IM5.1-17 | Liver Disease — Graded Quiz

Correct. Indications for liver transplantation include: MELD ≥15 (transplant benefit exceeds mortality without transplant), Child-Pugh Class C (score ≥10), or specific complications (recurrent SBP, refractory ascites, hepatopulmonary syndrome, portopulmonary hypertension, hepatocellular carcinoma within Milan criteria). For alcoholic cirrhosis, most transplant centres require 6 months of documented abstinence ('6-month rule') to assess hepatic recovery and commitment. Recurrent SBP and ongoing HE despite optimal medical therapy are strong indicators of need.

Liver transplant indications: MELD ≥15, Child-Pugh C, recurrent SBP, refractory ascites, hepatopulmonary syndrome, HCC within Milan criteria (single lesion ≤5 cm OR ≤3 lesions each ≤3 cm, no vascular invasion). Alcoholic cirrhosis: 6-month abstinence rule. Absolute contraindications: active alcohol/drug use, extrahepatic malignancy, severe cardiopulmonary disease.

MELD ≥15 is the threshold where transplant benefit outweighs mortality on the waiting list. For alcoholic liver disease, 6 months of abstinence is required by most programmes. Recurrent SBP and Grade II encephalopathy despite optimal therapy are indicators of disease severity that support listing. Alcoholic aetiology is not a contraindication — abstinence is required.

Correct. The pattern of predominantly conjugated hyperbilirubinaemia, markedly elevated ALP and GGT with only mild ALT elevation (cholestatic pattern), dilated intrahepatic ducts, and dilated CBD in the context of recent cholecystectomy localises to post-cholecystectomy biliary complication — either a bile duct injury or a retained common bile duct stone. ERCP is preferred when therapeutic intervention (stone extraction, stenting of a duct injury) is anticipated. MRCP is preferred when diagnosis alone is needed or the patient is high surgical risk.

Cholestatic pattern: conjugated bilirubin, ALP/GGT dominant, mildly elevated ALT. Hepatocellular pattern: ALT/AST dominant. Post-cholecystectomy cholestasis = bile duct injury or retained stone → ERCP (therapeutic) or MRCP (diagnostic). Key rule: dilated CBD on ultrasound always warrants further biliary imaging.

The cholestatic biochemical pattern (high ALP/GGT, mildly elevated ALT, conjugated bilirubin) with biliary dilatation on ultrasound after recent cholecystectomy points to a mechanical biliary obstruction from duct injury or retained stone. ERCP/MRCP is the investigation of choice. Liver biopsy and anti-mitochondrial antibody are for chronic liver disease and primary biliary cholangitis, not acute post-surgical obstruction.

Correct. Hepatorenal syndrome type 1 (HRS-AKI, now reclassified under AKI staging) is functional renal failure in cirrhosis. Diagnostic criteria: cirrhosis with ascites, rise in creatinine ≥0.3 mg/dL in 48 hours or >50% from baseline, no structural kidney injury (no casts, no proteinuria, no obstruction), and no response to a 48-hour albumin challenge (1 g/kg/day). Urine sodium <10 mEq/L reflects intense renal sodium avidity from splanchnic vasodilation. Treatment: terlipressin 0.5–2 mg IV every 4–6 hours (titrated to creatinine response) + IV albumin. Terlipressin reverses HRS in ~50% of cases. Liver transplant is the only cure.

HRS-AKI: functional renal failure in cirrhosis from splanchnic vasodilation → systemic hypotension → renal vasoconstriction. Key: urine Na <10 mEq/L, no structural kidney disease, no response to albumin challenge. Treatment: terlipressin + IV albumin. Noradrenaline + albumin is used in intensive care settings. Liver transplant is definitive.

HRS-AKI criteria: cirrhosis with ascites, creatinine rise ≥0.3 mg/dL in 48 hours, no structural kidney disease, no response to albumin challenge. The low urine Na (<10) reflects intense renal sodium retention from splanchnic vasodilation. Terlipressin + albumin is the specific pharmacological treatment. Pre-renal AKI would respond to volume; ATN would show casts.

Correct. In a pregnant woman with high HBV viral load (HBV DNA >200,000 IU/mL or >10^6 copies/mL), vertical transmission risk is ~90% even with infant immunoprophylaxis. Tenofovir disoproxil fumarate (TDF) started at 28–32 weeks reduces maternal viral load and lowers transmission risk. TDF is safe in pregnancy (FDA category B). Entecavir is FDA category C and should be avoided. At delivery: newborn receives HBIG (0.5 mL IM) plus first dose of HBV vaccine within 12 hours — this combination reduces transmission by >95%.

HBV in pregnancy: TDF (not entecavir, not interferon) from 28–32 weeks if viral load >200,000 IU/mL. Newborn: HBIG 0.5 mL + HBV vaccine within 12 hours of birth → >95% prevention. Vertical transmission is the dominant route of HBV transmission globally. Breastfeeding is NOT contraindicated with immunoprophylaxis.

Pegylated interferon is absolutely contraindicated in pregnancy. For highly viraemic HBV mothers (DNA >200,000 IU/mL), TDF from 28–32 weeks reduces transmission risk. Entecavir is category C and not preferred in pregnancy. Newborn immunoprophylaxis (HBIG + vaccine within 12 hours) is mandatory regardless.

Correct. The Charcot triad — fever, jaundice, and right upper quadrant pain — is the classic presentation of acute cholangitis (ascending infection of the biliary tree). Here it is caused by a CBD stone causing biliary obstruction with secondary bacterial infection. Management: IV antibiotics (piperacillin-tazobactam or meropenem in severe cases) AND urgent biliary drainage by ERCP with stone extraction within 24 hours (or 12 hours in Reynold's pentad — adds hypotension and altered consciousness). ERCP is the definitive treatment; antibiotics alone without drainage are insufficient.

Charcot triad = acute cholangitis: fever + RUQ pain + jaundice. Reynold's pentad adds hypotension + confusion = suppurative cholangitis (emergency). Treatment: IV antibiotics + urgent ERCP with stone extraction. CBD stone is the most common cause in India. If ERCP fails, percutaneous biliary drainage.

Charcot triad (fever + jaundice + RUQ pain) = acute cholangitis until proven otherwise. The dilated CBD confirms biliary obstruction. Antibiotics alone are insufficient; urgent biliary drainage by ERCP is the essential treatment. Reynold's pentad (adds shock and altered consciousness) indicates suppurative cholangitis requiring emergency decompression.

Correct. This pattern — HBsAg negative, anti-HBs positive, anti-HBc IgG positive — represents past resolved natural HBV infection. The presence of anti-HBc (core antibody) is the key discriminating marker: it appears only after natural infection (not vaccination). Vaccination produces ONLY anti-HBs (no anti-HBc). In the window period, both HBsAg and anti-HBs are negative while IgM anti-HBc is positive. Occult HBV has detectable HBV DNA despite negative HBsAg.

Hepatitis B serology: HBsAg = active infection; anti-HBs = immunity (vaccine or resolved); anti-HBc IgM = acute infection or reactivation; anti-HBc IgG = past exposure. Vaccination = anti-HBs positive ONLY. Natural resolved infection = anti-HBs + anti-HBc IgG. Window period = IgM anti-HBc only positive.

The key distinguishing marker is anti-HBc: present after natural infection, absent after vaccination. Past resolved natural infection = HBsAg negative + anti-HBs positive + anti-HBc IgG positive + HBV DNA undetectable. Vaccination alone gives only anti-HBs positive, anti-HBc negative. Window period: HBsAg negative, anti-HBs negative, IgM anti-HBc positive.

Correct. Primary biliary cholangitis (PBC, formerly primary biliary cirrhosis) is an autoimmune destruction of intrahepatic small bile ducts. Classic profile: middle-aged woman, progressive cholestasis (high ALP/GGT, conjugated bilirubin), pruritus, and a positive anti-mitochondrial antibody (AMA) in high titre (≥1:40 is diagnostic). AMA M2 subtype (against the pyruvate dehydrogenase complex) is 95% sensitive and specific. Treatment: UDCA 13–15 mg/kg/day improves transplant-free survival. Autoimmune hepatitis is characterised by hepatocellular pattern (high ALT) and ANA/anti-smooth muscle antibody.

PBC: chronic cholestasis in middle-aged women + AMA positive (titre ≥1:40) = diagnosis (no biopsy needed if both criteria met). UDCA 13–15 mg/kg/day is first-line treatment — slows progression. Second-line: obeticholic acid. Pruritus: cholestyramine or rifampicin.

PBC: middle-aged woman + cholestatic pattern (high ALP/GGT) + pruritus + positive AMA ≥1:40. AMA is the diagnostic marker. UDCA is the first-line treatment. Autoimmune hepatitis has hepatocellular pattern (high ALT, ANA or anti-SMA positive). These are distinct conditions.

Correct. LI-RADS 5 (arterial enhancement + washout on portal venous phase in a cirrhotic liver) is diagnostic of hepatocellular carcinoma (HCC) — biopsy is NOT required when imaging criteria are met in a cirrhotic liver. For a 3.2 cm lesion with no extrahepatic spread, the lesion exceeds the within-Milan criteria for transplant (single ≤5 cm OR ≤3 lesions each ≤3 cm). A single 3.2 cm lesion IS within Milan. Assessment for resection (non-cirrhotic or Child-Pugh A with adequate liver reserve) or transplant (within Milan, MELD-based priority) is the first step. If not eligible, locoregional therapies (TACE, ablation) extend survival.

HCC in cirrhosis: surveillance with 6-monthly ultrasound ± AFP. Diagnosis: LI-RADS 5 imaging (no biopsy needed). Milan criteria: single ≤5 cm OR ≤3 lesions each ≤3 cm, no vascular invasion. Treatment hierarchy: resection → transplant → locoregional (TACE/ablation) → systemic (sorafenib/lenvatinib). Child-Pugh score guides resection eligibility.

HCC diagnosis in cirrhotic liver: typical imaging (arterial enhancement + washout on CT/MRI) = no biopsy needed. Single 3.2 cm lesion is within Milan criteria (≤5 cm single lesion). Curative options: resection (Child-Pugh A, no portal HTN) or transplant. Sorafenib is for advanced HCC (vascular invasion or extrahepatic spread). Locoregional therapy (TACE/ablation) bridges to transplant or treats non-resectable disease.

Correct. Non-cirrhotic portal hypertension (NCPH) — either extrahepatic portal vein obstruction (EHPVO, common in children and young adults in India, often from neonatal omphalitis) or idiopathic non-cirrhotic portal hypertension — presents with portal hypertensive complications (variceal bleeding, splenomegaly, hypersplenism causing thrombocytopaenia) but with NORMAL or near-normal liver function tests. The preserved liver function (normal enzymes, mildly elevated bilirubin) and young age with no alcohol history should prompt consideration of NCPH rather than cirrhosis. EHPVO on Doppler shows portal vein cavernous transformation.

Non-cirrhotic portal hypertension: EHPVO (most common in young Indians, caused by neonatal umbilical sepsis or prothrombotic states) and idiopathic NCPH. Key: normal or near-normal LFTs, preserved hepatic synthetic function, splenomegaly, and hypersplenism. Doppler shows portal vein cavernous transformation in EHPVO. Prognosis better than cirrhotic portal HTN.

Normal liver enzymes with portal hypertension features (varices, splenomegaly, hypersplenism) in a young non-alcoholic patient = non-cirrhotic portal hypertension. EHPVO is the most common cause in India. Budd-Chiari involves hepatic venous outflow obstruction with tender hepatomegaly and ascites. Cirrhosis would show elevated enzymes and a small nodular liver.

Correct. Diuretic-induced complications (rising creatinine indicating AKI, hyponatraemia) are indications to reduce or stop diuretics. Diuretics should be stopped when: serum Na <125 mEq/L (or Na <130 mEq/L with symptoms), creatinine rising above 1.5 mg/dL, or encephalopathy occurs. This patient meets criteria for diuretic-induced AKI. If ascites is refractory (no response to maximum doses for 4 weeks, or recurs despite compliance), large-volume paracentesis (4–6 L) with albumin cover (6–8 g/L ascites removed) is the management. TIPS can be considered for refractory ascites in appropriate candidates.

Diuretic-induced complications: hyponatraemia Na <125 mEq/L, creatinine >1.5 mg/dL, encephalopathy, muscle cramps → reduce/stop diuretics. Refractory ascites defined as: no response to spironolactone 400 mg + furosemide 160 mg with Na restriction for 4 weeks, OR recurrence within 4 weeks. Management: serial LVP + albumin (8 g/L removed). TIPS reduces paracentesis frequency.

Diuretic complications: stop furosemide if creatinine rises >1.5 mg/dL; stop both diuretics if serum Na <125 or renal failure occurs. Increasing diuretics at this point would worsen renal function. Refractory ascites: LVP + albumin cover (8 g/L removed). TIPS for suitable candidates.

Correct. Tuberculous peritonitis: SAAG <1.1 (not portal hypertension), high total protein (exudate), lymphocyte-predominant cell differential, and elevated ADA (≥36 U/L in ascites is highly sensitive and specific for TB peritonitis in India). Rural Bihar has high TB endemicity. While elevated ADA strongly suggests TB peritonitis, the diagnostic gold standard is peritoneal biopsy via laparoscopy with histology showing caseating granulomas and/or culture for Mycobacterium tuberculosis. Treatment: standard NTEP 2HRZE + 4HRE, extended to 9 months for abdominal TB by many centres.

TB peritonitis: SAAG <1.1, exudate (protein >25 g/L), lymphocyte-predominant, elevated ADA ≥36 U/L. Diagnosis: laparoscopic peritoneal biopsy (gold standard). Culture of ascites has low yield. ADA has good sensitivity in India. Treatment: NTEP regimen (2HRZE+4HRE), often extended to 9 months for abdominal TB.

SAAG <1.1 excludes portal hypertension as the cause — cirrhosis causes SAAG ≥1.1. High protein exudate + lymphocyte predominance + elevated ADA in an Indian patient from a high-burden area = TB peritonitis. Diagnostic standard: laparoscopy with peritoneal biopsy. ADA ≥36 U/L in ascites has high sensitivity and specificity for TB in this setting.