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IgA Vasculitis (HSP) - Basics to Advanced Clinical

1. Nomenclature and Definition

IgA vasculitis is a small-vessel vasculitis characterized by palpable purpura (most commonly distributed over the buttocks and lower extremities), arthralgias, gastrointestinal signs and symptoms, and glomerulonephritis.

• Harrison's Principles of Internal Medicine 22E

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2. Epidemiology

• ROSEN's Emergency Medicine; Andrews' Diseases of the Skin

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3. Pathogenesis - From Molecular to Clinical

Step 1: Aberrant IgA1 Glycosylation (The Core Defect)

Step 2: Anti-glycan Autoantibodies (Second Hit)

Step 3: Immune Complex Deposition

• Skin (dermal capillaries and venules)
• Glomerular mesangium (kidneys)
• Synovium (joints)
• Intestinal submucosa (gut)

Step 4: Complement Activation and Inflammation

Additional Mediators

• Elevated TNF-alpha and IL-1beta
• Elevated vascular endothelial growth factor (VEGF) and endothelin
• Decreased factor XIII levels (associated with worse prognosis)
• High-titer IgA anti-endothelial cell antibodies (correlate with severe renal disease)

A high serum Ga-IgA1 level is not sufficient for the development of clinical symptoms. A "second hit" in the form of another environmental or inherited risk factor is required to produce IgA vasculitis.

• Firestein & Kelley's Textbook of Rheumatology

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4. Triggers and Precipitants

• Upper respiratory tract infections (most common - streptococcal pharyngitis, viral URIs) - precede disease in up to 50% of cases
• Helicobacter pylori infection (implicated in childhood and adult cases)
• Drugs (antibiotics and others)
• Insect bites, foods, immunizations
• Underlying malignancy (important in adults - see below)

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5. Clinical Features - The Classic Tetrad

A. Skin (100% of patients once fully established)

• Starts as mottled purpura on extensor extremities
• Becomes hemorrhagic within ~1 day
• Begins to fade in ~5 days
• New crops appear over weeks
• Distributed on lower extremities, buttocks, and posterior legs (dependent areas)
• May include urticarial lesions, vesicles, necrotic purpura, or hemangioma-like lesions
• Koebnerization: streaky/linear purpura from pressure on inflamed vessels (see image below)
• Purpura above the waist may be a marker of renal involvement

B. Joints (~63-82% of patients)

• Polyarthralgias progressing to arthritis
• Periarticular swelling around knees and ankles (most common joints)
• Usually without frank synovial effusion
• Non-destructive; resolves with the disease

C. Gastrointestinal Tract (~65-70% of patients)

• Colicky abdominal pain caused by gut vasculitis - typically occurs within 1 week after rash onset
• Nausea, vomiting, diarrhea, constipation
• Passage of blood and mucus per rectum (melena, hematochezia)
• Intussusception (classic risk - ultrasound required)
• Paralytic ileus, rebound tenderness, distension
• Endoscopy: purpura in upper or lower intestinal tract
• GI radiograph: "spiking" or "cobblestone" marbled appearance
• Important: GI symptoms may PRECEDE the rash in some cases, creating diagnostic difficulty and potentially leading to unnecessary exploratory surgery

D. Kidneys (10-50% in children; up to 70%+ in adults)

• Ranges from microscopic hematuria (+/- proteinuria) to nephrotic syndrome
• Red blood cell casts confirm glomerulonephritis
• Most cases are mild and self-limited in children
• Progressive glomerulonephritis and CKD/ESRD are uncommon in children but more prevalent in adults
• Nephrotic syndrome occurs in 20-30% of those biopsied
• AKI may develop from crescentic GN

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6. Histopathology

Skin Biopsy (Light Microscopy)

• Neutrophilic infiltration of vessel walls
• Nuclear dust (leukocytoclasis - fragmented neutrophil nuclei)
• Fibrinoid necrosis of vessel walls
• Extravasation of red blood cells

Skin Biopsy (Direct Immunofluorescence - DIF) - DIAGNOSTIC

Renal Biopsy (Light Microscopy)

• Mesangial proliferative GN (most common)
• Diffuse endocapillary proliferation
• Crescentic GN (severe, rapidly progressive cases)

Renal Biopsy (Immunofluorescence)

• Diffuse mesangial IgA deposits (identical to IgA nephropathy)
• C3 and IgG co-deposition
• The MEST scoring system for IgAN may apply but its predictive value for IgAV nephritis has not been validated

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7. Diagnosis

Clinical Diagnosis (especially in children)

1. Diffuse abdominal pain
2. Any biopsy showing predominant IgA deposition
3. Arthritis or arthralgia
4. Renal involvement (hematuria and/or proteinuria)

1990 ACR Classification Criteria (for epidemiologic use)

1. Age ≤20 years at disease onset
2. Palpable purpura
3. Acute abdominal pain
4. Granulocytes on biopsy

Laboratory Findings

Differential Diagnosis

• Septic purpura (meningococcemia) - thrombocytopenia present
• ITP / TTP - platelet count differentiates
• Streptococcal infection with rash + arthralgia
• Other systemic vasculitides (ANCA vasculitis, SLE vasculitis)
• Septic arthritis / reactive arthritis
• Acute surgical abdomen (when GI symptoms precede rash)

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8. Special Population: Adults vs. Children

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9. Prognostic Factors (Poor Prognosis)

• Nephrotic-range proteinuria (>1 g/day)
• Hypertension at presentation
• Crescents on renal biopsy
• Mesangial macrophages
• Tubulointerstitial fibrosis
• Decreased factor XIII levels
• Purpura above the waist
• Renal insufficiency at onset
• High-titer IgA anti-endothelial cell antibodies

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10. Treatment

Supportive (all patients)

• Rest, hydration, pain management
• Acetaminophen for arthralgias
• NSAIDs for joint pain (use cautiously - avoid with severe renal involvement or active GI bleeding)
• Close follow-up: urinalysis + blood pressure monitoring for at least 6 months

Skin-Limited Disease

• Dapsone 50-200 mg/day
• Colchicine 0.6-1.2 mg twice daily

Gastrointestinal Disease

• H2 blockers for GI symptoms
• Prednisone 1 mg/kg/day (more effective for abdominal pain than analgesics; does NOT reduce renal complication risk)
• IVIG for persistent abdominal pain refractory to steroids

Renal Disease - A Spectrum of Interventions

Despite this, it is prudent to treat aggressive renal involvement with an immunosuppressive regimen that includes high-dose glucocorticoids. Mycophenolate mofetil is an excellent option for severe renal disease.

• Firestein & Kelley's Textbook of Rheumatology

Malignancy-Associated IgAV

H. pylori-Associated IgAV (Adults with GI symptoms)

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11. Emergency Department Approach (Rosen's Framework)

• Cannot bear weight due to arthralgias
• Pain not controlled with oral medications
• Ongoing GI bleeding
• Renal involvement with fluid overload/AKI
• Severely elevated blood pressure

• Urinalysis (mandatory)
• BMP if hematuria or hypertension
• Abdominal ultrasound if GI bleeding/abdominal pain (rule out intussusception)
• CBC (normal platelets excludes ITP)

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12. Prognosis

• Overall prognosis is excellent, especially in children
• Mortality is exceedingly rare
• Most patients recover completely, often without therapy
• Illness duration: typically 6-16 weeks
• Children with gross hematuria usually do well
• Recurrent skin disease (multiple episodes over months) is not unusual but typically resolves over months to 1 year
• 1-5% of children progress to ESRD; in adults, up to 40% may develop CKD/ESRD at 15-year follow-up
• Persistent nephropathy (usually mild) in only ~8% of overall patients

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13. Transplantation

• ~50% of transplants: isolated IgA deposits in the graft
• Full-blown IgAN in the graft (clinically)
• Rarely: full systemic recurrence including rash
• Cadaveric donor may be preferable to living-related donor in children (controversial)
• Delaying transplantation after dialysis does not reduce recurrence risk

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14. Recent Evidence (2024-2026)

1. Rituximab in IgAV nephritis (Xiong et al., 2024 - PMID 39249581): Evaluates the role of B-cell depletion for refractory nephritis - emerging option for severe/refractory IgAV nephritis.
2. Tacrolimus vs cyclophosphamide in HSP nephritis in children (Jiang et al., 2025 - PMID 40696685): Compares calcineurin inhibitor vs alkylating agent approaches in pediatric nephritis.
3. IgAV with necrotizing arteritis (Ribereau-Gayon et al., 2026 - PMID 42192510): A French multicenter study describing the severe subtype with medium-vessel necrotizing involvement - distinct clinical phenotype with worse prognosis.

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Quick Reference Summary

HSP / IgA Vasculitis
├── Mechanism: Gd-IgA1 → anti-glycan IgG → ICs → vessel wall deposition
├── Trigger: URI, H. pylori, drugs, malignancy (adults)
├── Tetrad: Purpura + Arthralgias + Abdominal pain + Nephritis
├── DIF skin biopsy: Florid IgA deposition (DIAGNOSTIC)
├── Labs: Normal platelets, normal complement, elevated IgA (50%)
├── Kidney: Identical to IgAN on biopsy (MEST score)
├── Treatment:
│   ├── Mild: Supportive
│   ├── GI pain: Prednisone 1 mg/kg
│   ├── Renal: ACEi/ARB ± steroids ± MMF/CYC
│   └── Refractory: IVIG, rituximab (emerging)
└── Prognosis: Excellent in children; worse in adults (40% CKD at 15y)

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Internal Disease 4 - Viva Answers

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Q1. Systemic Sclerosis, CREST - Signs and Symptoms

• Limited cutaneous SSc (lcSSc) - skin involvement limited to hands, face, forearms below elbow
• Diffuse cutaneous SSc (dcSSc) - skin involvement extends to trunk and proximal extremities; more rapid organ damage

• C - Calcinosis (calcium deposits in soft tissue)
• R - Raynaud's phenomenon (vasospasm of digits: white → blue → red)
• E - Esophageal dysmotility (dysphagia, GERD)
• S - Sclerodactyly (thickening/tightening of finger skin)
• T - Telangiectasia (dilated vessels on skin/mucosa)

• Raynaud's phenomenon is often the first manifestation
• Skin: pitting edema → induration → atrophy; "mask-like" facies, microstomia
• Musculoskeletal: arthralgia, myopathy, tendon friction rubs
• Pulmonary: ILD (leading cause of death in dcSSc), pulmonary hypertension (leading cause in lcSSc)
• Cardiac: pericarditis, myocardial fibrosis, arrhythmias
• Renal: scleroderma renal crisis - abrupt hypertension, oliguric AKI (more in dcSSc)
• GI: dysmotility throughout, malabsorption, telangiectasias causing bleeding

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Q2. Idiopathic Pulmonary Fibrosis - Diagnosis, Pathogenesis, Symptoms

• Repeated micro-injuries to alveolar epithelium in genetically susceptible individuals
• Abnormal wound healing → aberrant fibroblast/myofibroblast activation
• Excessive collagen deposition → architectural distortion → honeycombing
• TGF-beta is the key pro-fibrotic mediator
• NOT primarily an inflammatory disease (unlike other ILDs)

• Insidious onset in patients >60 years
• Progressive exertional dyspnea (main complaint)
• Dry, non-productive cough
• Bibasilar fine "velcro" crackles on auscultation
• Clubbing in ~50%
• Cyanosis and cor pulmonale in advanced disease
• No fever or constitutional symptoms

• HRCT chest: bilateral peripheral, basal predominant honeycombing ± traction bronchiectasis (UIP pattern) - often diagnostic without biopsy
• PFTs: restrictive pattern (↓TLC, ↓DLCO, ↓FVC), low DLCO is earliest abnormality
• BAL: not diagnostic but helps exclude other ILDs
• Surgical lung biopsy: only if HRCT inconclusive
• Must exclude known causes of ILD (drugs, CTD, hypersensitivity pneumonitis)

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Q3. Dilated Cardiomyopathy - Signs, Symptoms, Diagnosis

• Heart failure: progressive dyspnea on exertion, orthopnea, PND
• Fatigue, weakness, reduced exercise tolerance
• Peripheral edema, ascites (right heart failure)
• Palpitations (arrhythmias - AF, VT/VF)
• Systemic or pulmonary emboli
• Physical exam: cardiomegaly, displaced apex beat (lateral/inferior), S3 gallop, mitral regurgitation murmur (functional), elevated JVP, hepatomegaly, edema

• ECG: LBBB, non-specific ST-T changes, arrhythmias
• Chest X-ray: cardiomegaly (cardiothoracic ratio >0.5), pulmonary vascular congestion, Kerley B lines
• Echocardiography (key): dilated LV, global systolic dysfunction (EF <40%), functional MR, possibly LV thrombus
• BNP/NT-proBNP: elevated
• Cardiac MRI: best for tissue characterization, detects fibrosis (late gadolinium enhancement)
• Coronary angiography: to exclude ischemic cause
• Endomyocardial biopsy: rarely needed (if giant cell myocarditis or sarcoid suspected)

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Q4. Cardiac Tamponade - Signs, Symptoms, Causes

• Malignancy (most common in developed world - lung, breast, lymphoma)
• Pericarditis (viral, idiopathic)
• Post-cardiac surgery / post-MI (Dressler's syndrome)
• Aortic dissection
• Trauma (hemopericardium)
• Hypothyroidism, uremia, SLE, TB

1. Hypotension (reduced cardiac output)
2. Elevated JVP / distended neck veins
3. Muffled heart sounds

• Pulsus paradoxus >10 mmHg fall in SBP during inspiration - cardinal sign
• Tachycardia (compensatory)
• Kussmaul's sign is typically absent (seen in constrictive pericarditis)
• Cool, clammy extremities; reduced urine output

• ECG: tachycardia, low voltage QRS, electrical alternans (pathognomonic - alternating QRS axis)
• CXR: "water bottle" heart silhouette
• Echocardiography (gold standard): pericardial effusion + right atrial/RV diastolic collapse

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Q5. Etiology, Pathophysiology and Examination Findings of Dilated Cardiomyopathy

• Idiopathic (50% of cases)
• Genetic (~25%): mutations in titin (TTN - most common), lamin A/C (associated with arrhythmias and sudden death), dystrophin (X-linked - Duchenne)
• Infective: viral myocarditis (Coxsackievirus B, HIV, Chagas disease - T. cruzi)
• Toxic: Alcohol (most common reversible cause), cocaine, anthracyclines (doxorubicin - dose-dependent)
• Metabolic: Hypothyroidism, thiamine deficiency (wet beriberi), selenium deficiency
• Peripartum: last month of pregnancy to 5 months postpartum

• Cardiomyocyte injury → myocardial dysfunction → ventricular dilation
• Compensatory neuro-hormonal activation: SNS, RAAS, ADH
• Ventricular remodeling (dilation + spherical shape) → worsens MR, increases wall stress
• Progressive decline in EF → low output state
• Dilation → stasis → risk of intracardiac thrombus

• Pulse: tachycardia, low volume, pulsus alternans
• BP: narrow pulse pressure
• JVP: elevated with prominent v-waves (functional TR)
• Precordium: laterally displaced, diffuse apex; palpable S3; systolic thrill (if MR)
• Auscultation: S3 gallop (hallmark of systolic dysfunction), holosystolic murmur of MR ± TR
• Chest: bibasal fine crackles
• Abdomen: hepatomegaly, ascites
• Legs: bilateral pitting edema

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Q6. Obstructive Sleep Apnea - Symptoms, Diagnosis, Treatment

• Loud snoring (most common - reported by bed partner)
• Witnessed apneas during sleep
• Non-restorative sleep, excessive daytime sleepiness (EDS)
• Morning headache (hypercapnia)
• Nocturia, nocturnal choking/gasping
• Cognitive impairment, irritability, depression
• Complications: hypertension (resistant HTN), AF, type 2 diabetes, pulmonary hypertension

• Screening: Epworth Sleepiness Scale (ESS >10 = excessive daytime sleepiness); STOP-BANG questionnaire
• Polysomnography (PSG): gold standard - measures AHI (Apnea-Hypopnea Index)
  • Mild: AHI 5-14; Moderate: 15-29; Severe: ≥30 events/hour
• Home sleep apnea testing: acceptable alternative in uncomplicated cases

• Lifestyle: weight loss, positional therapy (avoid supine), avoid alcohol/sedatives
• CPAP therapy (Continuous Positive Airway Pressure): first-line for moderate-severe OSA - maintains airway patency via pneumatic splinting
• Mandibular advancement device: for mild-moderate OSA or CPAP intolerant
• Surgical: uvulopalatopharyngoplasty, hypoglossal nerve stimulator (for CPAP failures)

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Q7. Pulmonary Embolism - Common Risk Factors, Signs and Symptoms

• Stasis: Immobility, prolonged travel, heart failure, obesity
• Hypercoagulability: Malignancy, oral contraceptives/HRT, pregnancy, inherited thrombophilia (Factor V Leiden, prothrombin mutation, antiphospholipid syndrome)
• Endothelial injury: Surgery, trauma, central venous catheters

• Dyspnea (most common - sudden onset)
• Pleuritic chest pain (peripheral PE - infarction)
• Hemoptysis (lung infarction)
• Tachycardia (most common sign), tachypnea
• Cough, fever, sweating
• Syncope or presyncope (massive PE)
• Signs of DVT: unilateral leg swelling, redness, calf tenderness
• Massive PE: hypotension, cardiogenic shock, cyanosis, raised JVP, loud P2, right heart strain

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Q8. Systemic Scleroderma - Major/Minor Criteria, Additional Signs, Treatment

• Skin thickening of the fingers of both hands extending proximal to the MCPs (sufficient alone for diagnosis = 9 points)
• Scoring system includes: skin thickening, fingertip lesions, telangiectasia, abnormal nailfold capillaries, ILD/PAH, Raynaud's, SSc-related antibodies

• Major: Proximal scleroderma (proximal to MCPs)
• Minor (2 of 3): Sclerodactyly, digital pitting scars, bibasal pulmonary fibrosis

• Raynaud's: calcium channel blockers (nifedipine), PDE5 inhibitors, prostacyclin analogs (severe)
• ILD: Mycophenolate mofetil (first-line), nintedanib, cyclophosphamide
• PAH: PDE5 inhibitors (sildenafil), endothelin receptor antagonists (bosentan), prostacyclins
• Scleroderma renal crisis: ACE inhibitors (captopril) - MANDATORY; control BP aggressively
• Skin/systemic: Methotrexate, mycophenolate mofetil
• GI: Proton pump inhibitors for GERD, prokinetics for dysmotility

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Q9. Cirrhosis - Causes, Pathogenesis, Complications

• Alcohol (most common in Western countries)
• Non-alcoholic fatty liver disease (NAFLD/NASH) - increasingly common
• Chronic viral hepatitis (HBV, HCV)
• Autoimmune hepatitis
• Primary biliary cholangitis, primary sclerosing cholangitis
• Wilson's disease, hemochromatosis, alpha-1 antitrypsin deficiency

• Chronic hepatocyte injury → inflammation → activation of hepatic stellate cells
• Stellate cells transform into myofibroblasts → deposit collagen → fibrosis
• Loss of normal sinusoidal architecture → portal hypertension
• Progressive loss of hepatocyte mass → synthetic failure

• Portal hypertension → esophageal/gastric varices (risk of life-threatening bleeding), splenomegaly, hypersplenism
• Ascites (most common complication) → spontaneous bacterial peritonitis (SBP)
• Hepatic encephalopathy
• Hepatorenal syndrome (type 1 = rapidly progressive; type 2 = chronic)
• Coagulopathy (↓clotting factors, thrombocytopenia)
• Jaundice, hypoalbuminemia, hyponatremia
• Hepatocellular carcinoma (HCC) - annual surveillance with ultrasound + AFP

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Q10. Hepatitis A - Etiology, Clinical Picture, Diagnosis, Management

• Incubation: 15-50 days (average 28)
• Prodrome (1-2 weeks): fever, malaise, anorexia, nausea, vomiting, right upper quadrant pain, dark urine, pale stools
• Icteric phase: jaundice, pruritis, tender hepatomegaly, splenomegaly
• Most cases self-limited; recovery in 4-8 weeks
• Fulminant hepatic failure: rare (<1%) but more common in elderly/pre-existing liver disease
• Cholestatic variant: prolonged jaundice, pruritis

• LFTs: markedly elevated ALT, AST (>10x ULN); elevated bilirubin (conjugated + unconjugated)
• Serology: Anti-HAV IgM = acute infection (positive for 3-6 months); Anti-HAV IgG = past infection/immunity
• PT/INR: prolonged in severe cases

• Supportive: rest, adequate nutrition, hydration; avoid alcohol and hepatotoxic drugs
• No specific antiviral therapy
• Hospitalize if: unable to maintain hydration, coagulopathy, encephalopathy
• Prevention: HAV vaccine (2-dose series); post-exposure immunoglobulin within 2 weeks

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Q11. Pathophysiology of Pericardial Effusion, Diagnostic Evaluation, Management

• Pericardial space normally contains 15-50 mL of fluid
• Excess fluid accumulation from: increased production (inflammation) or decreased resorption
• Rate of accumulation determines hemodynamic impact - slow accumulation allows pericardium to stretch (may accommodate 2L); rapid accumulation (200-300 mL) can cause tamponade
• Elevated intrapericardial pressure → impairs diastolic filling (first RV, then LV) → reduced stroke volume → compensatory tachycardia → if untreated, shock

• ECG: Low voltage, electrical alternans (tamponade), diffuse ST elevation (pericarditis)
• CXR: Enlarged cardiac silhouette ("water bottle" heart) if >250 mL
• Echocardiography (gold standard): Quantifies effusion; detects chamber collapse (tamponade); differentiates from constrictive pericarditis
• CT/MRI: Best for loculated effusions, malignancy staging, pericardial thickening
• Pericardiocentesis fluid analysis: LDH, protein (Light's criteria - differentiate exudate vs transudate), cytology, culture, AFB

• Treat underlying cause
• Hemodynamically stable: NSAIDs, colchicine (if pericarditis)
• Tamponade = medical emergency: immediate pericardiocentesis (echo-guided or subxiphoid approach)
• Recurrent effusions: pericardial window (surgical drainage)
• Malignant effusion: drainage + sclerotherapy

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Q12. Pulmonary Embolism - Causes, Symptoms, First Aid

• Sudden onset dyspnea, tachypnea
• Pleuritic chest pain (sharp, worse with breathing)
• Hemoptysis
• Cough, low-grade fever
• Syncope (massive PE)
• Symptoms of DVT (leg swelling, pain)

1. Call emergency services; place patient in sitting position (relieves dyspnea)
2. High-flow oxygen immediately (target SpO2 >94%)
3. IV access; IV fluid bolus (cautiously - 500 mL; excessive fluids worsen RV dilation)
4. Monitor: ECG, continuous pulse oximetry, BP
5. If massive PE with cardiac arrest: CPR + consider thrombolysis
6. Do NOT delay anticoagulation (LMWH or UFH) while awaiting imaging if clinical suspicion high
7. Emergency echocardiography/CT-PA as available

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Q13. Pulmonary Embolism - Causes, Signs/Symptoms, Diagnosis, Treatment

• Clinical probability: Wells score (DVT signs, HR>100, immobilization, prior DVT/PE, hemoptysis, malignancy, alternative diagnosis less likely)
• D-dimer: Sensitive but not specific; negative D-dimer in low probability excludes PE
• CT Pulmonary Angiography (CTPA): Gold standard - visualizes thrombus directly
• ECG: sinus tachycardia (most common); S1Q3T3 pattern (right heart strain); RBBB; AF
• ABG: hypoxemia, hypocapnia (respiratory alkalosis), widened A-a gradient
• Echo: RV dilation/dysfunction, McConnell's sign, TR, elevated PA pressures
• V/Q scan: alternative when CTPA contraindicated (renal failure, contrast allergy)
• Troponin, BNP: elevated in massive/sub-massive PE (RV injury markers)

• Anticoagulation (mainstay):
  • DOACs (rivaroxaban, apixaban) - first-line for most
  • LMWH + vitamin K antagonist (warfarin) - traditional
  • UFH: for massive PE or if thrombolysis planned
  • Duration: 3 months (provoked/transient risk), 6 months or indefinite (unprovoked, malignancy)
• Thrombolysis (systemic): For massive PE with hemodynamic instability (alteplase 100 mg IV)
• Catheter-directed therapy / Surgical embolectomy: For massive PE if thrombolysis fails or contraindicated
• IVC filter: only when anticoagulation absolutely contraindicated

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Q14. Atrial Fibrillation - Physical Examination, ECG, Management

• Irregularly irregular pulse (pathognomonic)
• Pulse deficit (apical rate > radial rate)
• Variable intensity S1
• Absent a-wave in JVP
• Signs of underlying cause (mitral stenosis murmur, thyrotoxicosis)
• Signs of heart failure if decompensated (elevated JVP, crackles, edema)

• Absent P waves (replaced by irregular fibrillatory "f" waves at 350-600/min)
• Irregularly irregular R-R intervals (hallmark)
• Narrow QRS complexes (unless aberrant conduction or pre-excitation)
• Rate: usually 100-160 bpm if uncontrolled

• Rate control (most patients): Beta-blockers (metoprolol), calcium channel blockers (diltiazem/verapamil), digoxin (in heart failure with reduced EF); target HR <80-110 bpm at rest
• Rhythm control: DC cardioversion (if hemodynamically unstable: immediate); antiarrhythmics: flecainide, propafenone (no structural disease), amiodarone (structural heart disease); catheter ablation for symptomatic patients
• Anticoagulation (stroke prevention):
  • CHA₂DS₂-VASc score ≥2 (male) / ≥3 (female): anticoagulate
  • DOACs preferred over warfarin (except mechanical valves/mitral stenosis)
  • Assess bleeding risk with HAS-BLED score
• Treat underlying cause (hyperthyroidism, sepsis, heart failure)

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Q15. Hepatitis - Types, Etiology, Signs/Symptoms, Complications

• Acute: Fulminant hepatic failure (highest with HBV + HDV, HEV in pregnancy)
• Chronic (B, C, D): Chronic hepatitis → cirrhosis → HCC
• Extrahepatic: HCV - cryoglobulinemia, membranoproliferative GN, vasculitis; HBV - polyarteritis nodosa, membranous nephropathy

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Q16. Virchow's Triad in PE, Diagnostic Methods, Examination Findings

1. Stasis of blood flow: Immobility, heart failure, long-haul travel, varicose veins
2. Hypercoagulability: Malignancy, pregnancy, OCP/HRT, thrombophilias (Factor V Leiden, antiphospholipid syndrome, protein C/S deficiency)
3. Endothelial injury: Surgery, trauma, central venous catheters, chemical injury

• Tachycardia (most common), tachypnea
• Hypoxemia, cyanosis (massive)
• Hypotension (massive PE - SBP <90 mmHg)
• Raised JVP, parasternal heave (acute cor pulmonale)
• Loud P2, tricuspid regurgitation murmur
• Leg: swelling, erythema, tenderness (DVT)
• Homan's sign (calf pain on dorsiflexion) - unreliable

• D-dimer (rule out), CTPA (gold standard), V/Q scan, echo, Doppler USS legs, ECG, ABG (see Q13)

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Q17. Myocardiodystrophy - Definition, Etiology, Pathogenesis

• Endocrine: Hypothyroidism, hyperthyroidism, diabetes mellitus, Cushing's disease, acromegaly, pheochromocytoma
• Nutritional/metabolic: Thiamine deficiency (beriberi), selenium deficiency (Keshan disease), obesity
• Toxic: Alcohol, cocaine, catecholamines
• Systemic diseases: Anemia, uremia, sepsis
• Dyselectrolytemia: Hypokalemia, hypocalcemia

• Metabolic derangement impairs myocardial energy production (oxidative phosphorylation, ATP synthesis)
• Ion pump dysfunction → calcium overload → impaired contractility
• Mitochondrial dysfunction → free radical damage to cardiomyocytes
• Lipid/glycogen accumulation → cytotoxicity
• Result: ventricular dysfunction (systolic ± diastolic) - potentially reversible if underlying cause treated

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Q18. Hemorrhagic Vasculitis (HSP/IgA Vasculitis) - Systemic Manifestations, Physical Findings, Criteria

• Skin: Palpable purpura (lower limbs, buttocks); non-blanchable; new crops over weeks
• Joints: Arthralgias/periarticular swelling (knees, ankles) - 63-82%
• GI: Colicky abdominal pain, nausea, vomiting, GI bleeding, intussusception - 65-70%
• Kidneys: Hematuria, proteinuria, GN - 10-50% (up to 70% in adults)
• Other: Scrotal edema (boys), CNS involvement (rare), pulmonary hemorrhage (rare)

• Non-thrombocytopenic palpable purpura (hallmark)
• Periarticular swelling (ankles, knees)
• Abdominal tenderness
• Normal platelet count, normal complement levels

• Mandatory: Palpable purpura (without thrombocytopenia)
• Plus at least 1 of:
  1. Diffuse abdominal pain
  2. Biopsy showing IgA deposition
  3. Arthritis or arthralgia
  4. Renal involvement (hematuria and/or proteinuria)

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Q19. Pulmonary Hypertension - Causes, Classification, Signs/Symptoms, Treatment

1. PAH: Idiopathic, heritable (BMPR2 mutation), drug/toxin-induced, associated (CTD, HIV, portal hypertension, congenital heart disease)
2. PH due to left heart disease: Heart failure (most common cause overall), valvular disease
3. PH due to lung disease/hypoxia: COPD, ILD, OSA
4. CTEPH: Chronic thromboembolic PH (persistent clot obstruction)
5. Miscellaneous: Sarcoidosis, histiocytosis, compression of pulmonary vessels

• Dyspnea on exertion (earliest symptom)
• Fatigue, syncope on exertion (low cardiac output)
• Chest pain, palpitations
• Hemoptysis
• Signs of right heart failure: elevated JVP, peripheral edema, hepatomegaly, ascites
• Loud P2, right-sided S3/S4, TR murmur, parasternal heave

• Treat underlying cause
• Group 1 (PAH) specific therapy:
  • Endothelin receptor antagonists: Bosentan, ambrisentan
  • PDE5 inhibitors: Sildenafil, tadalafil
  • Prostacyclin analogs: Epoprostenol, treprostinil (severe cases)
  • Riociguat: Soluble guanylate cyclase stimulator (also for CTEPH)
• Group 4 (CTEPH): Riociguat; surgical pulmonary endarterectomy (potentially curative)
• Supportive: diuretics, O2, anticoagulation (PAH, CTEPH)
• Lung transplantation for refractory cases

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Q20. AV Block 1st Degree - Causes, Signs, ECG

• Enhanced vagal tone (athletes, during sleep)
• Inferior MI (RCA supplies AV node)
• Drugs: digoxin, beta-blockers, calcium channel blockers, amiodarone
• Myocarditis, rheumatic fever, Lyme disease
• Electrolyte disturbances (hyperkalemia)
• Aging (fibrosis of conduction system)

• PR interval >0.20 seconds (>200 ms) or >5 small squares
• All P waves followed by QRS complexes (1:1 conduction)
• PR interval is constant (does not vary)
• Normal QRS morphology (unless coexisting bundle branch block)

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Q21. Pulmonary Hypertension - WHO Classification, Signs and Symptoms

• Auscultation: loud/accentuated P2 (pulmonary component of S2), ejection click, right-sided S4 (RV hypertrophy), TR murmur (pansystolic at LLSB, increases with inspiration), PR murmur (Graham Steell murmur)
• Inspection: raised JVP with prominent a-wave (RV hypertrophy) or prominent v-wave (TR), central cyanosis, peripheral edema
• Palpation: parasternal heave (RV hypertrophy), palpable P2, hepatomegaly, pulsatile liver (TR)

• Exertional dyspnea (hallmark, >95% of patients)
• Fatigue, exercise intolerance
• Syncope on exertion (fixed low cardiac output)
• Chest pain (RV ischemia)
• Palpitations
• Peripheral edema, abdominal distension (right heart failure)
• Raynaud's phenomenon (associated PAH)

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Q22. Cardiogenic Shock - Signs, Symptoms, Physical Findings, Management

• Severe dyspnea, extreme fatigue
• Confusion, agitation, altered consciousness (cerebral hypoperfusion)
• Oliguria/anuria
• Chest pain (if ACS is cause)

• Hypotension: SBP <90 mmHg for >30 min (or need for vasopressors)
• Tachycardia (compensatory) or bradycardia (if AV block/inferior MI)
• Cold, clammy, pale, mottled extremities (vasoconstriction)
• Elevated JVP (raised filling pressures)
• Bilateral crackles (pulmonary edema)
• S3/S4 gallop
• Murmurs (MR from papillary muscle rupture, VSD)
• Narrow pulse pressure (<25 mmHg)

1. Identify and treat underlying cause (ACS → urgent PCI; mechanical cause → surgery)
2. Oxygen + intubation if respiratory failure
3. Vasopressors: Norepinephrine (first-line); dopamine (alternative)
4. Inotropes: Dobutamine (for severe LV failure with low CO)
5. IV fluids: cautious small bolus (500 mL) only if dry (no pulmonary edema)
6. Mechanical circulatory support: Intra-aortic balloon pump (IABP), Impella, ECMO for refractory shock
7. Treat arrhythmias, correct electrolytes
8. Revascularization: immediate PCI/CABG for ACS-related cardiogenic shock

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Q23. Chronic Hepatosis - Pathogenesis, Clinical Picture, Treatment

• "Two-hit" hypothesis:
  1. First hit: lipid accumulation in hepatocytes (steatosis) from insulin resistance → impaired beta-oxidation, increased lipogenesis
  2. Second hit: oxidative stress, mitochondrial dysfunction, cytokine imbalance (TNF-alpha, IL-6) → hepatocyte injury and inflammation (NASH)
• Progressive: steatosis → NASH → fibrosis → cirrhosis

• Often asymptomatic (found incidentally)
• Fatigue, vague RUQ discomfort
• Hepatomegaly (smooth, non-tender)
• Acanthosis nigricans (insulin resistance)
• Features of metabolic syndrome: obesity, hypertension, dyslipidemia, DM2
• Advanced: signs of chronic liver disease

• Weight loss (>7-10% body weight) - most effective intervention
• Treat metabolic syndrome components: statins, metformin/SGLT2i, antihypertensives
• Vitamin E (non-diabetic, non-cirrhotic NASH)
• Resmetirom (THR-beta agonist) - recently approved for NASH with liver fibrosis
• Avoid alcohol, hepatotoxic drugs
• Screen for HCC if cirrhosis develops

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Q24. Pericarditis - Causes, Signs/Symptoms, Diagnosis, Treatment

• Idiopathic/viral (most common ~80%): Coxsackievirus A/B, Echo, EBV, CMV
• Bacterial: TB (important), Staph, Strep
• Post-MI: early (1-3 days, fibrinous) or late Dressler's syndrome (weeks-months)
• Post-cardiac surgery / post-ablation
• Systemic: SLE, rheumatoid arthritis, scleroderma, sarcoidosis
• Uremic pericarditis
• Malignancy, radiation

• Sharp, pleuritic chest pain - worse lying flat, better leaning forward (pathognomonic position)
• Low-grade fever, malaise
• Dyspnea
• Pericardial friction rub (3-component: atrial systole, ventricular systole, ventricular diastole) - best heard at LLSB, leaning forward; pathognomonic

• ECG: Diffuse saddle-shaped ST elevation in multiple leads; PR depression; evolves through 4 stages
• Echo: pericardial effusion (not always present)
• CRP/ESR: elevated
• Troponin: elevated if myopericarditis
• CBC: leukocytosis

• First-line: Aspirin (750-1000 mg TID) OR ibuprofen (600 mg TID) for 1-2 weeks
• Colchicine (0.5 mg BD): added to NSAID; halves recurrence rate
• Restrict physical activity until symptom-free and CRP normalized
• Corticosteroids: only if NSAIDs contraindicated or autoimmune cause
• Uremic pericarditis: intensify dialysis
• TB pericarditis: anti-TB therapy + corticosteroids (prevent constriction)

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Q25. Atrial Fibrillation - Clinical Presentations, ECG Findings

• Paroxysmal AF: Episodes <7 days, self-terminating
• Persistent AF: >7 days, requires cardioversion
• Long-standing persistent: >1 year
• Permanent AF: Accepted, no rhythm control attempted
• Asymptomatic (silent AF): Diagnosed incidentally or after embolic stroke
• Symptomatic: Palpitations, dyspnea, fatigue, lightheadedness, chest discomfort
• Hemodynamic compromise: Hypotension, acute heart failure (rapid AF + poor LV function)
• Thromboembolic: Stroke/TIA (most feared complication; 5x higher risk)

• No discernible P waves (replaced by irregular fibrillatory "f" waves)
• Irregularly irregular R-R intervals
• Narrow QRS (unless aberrant conduction or WPW)
• Ventricular rate 100-160 bpm (uncontrolled)

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Q26. Acute Pericarditis - Signs, Symptoms, Physical Findings

• Sharp, retrosternal chest pain - pleuritic in nature; radiation to trapezius ridge (pathognomonic)
• Pain worst supine; relieved sitting forward
• Low-grade fever, malaise, myalgias
• Dyspnea from pain or effusion

• Pericardial friction rub: Scratchy, high-pitched, 3-component sound; evanescent (may disappear and reappear); best heard at LLSB in held expiration leaning forward
• Tachycardia
• If effusion: muffled heart sounds, dullness to percussion at left base (Ewart's sign)
• If tamponade: Beck's triad + pulsus paradoxus

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Q27. Pericarditis - Definition, Classification, Signs, Treatment

• By time course: Acute (<4-6 weeks), Incessant (>4-6 weeks but <3 months), Recurrent (relapse after ≥4-week symptom-free interval), Chronic (>3 months)
• By etiology: Infectious, Non-infectious (autoimmune, metabolic, neoplastic, traumatic)
• By pathology: Fibrinous (dry), Effusive, Constrictive, Effusive-constrictive

• Acute: NSAIDs + colchicine
• Recurrent: NSAIDs + colchicine ± low-dose corticosteroids; anakinra (IL-1 blocker) for steroid-dependent recurrent cases
• Constrictive pericarditis: pericardiectomy (surgical stripping)

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Q28. AV Block 2nd Degree - Mobitz I and II - Causes, Symptoms, ECG

• ECG: Progressive PR interval lengthening until a P wave fails to conduct (dropped QRS); then cycle repeats
• Narrow QRS usually
• Block at level of AV node
• Causes: inferior MI (usually transient), increased vagal tone, drugs (digoxin, beta-blockers), myocarditis
• Usually benign; rarely needs treatment

• ECG: Constant PR interval with sudden, unexpected non-conducted P wave (dropped QRS); often wide QRS (infranodal block)
• Block at level of bundle of His or below
• Causes: anterior MI, Lev's disease (fibrocalcific degeneration), Lenegre's disease, sarcoidosis, myocarditis
• Clinically serious - high risk of progression to complete (3rd degree) heart block

• Mobitz I: usually asymptomatic
• Mobitz II: dizziness, presyncope, syncope, fatigue (reduced CO)

• Mobitz I: treat underlying cause; pacing if symptomatic
• Mobitz II: permanent pacemaker indicated (high risk of complete heart block regardless of symptoms)

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Q29. Hepatosis - Causes, Signs, Clinical Picture, Treatment

• Hepatomegaly (soft, non-tender)
• Signs of metabolic syndrome (obesity, acanthosis nigricans)
• No signs of acute liver failure unless advanced
• Splenomegaly if portal hypertension develops

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Q30. Pulmonary Embolism - Surgical and Pharmacological Management

• Anticoagulation (all non-massive PE):
  • DOACs: Rivaroxaban (15 mg BD x3 wks → 20 mg OD) or Apixaban (10 mg BD x7 days → 5 mg BD) - preferred for most
  • LMWH + warfarin: traditional; INR target 2-3
  • UFH: used for massive PE (easily reversible; dose-adjusted)
  • Duration: 3 months (provoked), extended/indefinite (unprovoked, active malignancy)
• Thrombolysis (massive PE): Alteplase 100 mg IV over 2 hours (tissue plasminogen activator); contraindicated in: recent surgery/stroke, active bleeding
• Catheter-directed thrombolysis: Lower dose thrombolytic directly into clot (lower bleeding risk)

• Surgical pulmonary embolectomy: For massive PE with contraindication to thrombolysis, failed thrombolysis; cardiopulmonary bypass required; high mortality
• ECMO: Bridge to definitive therapy or recovery in massive PE with cardiac arrest
• IVC filter: Absolute contraindication to anticoagulation, or recurrent PE despite adequate anticoagulation; retrievable filters preferred
• Pulmonary endarterectomy: Surgical treatment for CTEPH (chronic thromboembolic PH)

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Q31. Scleroderma - Pathophysiology, Types, Signs and Symptoms

1. Vascular injury: Endothelial cell injury → vasospasm (Raynaud's) → intimal proliferation → obliterative vasculopathy → tissue ischemia
2. Immune dysregulation: T-cell activation → TGF-beta, PDGF, connective tissue growth factor release → fibroblast/myofibroblast activation
3. Fibrosis: Excessive collagen (type I and III) deposition in skin, lungs, kidneys, heart, GI tract → organ dysfunction

• Limited cutaneous SSc (lcSSc): Skin thickening distal to elbows/knees; CREST features; anti-centromere antibody; PAH is major complication
• Diffuse cutaneous SSc (dcSSc): Widespread skin involvement including trunk; anti-Scl-70 antibody; ILD, renal crisis are major complications
• SSc sine scleroderma: Internal organ involvement without skin changes

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Q32. Portal Hypertension - Etiology, Pathogenesis, Clinical Picture, Complications, Management

• Pre-hepatic: Portal vein thrombosis, splenic vein thrombosis
• Intrahepatic: Cirrhosis (most common - any cause), schistosomiasis, hepatic fibrosis, nodular regenerative hyperplasia, sarcoidosis
• Post-hepatic: Budd-Chiari syndrome (hepatic vein thrombosis), right heart failure, constrictive pericarditis

• Cirrhosis → distorted hepatic architecture → increased resistance to portal flow
• Simultaneously: splanchnic vasodilation (NO-mediated) → increased portal blood flow
• Combined → sustained portal hypertension → portosystemic collaterals

• Splenomegaly (hypersplenism → thrombocytopenia, leukopenia, anemia)
• Ascites (most common)
• Portosystemic collaterals: esophageal varices (dilated veins at gastroesophageal junction), gastric varices, caput medusae (periumbilical), hemorrhoids, anorectal varices
• Caput medusae: veins radiating from umbilicus
• Fetor hepaticus, jaundice (hepatic decompensation)

• Variceal hemorrhage (most life-threatening; 30% mortality per episode)
• Ascites → SBP (spontaneous bacterial peritonitis)
• Hepatic encephalopathy
• Hepatorenal syndrome
• Hypersplenism

• Primary prevention of variceal bleed: Non-selective beta-blockers (propranolol, carvedilol); endoscopic band ligation
• Acute variceal bleed: IV octreotide/terlipressin (vasoconstrictor); endoscopic band ligation; IV antibiotics (prophylactic); TIPS (transjugular intrahepatic portosystemic shunt) for refractory
• Ascites: Dietary sodium restriction, spironolactone ± furosemide; therapeutic paracentesis + albumin (large volume); TIPS
• SBP: IV cefotaxime; primary prophylaxis with norfloxacin in high-risk patients
• Liver transplantation: Definitive treatment

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Q33. Chronic Hepatitis D - Diagnostic Criteria, Management

• HBsAg positive (prerequisite for HDV infection)
• Anti-HDV IgG: indicates past or current exposure
• HDV RNA (PCR): gold standard for active replication; confirms chronic infection
• HDV antigen (HDAg): detectable early in acute infection
• Liver biopsy: shows inflammatory activity, fibrosis staging
• LFTs: elevated ALT/AST, bilirubin

• More aggressive course than HBV alone
• Faster progression to cirrhosis (up to 70% within 10 years)
• High risk of HCC
• Patients may have flares mimicking acute hepatitis

• Pegylated interferon-alpha (Peg-IFN-alpha): only proven treatment; 48-72 weeks; achieves HDV RNA suppression in 25-40%; many relapse after stopping
• Bulevirtide (Hepcludex): approved in Europe (2020) - entry inhibitor blocking HBV/HDV attachment to hepatocytes; used with/without PEG-IFN
• Nucleos(t)ide analogs (tenofovir, entecavir) for HBV: suppress HBV DNA but have minimal effect on HDV alone; used if concurrent HBV replication
• Liver transplantation: for decompensated cirrhosis or HCC

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Q34. Systemic Sclerosis, CREST - Diagnosis, Management

• 2013 ACR/EULAR criteria (score-based system; ≥9 points = definite SSc):
  • Skin thickening proximal to MCPs: 9 pts (sufficient alone)
  • Skin thickening fingers: 4 pts
  • Fingertip lesions (pitting scars, ulcers): 2-3 pts
  • Telangiectasia: 2 pts
  • Abnormal nailfold capillaries: 2 pts
  • PAH/ILD: 2 pts each
  • Raynaud's: 3 pts
  • SSc-related antibodies (anti-centromere, anti-Scl-70, anti-RNA polymerase III): 3 pts
• Investigations: ANA (>95% positive), anti-centromere (lcSSc), anti-Scl-70 (dcSSc, ILD), anti-RNA pol III (dcSSc, renal crisis); nailfold capillaroscopy (dilated/absent capillaries); HRCT chest; echo; PFTs; renal function; esophageal manometry

• No disease-modifying drug treats all manifestations simultaneously
• Organ-specific therapy: Raynaud's, ILD, PAH, GI, renal crisis (ACEi for renal crisis = life-saving)
• Immunosuppression (MMF, methotrexate) for skin disease and ILD

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Q35. Etiology, Pathogenesis and Clinical Picture of Pulmonary Embolism

• Deep vein thrombosis (proximal leg) is source in >90%
• Less common: fat embolism (long bone fractures), amniotic fluid embolism, air embolism, tumor embolism, septic embolism

• Thrombus dislodges from deep vein → travels through right heart → lodges in pulmonary artery
• Mechanical obstruction: increased pulmonary vascular resistance → RV pressure overload → RV dilation → interventricular septal shift (D-shape on echo) → LV underfilling → reduced cardiac output
• V/Q mismatch: ventilated but non-perfused alveoli → hypoxemia; hyperventilation → hypocapnia (respiratory alkalosis)
• Humoral/reflex: serotonin, thromboxane A2 release → vasoconstriction and bronchospasm
• Infarction: occurs in peripheral PE (red wedge-shaped infarct)
• Massive PE: circulatory collapse from acute RV failure

• Massive (5%): hemodynamic collapse, shock, cardiac arrest
• Sub-massive (20-25%): RV dysfunction on echo/biomarkers but hemodynamically stable
• Low-risk (>70%): normal hemodynamics, no RV dysfunction

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Q36. Sudden Cardiac Arrest - Causes, Clinical Picture, Treatment

• Most common: Ventricular fibrillation (VF) / pulseless VT - usually in ischemic heart disease (85%)
• Structural: DCM, HCM, ARVC, myocarditis, valvular disease
• Electrical: Long QT syndrome (Torsades de Pointes), Brugada syndrome, pre-excitation (WPW + AF)
• Channelopathies: Short QT syndrome, catecholaminergic polymorphic VT
• Non-cardiac: PE, tension pneumothorax, cardiac tamponade, severe electrolyte abnormalities, drowning, asphyxia

• Sudden loss of consciousness, unresponsiveness
• No normal breathing (agonal breaths may occur initially)
• No palpable pulse
• Cyanosis
• Dilated pupils (after 3-5 min)

1. Immediate CPR: 30:2 compressions:ventilations; rate 100-120/min; depth 5-6 cm; minimize interruptions
2. Defibrillation: As soon as AED/defibrillator available for shockable rhythms (VF/pulseless VT) - 200 J biphasic
3. Advanced airway: Endotracheal intubation or supraglottic airway
4. IV/IO access: Epinephrine (adrenaline) 1 mg IV every 3-5 min for non-shockable rhythms; also given after 3rd shock in shockable rhythm
5. Amiodarone 300 mg IV (or lidocaine) for refractory VF/pVT
6. Reversible causes (4 H's and 4 T's): Hypoxia, Hypovolemia, Hypo/hyperkalemia, Hypothermia; Tension pneumothorax, Tamponade, Toxins, Thromboembolism
7. Post-resuscitation care: Targeted temperature management, coronary angiography (if suspected ACS), treat cause

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Q37. CPAP Therapy for Obstructive Sleep Apnea

• Moderate-severe OSA (AHI ≥15 events/hour)
• Mild OSA (AHI 5-14) with symptoms (EDS, impaired quality of life) or comorbidities (hypertension, cardiac disease)

• Eliminates apneas and hypopneas
• Improves sleep quality and reduces daytime sleepiness (reduces ESS)
• Reduces nocturnal hypoxemia and desaturation events
• Lowers blood pressure (especially in resistant hypertension)
• Reduces AF recurrence and cardiovascular events
• Improves cognitive function, mood

• Poor adherence (30-50% non-compliance) - threshold for benefit: >4 hours/night
• Side effects: mask discomfort/leaks, nasal congestion, skin pressure sores, claustrophobia
• Alternatives for intolerant patients: BiPAP, oral mandibular advancement device, positional therapy, weight loss

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Q38. Restrictive Cardiomyopathy - Clinical Picture, Diagnosis, Treatment

• Infiltrative: Amyloidosis (most common in adults), sarcoidosis, Gaucher's disease
• Storage diseases: Hemochromatosis, Fabry disease, glycogen storage diseases
• Endomyocardial: Hypereosinophilic syndrome (Loeffler endocarditis), endomyocardial fibrosis (tropical)
• Idiopathic

• Dominant right heart failure symptoms: peripheral edema, ascites, hepatomegaly, raised JVP
• Dyspnea on exertion (impaired LV filling → elevated LA pressure → pulmonary congestion)
• Exercise intolerance, fatigue
• Palpitations (AF common)
• Syncope (reduced cardiac output)

• Kussmaul's sign (JVP rises with inspiration - impaired RV filling) - seen in RCM and constrictive pericarditis
• S3 or S4
• Signs of right heart failure
• Peripheral neuropathy, proteinuria (amyloidosis)

• ECG: low voltage (amyloidosis), pseudo-infarction pattern, arrhythmias
• Echo: increased wall thickness, normal/small LV cavity, biatrial enlargement, diastolic dysfunction (restrictive filling: E/A >2, short deceleration time), "sparkling" myocardium (amyloid), preserved EF
• Cardiac MRI: late gadolinium enhancement patterns specific to etiology (diffuse subendocardial in amyloid, patchy in sarcoid)
• Cardiac biopsy: may confirm infiltrative disease
• Serum/urine protein electrophoresis, free light chains (amyloid); serum ferritin, transferrin saturation (hemochromatosis)

• Treat underlying cause: amyloidosis - tafamidis (TTR amyloid), chemotherapy (AL amyloid); hemochromatosis - phlebotomy; sarcoidosis - steroids
• Diuretics: Cautious use (reduce congestion but can cause hypotension due to preload dependence)
• Heart rate control: avoid tachycardia (preserves diastolic filling time)
• Anticoagulation for AF
• ICD if high arrhythmic risk (sarcoidosis, hemochromatosis)
• Cardiac transplantation: last resort; contraindicated if systemic amyloidosis

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Q39. Pneumonia - Etiology, Pathogenesis, Clinical Picture, Diagnosis, Treatment

• CAP (Community-Acquired): Streptococcus pneumoniae (most common overall), Mycoplasma pneumoniae (atypical), Haemophilus influenzae, Legionella pneumophila, viruses (influenza, SARS-CoV-2)
• HAP (Hospital-Acquired, >48h): MRSA, Pseudomonas aeruginosa, Klebsiella, gram-negative organisms
• Aspiration: Anaerobes, mixed flora
• Immunocompromised: Pneumocystis jirovecii (PCP), Aspergillus, CMV, Nocardia

• Fever, rigors, sweats
• Productive cough (rusty/purulent sputum), pleuritic chest pain
• Dyspnea, tachypnea
• Tachycardia
• Examination: dullness to percussion, increased tactile fremitus, bronchial breathing, crackles, pleural rub over consolidated area

• CXR: consolidation (lobar - typical; diffuse/bilateral - atypical/viral)
• CBC: leukocytosis (bacterial), normal/lymphopenia (viral/atypical)
• Sputum Gram stain and culture
• Blood cultures (moderate-severe)
• Urine antigen: Legionella and Pneumococcal antigen
• CT chest: if CXR inconclusive, complications suspected
• Severity: CURB-65 score (Confusion, Urea >7, RR ≥30, BP <90/60, Age ≥65 - each 1 point; 0-1 = home; 2 = hospital; 3+ = consider ICU)

• Mild CAP (outpatient): Amoxicillin + macrolide OR doxycycline
• Moderate-severe CAP (inpatient): Beta-lactam (amoxicillin-clavulanate/ceftriaxone) + macrolide OR respiratory fluoroquinolone (levofloxacin)
• HAP/VAP: Broad-spectrum (piperacillin-tazobactam, carbapenems) ± vancomycin/linezolid for MRSA
• Supportive: O2 therapy, fluids, antipyretics
• Duration: typically 5-7 days for CAP; 7-8 days for HAP

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Q40. Etiology and Clinical Picture of Acute Cardiac Arrest

• Cardiac (80%): Acute MI/ACS (most common - triggered by VF), pre-existing structural disease (DCM, HCM), severe valvular disease (AS), myocarditis, arrhythmia syndromes (Brugada, Long QT), WPW
• Non-cardiac (20%): Massive PE, tension pneumothorax, cardiac tamponade, severe hemorrhage, respiratory failure/airway obstruction, drowning, anaphylaxis, severe hyperkalemia, drug overdose (digoxin toxicity, cocaine)

• Sudden-onset unresponsiveness
• No breathing or only agonal gasping
• No palpable carotid/femoral pulse
• Cyanosis, pallor
• Dilated pupils (cerebral hypoperfusion after 3-5 min)
• Seizure-like activity may occur briefly (cerebral anoxia)
• If unwitnessed: found pulseless, unresponsive

• Shockable: VF (chaotic), pulseless VT
• Non-shockable: Pulseless electrical activity (PEA) - organized electrical activity but no pulse; Asystole (flat line)

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Q41. Clinical Manifestations and Epworth Score in OSA

• Nocturnal: Loud habitual snoring, witnessed apneas, choking/gasping, nocturia, nocturnal diaphoresis, restless sleep, frequent awakenings
• Daytime: Excessive daytime sleepiness (cardinal), non-restorative sleep, morning headache, dry mouth, cognitive impairment (poor concentration, memory), irritability, depression/anxiety, decreased libido
• Cardiovascular consequences: Systemic hypertension (in 50% of OSA), AF, resistant hypertension, stroke, pulmonary hypertension

• Self-reported questionnaire: rates likelihood of dozing in 8 situations (sitting reading, watching TV, in a car, lying down, sitting talking, after lunch, in traffic, in a meeting)
• Each rated 0-3; total score 0-24
• Normal: 0-10; Mild EDS: 11-12; Moderate: 13-15; Severe: 16-24
• ESS >10 is considered clinically significant excessive daytime sleepiness
• Used for screening, assessing treatment response to CPAP

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Q42. Arrhythmia - Mechanism, All Types, Classification

1. Abnormal impulse formation:
   • Enhanced automaticity (increased phase 4 depolarization) - sinus tachycardia, ectopic tachycardia
   • Triggered activity (early or delayed afterdepolarizations) - Torsades de Pointes, digitalis toxicity
2. Abnormal impulse conduction:
   • Re-entry (most common mechanism): requires two pathways with different refractory periods (AF, AVNRT, AVRT, VT in scar tissue)
   • Conduction block: AV blocks, bundle branch blocks

• Bradyarrhythmias (<60 bpm)
• Tachyarrhythmias (>100 bpm)

• Supraventricular (SVT):
  • Sinus tachycardia/bradycardia
  • AF, atrial flutter
  • AVNRT (most common true SVT)
  • AVRT (accessory pathway, WPW)
  • Atrial tachycardia
  • Junctional tachycardia
• Ventricular:
  • Premature ventricular contractions (PVCs)
  • Ventricular tachycardia (VT) - monomorphic/polymorphic
  • Torsades de Pointes (long QT)
  • Ventricular fibrillation (VF)
  • Accelerated idioventricular rhythm (AIVR)
• Conduction disorders:
  • SA node: sick sinus syndrome
  • AV node: 1st, 2nd (Mobitz I/II), 3rd degree block
  • Bundle branch blocks: LBBB, RBBB, fascicular blocks

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Q43. Cirrhosis - Clinical Picture, Etiology, Ascites

• Compensated: Often asymptomatic; spider angiomata, palmar erythema, leukonychia, Dupuytren's contracture, parotid enlargement (alcohol), muscle wasting, gynecomastia, testicular atrophy (males), menstrual irregularity (females)
• Decompensated (major events): Jaundice, ascites, variceal bleeding, hepatic encephalopathy, coagulopathy

• Hepatomegaly (early) → shrunken liver (late); splenomegaly
• Caput medusae (venous collaterals around umbilicus)
• Asterixis (liver flap) - hepatic encephalopathy
• Dupuytren's, spider nevi (>5 significant), palmar erythema

• Portal hypertension → splanchnic vasodilation (NO-mediated) → underfilling → RAAS/SNS/ADH activation → renal sodium and water retention → ascites formation
• Starling forces: Increased portal pressure + low oncotic pressure (hypoalbuminemia) → fluid transudation into peritoneum
• SAAG (Serum-Ascites Albumin Gradient): SAAG ≥1.1 g/dL = portal hypertension (transudate); <1.1 = other cause (malignancy, TB peritonitis)
• Treatment of ascites: Sodium restriction (<2 g/day), spironolactone 100-400 mg ± furosemide 40-160 mg; therapeutic paracentesis + albumin (8 g/L removed) for large volume; TIPS for refractory ascites

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Q44. Idiopathic Pulmonary Fibrosis - Causes, Symptoms, Diagnosis, Treatment

• Cigarette smoking (dose-dependent)
• Occupational exposures (metal/wood dust, farming, stone masonry)
• Viral infections (EBV, CMV - possible role)
• Gastroesophageal reflux disease (micro-aspiration theory)
• Genetic mutations: telomerase mutations (TERT, TERC), MUC5B promoter variant (most common genetic risk factor), SFTPC, SFTPA2

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Q45. Hepatic Encephalopathy - Etiology, Pathogenesis, Clinical Picture, Diagnosis, Treatment

• Cirrhosis (most common - spontaneous or triggered by precipitants)
• Precipitants (TIPS mnemonic): Toxins/drugs (sedatives, opioids), Infection (SBP, UTI, pneumonia), Protein overload (GI bleed - blood is protein), Portosystemic shunts, Hypokalemia/hyponatremia, Constipation, Renal failure, Dehydration

• Liver failure → inadequate clearance of gut-derived toxins (especially ammonia from intestinal bacteria)
• Ammonia enters systemic circulation → crosses blood-brain barrier
• Ammonia + glutamate → glutamine (by astrocytes) → astrocyte swelling → cerebral edema
• Increased GABAergic neurotransmission → neuroinhibition
• Neuroinflammation, oxidative stress, altered brain glucose metabolism

• Grade 0 (Covert): minimal - only detected by psychometric tests
• Grade 1: Subtle confusion, altered sleep-wake cycle, mood change, asterixis (mild)
• Grade 2: Obvious disorientation, lethargy, inappropriate behavior, asterixis
• Grade 3: Somnolence, marked confusion, incoherence, asterixis
• Grade 4: Coma (unresponsive to verbal/painful stimuli)

• Clinical (diagnosis of exclusion): check ammonia (elevated but not perfect correlate), liver function tests
• EEG: diffuse slowing, triphasic waves
• MRI brain: T1 hyperintensity in basal ganglia (manganese deposition in chronic)
• Number connection test, psychometric tests (covert HE)

• Identify and treat precipitants (most important step)
• Lactulose (first-line): non-absorbable disaccharide → lowers colonic pH → reduces ammonia production/absorption; titrate to 2-3 soft stools/day
• Rifaximin (non-absorbable antibiotic): reduces gut bacteria → ammonia production; used in addition to lactulose for secondary prevention
• Dietary protein: do NOT restrict (causes malnutrition); encourage 1.2-1.5 g/kg/day; prefer branched-chain amino acids and vegetable protein
• Zinc supplementation
• Treat acute liver failure with NAC
• Liver transplantation: definitive treatment for recurrent/refractory HE

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Q46. AV Block 3rd Degree (Complete Heart Block) - Causes, Clinical Picture, ECG

• Acute: Inferior MI (usually transient - RCA), anterior MI (usually permanent - LAD), Lyme disease, digoxin toxicity, hyperkalemia, cardiac surgery
• Chronic/Fibrotic: Lev's disease (calcification of left side of cardiac skeleton), Lenègre's disease (idiopathic fibrosis of conduction system), sarcoidosis, hemochromatosis, endocarditis

• Symptomatic bradycardia: severe fatigue, exercise intolerance
• Presyncope, syncope (Stokes-Adams attacks - sudden LOC due to ventricular asystole)
• Heart failure (from bradycardia and AV dyssynchrony)
• Angina (reduced coronary perfusion)
• Slow, regular pulse (ventricular escape rate 20-40 bpm if infranodal; 40-60 bpm if junctional)
• Large cannon a-waves in JVP (atria contract against closed tricuspid valve)
• Variable S1 intensity

• P waves and QRS complexes completely independent (P-P and R-R regular but not related)
• PP interval consistent; RR interval consistent; PR interval varies constantly (no relationship)
• Ventricular escape rhythm:
  • Junctional escape (AV node/His): rate 40-60, narrow QRS
  • Ventricular escape (below His): rate 20-40, wide QRS (>0.12s)

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Q47. Systemic Vasculitis - Classification, Systemic Manifestations, Physical Findings

• Large vessel: Giant cell arteritis (GCA), Takayasu's arteritis
• Medium vessel: Polyarteritis nodosa (PAN), Kawasaki disease
• Small vessel:
  • ANCA-associated: GPA (Granulomatosis with polyangiitis), EGPA (eosinophilic), MPA (microscopic polyangiitis)
  • Immune complex-mediated: IgA vasculitis (HSP), cryoglobulinemic vasculitis, anti-GBM disease

• Constitutional: fever, weight loss, fatigue, malaise
• Skin: palpable purpura, nodules, livedo reticularis, ulcers, digital ischemia/gangrene
• Musculoskeletal: arthralgia, arthritis, myalgia
• Renal: hematuria, proteinuria, rapidly progressive GN → AKI
• Pulmonary: DAH (diffuse alveolar hemorrhage), nodules (GPA), asthma (EGPA)
• Neurologic: peripheral neuropathy (mononeuritis multiplex), CNS involvement
• ENT (GPA): sinusitis, epistaxis, saddle nose deformity, subglottic stenosis
• GI: mesenteric ischemia, bowel infarction
• Ocular: scleritis, episcleritis, retinal vasculitis (GCA - blindness)

• Palpable purpura, skin ulcers
• Absent peripheral pulses, BP discrepancy (Takayasu's, GCA)
• Temporal artery tenderness, scalp tenderness (GCA)
• Mononeuritis multiplex (foot/wrist drop)
• Signs of GN (hypertension, edema)

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Q48. Restrictive Cardiomyopathy - Clinical Picture, Physical Findings, Diagnosis

• JVP: markedly elevated; Kussmaul's sign (JVP rises or fails to fall with inspiration, unlike normal)
• Pericardial knock: NOT present (seen in constrictive pericarditis); may have S3/S4
• Key distinction from constrictive pericarditis:

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Q49. AV Block 2nd Degree - Causes and Symptoms

• Mobitz I: Inferior MI, increased vagal tone, drugs (digoxin, beta-blockers, CCBs, amiodarone), myocarditis (Lyme disease, rheumatic fever), post-cardiac surgery
• Mobitz II: Anterior MI (LAD territory - bundle branch involvement), Lev's disease, Lenègre's disease, sarcoidosis, cardiomyopathy, myocarditis, cardiac surgery

• Mobitz I: Usually asymptomatic (benign); occasionally mild fatigue, palpitations
• Mobitz II: Symptoms vary with ventricular rate; dizziness, palpitations, presyncope, syncope (sudden dropped beats reduce cardiac output); fatigue, exercise intolerance; can progress to complete heart block with hemodynamic collapse

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Q50. Arrhythmia - Mechanism, Types, Classification

• Sinus tachycardia: Not a true arrhythmia - always look for the cause (fever, anemia, PE, hypovolemia)
• SVT management: Vagal maneuvers → adenosine IV → cardioversion
• VF: Only treatment is defibrillation - no drug works fast enough
• Torsades de Pointes: IV magnesium sulphate; correct electrolytes; stop QT-prolonging drugs

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Q51. IPF - Laboratory Tests and Diagnostic Methods

• Routine: CBC (mild leukocytosis, elevated ESR), CMP (hypoxemia on ABG), LDH (elevated in advanced disease)
• Autoimmune screen: ANA, RF, anti-CCP, ANCA, anti-Jo-1 (to exclude CTD-ILD and HP)
• Serum surfactant proteins SP-A, SP-D: elevated but non-specific
• KL-6 (Krebs von den Lungen-6): elevated glycoprotein; marker of ILD severity
• No specific serum biomarker for IPF

• PFTs: Restrictive pattern (↓FVC, ↓TLC); ↓DLCO (often earliest abnormality); ↓FEV1/FVC ratio normal or elevated
• HRCT Chest (most important): UIP pattern = bilateral peripheral, basal, subpleural honeycombing ± traction bronchiectasis (± GGO); typical UIP on HRCT in appropriate clinical context = diagnosis without biopsy; "probable UIP," "indeterminate," "alternative diagnosis" categories guide need for biopsy
• 6-Minute Walk Test: Assesses functional status, oxygen requirements
• Bronchoscopy + BAL: Lymphocytosis suggests HP; not diagnostic of IPF; helps exclude infection, malignancy
• Surgical Lung Biopsy (VATS): If HRCT inconclusive - shows UIP histology: temporal heterogeneity, fibroblastic foci, honeycombing, patchy fibrosis
• Transbronchial lung cryobiopsy: Less invasive alternative to surgical biopsy

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Q52. AV Block 1st Degree - Causes and ECG

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Q53. Hepatitis - Classification, Causes, Differential Diagnosis

• By duration: Acute (<6 months), Chronic (>6 months)
• By etiology: Viral (A, B, C, D, E), Alcoholic, Autoimmune, Drug-induced, Metabolic (NASH)
• By severity: Mild, Moderate, Severe, Fulminant (massive necrosis with encephalopathy)

• Viral (see Q15 table)
• Alcohol: AST:ALT ratio >2:1 (AST rarely >300); GGT markedly elevated
• Drug-induced (DILI): Paracetamol (most common acute cause), isoniazid, statins, NSAIDs, amoxicillin-clavulanate
• Autoimmune hepatitis: Young women; interface hepatitis; anti-smooth muscle antibody (SMA/ASMA), anti-LKM antibodies, elevated IgG; responds to corticosteroids
• Wilson's disease: <40y; Kayser-Fleischer rings; low ceruloplasmin, Coombs-negative hemolytic anemia
• Hemochromatosis: Middle-aged men; elevated ferritin/transferrin saturation; HFE gene mutation

• Right heart failure (congestive hepatopathy): elevated bilirubin, mildly elevated transaminases, elevated JVP
• Biliary obstruction (choledocholithiasis, cholangiocarcinoma): elevated ALP/GGT > ALT/AST; dilated bile ducts on ultrasound
• Ischemic hepatitis ("shock liver"): very high ALT/AST (>1000), rapid normalization
• Budd-Chiari syndrome: hepatic vein thrombosis, hepatomegaly, ascites, absent hepatic vein flow on Doppler

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Q54. Obstructive Sleep Apnea - Epworth Score and CPAP Therapy

• Mechanism: pneumatic airway splinting
• Titration: overnight PSG or auto-CPAP
• Benefits: eliminates apneas, improves EDS, reduces BP, reduces AF, cognitive improvement
• Adherence: defined as ≥4 hrs/night on ≥70% of nights; essential for benefit
• Follow-up: reassess ESS, compliance data download, AHI residual on machine

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Q55. Pulmonary Embolism - Signs/Symptoms and Gold Standard of Diagnosis

• CT Pulmonary Angiography (CTPA) is the current clinical gold standard:
  • Sensitivity ~83-90%, specificity ~95-98%
  • Directly visualizes intraluminal filling defect in pulmonary arteries
  • Allows visualization down to sub-segmental level
  • Also evaluates for RV dilation (prognostic), alternative diagnoses
• Historically: Conventional pulmonary angiography (invasive catheter-based) was the gold standard but now replaced by CTPA in clinical practice
• V/Q scintigraphy: Alternative gold standard when CTPA contraindicated (renal failure, contrast allergy, pregnancy concerns about radiation); interpreted as normal, low/intermediate/high probability using PIOPED criteria

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Q56. Bradycardia - Physical Examination Findings, Management

• Physiological (athletes, vagal tone, sleep)
• Intrinsic: Sick sinus syndrome, AV blocks, inferior MI, myocarditis, Lyme disease, sarcoidosis
• Extrinsic: Drugs (beta-blockers, digoxin, CCBs, amiodarone), hypothyroidism, hypercalcemia, hyperkalemia, hypothermia, obstructive jaundice, raised intracranial pressure (Cushing reflex)

• Slow, regular or irregular pulse (note: irregular suggests sick sinus syndrome, AF with slow rate)
• Low blood pressure (if hemodynamically compromised)
• Signs of low output: cool peripheries, pallor, diaphoresis
• JVP: cannon a-waves (complete heart block)
• Auscultation: varying S1 (CHB), S3 (heart failure), S4 (hypertrophy)
• Other signs of cause: hypothyroid signs (dry skin, myxedema, bradykinesia, cold intolerance), signs of inferior MI

• Hemodynamically stable: Investigate cause; review and stop causative drugs; treat underlying condition
• Hemodynamically unstable (hypotension, chest pain, syncope, heart failure):
  • Atropine 0.5-1 mg IV (first-line; repeat up to 3 mg total) - for vagally mediated or AV node level block
  • Transcutaneous pacing (external pacing via defibrillator pads) if atropine fails
  • Transvenous temporary pacing (if transcutaneous fails or ongoing)
  • Adrenaline/epinephrine infusion or dopamine as bridge
  • Permanent pacemaker if irreversible cause (sick sinus syndrome, AV block Mobitz II/complete)

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Q57. Cardiac Tamponade - Indicators for Pericardiocentesis

1. Hemodynamic instability/shock: Hypotension (SBP <90 mmHg), signs of cardiogenic shock (tachycardia, cold peripheries, confusion, oliguria)
2. Cardiac arrest or near-arrest due to tamponade
3. Clinical tamponade with rapidly deteriorating status

• Right atrial collapse (>1/3 of cardiac cycle)
• Right ventricular diastolic collapse (more specific)
• IVC plethora (>2.1 cm, <50% respiratory collapse)
• Marked respiratory variation in mitral/tricuspid inflow velocities (>25% and >40% respectively)
• "Swinging heart" (electrical alternans correlate)

• Large effusion (>20 mm on echo) with impending tamponade physiology
• Unknown etiology requiring fluid analysis (malignancy, TB, infection)
• Recurrent effusion (therapeutic drainage)

• Coagulopathy (correct before procedure if not emergency)
• Aortic dissection (hemopericardium from dissection - surgical management preferred)
• Loculated posterior effusion (surgical window preferred over blind approach)
• Small anterior effusion (<1 cm) - high risk of cardiac puncture

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Q58. Systemic Vasculitis - Symptoms, Diagnosis, Treatment

• Clinical: History of constitutional symptoms + organ-specific symptoms; examine for purpura, absent pulses, neuropathy, sinusitis
• Labs: ANCA (cANCA/PR3 - GPA; pANCA/MPO - MPA, EGPA), ANA, anti-GBM, CRP/ESR elevated, urinalysis (hematuria, RBC casts), renal function, CBC
• Imaging: CXR/CT chest (nodules, cavities, DAH), CT angiography (large vessel vasculitis), PET-CT (Takayasu's, GCA)
• Biopsy (gold standard for most): Skin (leukocytoclastic vasculitis + IF), kidney (crescentic GN + IF), temporal artery (GCA - granulomatous inflammation), lung/nerve depending on involvement
• Specific: Temporal artery biopsy (GCA, >2 cm length); angiography (Takayasu's, PAN)

• GCA: High-dose prednisone 40-60 mg/day immediately (to prevent blindness); taper slowly; tocilizumab (IL-6 receptor blocker) for relapsing/refractory disease
• GPA/MPA: Induction - IV methylprednisolone + cyclophosphamide or rituximab; maintenance - azathioprine or rituximab
• EGPA: Prednisone; mepolizumab (anti-IL-5) for relapsing eosinophilic disease
• PAN: Prednisone ± cyclophosphamide; if HBV-related: antiviral therapy
• Takayasu's: High-dose corticosteroids; methotrexate, azathioprine, or tocilizumab for refractory
• IgA Vasculitis: Supportive; steroids for GI symptoms; MMF for severe nephritis

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Q59. Research Methods and Treatment of Hepatic Encephalopathy

• Ammonia level: Elevated in most cases (venous or arterial); useful but imperfect - normal ammonia does not exclude HE; serial measurements may indicate trajectory
• EEG: Diffuse slowing; triphasic waves (high sensitivity, low specificity)
• Psychometric tests: Number connection test (NCT-A, NCT-B), digit symbol test - for covert HE
• Critical Flicker Frequency (CFF): Neurophysiologic test for covert HE
• MRI Brain: T1 hyperintensity in globus pallidus (manganese accumulation); T2 changes in acute hyperammonemia
• Neuropsychological Battery (PHES): Psychometric Hepatic Encephalopathy Score - standard for covert HE research

• Precipitant identification and treatment
• Lactulose (mainstay)
• Rifaximin (secondary prevention)
• Nutritional support (adequate protein)
• Zinc supplementation
• Liver transplant (definitive)

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Q60. Malabsorption Syndrome - Differential Diagnosis, Management

• Steatorrhea (bulky, greasy, floating, foul-smelling stools - fat malabsorption)
• Diarrhea (osmotic or secretory)
• Weight loss, failure to thrive (children)
• Abdominal bloating, flatulence
• Specific deficiency signs: anemia (B12, iron, folate), bleeding (vitamin K), neuropathy (B12), tetany (calcium, vitamin D), edema (albumin), night blindness (vitamin A), bone pain/fractures (vitamin D)

• Stool fat (72-h collection or qualitative Sudan stain)
• D-xylose test (mucosal absorption)
• Anti-tissue transglutaminase (anti-tTG) IgA + total IgA (celiac)
• Small bowel endoscopy + biopsy: villous atrophy (celiac), PAS-positive macrophages (Whipple's)
• CT abdomen/MRI enterography: Crohn's, lymphoma, pancreatic disease
• Breath tests: H2 breath test (lactase deficiency, SIBO), C14-urea (H. pylori)
• Fecal elastase: pancreatic exocrine insufficiency

• Treat underlying cause:
  • Celiac disease: strict gluten-free diet (lifelong)
  • Pancreatic insufficiency: oral pancreatic enzyme replacement + high-fat diet
  • Crohn's disease: steroids, biologics (infliximab), surgery
  • SIBO: antibiotics (rifaximin, metronidazole), treat underlying anatomic cause
  • Giardiasis: metronidazole or tinidazole
  • Whipple's disease: ceftriaxone IV → TMP-SMX orally (1-2 years)
• Nutritional supplementation: Fat-soluble vitamins (A, D, E, K), calcium, B12 (IM if terminal ileum disease), iron, folate, zinc
• Elemental/semi-elemental feeds if severe
• Parenteral nutrition if intestinal failure (short bowel syndrome)

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• Repeated topics (PE appears 6 times, AF twice, AV blocks 4 times, Cardiomyopathies 3 times) - memorize those answers cold; the examiner will ask follow-up questions on them.
• Overlapping answers - several questions share content (Q3 & Q5 = DCM; Q24 & Q26 & Q27 = Pericarditis; Q6 & Q37 & Q41 & Q54 = OSA; Q1 & Q8 & Q31 & Q34 = Scleroderma). Learn the full version once, then adapt.
• Don't-miss points examiners love:
  • Beck's triad + electrical alternans = tamponade
  • PR depression on ECG = pericarditis (before even asking about ST elevation)
  • Mobitz II → permanent pacemaker (unlike Mobitz I)
  • Complete heart block → Stokes-Adams attacks + cannon a-waves
  • SAAG ≥1.1 = portal hypertension ascites
  • Anti-centromere = lcSSc/CREST; Anti-Scl-70 = dcSSc + ILD risk
  • ACE inhibitors for scleroderma renal crisis = life-saving
  • Lactulose + rifaximin for hepatic encephalopathy