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CheatSheet: Hepatology

1. Viral Hepatitis

1.1 Hepatitis A (HAV)

1.1 Hepatitis A (HAV)

1.2 Hepatitis B (HBV)

1.2 Hepatitis B (HBV)

1.2.1 HBV Serology Patterns

1.2.1 HBV Serology Patterns

1.2.2 HBV Treatment Indications

  • HBeAg positive: HBV DNA >20,000 IU/mL + ALT >2× ULN or significant fibrosis
  • HBeAg negative: HBV DNA >2,000 IU/mL + ALT >2× ULN or significant fibrosis
  • First-line drugs: Entecavir, Tenofovir (high barrier to resistance)
  • Interferon-α: 48 weeks for HBeAg positive, contraindicated in decompensated cirrhosis
  • Prophylaxis in pregnancy: Tenofovir if HBV DNA >200,000 IU/mL from 28-32 weeks

1.3 Hepatitis C (HCV)

1.3 Hepatitis C (HCV)

1.4 Hepatitis D (HDV)

  • Defective RNA virus requiring HBsAg for replication
  • Coinfection with HBV: acute hepatitis, resolves with HBV
  • Superinfection in chronic HBV: severe chronic hepatitis, high cirrhosis risk
  • Diagnosis: Anti-HDV IgM, HDV RNA
  • Treatment: Pegylated interferon-α for 48 weeks

1.5 Hepatitis E (HEV)

1.5 Hepatitis E (HEV)

2. Cirrhosis

2.1 Definitions and Classification

2.1 Definitions and Classification

2.1.1 Child-Pugh Classification

2.1.1 Child-Pugh Classification
  • Class A: 5-6 points (1-year survival 100%, 2-year survival 85%)
  • Class B: 7-9 points (1-year survival 80%, 2-year survival 60%)
  • Class C: 10-15 points (1-year survival 45%, 2-year survival 35%)

2.2 Common Etiologies

  • Alcohol (most common in Western countries, macronodular)
  • Chronic HBV and HCV (most common worldwide)
  • NASH (Non-Alcoholic Steatohepatitis)
  • Autoimmune hepatitis
  • Primary biliary cholangitis (AMA positive)
  • Primary sclerosing cholangitis (pANCA positive, associated with IBD)
  • Wilson disease (Kayser-Fleischer rings, low ceruloplasmin)
  • Hemochromatosis (increased ferritin, transferrin saturation >45%)
  • α1-antitrypsin deficiency (PAS-positive globules)
  • Budd-Chiari syndrome (hepatic vein thrombosis)

2.3 Complications

2.3.1 Portal Hypertension

2.3.1 Portal Hypertension

2.3.2 Esophageal Varices

  • Develop when HVPG >10 mmHg, bleed when >12 mmHg
  • Primary prophylaxis: Non-selective beta-blockers (propranolol, carvedilol) or EVL if high-risk varices
  • Acute bleed management: Resuscitation, vasoactive drugs (terlipressin/octreotide), EVL, antibiotics (ceftriaxone)
  • Salvage therapy: TIPS (Transjugular Intrahepatic Portosystemic Shunt) if refractory
  • Secondary prophylaxis: Beta-blockers + EVL

2.3.3 Ascites

2.3.3 Ascites

2.3.4 Spontaneous Bacterial Peritonitis (SBP)

2.3.4 Spontaneous Bacterial Peritonitis (SBP)

2.3.5 Hepatic Encephalopathy (HE)

2.3.5 Hepatic Encephalopathy (HE)
  • Precipitants: GI bleed, infection, constipation, hypokalemia, diuretics, sedatives, high protein diet
  • Pathophysiology: Ammonia accumulation, GABA receptor alterations
  • Treatment: Lactulose (20-30g TDS to achieve 2-3 soft stools/day), Rifaximin 550mg BD
  • Acute management: Identify precipitant, lactulose enema, correct electrolytes

2.3.6 Hepatorenal Syndrome (HRS)

2.3.6 Hepatorenal Syndrome (HRS)

2.3.7 Hepatopulmonary Syndrome (HPS)

  • Triad: Liver disease + intrapulmonary vascular dilatations + arterial hypoxemia (PaO₂ <80mmhg or="" a-a="" gradient="">
  • Clinical features: Platypnea (dyspnea worse in upright position), orthodeoxia (hypoxemia worse upright)
  • Diagnosis: Contrast-enhanced echocardiography (bubbles appear in left atrium after 3-6 beats)
  • Treatment: Oxygen, liver transplant (only definitive treatment)

2.3.8 Portopulmonary Hypertension

  • Mean pulmonary artery pressure >25mmHg with pulmonary vascular resistance >240 dynes·sec·cm⁻⁵
  • Contraindication to transplant if mean PAP >45mmHg
  • Treatment: Prostacyclin analogues, endothelin receptor antagonists, phosphodiesterase-5 inhibitors

3. Acute Liver Failure

3.1 Definition and Classification

3.1 Definition and Classification

3.2 Common Etiologies

  • Viral: HAV, HBV, HEV (pregnant women), HSV, CMV
  • Drugs: Paracetamol (most common in West), anti-TB drugs, NSAIDs, valproate
  • Toxins: Amanita phalloides (mushroom), CCl₄
  • Vascular: Budd-Chiari syndrome, ischemic hepatitis
  • Metabolic: Wilson disease, acute fatty liver of pregnancy
  • Autoimmune hepatitis

3.3 King's College Criteria for Transplant

3.3.1 Paracetamol-Induced ALF

  • Arterial pH <7.3 after="" resuscitation="">
  • All three: INR >6.5, creatinine >3.4mg/dL, Grade III-IV encephalopathy

3.3.2 Non-Paracetamol ALF

  • INR >6.5 OR
  • Any three of: Age <10 or="">40 years, etiology (non-A non-B hepatitis, drug), jaundice to encephalopathy >7 days, INR >3.5, bilirubin >17.5mg/dL

3.4 Management

  • ICU admission, monitor vitals and mental status
  • N-acetylcysteine if paracetamol toxicity (loading 150mg/kg over 1h, then 50mg/kg over 4h, then 100mg/kg over 16h)
  • Correct coagulopathy only if active bleeding (not prophylactic FFP)
  • Lactulose for encephalopathy, avoid sedatives
  • Hypoglycemia monitoring and correction (10% dextrose)
  • Infection surveillance (broad-spectrum antibiotics if suspected)
  • Liver transplantation (definitive treatment if criteria met)

4. Alcoholic Liver Disease

4.1 Spectrum

4.1 Spectrum

4.2 Alcoholic Hepatitis Severity

4.2.1 Maddrey Discriminant Function (MDF)

  • MDF = 4.6 × (PT patient - PT control) + Bilirubin (mg/dL)
  • MDF ≥32: Severe, consider corticosteroids (prednisolone 40mg/day for 28 days)
  • Lille score at day 7: <0.45 (continue="" steroids),="">0.45 (stop steroids, poor responder)

4.2.2 MELD Score

  • MELD ≥21: Consider corticosteroids

4.3 Management

  • Abstinence (most important), nutritional support (high-calorie, high-protein diet)
  • Thiamine, folic acid, multivitamins
  • Prednisolone 40mg/day for 28 days if severe (MDF ≥32)
  • Pentoxifylline 400mg TDS (alternative if steroids contraindicated)
  • N-acetylcysteine may be added to steroids
  • Liver transplant: Minimum 6 months abstinence required

5. Non-Alcoholic Fatty Liver Disease (NAFLD)

5.1 Definitions

5.1 Definitions

5.2 Risk Factors

  • Metabolic syndrome (obesity, T2DM, hypertension, dyslipidemia)
  • Insulin resistance (central pathophysiologic mechanism)
  • PCOS, hypothyroidism, obstructive sleep apnea

5.3 Diagnosis

  • USG: Increased echogenicity (bright liver)
  • AST:ALT <1 (unlike="" alcoholic="" liver="">
  • Liver biopsy: Gold standard for NASH diagnosis
  • Non-invasive: FibroScan (transient elastography), NAFLD fibrosis score

5.4 Management

  • Weight loss (7-10% target), exercise, dietary modification
  • Tight control of diabetes, hypertension, dyslipidemia
  • Vitamin E 800 IU/day (non-diabetic NASH with fibrosis)
  • Pioglitazone (NASH with fibrosis, diabetic or non-diabetic)
  • Avoid hepatotoxic drugs and alcohol
  • No FDA-approved specific pharmacotherapy

6. Autoimmune Liver Diseases

6.1 Autoimmune Hepatitis (AIH)

6.1 Autoimmune Hepatitis (AIH)
  • Clinical: Young-middle aged females, insidious or acute hepatitis, hypergammaglobulinemia (IgG elevation)
  • Histology: Interface hepatitis (piecemeal necrosis), plasma cell infiltration
  • Treatment: Prednisolone + azathioprine (steroid-sparing), remission in 65-80%
  • Maintenance: Continue until remission (normal transaminases, IgG, histology), minimum 2-3 years
  • Transplant indication if decompensated cirrhosis or treatment failure

6.2 Primary Biliary Cholangitis (PBC)

6.2 Primary Biliary Cholangitis (PBC)

6.3 Primary Sclerosing Cholangitis (PSC)

6.3 Primary Sclerosing Cholangitis (PSC)

7. Metabolic Liver Diseases

7.1 Wilson Disease

7.1 Wilson Disease

7.2 Hereditary Hemochromatosis

7.2 Hereditary Hemochromatosis

7.3 α1-Antitrypsin Deficiency

  • Autosomal recessive, SERPINA1 gene (chromosome 14), PiZZ genotype (most severe)
  • Liver: Neonatal cholestasis, chronic hepatitis, cirrhosis, HCC
  • Lungs: Early-onset emphysema (panacinar, lower lobes), exacerbated by smoking
  • Diagnosis: Low serum α1-antitrypsin level, phenotyping, liver biopsy (PAS-positive diastase-resistant globules)
  • Treatment: Smoking cessation, α1-antitrypsin replacement (emphysema), liver transplant (definitive for liver disease)

8. Drug-Induced Liver Injury (DILI)

8.1 Patterns

8.1 Patterns

8.2 Common Hepatotoxic Drugs

8.2 Common Hepatotoxic Drugs

8.3 Management

  • Discontinue offending drug (most important)
  • N-acetylcysteine for paracetamol toxicity
  • Supportive care, monitor liver function
  • Corticosteroids if autoimmune-like DILI
  • Liver transplant if acute liver failure

9. Hepatocellular Carcinoma (HCC)

9.1 Risk Factors

  • Cirrhosis (80-90% of HCC), especially HBV, HCV, alcoholic, hemochromatosis
  • Chronic HBV (even without cirrhosis), HCV
  • Aflatoxin B1 exposure (Aspergillus flavus contamination)
  • NAFLD/NASH
  • Genetic: Hemochromatosis, α1-antitrypsin deficiency, Wilson disease, tyrosinemia

9.2 Surveillance

  • High-risk patients: Cirrhosis (any cause), chronic HBV (Asian males >40 years, Asian females >50 years, family history HCC, Africans >20 years)
  • Method: USG abdomen + AFP every 6 months
  • AFP >400 ng/mL is highly suggestive of HCC

9.3 Diagnosis

9.3 Diagnosis

9.4 Barcelona Clinic Liver Cancer (BCLC) Staging

9.4 Barcelona Clinic Liver Cancer (BCLC) Staging

9.5 Milan Criteria for Liver Transplant

  • Single tumor ≤5 cm OR
  • Up to 3 tumors, each ≤3 cm
  • No macrovascular invasion, no extrahepatic metastases
  • 5-year survival >70% if within Milan criteria

9.6 Treatment Options

  • Surgical resection: Solitary tumor, Child A, adequate liver reserve
  • Liver transplant: Best for small HCC with cirrhosis (Milan criteria)
  • Radiofrequency ablation (RFA): Tumors <3cm, not="" near="">
  • TACE: Intermediate stage, multinodular without vascular invasion
  • Sorafenib: Advanced HCC, portal vein thrombosis, extrahepatic spread

10. Liver Abscess

10.1 Pyogenic Liver Abscess

10.1 Pyogenic Liver Abscess

10.2 Amoebic Liver Abscess

10.2 Amoebic Liver Abscess

10.3 Differentiation

10.3 Differentiation

11. Miscellaneous Liver Disorders

11.1 Budd-Chiari Syndrome

11.1 Budd-Chiari Syndrome

11.2 Acute Fatty Liver of Pregnancy (AFLP)

  • Rare, 3rd trimester complication, microvesicular steatosis
  • Clinical: Nausea, vomiting, jaundice, abdominal pain, may progress to ALF
  • Labs: Hypoglycemia, elevated transaminases, low platelets, coagulopathy, elevated uric acid
  • Treatment: Immediate delivery (definitive), supportive care
  • Differentiate from HELLP syndrome (hemolysis, elevated liver enzymes, low platelets)

11.3 Gilbert Syndrome

11.3 Gilbert Syndrome

11.4 Crigler-Najjar Syndrome

11.4 Crigler-Najjar Syndrome

11.5 Dubin-Johnson Syndrome

  • Autosomal recessive, defective MRP2 (canalicular transport protein)
  • Conjugated hyperbilirubinemia, black liver (melanin-like pigment)
  • Benign, no treatment required

11.6 Rotor Syndrome

  • Autosomal recessive, defective hepatic uptake and storage
  • Conjugated hyperbilirubinemia, normal liver color
  • Benign, no treatment required

11.7 Ischemic Hepatitis (Shock Liver)

  • Acute hepatocyte injury due to hypoperfusion (shock, cardiac failure, sepsis)
  • Massive transaminase elevation (ALT/AST >1000 IU/L, often >3000)
  • Rapid rise and fall (peak 1-3 days, normalize in 7-10 days)
  • Treatment: Address underlying cause, supportive care
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