Liver Disease for NEET PG Medicine: Viral Hepatitis, Jaundice, Cirrhosis, Ascites, SBP, Encephalopathy, Liver Failure

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🎯 Exam priority: High. Expect: hepatitis viruses compared, HBV serology and the window period, vertical HBV, HCV and HEV facts, jaundice patterns, Gilbert and Dubin-Johnson, AST:ALT in alcohol, steroids in alcoholic hepatitis, SAAG, ascites and SBP treatment, encephalopathy precipitants and drugs, and the definitions of acute and acute-on-chronic liver failure.

CBME mapping: GM 5.1–5.17. Liver pathology is in Pathology; variceal bleeding in article 13; ATT hepatitis in article 7.

Hepatitis viruses, cirrhosis complications, encephalopathy, liver failure and jaundice. Drawn by TrackNation.

Viral Hepatitis

• Acute hepatitis: a viral prodrome, anorexia and nausea; jaundice often appears as other symptoms settle.

• HAV: faecal–oral, incubation 15–50 days, never chronic; diagnose with IgM anti-HAV.

• HBV: blood, sex and birth (infants of infected mothers have a 70–90% risk at delivery without HBIG and vaccine). Chronic = > 6 months; the younger the age at infection, the higher the chance of chronicity. Treat chronic HBV with entecavir or tenofovir. HCC risk rises even without cirrhosis.

• HCV: blood-borne, often chronic; pangenotypic sofosbuvir/velpatasvir or glecaprevir/pibrentasvir. Extrahepatic: mixed cryoglobulinaemia, glomerulonephritis, porphyria cutanea tarda.

• HDV replicates only with HBV (co-infection or superinfection). HEV: waterborne outbreaks; acute liver failure and death are rare except in pregnancy.

Jaundice and Alcohol

• Jaundice is visible at bilirubin about 2–3 mg/dL.

• ICMR patterns: isolated unconjugated rise with normal enzymes (haemolysis, congenital); obstructive — ALP > 4–5 × ULN with dilated ducts on ultrasound; hepatitis — AST/ALT usually > 5 × ULN (< 500 in alcoholic hepatitis). Refer if INR > 1.5, altered sensorium or bleeding.

• Gilbert: mild unconjugated hyperbilirubinaemia that rises with fasting or stress; harmless. Crigler–Najjar type I: severe unconjugated jaundice from birth, kernicterus. Dubin–Johnson: conjugated; the liver is deeply pigmented.

• Alcohol: AST:ALT ≥ 2 (vitamin B6 deficiency lowers ALT); Mallory hyaline. Severe alcoholic hepatitis (Maddrey DF ≥ 32) → prednisolone 40 mg/day for 4 weeks if no infection, GI bleed, renal failure or pancreatitis.

Cirrhosis, Portal Hypertension, Ascites, SBP

• Signs of chronic liver disease: spider angiomas, gynaecomastia, axillary hair loss, testicular atrophy, Dupuytren contracture; caput medusae is rare. Severity: Child-Turcotte-Pugh and MELD 3.0. HCC surveillance: ultrasound ± AFP every 6 months.

• Portal hypertension: normal portal pressure 5–10 mm Hg; cirrhosis is the commonest intrahepatic cause. Varices are managed with endoscopy and non-selective beta-blockers; TIPS if refractory.

• Ascites: SAAG ≥ 1.1 g/dL = portal hypertension. Treat with sodium restriction (2000 mg/day) first, then spironolactone ± furosemide; large-volume paracentesis > 5 L needs 6–8 g albumin per litre removed.

• SBP: ascitic neutrophils > 250/µL; usually E. coli or Klebsiella. Treat with ceftriaxone or cefotaxime plus albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 (prevents hepatorenal syndrome).

Encephalopathy and Liver Failure

• Hepatic encephalopathy: confusion, asterixis, coma, fetor hepaticus. Precipitants: infection, hypokalaemia, dehydration, diuretics, GI bleeding. Treat the cause plus lactulose and rifaximin.

• Acute liver failure: INR ≥ 1.5 with encephalopathy in someone without prior liver disease (MSD). ICMR: jaundice for < 4 weeks with encephalopathy and INR ≥ 1.5. Causes in India include viral hepatitis (HEV in pregnancy), drugs such as ATT, and acute fatty liver of pregnancy/HELLP (deliver promptly).

• ACLF (ICMR): known chronic liver disease with an acute insult — bilirubin ≥ 5 mg/dL and INR ≥ 1.5, plus ascites or encephalopathy within 4 weeks.

• ICMR management: IV N-acetylcysteine in drug-induced ALF (150 mg/kg over 1 h); tenofovir or entecavir for hepatitis B; no prophylactic FFP for the INR; ceftriaxone for SBP.

Traps the Examiner Sets

• Window period of HBV: only IgM anti-HBc is positive.

• HAV and HEV are faecal–oral; HEV kills in pregnancy.

• AST:ALT ≥ 2 suggests alcohol.

• SAAG ≥ 1.1 = portal hypertension; SBP = neutrophils > 250.

• Do not give FFP just to correct the INR in acute liver failure.

Memory Hooks & Shortcuts

Shortcuts to lock in this article's numbers and lists. Each one only re-packages facts proven above.

• 🧠 Vowels hit the bowels: hepatitis A and E are faecal–oral — hepatitis spread

• 🧠 HBV window: 'Core alone' — only IgM anti-HBc — window period

• 🧠 D is Dependent on B — HDV

• 🧠 E for Expecting mothers in danger — HEV pregnancy

• 🧠 Alcohol: 'S before L' — AST twice ALT — AST:ALT

• 🧠 SBP 250, SAAG 1.1 — ascites numbers

Rapid-Revision Cards

• HAV

  Faecal–oral, 15–50 d, never chronic; IgM anti-HAV.

• HBsAg

  Incubation; blood infectious.

• HBV window

  Only IgM anti-HBc positive.

• Anti-HBs

  Recovery or vaccine; lifelong.

• Vertical HBV

  70–90% without HBIG + vaccine.

• Chronic hepatitis

  > 6 months.

• Chronic HBV drugs

  Entecavir or tenofovir.

• HCV drugs

  Sofosbuvir/velpatasvir; glecaprevir/pibrentasvir.

• HCV extrahepatic

  Mixed cryoglobulinaemia, GN, PCT.

• HDV

  Needs HBV.

• HEV

  Waterborne; deadly in pregnancy.

• Visible jaundice

  Bilirubin ~2–3 mg/dL.

• Gilbert

  Unconjugated, rises with fasting.

• Crigler–Najjar I

  No enzyme; kernicterus.

• Dubin–Johnson

  Conjugated; deeply pigmented liver.

• Obstructive pattern

  ALP > 4–5 × ULN.

• Alcohol LFTs

  AST:ALT ≥ 2.

• Alcoholic hepatitis steroids

  DF ≥ 32 → prednisolone 40 mg × 4 wk.

• HCC surveillance

  US ± AFP 6-monthly.

• SAAG ≥ 1.1

  Portal hypertension.

• Ascites Rx

  Na 2000 mg/d → spironolactone ± furosemide.

• LVP albumin

  > 5 L: 6–8 g per litre.

• SBP

  PMN > 250; ceftriaxone + albumin 1.5 then 1 g/kg.

• HE drugs

  Lactulose + rifaximin.

• ALF

  INR ≥ 1.5 + encephalopathy, no prior liver disease.

• ACLF (ICMR)

  Bili ≥ 5, INR ≥ 1.5, ascites/HE ≤ 4 wk.

Sources

Facts in this article were checked against these documents.

• Standard Treatment Workflows: Jaundice; Liver Failure — Indian Council of Medical Research, DHR, 2020 (link)

• MSD Manual Professional: Hepatitis A–E; Cirrhosis; Ascites; Spontaneous Bacterial Peritonitis; Portal Hypertension; Portosystemic Encephalopathy; Acute Liver Failure; Jaundice; Inborn Metabolic Disorders Causing Hyperbilirubinemia; Alcohol-Related Liver Disease — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• Competency Based Undergraduate Curriculum, General Medicine (GM 5) — National Medical Commission, 2024

Test Yourself: Practice Questions

Thirty questions in NEET PG style, most of them clinical vignettes.

Practice Questions (NEET PG pattern)

Original questions written in the style of the exam: +4 for a correct answer, −1 for a wrong one. Every answer was checked against the sources listed above. NEET PG papers are not published by NBEMS, so these are not past-paper questions.

Q1. In a community with poor water treatment and sanitation, several people develop acute hepatitis. The virus that never causes chronic hepatitis and is diagnosed by IgM antibody is

• (a) hepatitis A

• (b) hepatitis C

• (c) hepatitis B

• (d) hepatitis D

Q2. In acute hepatitis B, HBsAg typically

• (a) appears in the incubation period before illness and means the blood is infectious

• (b) appears only after recovery

• (c) indicates immunity

• (d) is never detectable

Q3. A patient recovering from acute hepatitis B is HBsAg-negative and anti-HBs-negative, but IgM anti-HBc is positive. This is the

• (a) window period

• (b) chronic carrier state

• (c) vaccinated state

• (d) false-positive result

Q4. A person who recovered from hepatitis B years ago will usually have

• (a) HBeAg

• (b) anti-HBs, which persists for life

• (c) only IgM anti-HBc

• (d) HBsAg for life

Q5. Without immunoprophylaxis, an infant born to a mother with hepatitis B infection has a risk of acquiring HBV at delivery of about

• (a) 70–90%

• (b) 10%

• (c) 1–2%

• (d) 100%

Q6. The risk that acute hepatitis B becomes chronic is

• (a) higher the younger the age at infection

• (b) zero in children

• (c) the same at all ages

• (d) highest in the elderly

Q7. First-line oral treatment for chronic hepatitis B is

• (a) ribavirin

• (b) sofosbuvir

• (c) acyclovir

• (d) entecavir or tenofovir

Q8. A man with chronic hepatitis C asks about treatment. A first-line pangenotypic regimen is

• (a) tenofovir

• (b) lamivudine

• (c) interferon alone

• (d) sofosbuvir/velpatasvir

Q9. A patient with chronic hepatitis C has cutaneous vasculitis, arthralgia and glomerulonephritis. The likely extrahepatic association is

• (a) sarcoidosis

• (b) amyloidosis

• (c) mixed cryoglobulinaemia

• (d) polymyositis

Q10. Hepatitis D virus can cause infection only

• (a) after vaccination

• (b) in the presence of hepatitis B virus

• (c) in pregnancy

• (d) with hepatitis C

Q11. During a waterborne outbreak of acute hepatitis, the group with the highest risk of acute liver failure and death from hepatitis E is

• (a) children under 5

• (b) vaccinated adults

• (c) pregnant women

• (d) young men

Q12. A young adult has mild jaundice after fasting; bilirubin is mainly unconjugated and liver enzymes and blood counts are normal. The likely diagnosis is

• (a) acute hepatitis

• (b) Gilbert syndrome

• (c) obstructive jaundice

• (d) Dubin–Johnson syndrome

Q13. A neonate has severe unconjugated hyperbilirubinaemia from birth due to complete absence of the conjugating enzyme and is at risk of kernicterus. This is

• (a) Crigler–Najjar syndrome type I

• (b) Rotor syndrome

• (c) Gilbert syndrome

• (d) Dubin–Johnson syndrome

Q14. In Dubin–Johnson syndrome, liver biopsy shows

• (a) a deeply pigmented liver with otherwise normal histology

• (b) granulomas

• (c) fatty change

• (d) cirrhosis

Q15. Jaundice usually becomes clinically visible when serum bilirubin reaches about

• (a) 0.5 mg/dL

• (b) 20 mg/dL

• (c) 2–3 mg/dL

• (d) 10 mg/dL

Q16. A patient with jaundice, pruritus and clay-coloured stools has a markedly raised alkaline phosphatase. The pattern per ICMR is

• (a) hepatitic

• (b) obstructive (ALP > 4–5 × ULN; look for dilated ducts)

• (c) Gilbert

• (d) haemolytic

Q17. In alcohol-related liver disease, the AST:ALT ratio is typically

• (a) unrelated to alcohol

• (b) exactly 1

• (c) ≥ 2, because vitamin B6 deficiency lowers ALT

• (d) < 1

Q18. A heavy drinker has severe alcoholic hepatitis with Maddrey discriminant function 45, no infection, bleeding, renal failure or pancreatitis. The drug that may improve outcome is

• (a) prednisolone 40 mg/day for 4 weeks

• (b) propranolol

• (c) ursodeoxycholic acid

• (d) metformin

Q19. A patient with cirrhosis should be screened for hepatocellular carcinoma by

• (a) CT every 5 years

• (b) no screening

• (c) ultrasound with or without AFP every 6 months

• (d) AFP once at diagnosis

Q20. Ascitic fluid analysis shows a serum–ascites albumin gradient of 1.6 g/dL. This indicates

• (a) pancreatic ascites

• (b) peritoneal tuberculosis

• (c) peritoneal carcinomatosis

• (d) ascites due to portal hypertension

Q21. The first and lowest-risk treatment for cirrhotic ascites is

• (a) large-volume paracentesis

• (b) TIPS

• (c) dietary sodium restriction to 2000 mg/day

• (d) fluid restriction to 500 mL

Q22. During therapeutic paracentesis of 8 L of ascites, the patient should receive

• (a) 6–8 g of 25% albumin per litre removed

• (b) no albumin

• (c) FFP

• (d) normal saline 8 L

Q23. A cirrhotic patient with ascites has fever and abdominal pain. The ascitic neutrophil count that diagnoses spontaneous bacterial peritonitis is

• (a) > 50 cells/µL

• (b) > 10 cells/µL

• (c) > 250 cells/µL

• (d) > 1000 lymphocytes/µL

Q24. The usual organisms of spontaneous bacterial peritonitis are

• (a) anaerobes only

• (b) Escherichia coli and Klebsiella pneumoniae

• (c) Mycobacterium tuberculosis

• (d) Candida

Q25. Along with ceftriaxone or cefotaxime, a patient with SBP should receive albumin

• (a) 1.5 g/kg on day 1 and 1 g/kg on day 3

• (b) only if albumin < 1 g/dL

• (c) 10 g once

• (d) never

Q26. Normal portal venous pressure is

• (a) 25–30 mm Hg

• (b) 15–20 mm Hg

• (c) 5–10 mm Hg

• (d) 0–2 mm Hg

Q27. A cirrhotic patient becomes confused with a flapping tremor of the outstretched hands after starting diuretics; serum potassium is low. Treatment includes correcting the precipitant and giving

• (a) high-protein diet only

• (b) morphine

• (c) lactulose with rifaximin

• (d) benzodiazepines

Q28. Acute liver failure is diagnosed by

• (a) ascites in cirrhosis

• (b) raised ALP

• (c) INR ≥ 1.5 with encephalopathy in a patient without prior chronic liver disease

• (d) bilirubin > 2 mg/dL alone

Q29. A patient with known cirrhosis develops jaundice (bilirubin 9 mg/dL), INR 2.0 and ascites within 3 weeks after an acute insult. Per ICMR this is

• (a) acute-on-chronic liver failure

• (b) Gilbert syndrome

• (c) compensated cirrhosis

• (d) acute liver failure

Q30. In acute liver failure with a high INR but no bleeding, the ICMR workflow advises

• (a) vitamin K only and no monitoring

• (b) FFP to normalise the INR

• (c) platelet transfusion

• (d) no prophylactic fresh frozen plasma

Active Recall

From memory: compare hepatitis A–E, interpret HBV markers and the window period, give treatments for chronic HBV and HCV, describe jaundice patterns, Gilbert and alcoholic liver disease, outline HCC surveillance, SAAG, ascites and SBP management, and define hepatic encephalopathy, acute liver failure and ACLF.