organism )
- Tx: gram (-) coverage + Drainage

 Molluscum Contagiosum:
˗ Caused by Poxvirus
˗ Papules with central umbilication, Giemsa stain → inclusion body
˗ D/D: Cutaneous Cryptococcosis – red colored papules with central
umbilication (resembles Molluscum Contagiosum) – Dx: biopsy of lesions
˗ Tx: Freezing, electrocautery, curettage

 Osteomyelitis:
˗ Pain erythema, swelling, tenderness over the infected bone, draining sinus tract
˗ Hematogenously Spread
˗ Steph Aureus (MCC)
˗ Salmonella in pt with Sickle cell disease. [Order Hb electrophoresis to confirm
diagnosis of sickle cell disease if not previously diagnose of sickle cell disease]
˗ Best initial test → X ray → Periosteal elevation
˗ Earliest test → MRI / Bone Scan
˗ Most accurate test → Bone biopsy & culture
˗ Best empiric Treatment → Oxacillin / Neficillin + Aminoglycosides
˗ Chronic osteomyelitis → 12 weeks followed by 8-12 weeks orally
˗ ESR → useful to follow during treatment
˗ MRI – diagnosis of osteomyelitis in vertebrae and diabetic foot (most accurate
test) [C/I in patient with implanted pacemaker, defibrillators – Bone scan is
useful in those patient]

• Low-grade fever, elevated ESR, low backache, tenderness to gentle percussion

over the spinous process, diagnosis? Osteomyelitis of vertebrae; best test? MRI

 Gas Gangrene:
• Caused by Cl. Perfringens
• Deep , necrotic wound , without exit to the surface
• Crepitation over the site
• X – ray → gas bubbles
• Tx → High does penicillin / clindamycin
→ Surgical debridement / Amputation

Tetanus:
˗ caused by Cl. Tetani

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 ˗ Lockjaw , Respiratory arrest , dysphagia , flexion of arms & extension of lower
extremities
* Tetanus Prophylaxis: (TIG – Tetanus Immunoglobulin)
˗ Two Important factors – Vaccination history & Wound (clean or dirty)
˗ Last TT dose (< 10 yrs) & clean wound – No need to give tetanus prophylaxis
˗ Last TT dose (> 5 yrs) & dirty wound – Give TT prophylaxis
˗ No previous vaccination & clean wound – Give TT prophylaxis
˗ No previous vaccination & dirty wound – Give TT + tetanus immunoglobulins

 Blastomycosis → Broad base bud , rooting woods, skin lesions (crusted, heaped
up, warty lesion with violaceous hue) – Tx: Amphotericin B

 Histoplasmosis → Soil enriched with bird / bat feces, No skin lesions, found in
RES cells

 Coccidioides – California, spherules, skin lesions (Erythema multiforme and

Erythema nodosum)

 Aspergillosis → Neutropenia / steroid use / Cytotoxic drug, cavitatory lesion,

CXR – Abnormal, Sputum – Aspergillus, Acute 450 branching

 Babesiosis – hemolytic anemia with jaundice, no rash, tick-bite – Tx: quinine +

clindamycin / atovaquone + azithromycin

 Ehrlichiosis – tick-bite, “spotless – Rocky Mountain spotted fever”, fever,

malaise, headache, nausea and vomiting – Tx: Doxycycline

 Trichinellosis – Swelling around eye, severe muscle pain, splinter hemorrhage,

eosinophilia, no murmur

 Acquired Immuno Deficiency Syndrome (AIDS):

• Prophylaxis in AIDS → CD4+ < 200 cells → Trimethoprim / Sulfamethoxazole
(Pneumocystis Carinii - PCP)
+
CD4 < 50 cells → Azithromycin once a week for MAC
(Mycobacterium Avium Complex - MAC)
• Indication corticosteroid in PCP – alveolar-arterial O2 ratio >35 mmHg on room
air and/or Pao2 <70 mmHg on room air
• Start Antiretroviral therapy when CD4+ < 350 / viral load > 55000
• Post exposure prophylaxis – AZT + Lamivudin + PI (4-wks)
• Tx of HIV-associated thrombocytopenia – Zidovudine
• HIV virus load after initiation of HAART – within 4-wks [<5000 copies/ml], 8-
16 wks [<500 copies/ml], after 4-6 months [<50 copies/ml] After that viral load
can be reevaluated every 3 months
• CD4 count & HIV viral load monitoring for patient not on HAART – once
every 3-4 months

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 • Best indicator of immune status of HIV(+) patient – CD4 count
• Mx of Esophagitis in HIV positive – empiric Fluconazole; If doesn’t get better,
endoscopy
• Fluctuation of CD4 count and viral load in patient on HAART is common and is
self-limited
• CT scan of AIDS patient shows multiple hypodense, non-enhancing lesion with
no mass effect in the cerebral white matter, diagnosis? Progressive multifocal
leukoencephalopathy (PML) (JC virus) – without treatment, majority of patient
die within 3-6 months after onset of symptoms – Tx: HAART
• Dx of HIV during window period – measuring viral load by HIV RNA PCR
assay or by confirming presence of p24 antigen
• Pregnant Patient → AZT start at 14 wks. If serious disease ( very low CD4 /
very high viral load ) → start 3 drugs
• Only efavirenz is teratogenic
• AZT → Severe Anemia
• Didanosine (DDI ) & Zalcitabine (DDC) → Pancreatitis
• Stavudine → Peripheral neuropathy
• Indinavir → Nephrolithiasis
• All Protease Inhibitors → Central obesity, hyperlipidemia (Tx: Gemfibrozil),
hyperglycemia
• Nucleoside reverse transcriptase inhibitors can cause lactic acidosis by reduced
O2 utilization by tissue
• Disseminated Histoplasmosis in HIV  IV amphoterecin B, followed by lifelong
itraconazole
• Contact of saliva of patient with HIV has never shown to transmit infection so If
patient present with human bites from HIV-infected person, give standard wound
care and prescribe Ampicillin + Sulbactam

 Any newborn (<4 wks of age) with fever >38 C should be admitted to the hospital
and thoroughly evaluated (blood, urine & CSF culture) and start antibiotics

■ TORCH Infection:
 Toxoplasmosis – more serious in first trimester → intracranial calcifications,
IUGR, microcephaly, blindness – First trimester  Spiramycin / elective
abortion; In second & third trimester  pyrimethamine + sulfadiazine – Newborn
– Pyrimethamine and Sulfonamide & leucovorin.
 Other (Syphilis) – can be transmitted to fetus at any stage of pregnancy → fever,
anemia, failure to thrive, maculopapular rash, hepatosplenomegaly (<2yrs) →
Hutchinson teeth, saber skin, saddle nose, clutton joints (late manifestation)
 Rubella – IUGR, Cataract, PDA (Patent Ductus Arteriosus), Deafness,
blueberry muffin lesions.
 CMV – IUGR, Chorioretinitis, Periventricular calcification.
 Herpes – infection occur due to passage through an infected birth canal → first
time infection in mother has high rate of transmission → local (5-14days),
disseminated (5-7 days), CNS (3-4 wks). – Tx: Acyclovir, delivery by c-section.

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  Varicella – neonatal (Perinatal) disease is treated with VZIG if mother develop
varicella 5 days before to 2 days after delivery, Acyclovir in all perinatal
disease.

■ Pertussis:
- Whooping cough → forceful inspiratory gasp (whoop) after a paroxysmal cough.
- Children < 5 yrs of age.
- Catarrhal stage (infectious stage), paroxysmal stage, convalescent stage.
- Leukocytosis caused by absolute lymphocytosis.
- Direct fluorescent antibody testing of nasopharyngeal secretion (Rapid test).
- Tx: Supportive/Erythromycin.
- ALL contacts should receive prophylaxis with Erythromycin regardless of
their age & immunization status.

■ Cat Scratch Disease:

- Bartonella Hensalae.
- Chronic regional lymphadenitis, fever, headache, malaise.
- Resolve spontaneously in 2-4 months or Azithromycin for 5 days
- Bacillary Angiomatosis in AIDS patient.

■ Erythema Infectiosum:
- Fifth disease, Parvovirus B19
- “Slapped cheek” appearance (due to erythematous rash)
- Aplastic crisis in sickle cell anemia patient
- Infectious before the appearance of rash

■ Roseola (Exanthema Subitum):

- HHV (Human herpes Virus-6)
- High grade fever → resolve by 3-4 day → maculopapular rash appear.
- Supportive therapy.

■ Measles (Rubeola):
- Cough, coryza, conjunctivitis, koplik spots (grayish white dots on the buccal
mucosa), rash appear on face and spread towards trunk (rash pattern is same in
Rubella but patient looks more ill in Measles compare to Rubella)
- Supportive therapy, Vit-A supplementation.

■ Mumps:
- Contagious 1 day before and 3 days after the swelling.
- Swelling of the parotid gland, orchitis.
- Elevation of serum amylase – Tx : Supportive treatment

■ Rubella (German Measles):

- Contagious 2 days before the rash begin and 5 days after the rash
- Retroauricular, Posterior cervical & Postoccipital lymphadenopathy
- Supportive treatment.

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 - complication of Rubella – Arthritis, thrombocytopenia and encephalitis

■ Herpes Simplex:
- Burning rash followed by generalized eruption after 2-3 weeks, Vesicles on red
erythematous base – Tx: Acyclovir

■ Varicella (Chickenpox):
- Contagious 2 days before the rash begin and until all the lesions are crusted.
- Pruritic rash consisting of papules, vesicles, pustules and crusted lesions in
crops in various stages
- Varicella Zoster Immunoglobulin (VZIG), Acyclovir
- Varicella Post exposure prophylaxis  VZLG / Acyclovir (within 72 hrs only)
- Transmission of varicella from vaccinated individual to the organ transplant
household member is not typical. It can occur if rash appear after vaccination. If
rash appear, isolate the vaccinated person.

■ Scarlet Fever:
- Group A β-hemolytic Streptococci.
- “Strawberry” tongue, circumoral pallor, maculopapular/sandpaper rash,
pastia lines, military sudamina (small, vesicular lesions over the hands, abdomen
and feet), bilateral cervical lymphadenopathy
- Tx: Penicillins (DOC), Erythromycin, 1st generation cephalosporin.

■ Kawasaki Disease:
- Child with unilateral cervical lymphadenopathy, fever, desquamating rash on
palm, sole & mouth, Strawberry tongue, fissured lips
- Echocardiography (Best screening test – Coronary artery aneurism)
- Tx : IV Immunoglobulin (first step in treatment), High dose Aspirin [If need
arise to give continuous Aspirin, patient should receive influenza vaccine to
prevent Reye’s syndrome]

■ Hand, foot and mouth disease:

- Coxsackie A 16 virus
- Vesicular rash involve hand, foot & mouth.
- Supportive treatment

■ Scabies:
- Permethrin 5% cream / 1% lindane (>2 months of age).
- 6% sulfur in petroleum (<2 months of age)
- All family member & care taker should be treated.

■ Laryngotracheobronchitis (Croup):
● Parainfluenza virus
● Cold symptoms followed by brassy, barking cough & intermittent inspiratory
stridor
● X-ray: “steeple” signs indicate a narrow subglottic space.

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 ● Tx: steam from a vaporizer, continuous humidification (mild cases).
● Stridor at rest → epinephrine and corticosteroids systemically.
● give trial of epinephrine before intubation

■ Acute Epiglottitis:
- H.influenzae type B
- Acute onset of symptoms – high grade fever, stridor, drawling.
- Younger child sit in tripod position with neck hyperextended.
- X-ray: “thumb print” sign
- Tx: Intubation (1st step) (regardless of degree of respiratory distress), Antibiotic

■ Bronchiolitis: infection of lower respiratory tract

- Respiratory syncytial virus (RSV)
- around 6 months of age
- H/O URTI, rhinorhea, sneezing
- RSV infection increase the risk of asthma in later life
- CXR: hyperinflation of the lungs
- Antigen detection in nasopharyngeal secretion/culture.
- Criteria for hospitalization: premature, younger than 3 months old, RR>60/min,
PO2 <60 mmHg on room air , feeding difficulties
- Tx: respiratory isolation and supportive therapy (like IV fluids Antipyretics,
Humidified air and bronchodilators), Aerosolized epinephrine (no
corticosteroids), Ribavirin (aerosolized) (reserved for serious cases), Intubation.

 Rocky-Mountain Spotted Fever: headache, fever, rose-red maculopapular

rash (rosettes) on palms & soles → Tx: Doxycycline (benefits out weigh the
risk) (In Lyme, course of treatment is long that’s why we use Amoxicillin in
children less than 9 yrs of age)

 Lyme Disease: erythema chronicum migrans – The risk of acquiring Lyme

disease after tick’s bite is less than 1.5%. The most common complication of tick
bite is local inflammation and infection – Tx of classic early-localize Lyme
disease – oral Doxycycline for 28-days [It is clinical diagnosis, doesn’t require
serological test] – Dx of Lyme arthritis – ELISA antibodies in synovial fluid –
Prognosis of Lyme arthritis is good and more than 90% of patients are disease-
free one year after treatment – Early-disseminated-Lyme – do CSF examination
– If positive Lyme serology on CSF, give IV antibiotics – When pregnant patient
exposed to tick bite, prophylaxis of Lyme is necessary – give Amoxicillin orally
[All other patient doesn’t require any prophylaxis; Tick must be attached for more
than 24-hrs to transmit Lyme disease]

 Tx of UTI in newborn – fever, increase WBC, >20 hpf – Ampicillin +

Gentamicin (both IV)

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 ■ Eye discharge in Neonate:
- 1-3 day of life – Physiological
- 3-5 day of life (Mucopurulent discharge) – Gonococcal Conjunctivitis (Tx :
topical antibiotics)
- Few days after birth – Mucoid discharge – Chlamydia Conjunctivitis (Tx : Oral
(systemic) antibiotics to prevent pneumonia)

■ Eye discharge in child:

- Purulent discharge, crusting in the morning – Bacterial conjunctivitis
- Clear watery discharge (usually bilateral, h/o URTI) – Viral Conjunctivitis
- follicular conjunctivitis – trachoma (chlamydia)

 Otitis Media (infant is irritable) in patient with h/o conjunctivitis (red eye) is
caused by non-typable H. Influenzae so use Amoxicillin + Clavulanate acid (not
Amoxicillin alone)

■ IMMUNIZATION:
• Live Attenuated Vaccine :
- Viral: MMR, Yellow fever, Varicella
- Bacterial: BCG, oral typhoid

• Inactivated Vaccine :
- Viral: Polio, Rabies, Hepatitis A ( whole)
- Fractional
Protein based – Subunit → Hep B, Influenza, acellular Pertussis
Toxoid → Diphtheria, Tetanus
Polysaccharide based – Pure → Pneumococcal, Hib, meningococcal
Conjugate → Hib, Pneumococcal

• Influenza & Yellow fever vaccines are contraindicated in persons with

hypersensitivity to egg.
• IPV & MMR are contraindicated in persons with hypersensitivity to neomycin/
streptomycin.

• Contraindications to vaccines :
- severe allergic reaction to prior doses of vaccine ( or) to a component
- Encephalopathy following Pertussis vaccine
- Immunocompromised state & pregnancy
- Only MMR is contraindicated in HIV infected patient with severe
immunocompression & Symptomatic. All other vaccine can be given in HIV
positive symptomatic person.
- Previous febrile illness is not a contraindication (C/I) for giving MMR
- C/I to MMR are: pregnancy, severe immunodeficiency (asymptomatic HIV is
not a C/I), recent immunoglobulin administration, allergy to neomycin

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 • Immunization: Usually vaccines [DTaP, Hib, PCV, IPV] and Hep B (if not
given at birth) are given at 2, 4, 6 months and then boosters if appropriate.
• All pre-term infants should receive vaccines according to their chronological
age, not their gestational age. Hep B vaccine should be administer at birth (Wt
should be >2 kg)

- Hep-B vaccine → at birth.

- DTaP, Hib, PCV, IPV → Started at 2 months of age.
- MMR, Varicella → started at 12 months of age.
- Influenza → started at 6 months of age.
- DTaP → 2nd & 3rd dose 4-6 weeks apart, 4th dose 6 months after 3rd dose.
- Hib → All doses 4-6 weeks apart, if first dose is given after 15 months of age
then no need for other doses, booster b/w 12-15 months of age
- PCV → All doses 4-6 weeks apart, no doses for healthy child of ≥ 24 months of
age, booster b/w 12-15 months of age
- MMR → 2nd doses→ 4-6 weeks after 1st dose/at 4-6 yrs f age.
- Meningococcal Vaccine (serotypes A, C, Y, W - 135) → not protective for those
< 2 yrs of age. That means give vaccine after 2 yrs of age
- If mother is HBsAg positive → HBIG + HB Vaccine at birth.
- OPV (oral polio vaccine) is not used in USA

- Immunization in internationally adopted child without written

documentation – Give all necessary immunization according to recommendation
for unimmunized child + screen for Hep B, Hep C, HIV, Syphilis and TB

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 MUSCULOSKELETAL SYSTEM

 New born → Uneven gluteal folds → easy posterior dislocation of hip with
“click” and returned to normal position with “snapping” → positive family
history → Developmental dysplasia of Hip → sonogram of the Hip (not X-ray)
˗ Tx: Abduction splinting with Pavlik harness

 Legg calve Parthes disease →Avascular necrosis of the capital femoral epiphysis
→ around 6 yrs of age → Tx: keep femoral head in acetabulum by casting and
crutches

 Slipped capital femoral epiphysis → obese, around 13 yrs of age → sits with the
sole of the foot on the affected side pointing toward the other foot → Tx : Pin
the femoral head in place

 Osgood – Schlatter Disease → Osteochondrosis of the tibial tubercle

→ Persistent pain over tibial tubercle, aggravated by contraction of quadriceps →
Teenagers → Tx: immobilization of the knee in an extension (or) Cylinder cast
for 4 – 6 weeks.

 Spondylolisthesis → development disorder characterized by a forward slip of

vertebrae – palpable “step off” on examination if the disease is severe

 Flexible Kyphosis – postural round back which is correct on voluntary

hyperextension, no angular deformity and no neurological problem – it is a
common finding in adolescent and usually has no long term deformity

 Scoliosis – angularity in the thorax region on forward bending – Tx: Milwaukee

brace and spinal muscle exercises

Joint aspiration

↓ ↓
Cell count Gram stain Microscopic
↓ ↓ Polarization
 < 2,000 – OA, (+) organism (-) organism Needle-shaped / (-)
Traumatic birefringent – Monosodium
Urate (Gout)
 Up to 50,000 – Staph N. Gonorrhea Rhomboid / (+) birefringent –
Inflammatory Aureus Calcium Pyrophosphate
(RA, Gout, (Pseudogout)
Pseudogout)
 >75,000 (without
crystal) – Septic

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• Rheumatoid Arthritis (RA) • Osteo Arthritis (OA)
- Polyarticular Symmetric - Monoarticular Asymmetric
- Inflammatory synovitis - Non-inflammatory
- bone erosions - Non-erossive
- MCP & PIP involvement - PIP& DIP involvement
- Swan-neck deformity - Osteophytes & unequal joint space
- Boutonniere deformity - Bouchard’s node (PIP)
- radial deviation of the wrist with ulnar - Heberden’s node (DIP)
deviation of the digits - Tx: Acetoaminophen (NSAID)
- Tx: NSAID, Glucocorticoids, methotraxate, Capsaicin cream,joint Arthroplasty
Gold, Sulfasalazine, Infliximab, Hydroxychloroquine

• Best initial drug for Rheumatoid Arthritis (RA) – NSAID

• Best initial DMARDs – Methotraxate
• Patient on hydroxychloroquin – require frequent eye exam

■ Ankylosing Spondylitis: Positive HLA B-27, M>W, 2nd - 3rd decade

- chronic lower back pain, morning stiffness >1 hrs improve with exercise
- Anterior uveitis, Aortic insufficiency, 3rd degree heart block, Apical Pulmonary
fibrosis, Restrictive lung disease and Ig A nephropathy
- Best initial test: X-ray of lumbar spine → sacroilitis and eventual fusing of the
sacroiliac joint, bamboo spine – Repeat X-ray after 3-months & ESR (used to
monitor disease activity)
- Tx: NSAID, Physical therapy, exercise

• Next step in management of patient with low back pain who do NOT respond to
6-wks of conservative therapy – ESR; If increase in ESR, next step? – Imaging
studies (MRI / CT scan)

■ Reactive Arthritis: infectious diarrhea (C.Jejunii) + Arthritis

- Urethritis (Chlamydia) / conjunctivitis + Arthritis → Reiter Syndrome [Strong
association with HLA-B27 (80%); No HLA-B27 = no Reiter syndrome; negative
rheumatoid factor]
- Early Antibiotic use in urethritis decrease the chances of Reiter Syndrome

■ Psoriatic Arthritis: DIP joint + pitting of nail + skin lesions

■ Enteropathic Arthritis (Ulcerative colitis/ Crohn’s disease):

- Inflammatory Bowel disease + Arthritis + Pyoderma gangrenosum + erythema
nodosum

■ Gout: deposit of uric acid crystals in joints – most common site first toe
(podagra) – precipitating factors are alcohol, steroid withdrawal, diuretics,
Pyrazinamide, Ethambutol, following anti-cancer treatment

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 ■ Pseudo Gout: deposit of calcium pyrophosphate in joints – most common site
knee joints – pre-existing joint damage is a precipitating factor – causes:
Hyperparathyroidism, Hemochromatosis, Hypophosphatemia, Hypomagnesemia

■ Septic arthritis: Gonococcal: migratory polyarthropathy, Tenosynovitis

(inflammation of tendon sheath) Staphylococci: pre-existing joint damage (eg.
RA patient) – First step in Mx of septic arthritis – immediate surgical drainage
followed by IV antibiotics

 Inflammatory myopathies (polymyositis, Dermatomyositis, Inclusion body

myositis)
● Difficulty with task involving proximal muscles (lifting, combing hair, etc)
● ↑↑ Creatinine Kinase & Aldolase (most sensitive test)
● EMG→short duration, low amplitude myopathic potentials
● Muscle Biopsy (most specific test)
● Tx : Steroids→ polymyopathies & Dermatomyositis
● Inclusion body myositis→ Resistant to immunosuppressive therapy
• Fibromyalgia: chronic widespread pain (multiple tender points), fatigue,
women (20-50 yrs) – Tx: TCA or Cyclobenzaprine
• Polymyalgia rheumatic: pain & stiffness (at least 30 min) of the shoulder and
pelvic girdle, >50 yrs of age, ESR >50 mm/hr
• Polymyositis: c/o proximal muscles weakness (combing hair, difficulty raising
from chair)

■ SLE: anti-nuclear Ab, Anti-smith & Anti-ds-DNA Ab (most specific)

- non-erosive arthritis, malar rash, photosensitivity, Renal, CVS (Libman-Sack
endocarditis – sterile vegetation on MV), CNS involvement (psychosis)
- Anti-phospholipids antibody – anticoagulant, recurrent abortion
- Anti-cardiolipin antibody – give false VDRL & RPR test
- Absent of SLE symptoms, mildly high titer of ANA – No further work up require
- All SLE patients with renal involvement (Hematuria, Proteinuria) should have
renal biopsy to guide the treatment
- Tx of arthritis in SLE – NSAID
- Tx of SLE rash – cortisone cream
- Tx of Lupus Nephritis – pulse Cyclophosphamide

 Rosacea: facial rash same distribution as SLE, but rosacea has pustules &
papules & flushing of this rash by hot drinks – Tx: Metronidazole

■ Scleroderma: excessive collagen deposition – Raynaud’s phenomenon (blue

discoloration of fingers on exposure to cold), skin thickening, dysphagia – Anti-
scl-70 Ab; Tx of Scleroderma induce HTN – ACE inhibitors

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 ■ CREST Syndrome: Anti-centromere antibody
˗ Calcinosis, Raynaud’s phenomena, Esophagus (dysphagia), Scleroductly (claw-
like finger), Telangiectasia (dilated blood vessels) [Calcinosis is a feature of
CREST syndrome, not Scleroderma]

■ Raynaud’s Disease – Raynaud’s phenomena occurs independently without

connective tissue involvement – Tx: Nifedepine / Amlodepine

■ Sjogren syndrome: anti-Ro (SS-A) & Anti-La (SS-B) Antibodies, Dry eye
(constant sensation of foreign body in eye), dental caries, parotid enlargement
(lymphatic infiltration of glands – lip biopsy - most specific) – also gives
positive RA factor – Malignancy associated with Sjogren Syndrome – Hodgkin’s
Lymphoma (B-cell lymphoma)

 Juvenile Rheumatoid Arthritis: salmon pink evascent rash → Tx : NSAIDs

with monitoring of liver enzymes

 Adult Still’s disease – evanescent, salmon colored maculopapular rash that

involves the trunk & extremities typically develops with fever; Arthralgia /
Arthritis, significant leucocytosis – Tx: NSAID with monitoring liver panel

 Osteoporosis: hypogonadism, h/o taking steroids for long time – normal ALP
[Osteomalacia, Paget’s disease of bone – increase ALP] – Dx: Bone densitometry
[T-score: > -2.5 – osteoporosis; -1.5 to -2.5 – osteopenia] – Tx: Ca & Vit D (best
initial drugs), Bisphosphonates, Calcitonin, Estrogen [only when peri-
manopausal (c/o hot flashes) + osteopenia] Only Bisphosphonates has shown to
reduce incidence of hip fracture.
• Breast feeding increase bone resorption in women during post-partum period.
Breast feeding increase the level of PTHrP which is important for transferring
calcium in breast milk.

• Osteochondroma → most common benign tumor → Metaphysis

• Osteoma → Facial bones → associated with Gardner’s Polyposis Syndrome

• Giant cell tumor → Epiphysis → Females

• Osteogenic Sarcoma → Metaphysis of distal femur , Proximal tibia “sunburst”

appearance on X-ray → Male ( 10-25 yrs ) → Familial retinoblastoma

• Ewing’s Sarcoma → Diaphysis & metaphysis of proximal femur, ribs, pelvic

bones → “onion skin” appearance on X-ray

• Erb’s Palsy – upper trunk (C5, C6) → Axillary N. & Musculocutaneous N. →

muscles of shoulder & arm → Arm: medially rotated & adducted → Forearm:

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 extended & pronated (“waiter’s tip”) → Prognosis of obstetrical Erb’s palsy is
good, with 80% chance of full or near-full recovery

• Klumpke’s Palsy – lower trunk (C8, T11) → loss of muscles of Hand

• Open fracture – stabilization (eg. cast) + delayed primary closure (dressing of

wound for few days to prevent risk of osteomyelitis)

• Green stick fracture: one cortex break & another is intact Torus fracture :
impaction injury leads to buckling of cortex of long bones but on breach in
continuity
Plastic deformation: bones simply bend without any break in cortex
Physeal Injury: fracture across the growth plate of bone.

 Supracondylar Fracture → require appropriate casting / traction → tense &

tender forearm after casting → Volkmann contracture (complication)
→ immediate fasciotomy

 Fracture Clavicle → junction of middle and distal thirds → Tx: figure of 8

device for 4 –6 weeks.

 Anterior dislocation of shoulder – held arm close to the body – risk of Axillary
nerve damage →AP & Lateral view → Tx: reduction

 Posterior dislocation of shoulder → high-voltage electric burns, severe muscle

contraction (generalized seizure) → Axillary (or) Scapular view

 Frozen shoulder  joint stiffness & restriction of movement in all direction

(both active and passive)

 Rotator cuff tear or tendinitis  severe pain during mid arc abduction (passive
movement is normal); lidocaine injection  if movement improve  tendinitis; if
movement doesn’t improve  tear; diagnostic test?  MRI of shoulder

 Humeral shaft fracture →Radial nerve injury → Tx: reduction (If S&S of radial
nerve injury persist after reduction of the fracture → open reduction & remove
entrapped nerve)

 Colles Fracture → Osteoporosis, fall on outstretched hand → “ dinner fork

deformity → Tx: close reduction and long arm cast

 Monteggia fracture → direct blow to the ulna (eg. Someone hits you by stick) →
diaphyseal fracture of the proximal ulna , with anterior dislocation of the radial
head → Tx: close reduction of the radial head & open reduction and internal
fixation of the ulnar fracture

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  Galeazzi fracture → fracture of the distal radius and dorsal dislocation of the
radioulnar joint → Tx: open reduction and fixation of the radius & casting of the
forearm in supination to reduce dislocated joint.

 Carpel tunnel Syndrome: chronic use of hands (typist), DM, Hypothyroidism,

Acromegaly – eliciting pain by compressing median nerve at wrist / ask patient to
do forced and prolong flexion of the wrist [best initial test] – electromyography
[most accurate test] – Hand splinting at night [best initial treatment] – PO
prednisone has shown to improve symptoms

 Trigger finger → Acutely flexed finger → Tx: steroid injection / surgery

 de Quervain Tenosynovitis → young mother, holding baby’s head with hand →

pain occur when asking her to hold her thumb in her closed fist & forcing the
wrist into ulnar deviation → Tx: splint & NSAIDs / steroid injection

 Dupuytren contracture → contracture of the palm of the hand & palmar fascial
nodule on palpation (hand can not placed on a flat table) → Tx: surgery

 Felon → abscess in the pulp of a fingertip → throbbing pain →Tx: urgent

surgical drainage is require

 Scaphoid fracture → fall on outstretched hand → tenderness over anatomic

snuff – box → Tx: Thumb spica cast, with follow-up X-ray 3 weeks later (high
rate of nonunion). If displaced and angulated fracture of the scaphoid → open
reduction & internal fixation

 Gamekeeper Thumb → ulnar collateral ligament injury by forced hyper

extension of the thumb → collateral laxity at the thumb metacarpophalangeal
joint → Tx: cast

 Jersey finger → flex finger is forcefully extended – injury to flexor tendon →

Tx: splint

 Mallet finger → Extended finger is forcefully flexed → injury to extensor tendon

→ Tx: splint

 Compartment Syndrome → intense & persistent pain few hours after casting →
excruciating pain with passive movement of muscles → Tx: fasciotomy

 Fourth & fifth metacarpal neck fracture → hitting the wall with closed fist →
Tx: closed reduction & ulnar gutter splint (if mild) (or) K-wire / plate fixation (if
severe)

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  Externally rotated short leg → Hip fracture, femoral neck fracture,
intertrochanteric fracture → Tx: femoral head replacement with prosthesis in
femoral neck fracture & open reduction and pinning in intertrochanteric fracture

 Internally rotated short leg → Posterior dislocation of the Hip → typically in

car accident where knee hit the dashboard → Tx: emergency reduction (to avoid
avascular necrosis of femoral head)

 Medial collateral ligament injury: pain on direct palpation over the medial
aspect of the knee → Affected leg abducted more than normal leg (valgus stress
test) → MRI → Tx: Hinged cast / repair

 Avascular necrosis of femoral head: progressive hip pain with normal range of
movements – Causes: chronic steroid therapy, alcoholism, hemoglobinopathies –
diagnostic test? MRI of hip – Tx: Core decompression (stage 1 or 2 – positive
radiograph without femoral head collapse) / Total hip replacement (stage 4 –
flattening of femoral head with joint space narrowing)

 Lateral collateral ligament Injury: pain on direct palpation over the lateral
aspect of the knee → Affected leg Adducted more than normal leg (varus stress
test) → MRI → Tx: Hinged cast / repair

 Anterior Cruciate ligament Injury : leg can be pulled anteriorly (positive

drawer sign) → MRI → Tx: immobilization / repair

 Meniscal Tears → catching & locking that limit knee motion and a “ click ”
when the knee is forcefully extended → Tx: repair (complete meniscectomy →
degenerative arthritis)

 Posterior dislocation of knee → popliteal artery injury → Tx: reduction .

 Ankle fracture → falling on an inverted / everted foot → both malleoli break →

AP, lateral & mortise X-ray → Tx: open reduction and internal fixation

 Achilles tendon rupture → loud “pop” sound (like a gunshot) → palpation of

Achilles tendon reveals an obvious defect right beneath the skin → Tx : casting in
equines position for several months / open surgical repair

 Metatarsal Stress Fracture → H/O rigorous walking, marching

 Lumbar Spinal Stenosis: either the spinal canal (central stenosis) or vertebral
foramen (foraminal stenosis) becomes narrowed – compression of the nerves –
Elderly patient walking “like drunken sailor”, pain improves when lean forward
(bending forward increases the space in the spinal canal and vertebral foramen)
and gets worse by bending backward, best test? – MRI of spine

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  Spinal Nerve root irritation (Radiculopathy) – nerve may be inflamed or
pinched (spinal stenosis, osteoarthritis of spine, herniated lumbar disk,
osteoporosis, etc) – eg. Sciatica – shooting pain, weakness, numbness – pain
increased by bending forward and straining; decrease by lying down – SLR test is
positive at 60o or less

 Lumbargo (lower back pain): stiff & tender lower back muscles on palpation –
h/o recent heavy exercise – Tx: NSAIDs, apply heat & early mobilization

 Herniated Lumbar disk → L4 –L5 / L5 – S1 → Severe back pain (h/o heavy

weigh lifting recently) without neurological deficit & intact perianal area;
positive straight leg raising test, diagnosis?  Herniated disc; Treatment? 
NASIDs & early mobilization

 Cauda Equina Syndrome → Loss of bowel & bladder control & loss of
sensation in perianal area → Emergency decompression

 Motor Neuroma → inflammation of the common digital nerve at the 3rd

interspace between 3rd & 4th toes → pointed , high heel shoes → Tx: NSAIDS /
surgical excision

 Traumatically Amputed Digits → cleaned with sterile saline , wrapped in a

saline – moistened gauze , placed in a sealed bag (plastic) and then bag placed on
ice → surgically reattached

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 Nephrology

 Pre-renal Azotemia - ↑ BUN but creatinine near normal (N) (0.6 – 1.2)
 Post-renal Azotemia - ↑ BUN & ↑ creatinine
 Renal Azotemia – BUN/Cr ≤ 15 ( bcoz more ↑↑ in creatinine)
 Cortical necrosis of both kidney sparing medulla – DIC
 Sickle cell anemia – affect medulla most severly – can cause Papillary necrosis
 Renal papillary necrosis (SADD) – Sickle cell anemia, Acute pyelonephritis,
Drugs (Aspirin + acetaminophen), Diabetes

* Nephritic type Glomerular Disease : (moderate proteinuria & RBC cast)

 IgA glomerulonephritis (Berger’s disease) (Buerger’s disease –

thromboangitis obliterans – male – smoking cigarettes) (both are different
disease) – episodic bouts of hematuria 1-3 days following URTI, slow
progression to CRF (40-50%), mesangeal IgA deposit with granular
immunoflurocence
 Post-streptococcal – Hematuria 1-3 weeks following group A Strep Pyogens
infection
- Skin infection - ↑ anti-DNAase B titer
- Pharynx infection - ↑ ASO titer
- Diffuse proliferative (usually resolve, CRF is uncommon)
 Diffuse Proliferative (SLE) – subendothelial Immune Complex (IC) (anti-ds
DNA Ab) deposit with granular IF, “wire looping” of capillaries (CRF most
common cause of death in SLE)
 Rapidly Progressive – crescent formation, associated with Goodpasture
syndrome (linear IF) (Lower Resp Tract involvement, Hemoptysis followed
by ARF), Polyarteritis nodosa (p-ANCA) (GIT involvement – mesenteric
artery, bowel ischemia, bloody diarrhea), Wegner’s granulomatosis (c-
ANCA) (Upper & Lower Resp Tract involvement, perforation of nasal
septum)

* Nephrotic type Glomerular Disease: (proteinuria› 3.5 g/24 hrs & fatty cast)

 Minimal change disease – children – EM show fusion of podocytes

(selective proteinuria – Albumin not globulin), negative IF
 Focal Segmental – HIV, Heroin IV abuse, NSAID, Hodgkin’s lymphoma –
negative IF, non-selective proteinuria
 Diffuse Membranous – Adults – captopril, HBV, malaria, syphilis –
subepithelial deposit with granular IF – “spike and dome” pattern
 Type-1 MPGN – HCV, HBV, cryoglobulinemia – subepithelial deposit – EM
show “tram track” (progress to CRF)
 Type-2 MPGN – C3 nephritic factor (C3NeF), Ab binds to C3 convertase &
prevent its degradation & sustain activation of C3 leads to very low C3 level.
“dense deposit disease” (progress to CRF)

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  Only in SLE, there is subendothelial deposit. In all others, there is subepithelial
deposit
 Only in Goodpasture syndrome, there is linear deposit. In all others, there is
granular deposit.
 Patient with Nephrotic syndrome has accelerated athrogenesis
 Palpable purpura, hematuria, Proteinuria, Hepatitis C – diagnosis?  Mixed
essential cryoglobulinemia – Tx: Mix cryoglobulinemia associated with Hep C –
Anti-viral drugs (Ribavirin and alpha-interferon)
 Polyarteritis nodosa – p-ANCA – HbsAg (+) in 30% of cases
 Lichen planus – association with Hep. C

 Glomerular nodule – DM / Amyloid (chronic disease) both show red on H&E

stain but with Congo red stain – Amyloid – “apple-green” birefringence nodule.
DM nodule is composed of Type-4 collagen & protein

 Pathogenesis of DM: Nonenzymatic glycosylation (glucose + AA) → ↑vessel

permeability to protein and ↑athrogenesis; Osmotic damage → Aldolase
reductase (glucose → sorbitol) → sorbitol draws water into tissues causing damage
(eg. retinopathy); Diabetic microangiopathy → ↑synthesis of type-IV collagen in
basement membrane & mesangium
˗ Tight blood sugar control decrease the risk of development of microvascular
complication (retinopathy, nephropathy, neuropathy)
˗ ACE inhibitors has shown to reduce insulin resistance
 Screening test for nephropathy in DM: Random urine for microalbumin /
creatinine ratio (goal <30 mg/g)
 Earliest renal abnormality seen in diabetic nephropathy: glomerular hyper
filtration

 Ethylene glycol poisoning – Metabolic acidosis (↑ anion gap) + oxalate

crystalluria
 Cystinuria – staghorn calculi, positive nitropruside cyanide test
 Staghorn calculi – Proteus infection

* Acid-Base Disturbances

 (Na + K) – (HCO3 + Cl) = 8-14 (normal anion gap)

 Only chronic acidosis/alkalosis is compensated not acute
 Chronic Resp. Acidosis – compensated by Metabolic Alkalosis (HCO3 – 22-28)
PCo2 - › 45 mmHg, HCO3 - ≤ 30 mEq/L – Acute Resp. Acidosis
HCO3 - › 30 mEq/L – Chronic Resp. Acidosis
 Chronic Resp. Alkalosis – compensated by Metabolic Acidosis
PCo2 - ‹ 33 mmHg, HCO3 - ≥ 18 mEq/L – Acute Resp. Alkalosis
HCO3 - ‹ 18 mEq/L (but›12 mEq/L) – Chronic Resp. Alkalosis

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 * Renal Tubular Acidosis (Normal Anion gap Acidosis)

 Type-1 – secondary to autoimmune diseases, Lithium, analgesics, sickle cell

disease
Inability to secrete H+ in Urine, Urine pH - › 5.4
Patient usually gets Renal stone
Acid load Test – After giving ammonium chloride, urine pH still remain elevated
(normally it should be decreased)

 Type-2 – Renal threshold for absorbing HCO3 is lowered from normal of 24

mEq/L to 15 mEq/L
Initially pH › 5.5 and then it goes back to ‹5.5
Patient usually get bone lesion (osteomalacia, rickets)

Both Type-1 & Type-2 get Hypokalamia.

 Type-4 is the only renal tubular acidosis which produce hyperkalamia due to
destruction of JG apparatus - ↓ rennin - ↓ aldosterone
Causes – hyaline arteriosclerosis in afferent arteriole in DM, Legionaire’s disease

 Intake of salt = output of salt (95% renal & 5% sweat)

* Hyponatremia – Na ‹135 in the absence of hyperglycemia

 SIADH – Oral hypoglycemic & Carbamazapine
 Diagnosis – Urine osm › Serum osm (Urine osm › 40 is typical)
 Treatment – fluid restriction (hyponatremia due to volume overload like in CHF),
loop diuretics & normal saline, hypertonic saline, Lithium/Demeclocycline in
SIADH. Rapid correction of hyponatremia results in Central Pontine Myelinosis
– destruction of brain stem present with paraparesis, dysarthria or Dysphagia.
* Hypernatremia – loss of hypotonic fluids (sweating, burns, fever), central DI &
Nephrogenic DI – Best initial Tx of hypovolemic hypernatremia – normal saline
(0.9%)
* Hypokalamia – “U” wave on ECG, Alkalosis, ↑ Aldosterone
* Hyperkalemia – peaked T wave on ECG, Acidosis, ↓ Aldosterone – IV calcium
gluconate (first step) – In Hyperkalemia, removal of k+ from the body can be
achieved by dialysis, cations exchange resins (kayexalate) or diuretics.
* Hypercalcemia – IV normal saline infusion (first step). (except hypercalcemia is
due to Metastasis in which bisphosphonates preferred)
* Hypophosphatemia – continuous infusion of glucose is the leading cause of
hypophosphatemia; muscles weakness

* Hypercalcemia – Loop diuretics / Hypercalciuria – Thiazide diuretics

• Any time in question, hypokalamia, first step – IV potassium
• Any time in question, hyperkalemia, first step – IV calcium gluconate
• Hypocalcemia – hyperactive deep tendon reflexes
• Hypermagnesemia – loss of deep tendon reflexes
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 * Pheochromocytoma
 a neuroendocrine tumor of the medulla of the adrenal glands
 Signs & Symptoms of sympathetic hyperactivity (increase HR, HTN, etc)
 Diagnosis: urinary vanillylmandelic acid (VMA)
 CT scan/MRI – to localize tumor
 Confirmation of diagnosis with biochemical tests (24-hrs urine measurement of
VMA, metanephrines & catecholamine) is required before imaging studies. Once
diagnosis is confirmed, start alpha-blockers.
 Treatment – Alfa-blockade followed by surgical removal

* Renal Artery Stenosis

˗ Best screening test – US abdomen (renal Doppler US) / captopril renogram (best
non-invasive method)
˗ Most accurate method – MRI / CT angiography
˗ Best initial treatment – percutneous transluminal angioplasty

* MCC of secondary HTN in children – fibromuscular dysplasia (20% of all cases

of renal HTN) – angiogram typically show a “string of bead” appearance to the
renal artery

* Important Urinary Cast

 Waxy, broad cast – signs of End Stage Renal Disease
 WBC cast – Acute pyelonephritis, acute tubulointerstitial nephritis (drug)
 Renal tubular cell cast (muddy brown granular cast) - ATN

• First step in management of patient with hematuria – urine analysis

• Microscopic / gross painless hematuria, next step? – CT urogram / IVP (to look
kidney & ureter) and Cystoscopy (to look bladder)
• Most common cause of painless hematuria in adults in USA  Bladder mass then
Renal cell CA

• Patient with BPH doesn’t have hematuria. Presence of hematuria in a patient with
BPH present with irritative or obstructive voiding symptoms – always suspect
bladder CA

• Chronic pyelonephritis: h/o vasicoureteral reflux + bilateral focal parenchymal

scaring & blunted Calyces on IVP

 Chronic Renal Failure (CRF):

• Diabetic nephropathy, HTN and glomerulonephritis [These 3 = 75% of cases]
• Volume overload leads to HTN and CHF
• Uremia (Pericarditis and encephalopathy)
• Hyperkalemia, Hyperphosphotemia and Hypocalcemia (Vit-D3 deficiency) (renal
osteodystrophy)
• Metabolic acidosis and accelerated atherosclerosis
• Causes of bleeding in CRF – platelet dysfunction
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 • Increase Bleeding Time due to renal disease – IV Desmopressin (first choice)
• CRF patient should receive erythropoietin & iron supplementation
• Anemia in patient with end-stage renal disease is due to erythropoietin deficiency.
If there is no or minimal increase in hematocrit level after 4-6 wks treatment with
EPO, iron saturation, ferritin level and TIBC should be measure [Side effects of
Erythropoietin Therapy – worsening of hypertension, Headache, flu-like
syndrome, Red cell aplasia]
• Vitamin-D3 and calcium supplements, ACE inhibitors have been found to slow
the progression of CRF
• Protein restriction improve prognosis in CRF

 Kidney stones – plain X-ray KUB (first step); If KUB is normal but S&S
suggestive of renal stone, next step? – order CT scan without contrast; Pregnant
patient with S&S of renal stone, next step? – order U/S of abdomen

 Urethral Diverticulum – h/o frequent UTI, tender suburethral mass – classical

triad of dribbling, dyspareunia and Dysuria – order Cystourethrogram or
Urethroscopy

* Juvenile Polycystic Kidney Disease

 Autosomal recessive
 Bilateral enlarged kidney at birth
 Maternal oligohydramnios

* Adult Polycystic Kidney Disease

 Autosomal dominant
 Bilateral enlarged kidney around 20-25 yrs of age
 Cyst also present in liver (40%)
 Intracranial berry aneurysm (10-30%) (present with subarachnoid hemorrhage),
HTN, sigmoid diverticulosis (Before doing peritoneal dialysis in a patient with
APKD, patient should undergo colonoscopy first), MVP
 Follow up plan for patient with APKD – regular BP measurement
 Screening test for APKD – U/S

* Multiple contrast filled cyst on IVP, diagnosis?  Medullary Cystic kidney

(Autosomal dominant, No Hypertension)

* Unilateral flank mass in child > 3 yrs  Wilm’s tumor

Bilateral flank mass in child  polycystic kidney (infantile)
Unilateral flank mass in Adults  Renal cell CA
Bilateral flank mass in Adults  polycystic kidney (adult)

* Renal cell CA (clear cell CA, hypernephroma, Grawitz tumor)

 Derived from proximal tubule (PT)
 Risk factors – smoking, Von Hipple-Lindau syndrome, Adult polycystic kidney
disease (APKD)

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  Hematuria, flank mass & CVA tenderness
 Metastasize to lung [cannonball appearance on x-ray], Lt sided varicocele

* Wilms Tumor:
- Derived from mesonephric mesoderm (unilateral flank mass)
- Histology: abortive glomeruli, & tubules, primitive blastemal cells,
rhabdomyoblasts
- Hypertension in child, Autosomal Dominant (chromosome-11)
- WAGR Syndrome (Wilms tumor, Aniridia, Genital abnormalities, Retardation)

* Neuroblastoma:
- N-myc gene amplification.
- Small blue cell tumors (Ewing sarcoma, Lymphoma, Neuroblastoma, small cell
CA of Lung).
- Composed of malignant neuroblast, presence of Homer-Wright rosettes.
- Neurosecretory granules on electron microscopy.
- Hypertension in child.
- ↑↑↑ Urinary VMA (vanillylmandelic acid), HVA, metanephrines.

 Potter’s syndrome – absent of both kidney – oligohydroamnios – failure of

ureteric buds to develop

• Alport syndrome:
- X-linked dominant disorder
- Asymptomatic hematuria , Sensorineural hearing loss
- Renal biopsy: Glomerular Sclerosis , thickened basement membrane tubular
atrophy fibrosis and foam cells.

• Hemolytic Uremic Syndrome ( HUS ):

- E.Coli (0157 : HS) → produce Vero toxin → endothelial cell injury
- Endothelial injury of the kidney results in localized clotting → RBCs and intra-
renal platelate damage causes microangiopathic anemia and thrombocytopenia
- Approximately 1 week after E.Coli ( 0157 : H7 ) infection , patient develop
oliguria, sign & symptoms of anemia
- ↓ Hb level m drop in platelate count, Hematuria , proteinuria , Helmet cells on
peripheral smear
- D/D: TTP which involves CNS whereas HUS involves kidney.

• Henoch–Schonlein Purpura:
- IgA – mediated vasculitis of small vessels
- Non-thrombocytopenic purpura in children
- Usually follows an URI.
- Tetrad of Abd. Pain, Rash, Renal involvement & Thrombocytopenia.
- Palpable purpuric rash on buttocks
- Intussusception is more common in patient with HSP
- Tx: Corticosteroids

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 • Combination of obstruction & Infection of Urinary tract : Patient who is
being allowed to pass a ureteral stone spontaneously & who suddenly develop
chills , fever & flank pain. It is a medical emergency due to high chances of sepsis
so order CT scan without contrast to establish diagnosis after starting IV
antibiotics and hydration
˗ Tx : IV antibiotics & immediate decompression of the urinary tract above the
obstruction by either percutaneous nephrostomy or ureteral stent placement

■ Post- op – Zero urinary output → plugged / kinked catheter.

■ Post – op – Low urinary output with good perfusing pressure (SBP› 90 mm Hg)
↓
↓ ↓
Insufficient Fluid intake Acute Renal Failure
↓ ↓
Fluid challenge Test → 500 ml of RL/NS IV in 10-20 mins
↓ ↓
↑ urinary output no change in urinary output
↓ ↓
Na concentration → < 20 mEq / L
+
> 40 mEq /L

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 NEUROLOGY

 CSF: Lat ventricle → foramen of Monro → 3rd ventricle → Aqueduct of Sylvius →

4th ventricle [obstruction to CSF flow will give hydrocephalus]
 Arnold-Chiari malformation – herniation of cerebellum – hydrocephalus
 Arnold-Chiari malformation type 2 – syringomyelia, myelomeningocele
 Syringomyelia is associated with Arnold-Chiari malformation in most cases.
 Headache, 6th CN palsy, bilateral papilledema, empty sella & no mass lesion on
MRI, Diagnosis?  Pseudothmor cerebri (benign idiopathic intracranial hyper-
tension); next step?  Lumbar puncture (reduce intracranial pressure to prevent
vision loss); Tx: Acetazolamide

 Subfalcine herniation: cingulate gyrus herniates under falx cerebri [compress

anterior cerebral artery]
 Uncal herniation: medial portion of temporal lobe herniates through tentorium
cerebellli [compress midbrain & posterior cerebral artery]
 Tonsillar herniation: cerebellar tonsils herniates through foramen magnum [pro-
duce cardiorespiratory arrest]

■ Guillain – Barre Syndrome:

- Auto immune destruction of myelin
- Begins in lower extremities and move upward
- Patient usually c/o pain / tingling
- Associate with C.Jejunii
- Best Initial test: lumbar puncture for protein and cell count
- Most Accurate test: Electromyography (EMG)
- Treatment: IV immunoglobulin / plasmaphersis

• Progressive ascending paralysis with normal CSF finding – Tick-born paralysis

■ Myasthenia Gravis:
- Antibodies produce against Ach receptors
- C/o diplopia , ptosis , difficulty swallowing
- Symptoms are improved with rest
- Best Initial Test: Ach receptor antibody test
- Most Accurate Test: EMG → decremental decrease in muscle fiber contraction
on repetitive never stimulation
- Treatment : Anticholinesterase Drugs
- Glucocorticods / Azathioprine (take more time to reach peak action)
- Thymectomy (post-pubertal)
- Eaton-Lambert syndrome  Antibodies to voltage gated Ca+2 channels in the
presynaptic nerve terminal (pre-synaptic membrane damage), absent or
diminished reflex, ↑↑ muscle strength after repetitive task
- Myopathy in Lang CA  muscle membrane damage, Normal reflex

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 ■ Huntington Disease:
- Autosomal Dominant
- Affect Caudate nucleus
- CAG trinucleotide repeat expansion
- Chorea & behavioral disturbance
- Onset in 4th or 5th decade
- Diagnosis → Southern blot test to check DNA repeat expansion

■ Parkinson Disease:
- Degeneration of substantia nigra (↓ dopamine)
- Imbalance b/w dopamine (↓↓) and cholinergic (↑↑) transmitters
- Bradykinesia , Cogwheel Rigidity , Resting tremor (pill rolling) , postural
instability
- Shy-Drager Syndrome – Parkinsonism + orthostatic hypotension
- Diagnosis → clinical
- Treatment → 1st step is evaluating the patient’s functional status
- Intact functional status (less Bradykinesia) – Anticholinergics (Benztropin,
Trihexyphenidyl) (< 60 yrs of age) / Amantidine (> 60 yrs of age)
- Compromised functional status (significant Bradykinesia) – Carbidopa /
levodopa (best initial drugs), Selegiline (only drug which arrest progression of
disease), Surgery (pallidotomy, thalamotomy)
- Visual hallucination, confusion and agitation after starting treatment with
Levodopa is highly suggestive of Lewy body dementia

■ Multiple Sclerosis:
- Focal areas of demyelination
- Optic neuritis, scanning speech, intention tremor, nystagmus
- Bilateral internuclear ophthalmoplegia [demyelination of MLF] [pathognomic]
- Blurry vision and double vision → common initial manifestations of the disease
→ resolve spontaneously
- CSF show oligoclonal bands (70 –90 %)
- Best initial Test : MRI of the Brain
- Best Diagnostic Test : MRI of the Brain
- Relapsing – remitting disease → IFN-B1a, IFN-B1b, glatiramer acetate
- Secondary – progressive Disease → IFN-B1b, Mitoxantrone (cardiotoxicity )
- Primary – Progressive Disease → No approved therapy exist at this time
- Acute Exacerbation → IV steroid X 3 days followed by oral medication X 4
weeks plasma Exchange
- Patient with exacerbation of MS – IV steroids (study has shown that oral should
not be offered in patient with MS who present with optic neuritis) then start
interferon / glatiramer acetate (both are teratogenic) and follow-up with MRI after
3-months; optic neuritis as an initial presentation of MS has a good prognosis
- Spasticity → beclofen ; Nocturnal Spasticity → Diazepam , Tizanidine
- Trigeminal neuralgia → carbamazapine ; Fatigue → Amantidine / fluoxetine
- Bladder ltyperactivity → Oxybutynin; Urinary retention → Bethanechol

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 ■ Marcus-Gunn phenomenon – dilatation of Rt. Pupil with dilatation of Lt. Pupil
occur (Paradoxical dilatation) in patient with Rt. Optic neuritis/ Rt. retinal de-
tachment

 Alzheimer Disease: defect in degradation of β-Amyloid protein by secretase

leads to accumulation of Amyloid protein in neuron and damage neurons –
mutation in Tau protein (maintain microtubule in neuron) leads to formation of
neurofibrillary tangles – Microscopic [senile plaques (Amyloid protein) and
neurofibrillary tangles] – Problem in memory [affect hippocampus (old brain)
short term memory loss] & visuospatial abilities (early); Hallucination &
Personality change (late) – diagnosis of exclusion [rule out reversible cause of
dementia (first step) so order CBC, electrolytes, Ca+2,Creatinine, LFTS, Glucose,
TSH, Vit-B12 ,RPR, HIV – Tx: Donepezil (discontinue if no improvement within
3-6 months of treatment)
 Pick Disease: frontotemporal dementia → Pick body (Intracytoplasmic spherules
composed of paired helical filaments) → Present with Personality change
 Lewy body dementia: Lewy body (Intracytoplasmic spherules that stain brightly
eosinophilic) → fluctuating cognitive impairment [confusion and agitation]
which can be confused with delirium
 Creutzfeldt Jacob Disease (CJD): Shorter & more aggressive course, present
with dementia & myoclonus
 Vascular Dementia: h/o multiple strokes – multi-infarct dementia
 Extrapyramidal symptoms + dementia = subcortical dementia (Parkinsonism)
 Binswanger Disease: involve subcortical white matter, slow course
 Normal pressure hydrocephalus: dementia, gait abnormality and Urinary
incontinence
• Appearance of CT scan in different kind of dementia:
1. Enlargement of ventricle without cortical atrophy – normal pressure hydro-
cephalus
2. Hypodense images involving different brain regions – Multi-infarct
3. Marked atrophy of the frontal and temporal cortices – Pick
4. Diffuse cortical and subcortical atrophy – Alzheimer

 Krabbe’s Disease: presence of “globoid” cells (multinucleated histiocytic cells)

in degenerating white matter in brain – galactocerebrosidase deficiency

 Cerebrovascular Accident : Sudden onset of focal neurologic deficit

˗ Hypertensive (Lacunar stroke)  limited / mild neurologic deficit
˗ Large artery atherosclerosis / cardiac emboli  severe clinical manifestation
˗ Yong patient with TIA (neurologic deficit resolve in 24 hrs), cause?  Emboli
(MCC) investigation?  transthoracic echo (other cause vasculitis, dissection,
hypercoaguble state)
˗ Elder patient with TIA, cause?  Atherosclerosis & Emboli; investigation? 
Carotid Doppler ultrasonography
˗ Next step in management of patient with stroke whose carotid Doppler imaging is
normal – echocardiography
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 ˗ Best Initial Test / Next Step: Non-contrast CT Scan of the Head (detect blood
in the brain)
˗ Most Accurate Test : Diffusion – weighted MRI ( Detect ischemia)
˗ Treatment : tPA(within 3 hrs of onset of Symptoms if not contraindicates)
Heparin (if not contraindicated)
Anti-platelate Therapy (Aspirin / clopidogrel)
Carotid endarterectomy (Occlusion > 70 % & Symptomatic)
 Anti-hypertensive drugs should only be used in patient with h’gic stroke if BP is
over 220/120
 First step in management of patient with unconsciousness or Seizures or focal
neurologic findings [after stabilization]  CT scan without contrast
 Serum glucose level should be measured in all patients present with CNS
dysfunction [CNS dysfunction due to hypocalcemia, next step? - measure serum
glucose]

 Spinal Cord compression: neurologic emergency

˗ Pain which ↑ by action that ↑ intrathoracic pressure → ↑ CSF pressure
˗ H/O cancer, fever, bowel / bladder incontinence, UMN lesion sign below
compression
˗ High – dose dexamethasone → immediately once diagnosis is suspected
˗ X-ray Spine ( Best initial test )
˗ MRI Spine ( Most Accurate test )
˗ CT myelogram (when MRI is C/I)
˗ Surgical Decompression → Herniated disk, epidural abscess , Hematoma
˗ Hyperextension injuries in elderly patients with degenerative changes in
cervical spine – Central Cord Syndrome (Acute cervical spine cord injury) –
characterized by disproportionately greater motor impairment in upper compared
to lower extremities, bladder dysfunction, and variable degree of sensory loss
below the level of injury

■ Subacute Combined Degeneration: Vit – B12 deficiency

- deficit of vibration & proprioception

■ Ant Spinal artery Infarct:

- Acute onset of flaccid paralysis that evolves into a spastic paresis over days to
weeks
- Loss of pain & temp. Sensation with Sparing of vibration and position sense.

 Tabes Dorsalis: dorsal column of spinal cord – tertiary syphilis

 Seizures & Epilepsy :

˗ Postictal Symptoms (c/o disorientation, sleepiness, muscle aches) for mins to hrs
differentiate Seizure from Syncope

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 ˗ Todd’s paralysis: Acute onset of paralysis in patient gaining consciousness after
short period of unconsciousness and resolvement of paralysis after few hours,
Cause? – Seizure
˗ Child with febrile seizures have slightly increase risk of epilepsy in future
compare to general population
˗ Absence Seizures (Petitmal): Sudden, brief loss of consciousness without loss of
postural tone (stare in the space). EEG will show generalized, Symmetric 3-Hz
spike and wave discharge pattern
˗ EEG( electroencephalogram ) → best diagnostic test for epilepsy
˗ Treatment : Acute attack → Secure A,BC (first step )
˗ Lorazepam or Diazepam (IV) → Best initial drug
˗ Phenytoin / fosphenytion → Phenobarbitol → Midazolam / Propofol
˗ Generalized tonic–clonic (grandmal) → Valpronic acid / lamotrigine
˗ Absence Seizure → Ethosuximide or Valproic acid
˗ Partial Seizures (Simple / complex) → carbamazapine / phenytoin
˗ Myoclonic Seizures → Valproic acid
˗ Atonic Seizures → Valproic acid

• Patient with epilepsy which is well controlled with anti-epileptic drug comes to
you at 13-15 wks of pregnancy for first time for routine care, next step? –
continue her anti-epileptic drug and offer alpha-feto protein. [If there is a chance
of any malformation, pregnancy can be terminated] Breast feeding is not C/I
when patient is on anti-epileptic drugs

 Vertigo & Dizziness :

˗ Vertigo → c/o room (environment ) is spinning around
˗ Presyncope → c/o lightheadedness / feeling like I’m going to black out
˗ Central Vertigo (Cerebellar lesion/ Brain stem lesion) → gradual onset, Absent
tinnitus, no hearing loss, signs of CN lesions, vertical nystagmus
˗ Peripheral Vertigo → Sudden onset, tinnitus & hearing loss present, horizontal
nystagmus.

 Meniere disease → Tinnitus , Hearing loss & Episodic Vertigo

˗ Symptoms wax & wane as endolymphatic pressure rise & fall
˗ Tx: low salt diet & Diuretics [Syphilis can cause Meniere disease]

 Benign Paroxysmal Positional Vertigo → Head movements lead to vertigo (10-

60 sec) – Tx: Positional maneuvers

 Labyrinthitis → severe vertigo, hearing loss & tinnitus follows an URI

˗ Tx : meclizine & diazepam

 Temporal Arteritis (Giant Cell Arteritis) – vasculitis of superficial temporal

artery and ophthalmic artery → Unilateral pounding headache, Visual changes,

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 Jaw claudication, scalp tenderness, ESR >60 mm/hr → Tx: → High dose
Prednisone (1st step)

 Migraine Headache → unilateral throbbing, 4-72 hrs

- Scintillating scotoma → Migraine with Aura
- Tx : Acute attack → Sumatriptan / Ergotamine
- Prophylaxis (> 3 headache / month) → Propranolol / Valproic acid / methysergide

Tension –type Headache → bilateral tight band like headache with tightness of
posterior neck muscles .
˗ Tx : Relaxation Activities, Acetaminophen (NSAID), muscle relaxant

 Cluster Headache → excruciating , periorbital with rhinorhea , reddening of the

eye , nasal stuffiness , peaking in intensity in 5 min usually last 45-90 min , 1-3
times/day for 4-8 weeks
˗ D/D: Acute angle closure glaucoma & cluster headache may confuse, but halos
around light & fixed dilated pupils are seen in acute angle closure glaucoma.
Cluster headache are recurrent
˗ Tx : Acute attack → 100 % O2
Prophylaxis → Prednisone, lithium, Verapamil, methysergide, ergotamine

 Tuberous Sclerosis:
- Infantile spasm (Tx : ACTH & Prednisone)
- Rhabdomyoma of Heart (echocardiography)
- Ash leaf spots (Hyperpigmented lesions), shagreen patches (“orange-peel”
lesions), sebaceous adenomas.
- Angiofibroma on the face
- Angiolipomas in the kidney
- Astrocyte proliferations in subependyma (Look like “candlestick drippings” in the
ventricles)

 Neurofibromatosis (NF):
- Café au lait spots (tan/light brown flat lesion), Axillary freckling, Lisch nodules,
optic nerve gliomas, Acoustic Neuroma (CN-8)(feature of NF-2)(all other NF-1).
- Association with Pheochromocytoma, Wilms tumor

 Duchenne Muscular Dystrophy:

- Pseudohypertrophy of the calves.
- Gower Sign (child places hands on the knees for help in standing).
- Deficiency of dystrophin.

 Becker Muscular Dystrophy:

- Defective dystrophin
- Less serious than Duchenne muscular dystrophy

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  Warding – Hoffman Disease:
- Infantile spinal muscular atrophy.
- Atrophy of anterior horn cells in the spinal cord and of motor nuclei in the
brainstem.
- Severe hypotonia and absent tendon reflexes.
- Legs tend to lie in a Frog leg position.

 Charcot-Marie Tooth:
˗ Hereditary motor–sensory neuropathy.
- Peroneal muscular atrophy.
- Peroneal & Tibial nerve most commonly affected.
- Wasting of the lower legs giving them stork like appearance.
- Sural nerve biopsy → “onion bulb” formation (interstitial hypertrophic
neuropathy)

 Friedreich Ataxia:
- Expanded GAA triplet repeats
- Autosomal recessive
- male child with gait disturbance & dysarthria (speech difficulty)
- Cardiomyopaty (90% of cases)

 Ataxia Telangiectasia:
- Mutation in DNA repair enzyme, thymic hypoplasia
- Cerebellar ataxia, Telangiectasia of skin & eye

 CNS tumors: Adult (above tentorium cerebelli) Children (below tentorium

cerebelli) Most common [Adult – glioblastoma multiforme, meningioma;
Children – Astrocytoma, Medulloblastoma]

* Oligodendroglioma – “fried egg cell” round nuclei & clear cell – cerebral
hemisphere
* Choroid plexus papilloma – papillary growth in ventricle
* Ependymoma – pseudorosettes & structure resembling ependymal canal
* Glioblastoma multiforme – hemorrhagic tumor (multiple area of necrosis &
cystic degeneration)
* Pilocytic Astrocytoma – bipolar cells – cerebellum of young children
* Medulloblastoma – most common in children – only CNS tumor with both
neural & glial components – affect granular cell layer of cerebellum
* Meningioma – associated with neurofibromatosis – parasagital location
* Craniopharyngioma → remnant of Rathke’s pouch (Resembles to
Amblioblastoma) → calcified lesion above the sella on X-ray → bitemporal
hemianopsia
* Pineal gland tumor → loss of vertical gaze (“sunset eyes”) [Parinaud
Syndrome]
* Acoustic neuroma  MRI with gadolinium  surgery

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 ■ CNS bleeds:

* Epidural: skull fracture – rupture middle meningeal artery

* Subdural: tear of bridging veins – fluctuating levels of consciousness
* Atherosclerotic stroke: usually pale infarct (since no reperfusion)
* Embolic stroke: hemorrhagic infarct extends to surface of the brain
* Intracerebral bleed: hypertension most common cause – rupture of lenticulostriate
Charcot-Bouchard aneurysms – hematoma (not an infarct) – globus pallidus/putamen
area most common sites

˗ Hemorrhage in brain parenchyma:

˗ Putamen hemorrhage (most common site) – almost always involve internal
capsule. Hemiparesis, hemi-sensory loss, homonymous hemianopsia, stupor
and coma
˗ Pontine hemorrhage – pinpoint pupil, deep coma and paraplegia within few
min. There is decerebrate rigidity
˗ Cerebellar hemorrhage – ataxia, occipital headache, gaze palsy and facial
weakness (no hemiparesis)
˗ Subarachnoid hemorrhage – “worst headache of my life”

* Subarachnoid bleed: ruptured congenital berry aneurysm [junction of

communicating branch with anterior cerebral artery] – severe occipital headache –
common in patient with polycystic kidney disease – Major cause of morbidity
& mortality in a patient with subarachnoid hemorrhage (SAH)  Vasospasm
following SAH; Nimodipine is used to prevent vasospasm following SAH
˗ High RBC count without xanthochromia – traumatic LP
˗ RBC with xanthochromia and discoloration of centrifuged CSF due to Hb
breakdown – Subarachnoid h’ge

* Syncope (Loss of Consciousness): it may be acute or gradual – EKG (Best

initial test / first step in management) – causes of acute syncope [Arrhythmia,
Mitral valve prolapsed, Hypertrophic obstructiove cardiomyopathy and seizure]
gradual syncope [hypoglycemia, hypoxia, hypovolemai, vaso-vagal attack,
barbiturates, etc] – early regaining of consciousness is seen in syncope due to
heart problem which is helpful in differentiate acute syncope due to seizure
(gradual regaining of consciousness)

* Vasovagal syncope – Recurrent syncopal attacks provoked by emotions preceded

by prodrome (light headedness, blurred vision) – upright tilt table test

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 PSYCHIATRY

• IQ : Average(90 – 109) (50 % of population )

- Add 10 for High average , Superior , Very Superior (2.5 % population )

(110-119) (120-129) (over 130)

- Autistic children → IQ less than 70

• Commonly used IQ test:

- WAIS – R – Adult ( > 17 yrs )

- WPPSI – Pre – School & Primary ( 4 – 6 yrs )

- Stanford – Binet Scale – children ( 2 – 6 yrs )

- WISC – R – children ( 6 –17 yrs )

■ Mood Disorders: Depression or Mania (hyper)

• Dysthymia (non-psychotic depression) → chronic (atleast 2 yrs)

• Unipolar (Major depression) → Symptoms for atleast 2 weeks

- Early morning waking, pseudodementia in elderly

■ Cyclothymia (non-psychotic bipolar) → chronic (atleast 2 yrs)

- ego-syntonic

■ Bipolar – Manic Symptoms + Major depression

(bipolar-1) (bipolar-2)
- Presence of maniac symptoms put patient in bipolar category

■ Schizophrenia: Delusion, illusion, hallucination (Auditory 75 %), Blunted affect,

loose associations.

■ Differential: Schizophrenia - > 6 month of symptoms

Schizopheniform - < 6 month of symptoms
Brief Psychotic - < 1 month of symptoms
Schizoid Personality – life long pattern of social withdrawal seen by
others as eccentric, isolated
Schizotypal personality – Magical thinking, illusions, ideas of
Reference, very odd, strange, weird
Schizoaffective – Alteration in mood is present during substantial
Portion of illness + Sx of Schizophrenia

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 • Subtypes of Schizophrenia:
- Paranoid – Delusions of persecution (or) grandeur, hallucinations (voice)
- Catatonic – Rigidity of posture, Complete stupor, may be mute
- Disorganized – uninhibited, unrecognized (disorganized) behavior & speech,
poor personal appearance, little contact with reality.
- Undifferentiated – psychotic symptoms but doesn’t fit in above three category.
- Residual – Previous episode but no prominent psychotic symptoms at evaluation,
some negative symptoms.
• Positive Symptoms: Delusion, hallucination, bizarre behavior (dopamine)
• Negative Symptoms: Flat affect, apathy, mutism (muscarinic receptor)
• Brain structural and Anatomic abnormalities:
- Large ventricle size, cortical atrophy, smaller volume of left hippocampus and
amygdala, Atrophy of temporal lobe.
- Limbic system seen as the primary pathology site for schizophrenia
* Delusional Disorders: No hallucination, Delusions are not bizarre (like I’m a
millionaire (believable - could be possible) whereas in Schizophrenia bizarre
delusion like I’m a king of Moon (not believable) and patient is not functioning.

 Somatoform Disorder: Production of somatic symptoms (like abdominal pain,

headache, etc) – extensive diagnostic procedures fail to show any pathology –
constantly change their primary physicians – unconscious symptom production
 Factitious Disorder: intentional symptoms production but there is no motivation
to produce symptoms means symptom production is not for any gain
 Malingering: Intentional symptoms production for gaining something

• Munchausen Syndrome: Factitious disorder – usually medical field person

(nurse)
• Munchausen Syndrome by proxy: mother produce symptoms in her baby

• Conversion Disorder: One (or) more NEUROLOGIC symptoms (eg. paralysis

of half of the body) without any real organic cause.
- Loss of functioning is real & unfeigned

• Body dysmorphic disorder: persisten subjective feeling of ugliness or physical

defect

■ Post-Traumatic Stress Disorder: Flashback, Avoidance of associated stimuli –

Symptoms must be exhibited for > 1 month after passing few months of
traumatic event

• Acute stress Disorder: symptoms for < 1 month soon after traumatic event.

• Adjustment disorder – Symptoms must occur within 3 months of stressors and

must not last more than 6 months – Tx: Supportive Psychotherapy

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 ■ Substance Abuse:
- Cocaine, amphetamine, cannabis, hallucinogens and PCP (phencyclidine) →
paranoia (Schizopheniform delusion disorder)
- Cannabis, inhalants, hallucinogens and PCP do not have withdrawal reactions.
- Toxicology screening – urine immunoassay qualitative screen [rapid and
inexpensive]
* Cocaine – Intoxication → Paranoia, arrhythmias
Withdrawal → Depression
* Amphetamine – Intoxication → Paranoia, pupillary dilatation
Withdrawal → Depression
* Cannabis – Slowed reaction time, social withdrawal, injected conjunctiva
* Hallucinogens – Ideas of reference, brilliant color hallucination, pupillary
dilatation. Withdrawal – flash back (feels same as they are on drug without drug)
* Opiates – Intoxication → pupillary constriction, respiratory arrest, bradycardia,
hypotension (due to vasodilation)
Withdrawal → flu-like symptoms Tx: Clonidine, methadone

• IV drug abuser admitted in hospital and after few hours develop dilated pupils and
other symptoms (like piloerection, rhinorhea, abdominal cramps, etc) – opioid
withdrawal [Tx: Methadone / other opioids]

* PCP – violence, vertical nystagmus – Next step in management of patient with

PCP intoxication – put patient in low-sensory environment
* Benzodiazepines – Intoxication → inappropriate sexual / aggressive behavior
Withdrawal → seizures

■ Sleep: Sleep cycle is regulated by super chiasmatic nucleus.

- Non-REM → 1st half, REM → 2nd half (REM cycle → 90 mins)
- Adults wake out of REM / 2nd stage of non-REM
- REM → Rapid eye movement – eye is a part of brain so brain is active & body is
inactive (↑ eye movement, ↓ muscle tone)
- NREM → Opposite to REM means brain is inactive & body is active (↑muscle
tone)
- REM sleep is requiring for memory
- Melatonin → inhibited by Daylight (responsible for jetlag)
- Elderly → REM – 20 % (constant), stage - 4 (delta) – Vanish (↓)

• Neurotransmitters:
- Serotonin – initial sleep
- ACh – REM sleep
- Norepinephrine - ↓ in REM sleep
- Dopamine – Arousal & wakefulness

 Sleep Waves:
˗ Awake → low-voltage fast waves – Beta waves

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 ˗ Drowsy →Alpha waves (8-12 cps) (closing the eyes)
˗ Stage -1→Theta waves (3-7 cps)
˗ Stage -2→ Sleep spindles & K complexes. (12-14 cps)
˗ Delta sleep →Delta waves (1/2 –2 cps) [Delta – D means Deep sleep]
˗ REM sleep →low-voltage fast with saw tooth waves.

 Somnambulism: sleep walking –occur during stage-4 (Delta sleep).

 Nightmare: REM sleep – person often awake – dreaming (dreams of frightening

nature) – can recall

 Night terror: NREM sleep (stage 4) – person often impossible to fully awaken
– can’t remember

 Narcolepsy: excessive daytime sleepiness and abnormalities of REM sleep

greater than 3 months.
- REM sleep occurs in less than 10 mins
- Cataplexy → Sudden loss of muscle tone
- Sleep paralysis
- Falling asleep quickly at night
- Tx: Psychostimulant; If cataplexy present → Antidepressants

• Modeling / Observational Learning ( Social Learning ):

- victim of abuse is now abusing his/her own child

■ Defense Mechanisms:

• Projection – Paranoid behavior [Do not trust anyone!]

• Introjection – try to act like someone

- eg: Students act like the resident

• Denial – denies every thing

- eg: I know I don’t have cancer [even though patient have cancer]

• Isolation of Affect – no reaction on their face!

- Blunted affect (Schizophrenia)

• Splitting – split their behavior! Sometime very good Sometimes very bad
- Borderline personality

• Blocking – Transient block on our memory!

˗ eg: Oh! What’s his name? I can’t seem to remember his name

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 • Repression – nonretrievable forgetting
- eg: sexually abuse girl in her childhood doesn’t remember anything in her
adulthood

• Suppression – Forgetting is reversible

- eg: I went out for movie before the day of my anatomy exam but after coming
back I again started my reading [remembered that I have exam tomorrow!]

• Regression – Returning to an earlier stage of development

- eg: Enuresis in previously toilet train child after birth of another baby
• Somatization – productions of somatic symptoms [somatoform disorder]
˗ eg: Just thinking of six flag I get Butterflies in my stomach

• Displacement – source stays the same, target changes

- eg: My elder brother angry at me and I angry at my younger one

• Acting out – doing something to hide emotion!

- eg: Whistling in dark who is afraid of going in darkness

• Rationalization – Explanations are used to justify unacceptable behavior

- eg: USMLE step 1 exam was hard that’s why I failed [Not coz he / she didn’t
read!]

• Reaction formation – Unacceptable transformed into its opposite

- eg: Feel love but show hate

• Undoing – Action to symbolically reverse the unacceptable

- eg: I need to wash my hands whenever I touch something
- Obsessive- compulsive behavior

• Dissociation – Separating self form one’s own experience

- eg: Raped victim describe event as she is watching whole things form the roof
- Fugue, depersonalization

• Humor – A pleasant release from anxiety

- eg: Laughter hides the pain

• Sublimation – Unacceptable action transform into acceptable action

- eg: person who likes pornography becomes director of sensor board

• Altruism – Individual provides a helpful, gratifying service to others as a means

of quelling their own anxiety. Eg: Alcoholic cirrhotic patient works as a volunteer
for a non profit organization that assist patient with alcoholic cirrhosis

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 ■ Personality Disorders:

• Paranoid Personality – suspicious in nature

- Coldness & distance in most relationship
- Very hostile reaction to other people’s innocent or even positive act.

• Narcissistic personality – Person feels “entitled” to recognition. They often

believe they are so special that others are jealous of their talents. They do not
tolerate perceived rejection well.

• Histrionic Personality – excessive emotion and attention seeking

- Seductive behavior - Women > Men
• Borderline Personality – mood swings, unstable relationship, recurrent suicidal
behavior - Women > Men

• Anti–social Personality – continuous antisocial (or) criminal acts

- Men > Women

• Avoidant Personality – Social inhibition, fear of rejection, shy

• Dependent Personality – Submissive, gets others to assume responsibility, can’t

express disagreement.

• Obsessive–Compulsive Personality – Perfectionist, orderly, rigid, inflexible

• Obsessive-Compulsive anxiety disorder (OCD) – has Obsession (persistent

thoughts) and Compulsion (repetitive acts). Obsession and compulsion that are
focal and acquired and have functional impairment whereas obsessive-compulsive
personality disorder is life-long and less functional impairment

■ Impulse Control Disorders:

• Intermittent Explosive Disorder – Failure to resist aggressive impulses that

result in serious assaultive acts

• Kleptomania – Failure to resist impulses to steal objects that the patients does not
need
- Associated with Eating disorder, mood disorders, OCD

• Pyromania – characterized by deliberate fire setting on more than one occasion

• Trichotillomania – characterized by pulling one’s own hair, resulting in hair loss

patient may eat hair, resulting in bezoars stomach, obstruction & malnutrition

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 • Oppositional defiant disorder – frequently loss their temper, disobey their
elders, deliberately annoy others, no violation of rules

• Conduct Disorders – disregard rights and rules of the society, ‹18 yrs of age

• Anti-Social – disregard rights and rules of the society, › 18 yrs of age

• Selective Mutism – speak normally in other situation or at home

• Autism – ‹3 yrs of age, repetitive behavior, marked hearing impairment

• Childhood disintegrative disorder – period of normal development for atleast 2

yrs followed by loss of previously acquired skills like expressive or receptive
language, social skill, play & motor skills.

• Undetected hearing impairment – hereditary, repeated ear infection, symptoms

are same as autism but detected at later age compare to autism

* Kubler-Ross Stage of adjustment in dying patient:

1. Denial ( DABDA)
2. Anger
3. Bargaining • Any stage can occur first. (this order is not necessary)
4. Depression
5. Acceptance

• Fuge: Person has an abrupt change of geographic location (or) identity without
alteration in consciousness (or) memory change

* Delirium – Acute onset, impaired cognitive functioning, fluctuating & brief –

Reversible – Mx: order basic laboratory wok-up – Benzodiazepine for 3-5 days –
usually Haloperidol is not recommended as first-line drug but If patient become
more combative then use Haloperidol before applying restraints

* Suicide rate is high in native American adolescence

• Anorexia Nervosa – distorted body image (perception problem – even with

very thin body, patient looks herself as a fatty person), 15-20 % loss of body
weight – Complication: osteoporosis (Ca+2, estrogen deficiency), elevated
carotene and Cholesterol, euthyroid sick syndrome, amenorrhea (estrogen
deficiency), small for gestational age baby, Cardiac arrhythmia (due to
Hypokalemia) (hypomagnesemia is another electrolyte abnormality) – First step
in management of patient with Anorexia Nervosa – Hospitalization (weight gain
& prevent complication) – Refeeding syndrome – develop in second-third week
after initiation of feeding in patient with anorexia nervosa – patient develop
edema and heart failure – should be treated with Phosphate supplementation
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 ■ Bulimia Nervosa – Binge & purge – looks healthy compare to anorexia –
presence dental caries, excoriation on knuckle of hand due to repeated vomiting –
Level of serotonin is decreased in Bulimia that’s why SSRIs are good choice for
Bulimia.

■ Eating disorder, not otherwise specified: features suggestive of both anorexia

and bulimia, but doesn’t meet the criteria for one specific eating disorder

ANTIPSYCHOTIC MEDICATIONS

■ Mood Disorders :

■ Lithium ( DOC ) (C/I in pregnancy), Divalproex (2nd choice )

- In pregnancy → Clonazepam, Gabapentin
- M/A: ↓ PIP 2 → ↓IP3 & DAG → ↓ c AMP [ renal v2 receptor coupled to cAMP]
- AE : Goiter & Hypothyroidism, Teratogenic
Nephrogenic DI [Treat with Amiloride (K+ sparing) not Thiazide]
Low Na + → enhance toxicity
Concentration >4 mEq/L require emergent dialysis

■ Anti- Depressants : ( Depression → Functional deficiency of NE/5HT in Brain )

• MAO Inhibitors: (Phenelezine, Tranylcypromine)

- AE: Hypertensive crises with Tyramine
Severe drug reaction with Meperidine

• TCA s (Tricyclic Antidepressants ):

- MA : inhibit re-uptake of 5- HT and NE
- Amitriptyline, Imipramine, Clomipramine, Amoxepin, Doxepin
- USES: Major depression, Phobic & panic anxiety state, Neuropathic pain,
Enuresis (Imipramine), OCD (clomipramine)
- similar to Phenothiazines (M block , α block , sedation , ↓ seizure threshold)
- Cardiotoxicity (“quinidine like”), SIADH

• SSRIs: (Fluoxitine, Sertraline, Citalopram)

- It takes 5 wks to reach steady state & 6-8 wks to show adequate response
- Uses : PMS, Bulimia, OCD, Alcoholism
- AE : Agitation (need sedatives ), Weight loss (but regained after 12 months
treatment), Seizure , Sexual dysfunction (always discuss with patient)
- Serotonin Syndrome: diaphoresis, rigidity, hyperthermia, ANS instability,
myoclonus – occurs when it takes with MAOI.
- Pt on SSRI c/o sexual dysfunction, appropriate other drug? – Bupropion (MAOI
& TCA Can cause sexual dysfunction)

• Bupropion (Atypical): block DA reuptake – USE: Smoking Cessation

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 • Buspirone: partial agonist at 5HT 1A - USE: Generalize Anxiety Disorder

• Trazadone : block 5HT reuptake , 5HT2 antagonist – AE: Priapism

• Nefazodone: block both NE & 5HT reuptake

• Venlafaxime: similar to SSRI

• Mirtazapine: similar to TCAs

■ Anti-Psychotic Drugs :

• Phenothiazines (Typical): DA (dopamine ) receptor

- Chlorpromazine (rarely use now), Fluphenazine, Thioridazine.

- M block,α-block, Sedation, ↓Seizure threshold.
- Quinidine like cardiotoxicity (Thioridazine)
- Tardive dyskinesia (TD) → Extrapyramidal dysfunction

 Butyrophenone (Typical): DA receptor antagonist.

• Haloperidol
- Dystonia (torticolis – spasm of sternocleidomastoid, Occulogyric crisis – eyes
rolled upwards) (Within first few day) [Tx: Benztropine / Diphenhydramine]
- TD (Tardive dyskinasia) [involuntary rhythmic movements of jaw upper
extremity, lip, tongue protrusion, etc] (after long term use) [Tx: discontinue drug
and start atypical antipsychotic] [Akathisia – continuous restlessness and
inability to stay calm]
- ↑ Prolactin → gynecomastia
- Riversible pseudo-parkinsonism
- Neuroleptic Malignant Syndrome [Tx: Dentroline] [Benztropine is C/I because
anti-cholinergic drugs retain heat]

• Clozapine, Olanzepine, Risperidone [Atypical Anti-Psychotics]:

- Improve negative symptoms.
- Block 5HT2 receptors. (not DA receptor)
- Agranulocytosis (clozapine – that’s why it is not used as first-line drug)
- TD has not reported with clozapine and olanzapine.

• Pimozide: DOC for Tourette’s Syndrome

• Single episode of major depression – Anti-depressant should be continued for a

period of 6 months following patient’s response to the drug.

• First step in management of patient with major depression? – rule out

Hypothyroidism (order blood test)

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 • MAOI drug interaction – hypertensive crisis (Tyramine) and serotonin
syndrome (SSRI, Pseudoephedrine, Meperidine)

• For bipolar patient on lithium, maintenance therapy should be continued for at

least 1 yr following acute episode. If there are no relapses & patient attained good
symptomatic control then lithium can be gradually tapered off and discontinue.

• Alternative drug for bipolar – Valproic acid & Carbamazapine

• Lithium has been known to precipitate / exacerbate Psoriasis

• Treatment of choice for acute management of mania, psychosis or extreme
agitation – Haloperidol (rapid onset of action) or Lorazepam. Lithium takes 4-10
days.

• Drugs should be avoided in post-traumatic stress disorder? – Benzodiazepines.

Treatment of post-traumatic stress disorder – SSRIs, exposure or cognitive
therapy.

• Personality disorders – Individual Psychotherapy

• Anxiety disorders – Behavioral Therapy (breathing exercise, exposure therapy)
• Schizophrenia – Supportive Therapy (build up trust so they talk more with you)
• Drug addiction – Group Therapy

• First-line Treatment of Schizophrenia – Atypical Anti-psychotics (Risperidone)

• Problem with compliance – Give Fluphenazine (every 2 weeks) or Haloperidol
(every 4 weeks) (both comes in IM preparation)
• c/o Sedation – give Risperidone [side effects – movement problem likes EPS and
Parkinsonism]
• Side effect of Olanzepine – Obesity.
• Nothing works – Give Clozapine
• Treatment of catatonic Schizophrenia – Benzodiazepam (Lorazepam)
• Fluphenazine can cause hypothermia.

• Acute Treatment of Panic Attack – Alprazolam

• Chronic Treatment of Panic Attack – SSRIs

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 PULMONOLOGY

Obstructive Pulmonary Disease Restrictive Pulmonary Disease

• ↑ airway resistance • ↑ in lung recoil

• ↓ expiratory flow rate • ↓ in all lung volume
• ↑ TLC , ↓ FEV1 / FVC • ↑ or N FEV1/ FVC

PFT suggest obstructive pattern → Diffusing Capacity ← PFT suggest restrictive pattern

↓ ↓
↓ ↓ ↓ ↓

N/ Near N ↓↓↓↓ N / Near N ↓↓↓

↓ ↓ ↓ ↓
Chronic Bronchitis Emphysema Extrapulmonary Interstitial
Asthma Restriction lung disease
( eg. Kyphoscoliosis,
morbid obesity)

- A – a gradient = 150 – 1.25 X PCO2 – PaO2

- Normal → 5 –15 mmHg

Hypoxemia

N A-a gradient ↑ A – a gradient

↓ ↓
Extrapulmonary origin Pulmonary Origin

• PAO2 = % O2 ( 713) – arterial PCO2 / 0.8

• PAO2 = 0.21 ( 713) – 40 / 0.8 = 100 mmHg

• PaO2 = 95 mmHg
• A-a gradient = 5 mmHg

• Atelectasis – most common cause of fever in 1st 24-hrs post operatively

* CXR – best initial diagnostic test for pulmonary diseases

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 CXR

Calcified Pulmonary Nodule

Low Risk Patient High Risk Patient

(< 35 yrs old, non–smoker) (>50 yrs old, smoker)

C X R every 3 months x 2 yrs Open lung biopsy

Stop follow up, if no growth

CXR

Pleural Effusions

Thoracocentesis (Next Best Step)

↓
LDH & Protein level

Transudate Exudate
LDH effusion < 200 > 200
LDH E / S < 0.6 > 0.6
Protein E / S < 0.5 < 0.5
- All 3 value must meet to diagnose transudative effusion
- If atleast one criterion is not met, then exudative effusion
- low pleural fluid PH & glucose (<60 mg /dl) are an indication for chest tube
placement in patient with parapneumonic effusion

CXR
↓
Atelectasis
↓
Appears on CXR as volume loss / densely consolidated
↓
Bronchoscopy with subsequent removal of mucous plug (Best Treatment / next step)

• Bacterial Pneumonia → Consolidation → dull to percussion, ↑ vocal framitus

• Pneumothorax →Hyperresonant to percussion, ↓ Breath sound
• Pleural Effusion → dull to percussion, ↓ Breath sound, ↓ vocal framitus
• Atelectasis → dull to percussion, Absent Breath sound, loss of framitus
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 Pneumothorax → opposite side
• Deviation of Trachea
Atelectasis (upper lobe) → same side

• Atelectasis (lower lobe) → elevation of diaphragm (same side)

• Trachea → Rt & Lt main bronchus → terminal bronchioles → respiratory

bronchioles → alveolar duct (AD) → alveoli
• Foreign body inhalation in child, next step?  Direct laryngoscopy and rigid
bronchoscopy to remove foreign body

 Asthma: Reversible airway obstruction

˗ Cough induced by forceful expiration (characteristic of airway hyperactivity)
˗ Poor prognosis factors – Pulsus paradoxus, absent breath sounds, decrease
wheezing, cyanosis, bradycardia, normal PaCO2 in acute Asthmatic patient
˗ Best initial therapy – Beta-agonist(Albuterol)
˗ Exercise induced asthma – beta agonist / chromolyn (mast cell stabilizer)
˗ Acute exacerbation of Asthma – Oxygen (first-step) and Inhaled beta2-agonist
[steroids can be used when beta2-agonist fail. IV steroid is preferred over oral]
[oral steroid is only used if patient is not vomiting]; IV Steroids
˗ PFT should be done for documentation of Asthma
• Asthmatic patient present with c/o worsening of Asthma at night, night cough &
Wheezing, Diagnosis? GERD; next step?  proton pump inhibitors (omeprazole,
pentoprazole)
• Subcutaneous emphysema in asthamatic (crepitation over the face & neck), next
step? – CXR [it is benign in asthamatic patient. CXR should be order to rule out
pneumothorax]
• “Silent chest” (absent air entry bilaterally) in Acute asthmatic patient on IV
steroid, next step? Intubation
• Allergic bronchopulmonary Aspergillosis (ABPA) – skin prick test (first step)
should be done in all asthmatic patient who are suspected of having ABPA; Tx:
oral prednisone
• Chronic eosinophilic pneumonia – peripheral infiltrates that are photographic
negative of pulmonary edema on CXR is the pathognomonic feature of chronic
eosinophilic pneumonia – >40% of eosinophils on bronchoalveolar lavage

 COPD(Emphysema & chronic Bronchitis):

• Non-reversible airway obstruction
• ↓ Recoil & ↑ Airway resistance
• Emphysema: cigarette smoking & alpha1-anti-trypsin deficiency (AAT) -
↑compliance (more dilated alveoli) and ↓elasticity (failure to keep airway lumen
open – essential for expiration so air trapped during expiration) – Centriacinar
[distended respiratory bronchioles – air trapped in AD & alveoli] Panacinar
[distended whole respiratory unit (Resp bronchioles, AD & alveoli) – air trapped
in whole unit]

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 • Chronic Bronchitis: productive cough for at least 3 months for 2 consecutive
years – smoking cigarette & cystic fibrosis - ↑mucus in bronchi obstruct terminal
bronchioles & narrowing of lumen due to chronic inflammation and fibrosis
Emphysema Hyperinflation of bilateral lung fields
With flattening of diaphragm, small
CXR – Size heart

Chronic Bronchitis Increased pulmonary markings

• PFT – best diagnostic test
• FEV1 – Single most important factor to determine prognosis of COPD
• Treatment – Smoking cessation (Best treatment to slow progression)
• Acute Exacerbation → Oxygen, Systemic steroid, Antibiotics (Should cover
H.influenzae & Pneumococcus), Bronchodilators
• Out patient Tx option → Ipratropium (1st line drug) & Home O2
Bronchodilators (2nd line drug)
Vaccination [Influenza (yearly)]

• First step in management of massive hemoptysis  Rigid bronchoscopy (not

flexible)
• Copious in amount & foul smelling sputum, initial test?  CRX; next step? 
CT chest [Causes: Bronchiectasis, Lung Abscess, Anaerobic Pneumonia]

■ Lung Abscess: Alcoholic, Extremely bad odor ( like decomposing dead

animal)

 TB: Alveolar macrophage → CD4+ T-cells → Macrophage release IL-12

(stimulates TH1 cells) and IL-1 (fever; activate TH1 cells) → TH1 release IL-2 (self
stimulation of TH1) and ᵧ interferon (activate macrophage to kill tubercular
bacilli) → Inflammatory mediators release from macrophage are responsible for
tissue damage (no endotoxin or exotoxin) → Lipid from tubercular bacilli leads to
caseous necrosis

 Bronchiactasis:
- Permanent dilation of bronchi & bronchioles.
- Chronic infection [gram(-) organisms] [destruction of cartilage & elastic tissues]
- Persistent cough with purulent copious sputum production, wheezes, crackles
- Chest CT – Best noninvasive test
- Treatment → Bronchodilators, chest physical therapy, postural drainage, and
Antibiotics
- Vaccination (Pneumococcal – every 5 yrs & Influenza – yearly)

 Idiopathic pulmonary Fibrosis:

- Involve only lung except clubbing
- Unknown etiology, occur in 5th decade
- CXR – Reticular / Reticulonodular disease

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 - Chest CT – ground glass appearance
- PFT- restrictive pattern
- Treatment – steroid with / without Azathioprine (help in only 20% of pt)

 Sarcoidosis:
- 20 – 40 yrs. Old women
- Presence of nonspecific non-caseating granuloma in the lung and other organs
- CXR – bilateral hilar adenopathy (90% of cases)
- Hypercalcemia (↑ 1-α-hydroxylase by macrophage leads to ↑ Vit–D)
[Hypercalciuria is occur in around 50% of cases whereas Hypercalcemia is seen
in around 10-20% of cases of Sarcoidosis]
- ↑ ACE (60 % of patients)
- Decrease cellular immunity [low helper/suppressor T-cell ratio] and activation of
humoral immunity [increase CD4/CD8 ratio]
- Ophthalmoscopic examination (uveitis & conjunctivitis - >25% of the cases)
- Treatment – systemic steroids when it involve uveitis / CNS / Hypercalcemia
- Tx of Hypercalcemia in Sarcoidosis – hydration + glucocorticoids

- Pulmonary pathology in Sarcoidosis  inflammatory granuloma

- Pulmonary pathology in Systemic Sclerosis (Scleroderma)  interstitial fibrosis

 Pneumoconiosis:
- CXR – small irregular opacities, interstitial densities, ground glass appearance,
honey combing
- Asbestosis → H/O exposure, usually involve lower lung fields
- CXR – diffuse /local pleural thickening, pleural plaques, calcification at the level
of diaphragm
- Lung biopsy – barbell shaped asbestos fiber (Best diagnostic test)
- ↑↑↑ Risk of Bronchogenic CA
- ↑ Risk of pleural / peritoneal mesothelioma

 Coal miner’s / coal worker’s pneumoconiosis (CWP):

- Usually involve upper half of lung
- Increase Levels of IgA, IgG, C3 , anti-nuclear Ab, RF
- Caplan syndrome – Rheumatoid nodule in the periphery of the lung in a patient
with RA & CWP

 Silicosis Hyaline nodule, usually involve upper lobe

- Strong association with TB, Pt should go yearly PD & if PPD >10mm then INH
for 9 months

 Pulmonary Thromboembolism:
- Sudden onset of dyspnea along with tachycardia
- ECG Right Axis Deviation
- h/o long term immobility
- Ventilation – perfusion (V /Q) scan (Best initial test)

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 - Pulmonary Angiogram (most accurate test)
- V/Q scan → Doppler U/S of lower limb or CT angiogram of chest → Pulmonary
angiography
- Treatment: continuous Heparin therapy x 5 days + Warfarin x 6 months. If
Hemodynamically unstable → THROMBOLYTICS, EMBOLECTOMY (IF
THROMBOLYTICS ARE CONTRAINDICATED )
- Pregnant patients → low molecular weight Heparin x 6 months

• Pleuritic chest pain (pain increase on inspiration), tachycardia & dyspnea in

patient on contraceptive pills, diagnosis?  Pulmonary embolism / infarction

 Adult Respiratory Distress Syndrome (ARDS):

- ↑ Permeability of the alveolar – capillary membrane & Pul.edema
- Alveolar macrophage → cytokines → Neutrophil → damage capillary membrane
- CXR – diffuse interstitial infiltrates; whiteout of both lung fields
- Swan-Ganz Catheter – normal cardiac output & capillary wedge pressure
↑ Pulmonary artery pressure
˗ Mx of ARDS: PEEP (around 8-9 cmH2O), High oxygen and low tidal volume;
Oxygen flow should be decrease after patient improve to prevent oxygen toxicity

 Sleep Apnea: Daytime Somnolence

- Obstructive sleep Apnea → floppy airway, obese patient
- Central sleep Apnea → inadequate ventilatory drive
- Treatment → Acetazolamide, progesterone and supplemental O2

 Bronchogenic Carcinoma:
- Squamous cell CA → Centrally located → Hypercalcemia – PTH-like substance
- Small cell CA → Centrally located → SIADH, Eaton-Lambert, Venocaval
obstruction Syndrome, Hornor’s syndrome
- Large Cell CA → Peripherally located
- Adenocarcinoma → peripherally located → Pleural effusion with high
hyaluronidase level in effusion fluid. Bronchoalveolar CA is subtype
- Popcorn calcification, concentric, central, or diffuse homogenous calcification on
CXR is suggestive of a benign pathology of pulmonary nodules
• Diagnosis : Sputum Cytology (SCC - >80%), Bronchoscopy (>90% for centrally
located)
- Needle Aspiration Biopsy → peripheral nodule with effusion
- Treatment : Resection (when possible), etoposide & platinum for small CA,
- Non-small cell CA – Cyclophosphamide, Adriamycin and platinum
- Effusions can be sclerosed with Tetracycline
• Pancoast tumor – Hornor’s syndrome, Phrenic N involvement [Chest movement
asymmetry] [a dangerous sign in patient with Pancoast tumor]; Radiation therapy
is the treatment of choice for Pancoast tumor with distant metastasis

• Hornor’s syndrome in smoker, next step? – CXR (to rule out lung CA)

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 REPRODUCTIVE SYSTEM

 Cryptorchidism: undescended testis – usually resolve by 1 year of age – increase

risk for seminoma, infertility

 Vericocele: “bag of worms” appearance – Lt sided most common – infertility

 Hypospadias → urethral opening on ventral side of the penis → never do

circumcision → Tx : surgical repair

 Epispadias → urethral opening on dorsal side of the penis

 Posterior Urethral valves → newborn boy, not urinate during the first day of life
or distended bladder and weak urinary stream – thickened urinary bladder wall on
U/S → Dx: voiding cystogram → Tx: Endoscopic fulguration .

 Hydrocele – fluid collection b/w layer of tunica vaginalis, transillumination

positive → usually resolve by 1 year of age. If it is not resolved by 1 year of age
then surgical intervention

 Testicular Tumors: unilateral painless testicular mass in young person

˗ Germ cell (95%) – malignant
˗ Sex-cord (5%) – benign
˗ Germ cell – Seminoma (40%) and Non-seminoma (60%)
˗ Seminoma – metastasis [para-aortic → hematogenous (lung)]
˗ Seminoma (↑hCG) & Non-Seminoma (↑ AFP & hCG)
˗ Tx: inguinal exploration & high ligation of the spermatic cord with removal of
the testicles and spermatic cord (radical orchiectomy) (best initial treatment)

• Large mediastinal mass with elevated hCG & AFP, diagnosis? non-seminomatous
germ cell tumor

• Nodule on prostate [not enlarge prostate (BPH)] and/or PSA >4 ng/ml, next step?
– biopsy of prostate

 BPH (Benign Prostatic Hypertrophy): DHT (dihydrotestosterone) causes

hyperplasia of glandular and stromal cells – develop in central zone so do not
palpable by digital rectal examination (DRE) – trouble initiating & stopping
urinary stream, dribbling, nocturia, dysuria – no relation with prostate CA –
Complication: UTI (most common), Sepsis (E.coli), Post-obstruction renal failure
– Tx: Finasteride (5-α-reductase inhibitor) (act on epithelial component of
prostate gland); TURP (Transurethral resection of prostate) [Most common
complication of TURP is Hyponatremia, cause? fluid containing glycine,
mannitol or sorbitol is used to flush during TURP] [Most common long-term
complication of TURP – retrograde ejaculation]

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 • Patient [pt.] with BPH present with irritative symptoms, next step? Urine analysis
& serum creatinine

 Prostate CA: DHT dependent – develop in peripheral zone so palpable by DRE

– usually asymptomatic until advanced – PSA >10 ng/ml highly predictive – bone
metastasis (common) [it is the only tumor which has osteoblastic activity where
as other tumor has osteoclastic (ostolytic) activity when metastasize to bone]
• First line Tx of Metastatic prostate CA – Leuprolide [LHRH agonist], [must be
given with Androgen blockers (Flutamide) initially to prevent flare up reaction] +
Radiation

 Prostatitis: urine analysis and urine culture – non-bacterial Prostatitis

(Prostatodynia) is more common than acute and chronic bacterial Prostatitis –
clinical picture is similar in both bacterial and non-bacterial Prostatitis and WBCs
are >20/hpf in prostatic secretion in both but in non-bacterial, culture of
prostatic secretion is negative and no h/o past UTI. Tx of non-bacterial
Prostatitis – sitz baths and anti-inflammatory drugs

• Afebrile patients with prostatic tenderness and irritative voiding symptoms, no

H/o past UTI, diagnosis?  Prostatodynia

 Acute bacterial prostatitis  gram stain & culture of a mid stream urine sample
(prostatic massage is contraindicated due to the possibilities of disseminating the
infection) – Tx: Ciprofloxacin / TMP-SMX

 Testicular Torsion: severe testicular pain of sudden onset without fever, pyuria
(or) h/o recent mumps → swollen, extremely tender high riding horizontally lie
testis → Emergency surgery

 Acute epididymitis: severe testicular pain of sudden onset with fever, pyuria →
swollen, extremely tender testis in normal lie → Tx: Antibiotics [Ceftriaxone +
Doxycycline] (USG → to rule out torsion)

 Recurrent, Painful oral & genital ulcers + erythema nodosum, diagnosis? 

Behcet’s Syndrome (Autoimmune mechanism)

 Penis fracture, next step?  Retrograde urethrogram fallowed by Surgical repair

 Penile CA in situ – Bowen’s disease – one lesion (thicken whitish plaque with a
slight ulcerated surface) – risk for SCC (squamous cell CA)
- Bowenoid Paulosis – multiple reddish brown popular lesion – No risk for
SCC
- Erythroplasia of Queyart – multiple shiny red plaques – risk for SCC

 Pearly penile papules are considered a normal variant and are not transmitted
through sexual contact and has no malignant potential

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 ■ Embryology:
* Post-conception week 1: Implantation of blastocyst
 Intra-tubal phase: first half of the week 1
 Intra-uterine phase: entery of the morula into the uterus
Morula differentiate into a hollow ball of cells
Outer layer – trophoblast (Placenta)
Inner layer – embryo

* Post-conception week 2: Development of the bilaminar germ disk with epiblast

and hypoblast layer
 Invasion of maternal sinusoids by syncytiotrophoblast (β-HCG test becomes pos-
itive)
* Post-conception week 3: Migration of cells through the primitive streak between
the epiblast and hypoblast to form the trilaminar germ disk with ectoderm, meso-
derm and endoderm layers

* Post-conception week 4-9: Organs & organ systems development

 Chorionic villous sampling (CVS): fetal Karyotyping (9-12 weeks)

 Amniocentesis: genetic purpose (15-20 weeks), Rh-isoimmunization (after 24
weeks), fetal maturity (after 34 weeks)
 Percutaneous Umbilical blood sampling: fetal Karyotyping, IgM antibody de-
tection, blood typing, intra-uterine blood transfusion (after 20 weeks)

 Placental Hormones: β-HCG, Human Placental Lactogen (HPL)

 Progesterone sources: corpus luteum of pregnancy (6-7 weeks), corpus luteum
& placenta (7-9 weeks), Placenta (after 9 weeks)
 Estrogen sources: Estradiol (non-pregnant reproductive period): follicular
granulosa cells; Estriol (during pregnancy): DHEA-S from fetal adrenal gland
convert into Estriol by placental sulfatase; Estrone (menopause): peripheral
adipose tissues

 Steroid binding globulins increase during pregnancy, so total hormone level in-
crease but free hormone level remains unchanged (same thing happen in person
on anabolic steroids, OCP) therefore hypothyroid patient should increase dose of
thyroxine.

 Braxton-Hicks Contraction: painless, low intensity, long duration contraction

(during 2nd trimester)
 Maternal Serum AFP (MS-AFP): [0.85 – 2.5 MoM]
Elevated MS-AFP – obstetric US to confirm gestational date (1st step)
Low MS-AFP – obstetric US to confirm gestational date (1st step)
 Triple marker screen: MS-AFP, hCG & Estriol (15-20 weeks)
↓↓ MS-AFP & Estriol, ↑ hCG – trisomy-21 – next step? – Amniocentesis for
Karyotyping
↓↓↓ All three – trisomy-18 – next step? – Amniocentesis for Karyotyping

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  Gestational Diabetes Screen – b/w 24-28 wks – 1-hr 50g oral GTT (screening
test) – If level >140 mg/dl, do definitive test (3-hrs 100g oral GTT done after
overnight fasting) – FBS (<126 gm/dl), After 100g oral GTT – at 1-hr (<180
gm/dl), at 2-hrs (<155 mg/dl), at 3-hrs (<140 mg/dl)

 c/o ↓ fetal movement, no fetal heart tone on Doppler, next step? ultrasonography
 c/o ↓ fetal movement, fetal heart tone heard on Doppler, next step? Non-stress
test
 Ultrasonography (Biophysical profile) – FHR (without any stressor like oxytocin),
fetal body movement, tone, breathing, amniotic fluid index

 c/o decrease fetal movement, next step? – NST (non-stress test)

Reactive Non-reactive
Reassuring
> 10 beats / min (< 32 weeks) Next step?
> 15 beats / min (> 32 weeks)
Two acceleration in 20 mins Vibroacoustic Stimulation

Still non-reactive,
next step?

Biophysical Profile (US)

4-6 8-10 0-2

Perform CST Highly reassuring Prompt delivery

Negative Positive (late deceleration)

Highly reassuring Worrisome (deliver if >36 weeks)

■ Perinatal Infections:

 Group B beta-hemolytic streptococci (GBBS): candidates for intra-partum

Penicillin G prophylaxis – positive GBBS urine culture, previous baby with
GBBS sepsis, positive 3rd semester vaginal culture, preterm gestation, maternal
fever, membrane rupture > 18 hrs

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  Toxoplasmosis: 3rd trimester primary infection with T.gondi – high risk of vertic-
al transmission
 Cesarean section: genital HSV lesions & HIV positive patients [Condylomata
acuminata is a manifestation of HPV infection and it is not a C/I for vaginal de-
livery]

■ Important Pregnancy changes: Increase – plasma volume, RBC mass (less

compare to plasma), factors 7,8,9,10, cardiac output, tidal volume, renal blood
flow, GFR, pituitary & thyroid gland size
 Respiratory alkalosis occur during pregnancy
 ↓ Renal glucose threshold
 ↓ gastric & bowel motility

* Herpes Gestationis: autoimmune (not due to virus) – rash and vesicles around
umbilicus in second / third trimester, recur during subsequent pregnancy – Tx:
topical triamcinolone

* Pruritic urticarial papules and plaques of pregnancy (PUPPP): it typically de-

velops on the abdomen, especially with periumbilical striae distensae, while the
umbilicus is usually spared (contrast to Herpes Gestationis)

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 Pregnancy Bleeding

Who is compromising?

Mother (low BP, shock) Fetus (bradycardia)

Next step?
Vasa Previa
Stabilize mother
(IV line with large bore needle) Next step?

Important causes Emergency C-section

Abruptio Placenta Placenta Previa

Painful vaginal bleeding Painless vaginal bleeding
h/o cocaine abuse, h/o trauma Management depends upon
increase fundal heights, abnormal Maternal or fetal jeopardy, fetal
shape (in conceal bleeding) maturity
Management depends upon Complications: Shock with ATN,
Maternal or fetal jeopardy, fetal Sheehan’s Syndrome
maturity Never perform a digital or
Complications: DIC, shock with speculum examination until US
ATN (acute tubular necrosis) rules out placenta previa
D/D: Abruptio placenta & Placenta accreta
Uterine rupture can be difficult Placenta invades the myometrium,
to distinguish when present but does not penetrate the entire
with h/o trauma, but thickness of the muscle.
culdocentesis suggestive of Placenta increta
hemoperitoneum is seen in Occurs when the placenta further
uterine rupture and helpful in extends into the myometrium
diagnosis Placenta percreta
The worst form of the condition,
The placenta penetrates the entire
myometrium to the uterine serosa
(invades through entire uterine
wall).

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 Abortion

No cervical dilatation Cervical dilatation present

Missed Inevitable Incomplete

Threatened Some Product
Non-viable Product of
Viable pregnancy of conception
pregnancy conception
No intervention is has passed
Suction D&C not passed
generally Emergency
or Emergency
indicated. suction D&C
Conservative until suction D&C
Mx: Regular out
spontaneously
patient follow-up
aborted

 Complete Abortion: All products of conception passed, US show no intrauterine

contents.

Fetal Demise

Uterine fundus less than dates (< 20 weeks)

Absence of fetal movement (> 20 weeks)
Absent heart activity on US

Management

DIC present DIC absent

Emergency delivery Suction D&C (< 20 weeks)
Induction of labor (> 20 weeks)

■ Rh-Isoimmunization: Mother Rh-negative, fetus Rh-positive

 Indirect Coomb’s test (screening test) – at 28 weeks of gestation
 Atypical antibody titer – >1:8 – risk for fetus
<1:8 – no fetal risk
 Tx: Intrauterine transfusion if gestational age <34 weeks
 Delivery if gestational age >34 weeks

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  Prevention: RhoGAM is given to Rh-negative mother at 28-weeks of gestation,
within 72-hrs of amniocentesis, D&C, chorionic villous sampling and delivery of
Rh-positive baby
 Kleihauer-Betke test: measure the volume of fetal RBCs in maternal circulation

■ Premature Rupture of Membrane (PROM):

 Pooling positive, Nitrazine positive (paper turns blue), fern positive
 If uterine contraction present, Tocolysis is contraindicated
 If infection present – cervical culture, antibiotics, prompt delivery
 If infection absent – management depends upon fetal maturity
 <36 wks – Hospitalize, cervical culture, steroids, antibiotics
 >36 wks – prompt delivery
 Chorioamnionitis signs & symptoms: maternal fever, uterine tenderness, PROM,
absence of UTI or URI

■ Preterm labor: gestational age (20-37 wks), atleast three contractions in 30 mins,
cervical dilation (>2 cm) / effacement
 Bed rest & IV hydration (first step), IV MgSO4, steroids, cervical cultures, antibi-
otics
 Ritodrine (only FDA approved tocolytics) – beta-agonist [side effects – hypoten-
sion, tachycardia, hyperglycemia, hypokalamia, pulmonary edema]

■ Post term labor: >42 wks of gestation

 Dates sure, favorable cervix – aggressive management
 Dates sure, unfavorable cervix – cervical PGE2 followed by IV oxytocin
 Dates unsure – conservative management & await spontaneous labor

HTN in Pregnancy

Gestational HTN
Mild Preeclampsia Severe Preeclampsia
BP - 140/90 mm of Hg
BP - 140/90 mm of Hg BP - 160/110 mm of Hg
after 20 wks without
1-2 + proteinuria 3-4 + proteinuria
proteinuria
Hemoconcentration Hemoconcentration
Conservative
Delivery is the only Thrombocytopenia
management
definitive cure Elevated liver enzymes
< 36 wks – Aggressive prompt
conservative in the delivery at any
hospital gestational age
> 36 wks – delivery IV IV MgSO4 to prevent
oxytocin + IV MgSO4 Eclampsia

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 ■ Eclampsia: Preeclampsia + seizure
 Aggressive prompt delivery at any gestational age after stabilization of mother
 Intracerebral hemorrhage – most common cause of death in eclampsia

■ Chronic HTN: BP - 140/90 mmHg before 20 wks of gestation; conservative

management for mild-moderate HTN / Methyldopa; DBP should be maintain b/w
90-100 mmHg – Drug of choice for chronic HTN & diabetic nephropathy in
pregnancy: Labetalol (ACE inhibitors are contraindicated)

 DOC for hypertensive emergency in pregnant women – Labetalol / Hydralazine

■ HELLP syndrome: Hemolysis, Elevated Liver enzymes and Low Platelets

count; Tx: aggressive prompt delivery at any gestational age + IV MgSO4 to pre-
vent eclampsia

■ Symmetric IUGR – both head & body – usually before 28 wks. (chromosomal
abnormality, infection)

■ Asymmetric IUGR – Head is spare & body affected – usually after 28 wks.
(Mother’s factors  hypertension, preeclampsia, chronic renal disease)

■ Overview of Labor:
 More than 3 contractions in 10 mins, each lasing >30 sec
 Engagement → Decent → Flexion → Internal Rotation → Extension → External Ro-
tation → Expulsion (First 3 steps occur simultaneously)

 Stage-1: Onset of contraction to complete cervical dilation (10 cm)

 Latent Phase: ends with the acceleration with cervical dilation (3-4 cm); No des-
cent of fetus occur; 20-hrs in Primipara & 14-hrs in Multipara
 Active Phase: ends with complete cervical dilation (10 cm); descent of fetus oc-
cur; 1.2 cm/h in Primipara & 1.5 cm/h in Multipara

 Stage-2: ends with delivery of fetus

 Up to 2-hrs in Primipara & 1-hr in Multipara

 Stage-3: ends with expulsion of placenta (gush of blood vaginally, decrease

fundal heights, “lengthening” of umbilical cord); up to 30-mins in all women

 Stage-4: close observation of parturient for 1-2 hrs after delivery

 Oxytocin (similar to ADH) can cause water intoxication by retention of water

[which dilute Na and produce hyponatremia]

 Prolong active phase of stage-1: Oxytocin if hypotonic contraction; Emergency

C-section if contractions are adequate

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  Prolong stage-2: IV Oxytocin if hypotonic contraction
 If adequate contraction, check fetal head is engage or not
 If head engage, consider trial of forceps or vacuum
 If head is not engaged, emergency C-section

 Prolong stage-3: IV Oxytocin / IM Methylergomatrin / manual removal of pla-

centa / hysterectomy (rarely)

 Prolapsed umbilical cord: Emergency C-section

 Preferred contraception in early post-partum period – sterilization, condom & pro-

gesterone only pills (mini pills)

 Non-reassuring FHR (fetal heart rate) tracing: Baseline rate show tachy- /
bradycardia without explanation, absent acceleration, repetitive variable decelera-
tion, repetitive late deceleration, absent variability
˗ Variable deceleration (without contraction) – fetal cord compression
˗ Early deceleration (with contraction) – fetal head compression
˗ Late deceleration (after contraction) – uteroplacental insufficiency

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 Cervical Cancer

How will it present to us?

Abnormal routine Pap smear c/o Post-coital bleeding

(Atypical Sqmaous Cells)
Next step?
Next step?

HPV DNA testing & Cervical Biopsy

Colposcopy

If abnormal findings If biopsy confirms

(mosaicism, punctuation, invasive CA, Next
white lesions, abnormal step?
blood vessels), Next step?

Ectocervical biopsy of above Metastatic work-up

colposcopic findings
Endocervical curettage (ECC)
(All non-pregnant women) Managements
If Pap smear finding is worse than
histology or If abnormal ECC, Next
step?

Cone Biopsy

 HPV subtypes associated with cervical CA – 16, 18, 31, 33, 35

 Atypical squamous cells (ASC) on pap smear – ASC-US or ASC-H (can’t ex-
clude HSIL)

 Classifications: Pre-cancerous stages

Dysplasia CIN Bethesda CIN = cervical intraepithelial neoplasia

Mild I LSIL CIS = carcinoma in situ
Moderate II HSIL LSIL = low grade squamous intraepithelial lesions
Severe III HSIL = high grade squamous intraepithelial lesions
CIS

That means: Mild dysplasia = CIN-I = LSIL

Moderate dysplasia = CIN-II = HSIL
Severe dysplasia / CIS = CIN-III = HSIL

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 ■ Management of Pre-cancerous lesions:

 ASC-US, CIN-I: repeat Pap smear in 4-6 months (If patient is unreliable for fol-
low-up, do Colposcopy instead of waiting for patient to come back for Pap
smear)
 CIN-I, CIN-II, CIN-III: Cryotherapy, laser, LEEP, cold-knife conization
 Biopsy confirmed recurrent CIN-II,III: Hysterectomy

■ Management of Invasive Cervical CA: Depend upon stage

• Stage 0 - full-thickness involvement of the epithelium without invasion into the
stroma (carcinoma in situ)
• Stage I - limited to the cervix
o IA - diagnosed only by microscopy; no visible lesions
 IA1 - stromal invasion less than 3 mm in depth and 7 mm or less in
horizontal spread
 IA2 - stromal invasion between 3 and 5 mm with horizontal spread
of 7 mm or less
o IB - visible lesion or a microscopic lesion with more than 5 mm of depth
or horizontal spread of more than 7 mm
 IB1 - visible lesion 4 cm or less in greatest dimension
 IB2 - visible lesion more than 4 cm
• Stage II - invades beyond cervix
o IIA - without parametrial invasion, but involve upper 2/3 of vagina
o IIB - with parametrial invasion
• Stage III - extends to pelvic wall or lower third of the vagina
o IIIA - involves lower third of vagina
o IIIB - extends to pelvic wall and/or causes hydronephrosis or non-func-
tioning kidney
• Stage IVA - invades mucosa of bladder or rectum and/or extends beyond true pel-
vis
• Stage IVB - distant metastasis

 Stage-Ia1: simple hysterectomy

 Stage-Ia2: hysterectomy + lymphnodes removal
 Stage Ib1 and IIa less than 4 cm: radical hysterectomy with removal of the
lymph nodes or radiation therapy.
 Stage Ib2 and IIa more than 4 cm: radiation therapy and cisplatin-based chemo-
therapy, hysterectomy or cisplatin chemotherapy followed by hysterectomy
 Stage-IIb, III, IV: Radiation and Chemotherapy (cis-platinum)

 Pregnancy & Cervical CA: Diagnosis & management is same as in non-preg-

nant women except ECC is not done in pregnant women

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 ■ Endometrial CA:
 Prolong Estrogen (E) exposure without Progesterone (P)
 Post-menopausal bleeding (most common presentation)
 Next step? – Endometrial sampling
 If negative histology – Hormone replacement therapy
 If positive histology – Surgery, Radiotherapy, Chemotherapy

■ Leiomyomas:
 most common benign uterine tumor
 Intramural – within the wall of the uterus
 Submucous – located beneath the Endometrium; causes Menorrhagia (heavy
bleeding) and Metrorrhagia (irregular bleeding in between menses)
 Subserosal – located beneath uterine serosa
 Asymmetric, Non-tender, enlarged uterus in the absence of the pregnancy
 Tx: GnRH analog (3-6 months), myomectomy, embolization, Hysterectomy

■ Adenomyosis:
 endometrial glands and stoma located within the myometrium of the uterine wall
(uterus)
 Pain immediately before and during menses
 Symmetric, tender, enlarged uterus in the absence of the pregnancy
 Tx: levonorgestrel intrauterine system

■ Endometriosis:
 endometrial glands and stoma located outside the uterus
 Chocolate cyst of the ovary, utero-sacral ligament nodularity, pain during inter-
course (dyspareunia), infertility
 Dx: Laparoscopy
 Tx: OCPs (oral contraceptive pills)

■ Vulvar neoplasm:
 c/o intense vulvar pruritus
 Melanoma – black lesions – biopsy & excision
 Paget’s disease – red lesions – biopsy & excision
 Squamous cell CA – HPV association – whitish lesions – biopsy & excision
 Hypertrophic dystrophy of the Vulva – corticosteroid ointment
 Atrophy of Vagina – Estrogen cream

 Paget’s disease (of breast, cervix) – Adenocarcinoma

 Paget’s disease of bone – isolated elevation of Alkaline phosphate in elderly
Patient with normal Ca+2, Po4 & amino transferase level - Worrisome changes
in Paget’s disease of bone – sarcomatous (1-3%) – Tx: asymptomatic Paget’s dis-
ease of bone – nothing; symptomatic – bisphosphonates

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 Adnexal Mass

Pre-Pubertal Reproductive Age Post-Menopausal

Germ cell tumors Simple cyst Ovarian Cancer

Complex mass
[Teratoma (Dermoid
Next step? cyst)] Next step?
Ectopic Pregnancy
Obtain tumor markers Next step?
Find GI tract and
LDH – Dysgerminoma Urinary tracts
β-HCG – β-HCG lesions
Choriocarcinoma US (ultrasonography)
AFP – Endodermal
sinus tumors (Yolk-
sac tumors)

 Simple Cyst on US: <7 cm, next step? – observe for 6-8 wks, resolved spontan-
eously, start OCPs to prevent further functional cysts fro forming; >7 cm or
already on OCP (for atleast 2-months), next step? – Laparoscopy
 Complex mass on US: Cystectomy (to preserve ovarian function); Oophorec-
tomy if conservative failed
 Any cyst in pregnancy which is greater than 5 cm should be removed during
second trimester of pregnancy

 Most common benign ovarian tumor – serous cystadenoma

 Most common malignant ovarian tumor – serous cystadenocarcinoma
 Granulosa-theca cell tumors – secrete estrogen
 Sertoli-Leyding cell tumors – secrete testosterone
 Krukenberg’s tumor – contains signet ring cells from Metastatic stomach cancer
 Dysgerminoma – resembles Seminoma of the testis
 Meig’s Syndrome – Ovarian fibroma, Ascites & right sided pleural effusion
 Abdominal pain + Adnexal mass, diagnosis? – Torsion of the ovary, next step? –
surgical intervention (exploratory laparotomy)

 Immature teratoma – primitive epithelial cells & developing skeletal muscles,

potentially malignant [teratoma – derivatives of all 3 germ layers [ectoderm,
mesoderm and endoderm – hair, tooth, thyroid gland, etc]

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  Dermoid cyst: A dermoid cyst is a mature cystic teratoma containing hair and
other structures characteristic of normal skin and other tissues derived from the
ectoderm. The term is most often applied to teratoma on the skull sutures and in
the ovaries of females.
 Struma ovarii: mature teratoma that contains mostly thyroid tissue.

 Gestational Trophoblastic Neoplasia (GTN):

 HTN in the first trimester, fundus larger than dates, “snowstorm” appearance on
US, grape-like vesicles, high beta-hCG, hyperthyroidism
 Complete Mole: empty egg, 46XX (parental), No fetus, progression to malig-
nancy (20%)
 Incomplete Mole: 69(XXX), fetal parts present, progression to malignancy
(10%)
 Lung most common site of metastasis, Tx: Suction D&C
 After D&C for molar pregnancy, patient should be put on OCP so they don’t get
pregnant and beta-hCG level monitor effectively
 Follow-up with beta-hCG [upto 1-yr – if benign; upto 5-yrs – if malignant]

■ Uterine Incontinence:

 α & β receptors – prevent micturation

 cholinergic receptors – enhance micturation
 Urethra – α receptors (estrogen)
 Bladder – β receptors (progesterone) & cholinergic receptors

 Genuine stress incontinence:

 Cystocele, positive Q-tip test [Q-tip rotate >300 when intra-abdominal pressure in-
crease, eg. Cough]
 Mx: Kegel exercise, estrogen replacement, urethropaxy

 Irritative incontinence:
 Infection, stone, tumor, foreign body
 Mx: treat the cause

 Hypertonic incontinence:
 Idiopathic detrusor contraction
 Urgency (most common symptoms)
 Mx: Anticholinergic medication

 Hypotonic incontinence:
 Denervated bladder (DM, Multiple Sclerosis)
 c/o pelvic fullness, ↓ pudendal nerve sensation
 Mx: Intermittent self catheterization, cholinergic medications
 Fistula, Bypass incontinence:
 h/o radical pelvic surgery or h/o pelvic radiation therapy, c/o continuous leaking
 Mx: Surgical repair

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 ■ Ectopic Pregnancy:
 Amenorrhea, vaginal bleeding and unilateral pelvic-abdominal pain
 Positive beta-hCG, no intrauterine pregnancy (IUP) on US
 IUP detected with vaginal sonogram at 1500 mIU beta-hCG titer
 IUP detected by abdominal sonogram at 6500 mIU beta-hCG titer
 Beta-hCG level in normal IUP doubles every 58-hrs
 Age is an important risk factor for an ectopic pregnancy besides PID (35-44 age
group, 3 fold increase in risk for ectopic pregnancy)
 Mx: Confirm diagnosis (first step) (beta-hCG titer >1500 mIU, no IUP)
 Ruptured ectopic: immediate surgical intervention (salpingectomy)
 Unruptured ectopic: pregnancy mass <3.5 cm, beta-hCG level <6000 mIU, absent
fetal heart motion, no folic acid supplementation – Methotraxate
 If above criteria not met – Laparoscopy (salpingostomy)
 Rh-negative mother should receive RhoGAM, follow-up with beta-hCG titer
 Beta-hCG routinely drawn on day 4 and day 7 of treatment of ectopic pregnancy
with Methotraxate. If it drops 15% from day 4 to day 7, treatment of ectopic preg-
nancy is thought to be successful and patient returns for beta-hCG blood draw un-
til it is negative

 Bacterial Vaginosis: thin, grayish-white discharge, fishy odor, vaginal pH above

5, epithelial cells with smudged borders (“clue” cells) due to bacteria adherent to
cell membranes – Tx: Metronidazole (contraindicated in pregnancy, use Clinda-
mycin during pregnancy)

 Trichomonas Vaginitis: frothy, green discharge, itchy, burning pain with inter-
course, vaginal pH above 5, sexually transmitted disease (STD), “trichomon-
ads” on microscopic examination – Tx: Metronidazole (treat both partners) - Tx
of trichomoniasis in lactating women – 2 g of Metronidazole single dose and ask
her to discontinue breast feeding for 12-24 hrs

 Yeast Vaginitis: curdy, white discharge, pH <4.5, not a STD, Pseudohyphae on

microscopic examination – Tx: single dose Fluconazole

■ Menstrual Cycle Hormones:

 FSH: stimulate granulosa cells to secrete E & Inhibin (inhibits FSH release)
 Estrogen: Negative feedbacks to FSH
Low E – Negative feedbacks to LH
High E – Positive feedbacks to LH
 LH: stimulate production of androgens from theca cells, LH surge stimulates syn-
thesis of prostaglandins to enhance follicular rupture & ovulation
 Progesterone: secreted by corpus luteum, prepare Endometrium for blastocyst
implantation

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 Abnormal Vaginal Bleeding

Premenarchal Reproductive Age Post-Menopausal

Vaginal foreign body Pregnancy Atrophic changes

Sexual abuse Anatomic causes Endometrial
Precocious puberty DUB (Dysfunctional carcinoma
Sarcoma botryoides Uterine Bleeding)
(grape like
protrusion through
vagina)

■ Puberty changes:
 Thelarchy (breast development) – 9-10 yrs (E from the ovary)
 Adrenarchy (pubic & Axillary hair) – 10-11 yrs (Adrenal hormones)
 Maximal growth rate – 11-12 yrs
 Menarchy (onset of menses) – 12-13 yrs

■ Precocious Puberty: development of puberty before age 8 in girls and before age
9 in boys
 GnRH stimulation test – helpful to differentiate central Vs peripheral cause of
precocious puberty - ↑↑ LH after GnRH injection indicates central cause
 Central: hypothalamic-pituitary-ovarian axis disturbance
 Peripheral: ovarian tumor, adrenal tumor, exogenous estrogen, McCune-Albright
 Management of patient with precocious puberty  GnRH agonist to inhibit se-
cretion of estrogen to prevent premature fusion of the epiphyseal plates

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 Precocious Puberty

Gonadotropin Dependent Gonadotropin Independent

CNS Pathology Idiopathic McCune–Albright Granulosa cell tumor

Sarcoidosis 80% of cases Syndrome Secrete estrogen
Meningitis Tx: Leuprolide Autonomous Tx: Surgical removal of
Other causes stimulation of tumor
Tx: treat aromatase enzyme
pathology which ↑↑ estrogen
production from
ovary
Café-au-lait skin spots
Multiple cystic bone
lesions (Polyostic
fibrous dysplasia)
Tx: Aromatase
enzyme inhibitors
McCune Albright
syndrome has
association with
Cushing’s
syndrome, not
Cushing’s disease
(which is due to
Pituitary tumor)

■ Dysfunctional Uterine Bleeding: Anovulation (So no progesterone effect

which left estrogen unopposed), no secretory phase, no mid-cycle rise in temper-
ature – Biopsy: Proliferative Endometrium with stromal breakdown. No secret-
ory endometrium – Tx: OCPs
■ First step in management of heavy unremitting endometrial hemorrhage through
menarche and perimenopause period  high dose unconjugated estrogen (to
suppress bleeding); Once stabilize D&C should be performed & pt should be put
on OCP
■ If perimenopausal women c/o an episode of heavy dysfunctional bleeding or ir-
regular menses, then do endometrial surveillance in the form of vaginal ultra-
sound (to ensure endometrial thickness <4mm) or endometrial biopsy

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 Primary Amenorrhea

Breast Present (secondary sexual Breast Absent

characteristics present) Uterus Present
Uterus Absent
Next step? – Karyotyping
and FSH level
Next step? – Karyotyping
and Testosterone level

Mullerian Androgen Turner’s Hypothalamic

Agenesis Insensitivity syndrome Pituitary
(Rokitansky – (Testicular failure
Kuster – Hauser feminization)
45 (XO)
Syndrome) ↑↑ FSH ↓↓ FSH
Genetically male Streak ovary, Absent
(XY) cystic hygroma secondary
Normal female
Secondary female (web neck) sexual
(XX)
sexual Tx: OCP (oral characteristic
Normal
characteristics contraceptive
Testosterone
Tx: Remove testis pills)
Tx: Surgical
and give estrogen
elongation of
supplement
vagina

■ Kallman Syndrome: anosmia + absent GnRH – Tx: OCPs

■ Secondary Amenorrhea: absence of menses for 3 months if previously regular

menses or for 6 months if previously irregular menses
 Hypogonadotropic (Hypothalamic or Pituitary dysfunction)
 Hypergonadotropic (ovarian follicular failure)
 Eugonadotropic (pregnancy, Anovulation, out-flow obstruction)
 First step in management – beta-hCG titer to rule out pregnancy
 Next step? – TSH level (hypothyroidism) Prolactin level (Hyperprolactinemia)
 Next step? – Progesterone challenge test (PCT)
 If PCT positive – diagnosis of Anovulation [Estrogen production is adequate]
 If PCT negative – inadequate Estrogen / Out-flow obstruction
 Estrogen – Progesterone challenge test (EPCT)
 If EPCT positive – inadequate Estrogen [Y-chromosome mosaicism, savage syn-
drome (ovarian resistant syndrome)]
 If EPCT negative – out-flow obstruction

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  Cause of amenorrhea in patient who lost more weight – estrogen deficiency (due
to low LH and GnRH). They are also at risk of developing Osteoporosis

 Premenstrual Syndrome (PMS): wide range of physical & emotional symptoms

occur, typically two weeks before menstruation and disappear with menses for
atleast 3 consecutive cycles
 Tx: SSRIs (fluoxetine); If it fails, give Alprazolam; Diuretics, Vit-B6

c/o ↑↑ hair growth in female

Hirsutism Virilization
(Hirsutism + Musculinizing signs like
clitorimegaly, baldness, etc.)
Congenital Adrenal
Hyperplasia
Gradual onset Adrenal Tumor
↑↑ 17-OH progesterone Rapid onset
Tx: Corticosteroid ↑↑ DHEAS level
replacement Tx: Surgical removal

Ovarian Tumor
PCO (Polycystic Ovarian
Rapid onset
Syndrome) (Stein-
↑↑ Testosterone level
Leventhal Syndrome)
Tx: Surgical removal
↑↑ LH:FSH, Obese, ↑
Testosterone
Cystic appearance of ovary
(neckless) on US
Tx: OCP, Metformin

Idiopathic
Positive family history
Normal level of all
hormones
Tx: Spironolactone

 First step in management of infertility in patient with PCOD – weight loss; If it

fails, try Clomiphen citrate or Metformin
 Metformin has shown to induce ovulation in patient with PCOD. It should be
discontinued during pregnancy once pregnancy is documented

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 ■ Infertility:
 First step in management – semen analysis
 Screening test for ovulation – BBT (basal body temp) & mid-cycle progesterone
level
 Luteal phase Defect  Abnormal basal body temperature curve & low mid-luteal
progesterone level. Confirmation of diagnosis?  Endometrial biopsy. Initial
Treatment?  Progesterone supplement; if it fails, then?  Clomiphene citrate /
hMG (human menopausal gonadotropin)
 Best measure for pt with premature ovarian failure who still want to conceive
 egg donation
 Once diagnosis of premature ovarian failure is made (< 35 yrs of age, low estro-
gen, high FSH) next step?  Chromosome analysis to rule out presence of Y
chromosome

■ Hormone replacement therapy in Menopause:

 Women with uterus – Estrogen + Progesterone
 Women without uterus – Estrogen
 Indication: vasomotor symptoms only (optimally do not exceeded 4 yrs)
 Estrogen alternatives: Tamoxifen, Raloxifen
 Raloxifen can be given in patient with positive family history for Breast CA to
prevent osteoporosis
 First-line drug to prevent osteoporosis – Bisphosphonates

 Conclusion from WHI trial for HRT (Hormone Replacement Therapy)

No cardiovascular benefit
Increased risk for stroke with long – term use
Increased risk for Breast CA [but not with unopposed estrogen]

 Contraception: Estrogen causes Thromboembolism, not progestin

 Contraception of choice in patient with bleeding disorders – Depot
Medroxyprogesterone acetate. (it is ideal for h/o PID, heavy menstrual bleeding,
heavy smoking, fibroids, sickle cell disease) [Menorrhagia is the most common
complication in women using “Norplant” (six capsules of levonorgestrel)]
 Emergency contraception – levonorgestrel within 12-hrs (good efficacy within
48-hrs; appears to work up to 120-hrs after intercourse)
 OCP decrease chances of ovarian CA
 Pregnancy decrease chances of ovarian and breast CA
 OCP decrease the risk of Gonococcal PID [Basis – it increases thickness of
mucous & prevent gonococci to enter in fallopian tube]
 Advise regarding contraception in adolescents – use barrier methods in addition to
OCP (barrier method is useful to prevent STDs)

 Identical twins (monozygotic twins – embryo split during blastomere &

blastocyst stage) – monochorionic, monoamniotic & monochorionic, diamniotic
 Lactation suppression  tight lifting bra & ice packs

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 BREAST DISEASES

■ Fibroadenoma → young woman ( child baring age ) → firm, rubbery mass,

moves easily on palpation (Breast mouse ) → sonogram of breast (best
diagnostic Test ) → Tx: Surgical Excision (optional)

■ Cystosarcoma Phyllodes → young woman → very large mass → benign but has
potential to become malignant → core / Incisional biopsy → Tx: Surgical
removal (mandatory)

■ Fibrocystic Disease → multiple bilateral breast cysts “come & go” at different
time in menstrual cycle → mammogram (first step) → if persistent / dominant
mass → Aspiration (not FNA) → still persist → biopsy; if bloody fluid on
Aspiration → cytology

■ Intraductal Papilloma → young woman with bloody nipple discharge →

mammogram → galactogram guided surgical resection

■ Breast Abscess → lactating mother → fever, leucocytosis, fluctuating red, hot,

tender mass in breast → Tx: Incision & Drainage with biopsy of the abscess
wall

■ Breast cancer → mammogram (irregular area of increased density with fine

microcalcification) with core biopsy → Lumpectomy with Axillary node
sampling + Post-op-radiation ( small tumor , away from nipple and areola ) /
Modified radical mastectomy (best choice)
 If unresectable → chemotherapy
 If Axillary node positive → chemotherapy
 If hormone receptor sensitive → Add Tamoxifen (Pre-menopausal) /
Anastrazole (post-menopausal)
 Breast cancer signs & Symptoms → palpable breast mass, retraction of
overlying skin, retraction of nipple, (“orange peel” skin), palpable Axillary nodes.
■ Ductal carcinoma in situ → cannot metastasize ( No Axillary sampling ) .
˗ Tx: Total simple mastectomy / Lumpectomy + Post-op- radiation
 Tubular Breast CA → Best prognosis
 Inflammatory Breast CA →worst prognosis
 Infiltrating Ductal CA → most common
 Lobular CA → high incidence of bilateral involvement
 Other types → Medullary, Mucinous
 Breast CA during pregnancy: same procedure for diagnosis as without
pregnancy
● Tx : same as without pregnancy except No chemotherapy in first trimester ,
No Radiotherapy during entire pregnancy .
● There is no need for termination of pregnancy

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 TOXICOLOGY

 Ipecac – to induce vomiting-within 1-2 hrs-conscious patient

 Gastric lavage – patient with altered mental status/unconscious-within 1st hour
except TCA ingestion in which anticholinergic action delay gastric emptying
 Both ipecac & lavage are contraindicated in caustic substance ingestion
 Charcoal – administer every 2-4 hrs – not effective in metal poisoning and
different alcohol Poisoning
 Whole bowel irrigation – for large volume pill ingestions in which the pills can be
seen on an x-ray
 Dialysis – When serious symptoms are present (coma, hypotension, etc.)
 Forced Alkaline Diuresis – Salicylates (Aspirin), Barbiturate
 Sodium Bicarbonate- TCA (Tricyclic Antidepressants)
 Naloxone + Dextrose + Thiamine – any patient who present with altered mental
status (or) coma with unknown drug ingestion

 Acetaminophen: (140 mg / kg toxic dose)

˗ N-acetyl Cystine → as early as possible
˗ When more than 24 hrs have elapsed since ingestion, there is no specific
therapy that can prevent OR reverse the toxicity.

 Alcohols (methanol, Ethylene glycol, Isopropyl alcohol):

˗ Methanol – paint thinner, solvents, windshield washer- visual disturbances,
blindness - ↑anion gap metabolic acidosis
˗ Ethylene glycol – automotive antifreeze – Renal failure & Oxalate crystals -
↑anion gap metabolic acidosis
˗ Isopropyl alcohol – Ketosis without elevated anion gap acidosis
˗ Tx: ethanol infusion followed by hemodialysis, Fomepizole (alcohol
dehydrogenase inhibitor) can be used instead of ethanol infusion.
˗ Fomepizole infusion is now proffered for Tx of ethanol, methanol and ethylene
glycol poisoning. Fomepizole should not be used simultaneously with ethanol
during treatment of methanol and ethylene glycol poisoning

 Carbon monoxide (CO) poisoning: burn around face, entrapment in fire, winter
season; c/o headache, absent fever and negative meningeal signs, involvement of
other family members at home
˗ carboxyhemoglobin level (Best initial test / next step)
˗ Tx: 100% O2 administration / hyperbaric O2 in severe cases.

 Acids and Alkali ingestion: Upper Endoscopy (most important / next step in
management) – never try to neutralize (Acid by Alkali (or) Alkali by acid )

 Digoxin Toxicity:
˗ GI symptoms, Neurologic & Visual Symptoms, Cardiac disturbance (Arrhythmia)

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 ˗ Hypokalemia→↑ Toxicity (K+ & digoxin, both compete for Na+-K+ ATPase
pump)
˗ EKG→ atrial tachycardia with AV block (specific for digoxin toxicity)
˗ Tx: Repeated doses of charcoal, Digoxin-specific antibodies, correction of
electrolyte abnormalities, phenytoin / lidocaine for ventricular arrhythmic

 Lead poisoning: paint, soil, drinking water contaminated with lead –

Sideroblastic anemia, Lead lines on x –rays, Neuropathies (wrist drop)
Tx: environmental / behavior intervention; If blood level >44 – EDTA / succimer
+ environment intervention; If blood level >70 – Hospitalization + IV BAL
(Dimercaprol) [BAL is fast acting than EDTA] [Penicillamine in adults] [oral
succimer in children]; for Dx use venous blood sample

 Mercury Poisoning: thermometer, Sphygmomanometer

Tx: Dimercaprol (BAL) / Penicillamine / Succimer

 Arsenic Poisoning: garlic smell , watery diarrhea ( like in Cholera )

Tx: Symptomatic treatment

 Cyanide Poisoning: Bitter Almond smell

Tx: Amyl nitrate

 Salicylates: Tinnitus (more specific complain)

 TCA: H/O depression, Anticholinergic symptoms, Torsade de pointes [wide

QRS complex (Indicators of severity of TA overdose), QT prolongation].
Tx: Immediate sodium bicarbonate (first step / next step in management) [M/A:
alleviate cardio depressant action on sodium channel]

 Opiates: pin point pupils, respiratory depression.

˗ Tx: Naloxone

 Cocaine: inhibit re-uptake of NE & DA.

˗ Hypertension, Arrhythmia, Seizure, Abortion
˗ Tx: Diazepam, Labetalol (anti-hypertensive) .

 Benzodiazepines: somnolence, dysarthria, ataxia, stupor

˗ Tx: Flumazenil (prepare to treat seizure from acute withdrawal from
benzodiazepines antagonism)

• Slurred speech, unsteady gait and drowsiness in young patient  Benzodiazapine

Overedose [look for distinguishing features of other drugs present same way 
Opioid (miosis), Alcohol & phenytoin (nystagmus, Hand tremor)]

 Barbiturates: Respiratory depression, absent EEG activity

˗ Tx: Forced alkaline diuresis, supportive
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  Hallucinogens: Marijuana, LSD, PCP (angel dust)
˗ Tx: Benzodiazepines (eg. Diazepam)

 Bradycardia, AV block, Hypotension & diffuse wheezing in Hypertensive Patient

attempt suicide, diagnosis?  Beta-blockers toxicity; Tx?  Glucagon

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 TRAUMA

■ First thing to do is maintain Airway, Breathing & Circulation.

 Airway : must be secured first if there is expanding hematoma (or) emphysema

in the neck
 Cricothyroidotomy (field) / Orotracheal intubation (ER, most preferred route)
 Cervical spine injury → orotracheal (if head is secured) / nasotracheal
 Maxillofacial injury (in adult) → Cricothyroidotomy / percutaneous
transtracheal ventilation
 Maxillofacial injury (in child) → Percutaneous needle Cricothyroidotomy (not the
classic with tube which causes subglottic stenosis in child) followed by
tracheostomy
 Cricothyroidotomy tube can be kept only for 48-hrs in adult. If ventilatory support
required beyond 48-hrs, Tracheostomy should be done.

 Breathing: Breath sound on both sides of chest / pulse oxymatory

 Circulation: SBP should be > 90 mmHg, Palpable pulse

Shock in Trauma

↓ ↓ ↓
Bleeding Cardiac Temponade Tension Pneumothorax
↓ ↓ ↓
Low CVP High CVP High CVP
↓ ↓ ↓
Treatment - No respiratory distress - Respiratory distress
- Tx: Pericardiocentesis - No breath sound &
OR Hyperresonant to percussion
Pericardial window - Tracheal deviation
- Tx: big needle inserted in
upper pleural space
followed by chest tube
connected to underwater
seal
Trauma center Trauma center
Near by far away

Transportation IV fluids (Ringer lactate/Normal Saline)

 Any penetrating injury require surgical intervention and repair of the damage

 Unconscious patient with Head trauma → CT scan (1st step in management)

 Linear skull fracture(closed) → left alone / observe
 Linear skull fracture (open) → wound closure only (ER)

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  Comminuted/ depressed skull fracture → repair in OR (Operating Room)

■ Acute Epidural Hematoma → Middle meningeal artery → hit on side of the

head→ unconsciousness → lucid interval → unconsciousness; CT scan →
biconvex, Lens-shaped Hematoma Tx: Craniotomy

■ Acute Subdural Hematoma → Tear of bridging veins → bigger trauma and

much sicker & severe neurological damage → CT scan → semilunar, crescent-
shaped hematoma Tx: craniotomy

 Chronic Subdural Hematoma: elderly / severe alcoholics → Tearing bridging

vein → mental function deteriorates over several days to Weeks → Tx →
Surgical evacuation.

 Diffuse Axonal Injury → CT scan shows diffuse blurring of the gray–white

matter interface and multiple small punctate hemorrhages → Tx : Prevent rise in
ICP

Gunshots in Neck
↓

Middle Zone Upper / lower Zone

↓ ↓
Surgical Exploration Diagnostic procedures
( even though patient is asymptomatic ) then Surgery
↓
↓ ↓
Upper Zone Lower Zone
↓ ↓
Arteriography for Arteriography
Diagnosis & embolization . Esophagogram
Bronchoscopy
↓
Surgery

 Stab wound to Neck → Observe (if asymptomatic)

 Stab wound to Neck, Crepitation at the base of neck → Bronchoscopy (1st step)
followed by bronchoscopy guided intubation (best choice) / orotracheal intubation

 Blunt Trauma to the Neck → X-ray / CT scan (tenderness over cervical spine,
neurological deficits) → Intervention

 Signs & Symptoms of Spinal cord injuries → High-dose prednisone → MRI

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  Rib fractures → pain relief by nerve block (no strapping / binding)

 Plain Pneumothorax (not tension) → CXR → Tx

 Sucking Chest wound ( flap ) → occlusive dressing (taped on 3 sides)

 Hemothorax → CXR → Chest tube / Thoracotomy (> 1500 ml blood / > 600 ml
in 6 hrs)

 Flail chest → segment of the chest wall cave inside during inspiration and bulge
out during expiration in multiple ribs fractures – Tx: fluid restriction, Diuretics,
use of colloids, Respirators with bilateral chest tubes. (to prevent tension
pneumothorax)

 Pulmonary contusion → “white out” of the lungs on CXR → Tx: same as

above

 Traumatic rupture of Diaphragm → bowel in the left chest on X-ray → Tx :

Surgical repair from the abdomen

■ Subcutaneous Emphysema → CXR → Bronchoscopy → Surgical repair

■ Traumatic rupture of Aorta → deceleration injury / 1st rib /sternum fracture

CXR (wide mediastinum) → transesophageal echo / spiral CT → Aortogram
(if 2nd fail) → surgical repair

■ Air embolism: subclavian vein is opened to the air which sucks air during
inspiration (hissing sound) → sudden death (Supraclavicular node biopsy , CV
line placement , CV line disconnected and leave it open to the air) → Tx:
Immediate head down and raised right shoulder

■ Fat embolism → long bones fracture (femur) → CXR : Bilateral patchy

infiltrates → fever , tachycardia → Tx : Respiratory Support

■ Gunshot wound to the Abdomen (any entrance / exit wound below the level of the
nipple) → exploratory laparotomy

■ Stab wound to the Abdomen (Stable patient with no protruding viscera) →

observe & Standard wound care

■ Stab wound to the Abdomen (unstable patient / protruding viscera) → exploratory

laparotomy

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 ■ Blunt abdominal Trauma → Signs & Symptoms of peritoneal irritation →
Exploratory laparotomy

■ Blunt Abdominal Trauma → Signs & Symptoms of internal bleeding (shock) →

Stable patient → CT scan → Intervention

■ Above scenario → unstable patient → Diagnostic peritoneal lavage /

sonogram → intervention

■ Fractures of lower ribs on Left side → rupture spleen

■ Coagulopathy during operation → FFP + platelate transfusion

■ Prolonged laparotomy → more IV fluids given → Abdominal compartment

Syndrome ( Abdomen can’t close without tension ) → Tx : temporary cover
with absorbable mesh / non – absorbable plastic

■ Pelvic Fracture → External fixation / arteriographic embolization.

■ Hemodynamically unstable with pelvic fracture due to blunt trauma – first step?
USG abd or Diagnostic peritoneal lavage to rule out intraperitoneal hemorrhage
(h’ge) – If negative, next step? Pelvic angiogram to rule out retroperitoneal h’ge –
if h’ge present, prepare for appropriate embolization

■ H/O Trauma → Blood in the Urine (urological injuries)

Gross Hematuria Microscopic Hematuria

↓ ↓
sonogram ( Best ) / IVP ↓ ↓
Children Men ( Adults )
↓ ↓
Asymptomatic / Symptomatic Asymptomatic
↓ (do nothing)
Sonogram / IVP ↓
(When ask best diagnostic test for suspecting renal damage, Symptomatic
Answer CT scans of abdomen) ↓
Sonogram / IVP

- Penetrating urologic injuries (gunshot in lower abdomen) – surgical exploration &

repair

- Pelvic Fracture + Hematuria (Blood at urethral meatus) → retrograde

urethrogram → surgical repair

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 - Pelvic fracture + gross blood on catheterization → retrograde cystogram then
surgical repair

- Rib fractures, Abdominal contusion + Gross hematuria and normal retrograde

cystogram → CT scan Abdomen (Renal damage)

- H/O Renal damage + few weeks after develop CHF & Flank bruit → Traumatic
arteriovenous Fistula & subsequent CHF

- Blunt Renal trauma doesn’t require operation unless avulsion of renal pedicles
which can be complicated by arteriovenous fistula later
.
■ Sensation that patient wants to urinate but he can’t → Posterior urethral injury

■ Hematoma of penile shaft (corpora cavernosa fracture) → urological emergency

→ immediate surgical repair

 Gunshot wound to Extremities

↓ ↓ ↓
No or vascular injury possibility of vascular definite vascular
Unlikely injury injury
↓ ↓ ↓
Standard wound care Arteriogram / Doppler surgical exploration
And repair
↓
Surgical repair if
Injury present

 Complex extremity Injury → 1st fracture stabilization → 2nd vascular repair →

lastly nerve repair

 Crushing Injury → Tx: plenty of fluids, diuretic, Alkalization of urine

 Compartment Syndrome → Fasciotomy

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 MISCELLANEOUS

 Edema: Transudate (↑ Hydrostatic pressure & ↓ Oncotic pressure) Exudates (↑

vascular permeability)

 Shock: Low perfusion pressure to tissues – Hypovolemic (low circulatory

volume); Cardiogenic (heart is not pumping well) and Septic (vasodilation leads
to blood flow too quickly and give less time for tissue to extract oxygen)
 Cardiogenic shock – low CO & High PCWP
 ARDS – Normal PCWP [PCWP = pulmonary capillary wedge pressure]
 Septic shock – High CO, Low PCWP & Normal mixed venous O2
 Hypovolemic shock – low CO, low PCWP, low mixed venous O2

 High PCWP & low CVP – LV dysfunction [CVP = central vein pressure]
 High PCWP & high CVP – Cardiac temponade
 Respiratory distress & high CVP – Tension Pneumothorax

• Abdominal Aortic Aneurysm – Atherosclerosis – (rupture - left flank pain ,

hypotension, pulsatile mass) – below renal artery origin is most common site

• Syphilitic Aneurysm – Aortic arch aneurism, tertiary syphilis, vasculitis of vasa-

vasorum, Aortic valve regurgitation, brassy cough due to stretching of Lt.
recurrent laryngeal N by aneurysm

• Ehler-Danlos Syndrome: defect in type-I and type-III collagen – poor wound

healing, aortic dissection (MCC of death), hyper mobile joints

• Chrug Strauss Syndrome – Vasculitis + eosinophilia – Asthma (nocturnal chest

tightness, short of breath, etc) – Nephritic syndrome, positive p-ANCA –
Leukotrines inhibitors can cause Chrug Strauss Syndrome

• Capillary Hemangiomas in newborn regress with age

• Sturge-Weber syndrome – Nevus flammeus (birth mark) on face in distribution

of Ophthalmic branch of CN 5 – Ipsilateral malformation of pia matter vessel
overlying occipital & parietal lobes

• Takayasu arteritis (Pulseless disease) – young asian girl – granulomatous vas-

culitis of aortic arch

• Kaposi sarcoma – HHV-8 – malignant tumor of endothelial cells – raised, red-

purple flat lesion to plaque & nodules

• Bacillary angiomatosis – benign capillary proliferation involving skin & viscera

in AIDS – simulate Kaposi sarcoma – Bartonella Henselae (causative agent)

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  Von Hippel Lindau – Autosomal Dominant – cerebellar hemangioblastomas,
Pheochromocytoma, renal adenocarcinoma (high incidence)

• Kartagenar Syndrome:
˗ Immotile cilia syndrome
˗ Recurrent sinusitis, infertility & situs inverses

• Rhabdomyosarcoma:
- Tumor of striated muscles.
- Head & Neck and genitourinary tract.
- Grape-like mass protruding through vagina (Sarcoma botryoides)

• Osteogenesis Imperfecta:
- Blue sclera, brittle bones
- Defective synthesis of type-I collagen

■ HLA association with Diseases:

• HLA-A3 – Hemochromatosis
• HLA-B27 – Ankylosing Spondylitis
• HLA-DR2 – Multiple Sclerosis, Goodpasture, Narcolepsy, Hay fever
• HLA-DR2,DR3 – SLE
• HLA-DR3 – Celiac Sprue, Dermatitis Herpatiformis
• HLA-DR3,DR4 – Type-1 DM
• HLA-DR4 – Rheumatoid Arthritis(RA), Pemphigus Vulgaris
• HLA-DR5 – Pernicious Anemia, Juvenile RA
• HLA-DR7 – Steroid-responsive Nephrotic Syndrome

• Hereditary Angioedema – C1 esterase deficiency

• Paroxysmal Nocturnal Hemoglobinuria – Defect in molecule anchoring decay
accelerating factor(DAF) which normally degrade C3&C5 convertase on
hematopoetic cell membranes therefore in the absence of DAF complement
mediated Intravascular lysis of RBC occur(Hemoglobinuria)
• Bruton’s Agammaglobulinemia & Wiskott-Aldrich Syndrome are the only X-
linked recessive immune deficiency syndromes.
• Bruton’s Agammaglobulinemia – tyrosine kinase deficiency.
• Wiskott-Aldrich Syndrome – Eczema, Thrombocytopenia, deletion of T & B
cells, Low IgM, Non-Hodgkin Lymphoma
• Phagocyte Dysfunction [CGD (Chronic Granulomatous Disease), Chediak-
Higashi Syndrome] – Extracellular Bacteria (Staph. Aureus) + Fungi
(Aspergillosis)
• T-Cells Deficiency (DiGeorge Syndrome) – Intracellular Organisms (Virus,
Candida, TB) but NOT Staph. Aureus, Hypocalcaemia due to absent parathyroid
glands; 3rd&4th pouch defect, absent thymus too.
• B-cells Deficiency(Bruton’s Agammaglobulinemia) – Extracellular Pyogenic
Bacteria but NOT intracellular

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 • SCID – Bacteria, Virus, Fungus; Adenosine Deaminase deficiency; Neutrophils
- ↑ or normal, B&T cells - ↓↓↓
• C3 deficiency – Pyogenic Bacteria
• C1,C4 or C2 deficiency – Opsonization not efficient
• C6-8 deficiency – Neisseria Infections
• ↑IgM but deficient IgG & IgA – CD40 ligand deficiency on activated T-cells
• At blood transfusion, blood types are appropriate to ABO & Rh typing, but still
person develop Anaphylaxis → Selective IgA deficiency. Patient may have h/o
recurrent sinopulmonary infections.
• Leukocyte Adhesion Deficiency – deficiency of selectins or β2 integrins
(CD11a:CD18) – delayed separation of umbilical cord in newborn
• NADPH oxidase produce free radicals of oxygen – Superoxide dismutase
converts it in to H2O2 (called respiratory burst) – Myeloperoxidase combine it with
Cl and form hypochlorus free radicals which kills organisms
• Chronic Granulomatous Disease – absent NADPH oxidase – absent respiratory
burst [negative NBT (Nitro-blue tetrazolium)]
• Myeloperoxidase deficiency – respiratory burst occurs – so able to kill
streptococcus species (catalase negative) but not staphylococci (catalase positive)
• Job’s syndrome – defective Chemotaxis (staph infection) and ↑ IgE (eczema)

• Decompression sickness (Caisson’s Disease) – rapid ascent of deep sea drivers

leads to formation of nitrogen gas bubble which occludes vessels lumen and
causes thrombo-embolic events – Tx: recompression by forcing nitrogen to
solution again by increasing pressure and slow decompression

• Prader-Willi syndrome – Microdeletion syndrome with

hypogonadism, mental retardation, short stature, and obesity
(chromosome 15 deletion is of Paternal origin)
• Angelman syndrome – chromosome 15 deletion is of maternal
origin (child continuously laughing)
• Cancers caused by radiation – Acute Leukemia, Papillary CA of Thyroid
• CA due to smoking: mouth, larynx, esophagus (SCC), pancreas, Urinary bladder
• CA due to alcohol: oropharyngeal, upper to mid esophageal, HCC

• Ectopic Hormones & Tumor relationship:

 ACTH: most common ectopic secretion – secreted in Small cell CA of Lung and
Medullary CA of thyroid – produce Cushing Syndrome
 ADH: secreted in Small cell CA of lung – produce SIADH
 β–hcg: secreted in Trophoblastic tumors and germ cell tumors – produce
Gynacomastia and hyperthyroidism (similar to TSH)
 Erythropoietin: secreted in Renal cell CA and HCC (hepatocellular CA) –
produce secondary polycythemia
 Insulin-like peptide: secreted in HCC – produce hypoglycemia
 Calcitonin: secreted in Medullary CA of thyroid – produce hypocalcemia

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  PTH-like peptide: secreted in Small cell CA of Lung, Renal cell CA, Breast CA,
Ovarian CA – produce Hypercalcemia (low PTH)
 Serotonin: secreted in Carcinoid syndrome, SCC, Medullary CA of thyroid –
produce diarrhea, flushing, Valvular insuffiency (tricuspid insufficiency &
Pulmonic stenosis)

 Prostate cancer – osteoblastic metastasis (↑ Alkaline phosphate) All other can-

cers which metastasize to bone has osteoclastic effect.

 Down Syndrome (trisomy - 21) – endocardial cushion defect (Atrial & ventricu-
lar septal defect)
- ↑ risk of Hurschprung disease & duodenal atresia
- ↑ risk for leukemia (Acutemegakaryocytic - ‹ 3yrs, ALL - › 3yrs)
- Alzheimer’s disease by age of 35yrs.
 Edward’s Syndrome (trisomy – 18) – VSD, clenched hands with overlapping
fingers, “Rocker bottom feet”
 Patau’s Syndrome (trisomy – 13) – VSD, cleft lip & cleft palate
 D E P – 21, 18, 13

 Turner’s Syndrome – Pre-ductal coarctation & bicuspid aortic valve, primary

amenorrhea, cystic hygroma

 Most of the spontaneous abortions are due to trisomy 16

• Marfan Syndrome:
- Defect in synthesizing fibrillin
- Mitral valve Prolapse, Aortic dissection.
- Subluxated lens, arachodactyly.
- Most common finding in patient with Marfan syndrome – dural ectasia (90% of
cases) [require MRI of spine for diagnosis] [lens dislocation and aortic dilatation
– 80% of cases]

• Klinefelter Syndrome:( 47,XXY):

- Hypogonadism, Infertility, Gynacomastia
- ↑↑ FSH & LH, ↓ ↓ Testosterone

• Kartagenar Syndrome:
˗ Immotile cilia syndrome
- Recurrent sinusitis, infertility & situs inverses
• Fragile X-Syndrome:
˗ CGG repeat sequence
˗ Mental retardation, enlarge testis, prominent jaw, large ears

 Low protein diet should be given in patient with renal failure and cirrhosis
 Kwashiorkor – inadequate protein intake – edema
 Marasmus – inadequate calorie intake – extreme muscle wasting

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  Anorexia nervosa – distorted body image
 Bulimia nervosa – binging & purging (self induce vomiting)
 Vit-E – decrease synthesis of Vit-K dependent coagulation factor

■ Lesch – Nyhan Syndrome:

- Defective purine metabolism
- Deficient HPRT (HGPRT)
- Child tendency to compulsively bite his finger (self mutilation)
- Mental retardation
HPRT
- Hyperuricemia is due to ↓ IMP (Hypoxanthine > IMP)

■ Tay Sachs Disease:

˗ Hexosaminidase A deficient
˗ Ganglioside accumulate in cells
˗ Charry red macula, No Hepatomegaly and cervical lymphadenopathy

■ Niemann – Pick:
- Sphingomyelinase deficiency
- Sphingomyelin accumulate in cells
- Characteristic foamy macrophage, charry red macula but Hepatomegaly, &
cervical Lymphadenopathy present

■ Gaucher’s Disease:
˗ Gluocerebrosidase deficiency
˗ glucocerebroside accumulate in cells
˗ characteristic Macrophage (crumpled paper inclusion)

■ Klein- Waaredenberg Syndrome:

- mutation in PAX gene
- Dystonia Canthorum ( Lat. displacement of inner corner of eye )
- Pigmentary abnormality
- Congenital Deafness, Limb abnormalities

■ Phenylketonuria:
˗ Phenylalanine Hydroxylase Deficiency (Phenylalanine → tyrosine)
˗ Musty odor from child, mental retardation
˗ Aspartame (artificial sweeteners) must be strictly avoided by phenyketonurics
˗ ↑ Phenylalanine level in pregnant woman → mental retardation in Infants

■ Homogentisate Oxidase Deficiency:

- accumulation of homogentisic acid in blood & excretion in urine
- Ochronosis (accumulation of pigments in cartilages)

■ Maple Syrup Urine Disease:

˗ Branched chain ketoacid dehydrogenase deficiency

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 ˗ impaired metabolism of Valine, Leucine, Isoleucine
˗ Maple syrup odor in urine, Ketosis, coma, & death if not treated

■ Acute Intermittent Porphyria:

˗ Uroporphyrinogen – 1 synthase deficient
˗ Episodic variable expression
˗ Acute abdomen (“belly full of scars”) , brief psychosis
˗ No photosensitivity (↑δ ALA , PBG)
˗ Never give Barbiturates, Pyrazinamide, Gresiofulvin

■ Porphyria Cutanea Tarda:

- Uroporphyrinogen decarboxylase deficient
- Photosensitivity (↑ uroporphyrin 1) [urinary uroporphyrin - diagnostic test]
- Painless blistering on sun exposed area – Tx: stop alcohol & estrogen use

■ Homocystinuria: Marfan’s features, Arthrosclerosis in childhood, recurrent DVT

Cystathione Synthase
(Homocystine Cystathione)
Vit-B6

 Causes: Cystathione synthase deficiency, Vit- B6 deficiency, Homocystine

methyltransferase deficiency, Folic acid & Vit- B12 deficiency
 Methionine is degraded via the Homocystine–Cystathione Pathway; so
methionine is elevated in patient with cystathione synthase deficiency via
activation of Homocystine methyltransferase by excess substrate homocystine.

Galactosemia/Galactosuria Fructosemia/Fructosuria
 galactokinase deficiency  Fructokinase deficiency

- ↑galactose in blood - ↑ fructose in blood

- cataract (Aldose reductase) - No cataract
- galactokinase trap galactose in cell by - fructokinase trap fructose in cell by
phosphorylation as galactose-1-phosphate phosphorylation as fructose-1-phosphate
 Gal-1-Uridyltransferase Deficiency  Aldolase B Deficiency

- convert galatose-1-phosphate into - convert fructose-1-phosphate into DHAP

glucose-1-phosphate & Glyceraldehydes
- If it deficient, galactose-1-phosphate -If it deficient, fructose-1-phosphate
accumulate in cells and produce symptoms accumulate in cells and produce symptoms.
- Liver, Brain & other tissue. - Liver , kidney
- Symptoms evident while on Breast milk, - Symptoms are not evident while on
so early onset of symptoms after birth Breast milk, so late onset of symptoms
after birth
- cataract - No cataract

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- Hypoglycemia, Lactic acidosis, Jaundice, - Hypoglycemia, Lactic acidosis, Jaundice,
Mental retardation Proximal Renal tubular disorder
resembling Fanconi’s syndrome
- Avoid milk & milk product - Avoid Honey, table sugar which contain
sucrose

• Cretinism – hypothyroidism in child – protruding tongue, prominent fontanels,

chubby, umbilical hernia, short stature

• Short Stature: Half of adult height should be achieved by age of 2 yrs. – short
stature could be due to constitutional delay or due to genetic cause – X-ray of
hand & wrist (best test) – Constitutional delay [Bone age – 5 yrs old in 8 yrs old
child] Genetic cause [Bone age 8 yrs in 8 yrs old child] [Low dose of testosterone
can be used for Tx of constitutional delay, but only used for short time]

• Failure to thrive – dietary modification is the best initial Tx. If history and
physical finding suggestive of any organic cause, order lab test. If patient doesn’t
improve within 4-6 wks of oral feeding, admit to the hospital and start nasogastric
feeding. If child neglect / abuse are suspected, admit to the hospital. Daily calories
up to 1 years of age is 100 kcal/kg

• Bilious vomiting in an infant means there is a malrotation with Volvulus until

proven otherwise – Tx: laparotomy

• Mongolian spots: flat blue (or) gray lesions with well-defined margins; disappear
in first few years of life.
- Most common over the presacral area
- D/D: bruises of child abuse – fade into surrounding skin and have different
colors

• Epstein’s pearls (Milia) : pearly white small inclusion cysts.

• Cutis Marmorata : vasomotor response to cold stress.

- Skin assumes a lacy pattern similar to cobblestones.
- Persistent form is seen in trisomy 21, trisomy18.

 Erythema toxicum: Eosinphilis filled small papule(or)pustules on an

erythematous base.
- D/D: Staphylococcal scalded skin syndrome : very ill looking infants, culture
positive for Staph.Aureus, neutrophils in the lesions.

• Salmon Patch: flat vascular lesion that disappear with time.

- glabella, eyelids, nuchal area
- D/D: Sturge-Weber Syndrome (Port wine stains): (“birth mark”) on face in the
distribution of the ophthalmic branch of CN-5. Remains permanently

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 • Capillary Hemangiomas: bright red, reminiscent of a strawberry which regresses
spontaneously.

• Nevus Sebaceous (of Jadassohn): yellow-orange hairless plaques resembling flat

warts located on the scalp
- Removed in adolescence because of potential to become malignant

• Cephalhematoma – subperiosteal bleed, does not cross suture lines, resolve

spontaneously.
• Caput Succedaneum – swelling of scalp, cross suture lines, resolve
spontaneously.

• Subcutaneous fat necrosis → rubbery, firm nodules on cheeks (or) buttocks occur
during difficult labor, particularly forceps (or) vacuum extraction, resolve
spontaneously.

• Neonatal drug withdrawal: Infants born to actively addicted mothers

- Most common drugs – Heroin (48 hrs) & Methadone (2-6 weeks)
- hyperactivity, irritability, fever, tremors/jitters, high-pitched crying, vomiting,
poor feeding, seizures
- Tx: narcotics, sedatives and hypnotics as well as swaddling and reducing noxious
stimulation

• Adrenal hemorrhage is seen almost exclusively in newborn and is an indicator of

birth trauma, stress, anoxia or dehydration. Follow up with US in 1-2 wks

• Newborn can lose up to 10% of wt during first week

• Facial Palsy in Infant : affected part of face doesn’t move when baby cry

• GERD in Infants : h/o spitting on burping, h/o aspiration pneumonia (Rt. lung
pneumonia), wheezing

• Breast Milk: immunologic factors: IgA, lactoglobulins and maternal macrophage

- Low Vit-k → All newborn infants should receive Vit-k at birth to prevent
hemorrhagic newborn disease.
- Vit-D supplementation → if mother’s intake is inadequate / if there is a limited
sun exposure to baby.
- Iron supplementation for baby on cow milk (whole milk).
- Folate & vit-B6 supplementation for baby on goat milk
- Mother with HBsAg positive can breast feed her child immediately after birth
- Contraindication to breast feeding – HIV positive mother, Lithium, mother
taking cocaine, heroin, PCP, marijuana, nicotine
- Breast feeding should continue until age of 1 yr, start iron supplementation at age
of 6 months
- Mother should breastfeed infant atleast every 4-hrs
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  Attention Deficit Hyperactive Disorder (ADHD)
- Inability to attend to the task at hand, increased motor activity and impulsivity.
- Tx: methylphenidate / Dextroamphetamine & psychological therapy.

 Enuresis:
- Day & night bladder control is usually attained by age 5 yrs.
- first step in management of pt with enuresis  urine analysis
- Causes – UTI, urinary tract abnormality, Psychogenic, developmental delay of
the bladder, Diabetes, Stress incontinence, waiting too long to void
- Tx: Non pharmacological → ↓ water intake at night, alarm system, reward
system.
Pharmacological → Imipramine, Desmopressin

 Asperger Syndrome: more communicative, appear more socially aware; do not

have language impairments, repetitive behavior.
 Rett syndrome: neurodegenerative disorder, only affect females.
- Stereotypic hand movement (hand wringing) & Acquired microcephaly.

■ ENT: Tx of benign positional vertigo – canalith repositioning procedures

• Non-sedating nasal decongestant (Pseudoephedrine) before diving has been
shown to reduce the ear and sinus barotraumas by 75%
• Adolescent with nasal mass & epistaxis – angiofibroma (MCC of nasal mass)
• Ingestion of button battery in child should be removed immediately with
endoscopy because it contains heavy metals which can produce tissue damages.
For other foreign body ingestion, wait and watch (comes out in stool)
• Tx of external otitis – cleaning of ear canal with cerumen wire loop or cotton
swab (first step) [cleaning with hydrogen peroxide is an alternative method if
tympanic membrane is visualize and it is intact]
• Nasal cytology is the best step in management of patient with rhinitis
• Patient c/o aural fullness, audible popping sound while swallowing, intermittent
ear pain and hearing loss, diagnosis? – Eustachian tube dysfunction
• Hereditary hearing loss – sensorineural
• Osteosclerosis – Autosomal dominant, conductive hearing loss, absent stapedial
reflex

■ Ophthalmology: Orbital cellulitis – admit the patient in the hospital – start IV

broad spectrum antibiotics (for at least 3 days) then continue on oral regimen for
few days as an out-patient follow up
• Orbital cellulitis – unilateral proptosis, normal fundoscopy
• Cavernous sinus thrombosis – bilateral proptosis, papilledema
• Tx of Diabetic retinopathy – Proliferative (disc neovascularization) – immediate
laser photocoagulation; Non-proliferative – Retinoscopy (to check any macular
edema) followed by elective laser photocoagulation
• Ocular Melanoma – ocular ultrasound (for diagnosis) and MRI (to check
extrascleral extension) – Tx: Enucleation

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 • Blepharospasm – periodic involuntary closure of eye (form of focal Dystonia) –
Tx: Botulinum toxin injection
• Anterior Uveitis (iritis) – pain, redness, photophobia, irregular pupils and
leucocytes in anterior chamber – around 25% of patient with Sarcoidosis have
uveitis
• Endophthalmitis – ophthalmic emergency – intraocular surgery, h/o eye injury;
c/o light flashing, severe pain, on examination hypopyon and failure to visualize
retinal vessels (80% of cases) – urgent ophthalmic referral is necessary – Tx:
Vitreous or Aqueous culture and Intavitreal antibiotics; Vitrectomy; Enucleation
• Tx of Candida Endophthalmitis – vitrectomy + IV Amphotericin B
• Amblyopia → vision impairment resulting from interference with the processing
of images by the brain during the first 6-7 yrs of life → Strabismus / Congenital
cataract / Retinoblastoma → Initial treatment of Amblyopia: occlusion therapy
(continuous covering of normal eye) → correction of problem needed as early
as possible
• Intermittent painless loss of Vision in elder (Amaurosis fugax), next step?
Duplex study of neck. Cause? – emboli
• Dacryocystitis – infection of lacrimal sac
• Hordeolum (Stye) – Abscess located over the upper or lower eyelid
• Herpes simplex Keratitis  corneal vesicle & dendritic ulcers
• Herpes zoster ophthalmicus  elderly patient – burning & itching sensation in
periorbital area, vesicles in the distribution of the cutaneous branch of the first
branch of trigeminal nerve (Ophthalmic N)
• HSV keratitis in HIV  painful lesion, fundoscopic findings of peripheral Pale
lesions & central retinal necrosis
• CMV retinitis in HIV  painless, fundoscopic findings of hemorrhage and
fluffy or granular lesions around the retinal vessels
• Grade of Hypertensive Ratinopathy (I  IV): Av nicking  copper wiring 
silver wiring, flame shaped hemorrhage (h’ge), Exudates  papilledema
• Central Retinal Vein Occlusion: painless – disc swelling, vein dilated &
tortuous, retinal hemorrhage & cotton wool spots
• Central Retinal Artery Occlusion: painless – pallor of optic disc, cherry red
fovea and boxcar segmentation of blood in the retinal vein
• Follicular conjunctivitis & neovascularization of cornea (pannus), diagnosis? –
Trachoma
• Sympathetic Ophthalmia: “spared eye injury” – immune mediated inflammation
of one eye (the sympathetic eye) after a penetrating injury to the other eye –
mechanism? “uncovering of hidden antigen”
• Open angle glaucoma – central vision spared
• Macular degeneration – peripheral vision spared (Tx: laser photocoagulation)

■ Preventive Medicine: Mx of exposed health care worker to TB – place PPD now

and repeat it in 3-wks
• Nicotine replacement is preferred over buproprion for the management of nicotine
withdrawal during early stage of smoking cessation – give behavioral counseling

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 and nicotine patch [First counseling then treatment; If you have never counseled
patient regarding smoking cessation, do not pick prescribe nicotine patch or any
other treatment for smoking cessation (most probably wrong answer)]
• CXR is not done routinely for screening purpose for lung cancer
• There are no screening test indicated routinely for many cancers like bladder CA,
Ovarian CA, pancreatic CA, lung CA, Hepatocellular CA, etc so do not pick
answer telling you order this screening test to rule out this CA
• Prophylaxis of meningococcal meningitis – Rifampin
• Prophylaxis of meningococcal meningitis in women taking OCP – ciprofloxacin
• HRT can cause significant elevation in triglyceride. If hypertriglyceridemia
doesn’t solve after discontinuation of HRT and dietary modification , start
treatment
• Smoking cessation has shown benefit in patient with osteoporosis
• Cigarette smokers have been shown to have more wrinkles than do nonsmokers
• Dehydration aggravate skin damage and therefore patient going on vacation in a
area with lot of sun exposure should be educated to drink more water and wear
protective clothes
• Prevention of malignant melanoma – Protective clothing
• Most important risk factor in stroke – HTN
• A clear association has been found b/w excessive alcohol intake & development
of hypertension
• Several studies has suggested strong correlation b/w alcohol intake and colon CA
• Colonoscopy should be started at age of 50 yrs in a general population with
average risk and at age of 40 yrs or 10 yrs earlier than detection of colon CA in
family member, whichever come first
• Patient with ulcerative colitis and pancolitis should begin surveillance
colonoscopy after 8 yrs of having the disease
• Do nothing after complete resection of <2cm pedunculated adenomatous polyp;
surveillance – colonoscopy after 3 yrs; If negative at 3 yrs follow up,
surveillance colonoscopy period can be extended to 5 yrs.
• Mammography screening – started b/w 40-49 yrs of age – every 2 yrs; After 50
yrs of age – annually [The American Medical Association, American College of
Radiology, American Cancer Society, American College of Obstetricians and
Gynecologists, and the USPSTF all support mammography screening beginning
at age 40; In patient with h/o breast CA in first degree relative, begin at 10 yrs
earlier than detection of breast CA in family member]
• Pap smear – within 3 yrs after onset of sexual activity or age of 21 yrs,
whichever occur first [some says age of 18 yrs] [If 3 annual pap smears are
negative, then do pap smear every 2 yrs until age of 70 yrs] [Annual pap smear
screening is recommended for all women regardless of their sexual orientation
(hetero/homosexual women)]
• Prostate CA screening – African-American and individual with family h/o
prostate CA should begin annual screening (PSA level and digital rectal exam) at
age of 40 yrs; at age of 50 yrs for everyone else
• Screening of DM is indicated in everyone aged 45 yrs or older. [FBS]

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 • Gestational Diabetes Screen – b/w 24-28 wks – 1-hr 50g oral GTT (screening
test) – If level >140 mg/dl, do definitive test (3-hrs 100g oral GTT done after
overnight fasting) – FBS (<126 gm/dl), After 100g oral GTT – at 1-hr (<180
gm/dl), at 2-hrs (<155 mg/dl), at 3-hrs (<140 mg/dl)
• Triple marker screen – b/w 15-20 wks – MS-AFP, hCG, Estriol - ↓↓ (MS-AFP
& Estriol), ↑ hCG → Trisomy 21 (Down syndrome), next step? – Amniocentesis;
↓↓↓ (All three) → Trisomy 18, next step? – Amniocentesis for karyotyping
• Rh-isoimmunization – Blood typing at first prenatal visit – If Rh-negative
mother, Indirect Coomb’s test at 28 wks of gestation [<1:8 – no fetal risk]; give
RhoGAM to all Rh-negative mothers at 28-wks of gestation
• RhoGAM is given to Rh-negative mothers at 28-wks of gestation, after delivery
of Rh-positive infant, within 72-hrs of amniocentesis, D&C, chorionic villous
sampling
• Chlamydia Trachomatis Screening – All sexually active women age 24-yrs
and younger and in other women who are at increased risk of STDs
• CDC recommended vaccination id Adult – Td (every 10 yrs after age of 18 /
last booster at age of 50), acellular Pertusis (booster b/w age of 19-64), Influenza
(All adults >50 yrs of age – IM route; Healthy 5-49 yrs of age, non-pregnant
women – Intranasal), Pneumococcal (All adults >65 yrs of age)
• Vaccination in HIV positive patient – Influenza (IM), MMR, S. pneumoniae,
Hepatitis
• First trimester screening tests – CBC, Rubella IgG antibody, Hep B, Blood
type, Rh & Antibody screen, cervical culture, urine culture, PPD, VDRL/RPR,
Pap smear and HIV ELISA [require specific consent]
• Screening tests for All newborn – Hypothyroidism, Galactosemia,
Phenylketonuria
• Voiding after intercourse has been shown to decrease the risk of UTI in sexually –
active females
• Breast cancer prevention trial suggest that Tamoxifen reduce the risk of breast
cancer in patients who have an increased risk of developing breast cancer
• [Ideal body weight for female – 5 feet height = 100 lbs then add 5 lbs for each
inch increase in height; Ideal body weight for male – 5 feet height = 106 lbs then
add 6 lbs for each inch increase in height]

Drugs Decrease long term mortality in different condition

ACE inhibitors CHF, Prevent diabetic nephropathy, reduce insulin resistance
Beta blockers Acute MI, Perioperative period
Aspirin Acute MI
Home Oxygen COPD, Right sided heart failure due to pulmonary hypertension
Spironolactone With ACE inhibitors in CHF

Good Luck

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