IM5.1-17 | Liver Disease — Practice Quiz

Correct. Gilbert syndrome is caused by a UGT1A1 promoter polymorphism that reduces UDP-glucuronosyltransferase activity by ~30%. It presents with mild unconjugated hyperbilirubinaemia, worsened by fasting or physiological stress, with normal liver enzymes and no haemolysis. It is benign and requires no treatment.

Isolated unconjugated hyperbilirubinaemia with normal liver enzymes and no haemolysis, worsened by fasting = Gilbert syndrome. SAAG is irrelevant here; this is a prehepatic/hepatic conjugation defect, not portal hypertension.

The key features here are isolated unconjugated hyperbilirubinaemia, normal liver enzymes, normal haemogram/reticulocyte count, and worsening with fasting — all pointing to Gilbert syndrome. Haemolysis would show raised reticulocytes; Crigler-Najjar type I presents in neonates with severe unconjugated jaundice; Dubin-Johnson causes conjugated hyperbilirubinaemia.

Correct. An AST:ALT ratio >2:1 (here 120:55 = approximately 2.2:1) is characteristic of alcoholic liver disease. The mechanism is twofold: alcohol depletes pyridoxal phosphate (ALT is more dependent on it), and alcohol induces mitochondrial AST release preferentially. This ratio is diagnostically significant only when absolute enzyme values are elevated.

AST:ALT ratio >2:1 = alcoholic liver disease (alcohol depletes pyridoxal phosphate, reducing ALT synthesis; alcohol also induces mitochondrial AST release). The ratio is only meaningful when absolute enzyme values are elevated.

The AST:ALT ratio >2:1 is a well-established pattern in alcoholic liver disease. In acute viral hepatitis, the ratio is typically <1 with ALT often dominating. The ratio 2:1 in the context of chronic heavy alcohol use and elevated absolute enzyme values strongly supports alcoholic aetiology.

Correct. Hepatitis E (caused by HEV, transmitted faeco-orally via contaminated water) is endemic in India and causes sporadic/epidemic jaundice. It has a case fatality rate of 0.5–1% in the general population but dramatically higher mortality (20–25%) in pregnant women, particularly in the third trimester, where it can cause fulminant hepatic failure. Diagnosis requires IgM anti-HEV serology.

Hepatitis E is the most dangerous hepatitis in pregnancy — case fatality rate rises to 20–25% in the third trimester. In India, HEV is a leading cause of acute fulminant hepatic failure in pregnant women. Always test IgM anti-HEV in jaundiced pregnant women.

The combination of acute jaundice in a pregnant woman in India, with HBsAg negative, anti-HCV negative, and IgM anti-HAV negative, makes Hepatitis E (HEV) the most likely diagnosis. HEV has dramatically elevated mortality (up to 20–25%) in pregnancy, especially the third trimester — this is the key distinguishing clinical fact.

Correct. Confusion, flapping tremor (asterixis), and slurred speech with a clear precipitant (high protein intake) represent West-Haven Grade III hepatic encephalopathy (marked confusion, disoriented, responds to stimuli but cannot do purposeful tasks). Management: lactulose titrated to 2–3 soft stools per day + rifaximin 550 mg twice daily. Identifying and treating the precipitant (here, protein load; other precipitants: GI bleed, infection, constipation, diuretics) is equally important.

West-Haven grading: Grade I = sleep-wake reversal/subtle; Grade II = asterixis/moderate confusion; Grade III = marked confusion, responds to stimuli; Grade IV = coma. Lactulose + rifaximin are first-line. Always identify the precipitant (TIPS mnemonic: Toxins/medications, Infection, Protein load, portosystemic Shunting).

Confusion, asterixis (flapping tremor), and slurred speech = West-Haven Grade III hepatic encephalopathy. The immediate management is lactulose (titrate to 2–3 soft stools/day) + rifaximin, plus identifying and correcting the precipitant. Neomycin is no longer routinely used due to nephrotoxicity.

Correct. SAAG = serum albumin − ascitic albumin = 2.8 − 0.8 = 2.0 g/dL. A SAAG ≥1.1 g/dL indicates portal hypertension-related ascites (cirrhosis, cardiac failure, Budd-Chiari). SAAG ≥1.1 is more reliable than total protein for this distinction. First-line management: spironolactone 100 mg/day (titrate up to 400 mg) ± furosemide 40 mg/day (ratio 100:40 to maintain normonatraemia), combined with dietary sodium restriction to <2 g/day.

SAAG = serum albumin − ascitic albumin. SAAG ≥1.1 = portal hypertension (cirrhosis, right heart failure, Budd-Chiari). SAAG <1.1 = non-portal hypertension (TB peritonitis, malignancy, pancreatitis). Always use same-day serum albumin for accuracy.

SAAG = serum albumin − ascitic albumin = 2.8 − 0.8 = 2.0 g/dL. SAAG ≥1.1 = portal hypertension-related ascites. The formula uses serum minus ascitic albumin, measured on the same day. First-line management is spironolactone ± furosemide with sodium restriction.

Correct. In acute variceal haemorrhage, terlipressin (2 mg IV every 6 hours) is the vasoactive drug of choice — it reduces portal pressure by splanchnic vasoconstriction and reduces mortality. Prophylactic antibiotics (ceftriaxone 1 g IV daily or norfloxacin 400 mg BD) must be started simultaneously because bacterial infection occurs in 35–65% of cirrhotics with GI bleeding and significantly worsens outcomes. Both must be started at presentation, NOT after endoscopy.

Acute variceal bleed management: (1) resuscitate (target Hb 7–8 g/dL; avoid over-transfusion as it increases portal pressure); (2) terlipressin 2 mg IV bolus immediately; (3) prophylactic ceftriaxone immediately; (4) urgent endoscopy within 12 hours for band ligation. BOTH terlipressin and antibiotics before endoscopy — this is the most common management error.

The critical teaching point: in acute variceal haemorrhage, terlipressin AND antibiotics must start at presentation, not after endoscopy. Propranolol is for secondary prophylaxis, not acute bleeding. Omeprazole is for peptic ulcers. FFP alone is insufficient and delays definitive management.

Correct. Spontaneous bacterial peritonitis (SBP) is diagnosed by ascitic fluid PMN count ≥250 cells/mm3, even without a positive culture (culture-negative SBP is common due to low bacterial density). Treatment must NOT wait for culture results: cefotaxime 2 g IV every 8 hours (5 days) is first-line. Albumin infusion (1.5 g/kg at diagnosis and 1 g/kg on day 3) reduces hepatorenal syndrome risk in patients with creatinine >1 mg/dL, bilirubin >4 mg/dL, or BUN >28 mg/dL.

SBP diagnosis: ascitic PMN ≥250 cells/mm3 (not culture). Treat empirically with cefotaxime 2 g 8-hourly for 5 days. Add albumin (1.5 g/kg day 1, 1 g/kg day 3) when creatinine >1, bilirubin >4, or BUN >28 to prevent HRS. After resolution, secondary prophylaxis with norfloxacin 400 mg daily.

SBP is diagnosed when ascitic PMN count is ≥250 cells/mm3 — do not wait for culture (culture-negative SBP is common). Treat immediately with cefotaxime. Adding albumin infusion reduces HRS risk in high-risk patients. Secondary peritonitis (surgical cause) is suspected when total protein >10 g/L and LDH is high — this patient does not fit that profile.

Correct. Anti-tubercular therapy (isoniazid, rifampicin, pyrazinamide) is the most common cause of DILI in India. The threshold for stopping hepatotoxic ATT is: ALT >3x ULN with symptoms (jaundice, nausea), or ALT >5x ULN regardless of symptoms. This patient has 8x ULN with jaundice — all hepatotoxic drugs (H, R, Z) must be stopped immediately. Re-introduce sequentially under monitoring when LFTs recover. Ethambutol and streptomycin (non-hepatotoxic) can be continued.

ATT-DILI: isoniazid and pyrazinamide are most hepatotoxic (idiosyncratic), rifampicin less so. Stop H, R, Z when ALT >3x ULN + symptoms or >5x ULN. Ethambutol is non-hepatotoxic. Re-introduce sequentially (R first, then H, then Z) after LFTs normalise.

ATT-DILI threshold: stop hepatotoxic drugs (H, R, Z) if ALT >3x ULN with symptoms or >5x ULN regardless. This patient has 8x ULN with jaundice — stop H, R, Z immediately. Continuing with dose reduction is dangerous. Ethambutol can be continued as it is not hepatotoxic.

Correct. NAFLD is the most common cause of incidentally raised liver enzymes in patients with metabolic syndrome (obesity, diabetes, hypertension, dyslipidaemia). The diagnosis is one of exclusion: negative viral markers, negative autoantibodies, and no significant alcohol intake, with hepatic steatosis on imaging. The echogenic 'bright liver' on ultrasound confirms fatty infiltration. GGT elevation disproportionate to ALP is a pattern seen in fatty liver, but also in alcohol use — history of alcohol intake must be excluded.

NAFLD diagnosis requires: (1) hepatic steatosis on imaging/biopsy; (2) exclusion of other causes (viral, autoimmune, metabolic); (3) absence of significant alcohol intake (<20 g/day women, <30 g/day men). NAFLD spectrum: simple steatosis → NASH → fibrosis → cirrhosis. Metabolic syndrome is the strongest risk factor.

NAFLD is the most common cause of incidental liver enzyme elevation in patients with metabolic risk factors (obesity + diabetes). The exclusion criteria are met (negative HBsAg, anti-HCV, autoantibodies) and the ultrasound confirms hepatic steatosis. Alcoholic fatty liver requires a significant alcohol history.

Correct. This patient has HBeAg-negative chronic hepatitis B (anti-HBe positive, HBV DNA 2.5 × 10^4 IU/mL with raised ALT and moderate fibrosis on biopsy). Treatment is indicated: HBV DNA >2000 IU/mL + raised ALT + significant fibrosis (F2 or above). TDF (tenofovir disoproxil fumarate) 300 mg/day or entecavir 0.5 mg/day are first-line oral antivirals, continued lifelong (or until seroconversion in HBeAg-positive disease). TDF is safe in pregnancy.

Chronic HBV treatment indications: HBV DNA >2000 IU/mL AND (raised ALT OR significant fibrosis ≥F2). TDF preferred (safe in pregnancy, no resistance). Entecavir 0.5 mg/day is equivalent. Treatment is lifelong in most patients. HBeAg-negative CHB is as serious as HBeAg-positive disease.

HBeAg-negative CHB with HBV DNA >2000 IU/mL + raised ALT + bridging fibrosis meets treatment criteria. TDF or entecavir are first-line; treatment is lifelong. HBeAg negativity does not exclude active disease — HBeAg-negative CHB is the predominant form in India.