IM5.1-17 | Liver Disease — Glossary

An enzyme elevated in ascitic fluid in tuberculous peritonitis (typically >30 IU/L); used as a screening test for TB peritonitis in patients with low-gradient (SAAG <1.1 g/dL) lymphocyte-predominant ascitic fluid; high sensitivity in TB peritonitis but low in the presence of cirrhosis.

An acute inflammatory syndrome in the context of heavy alcohol use, characterised by acute jaundice, fever, hepatomegaly, AST:ALT ratio >2:1, and histological features of hepatocyte ballooning, Mallory-Denk bodies, and neutrophilic infiltrate with zone 3 necrosis; severe disease defined by Discriminant Function >32.

An enzyme found in bile canaliculi, bone, placenta, and intestine; elevated in cholestatic liver disease and bone diseases; GGT elevation confirms the hepatic origin of ALP elevation when the source is ambiguous (GGT is not elevated in bone disease).

A cytoplasmic hepatocyte enzyme; the most liver-specific transaminase; elevated in hepatocellular injury or necrosis; used as the primary marker of hepatocellular pattern in liver function tests; also mildly elevated in skeletal muscle disease and haemolysis.

Immunoglobulin M antibody to hepatitis B core antigen; the diagnostic marker of acute HBV infection; appears early in the acute phase and remains positive for 6–12 months; critical for diagnosing acute HBV in the window period when HBsAg may have cleared but anti-HBs has not yet appeared.

A hepatocyte and mitochondrial enzyme also present in cardiac and skeletal muscle and red cells; less liver-specific than ALT; AST:ALT ratio >2:1 with heavy alcohol history indicates alcoholic liver disease (mitochondrial injury and pyridoxal-5'-phosphate depletion preferentially reduce ALT).

The ratio of serum aspartate aminotransferase to alanine aminotransferase; a ratio >2:1 in the context of elevated transaminases and heavy alcohol history strongly suggests alcoholic liver disease (due to mitochondrial damage and pyridoxal-5'-phosphate depletion preferentially reducing ALT); <2 favours viral hepatitis or NAFLD.

Brief, involuntary lapses of sustained posture resulting from sudden loss of postural muscle tone; elicited by asking the patient to extend both arms with wrists dorsiflexed; the cardinal sign of hepatic encephalopathy grade II; also present in uraemic and hypercapnic encephalopathy (metabolic flap).

Involuntary lapse of sustained posture due to brief loss of postural muscle tone; demonstrated by asking the patient to extend arms with hands dorsiflexed ('stopping traffic'); the cardinal physical sign of hepatic encephalopathy Grade II; also seen in uraemia and respiratory failure (metabolic flap).

The internationally recommended staging system for hepatocellular carcinoma that integrates tumour burden, liver function (Child-Pugh), and patient performance status to guide treatment selection; stages 0/A (curative: resection/ablation/transplant), B (TACE), C (systemic therapy: sorafenib/lenvatinib), D (best supportive care).

Treatment allocation system for hepatocellular carcinoma: Stage 0/A (very early/early) = curative (resection/ablation/transplant); Stage B (intermediate) = TACE; Stage C (advanced, vascular invasion or extrahepatic) = sorafenib/lenvatinib or atezolizumab + bevacizumab; Stage D (end-stage) = best supportive care.

A validated four-question alcohol screening tool: (C)ut down — 'Have you ever felt you should cut down on your drinking?'; (A)nnoyed — 'Have people annoyed you by criticising your drinking?'; (G)uilty — 'Have you ever felt bad or guilty about your drinking?'; (E)ye-opener — 'Have you ever had a drink first thing in the morning to steady your nerves?'; 2+ positive answers suggests probable alcohol use disorder.

Dilated paraumbilical veins visible on the abdominal wall, radiating from the umbilicus in a radial pattern; caused by portal hypertension forcing blood through paraumbilical portosystemic collaterals; flow is away from the umbilicus (distinguishes it from IVC obstruction where flow is upward).

The classical triad of ascending cholangitis: fever/rigors, jaundice, and right upper quadrant pain; caused by bacterial infection of an obstructed bile duct (commonly from choledocholithiasis); Reynolds' pentad adds shock and altered consciousness in severe cases.

A 15-point scoring system for cirrhosis severity incorporating five parameters: serum bilirubin, serum albumin, INR/prothrombin time, degree of ascites, and grade of hepatic encephalopathy. Class A (5–6) = well-compensated; Class B (7–9) = significant dysfunction; Class C (10–15) = decompensated.

Gallstones present in the common bile duct (as opposed to the gallbladder); causes obstructive jaundice, elevated ALP and GGT, and if secondarily infected, ascending cholangitis (Charcot's triad: fever + jaundice + RUQ pain); treated by ERCP with sphincterotomy and stone extraction.

A pattern of liver function test abnormalities characterised by predominantly elevated ALP and GGT (ALP >3× ULN) with relatively preserved transaminases; indicates obstruction to bile flow (intrahepatic or extrahepatic); causes include choledocholithiasis, primary biliary cholangitis, primary sclerosing cholangitis, and drug-induced cholestasis.

Bilirubin glucuronide formed by UDP-glucuronosyltransferase 1A1 in hepatocytes; water-soluble; excreted in bile; elevated in cholestatic and hepatocellular disease; detectable in urine (bilirubinuria) when serum level is elevated.

Liver injury caused by medications, herbal preparations, or toxins; classified as intrinsic (dose-dependent, predictable — prototype: paracetamol) or idiosyncratic (unpredictable, immune or metabolic mechanism — prototype: isoniazid); RUCAM score assesses causality.

A class of oral antivirals that directly inhibit specific steps in the HCV replication cycle (NS3/4A protease, NS5A replication complex, NS5B polymerase); pan-genotypic regimens (sofosbuvir/velpatasvir, glecaprevir/pibrentasvir) achieve sustained virological response (SVR) in >95% of patients; effectively cures HCV in most cases.

Fibrosis and contraction of the palmar fascia causing progressive flexion deformity of the ring and little fingers; associated with chronic alcoholism, cirrhosis, and other conditions; caused by fibroblast activation, possibly through a mechanism related to alcohol-induced growth factor dysregulation.

A combined endoscopic and fluoroscopic procedure allowing access to the biliary system via the ampulla of Vater; primarily a therapeutic procedure (sphincterotomy, stone extraction, stenting); not indicated as a purely diagnostic procedure when MRCP is available; complications include post-ERCP pancreatitis, cholangitis, perforation.

Endoscopic rubber band ligation of oesophageal varices; the standard endoscopic treatment for acute variceal haemorrhage and for secondary prophylaxis; achieves variceal obliteration more quickly and with fewer adverse effects than sclerotherapy.

A sensitive but non-specific marker of hepatic injury, particularly cholestasis and alcohol use; not elevated by bone disease; used to confirm hepatic origin of ALP elevation; elevated in isolation may reflect alcohol use, fatty liver, or enzyme induction by anticonvulsants.

Benign glandular breast tissue enlargement in males; in chronic liver disease, caused by hyperoestrogenaemia from impaired hepatic oestrogen metabolism and reduced testosterone production; distinguished from pseudogynaecomastia (fatty breast enlargement) by the presence of firm, glandular breast tissue palpable beneath the areola.

A secreted antigen reflecting active HBV replication; presence indicates high viral load and high infectivity; its clearance (HBeAg seroconversion to anti-HBe) marks transition to a lower-replication phase in chronic HBV and is a therapeutic goal.

The first serological marker to appear in acute HBV infection; defines current HBV infection; persistence beyond 6 months = chronic HBV; its clearance (followed by appearance of anti-HBs) = resolved HBV. HBsAg-positive individuals are infectious.

Quantitative PCR test for active HCV infection; becomes detectable 1–2 weeks after acute infection; used to confirm active infection after a positive anti-HCV screening test; anti-HCV remains positive lifelong (both in active and resolved infection), so HCV RNA is essential to distinguish the two.

Neuropsychiatric dysfunction caused by inadequate hepatic clearance of nitrogenous waste products, principally ammonia, in cirrhosis; classified by West-Haven criteria: Grade I (subtle personality change), Grade II (obvious confusion, asterixis), Grade III (gross confusion, somnolence), Grade IV (coma); precipitants include GI bleed, infection, diuretic excess, constipation.

See asterixis; the term 'hepatic flap' specifically emphasises its association with hepatic encephalopathy, while 'asterixis' is the generic term for the sign regardless of cause.

Passive immunisation using anti-HBs antibodies derived from human plasma; used for post-exposure prophylaxis (needle-stick, sexual exposure) and for neonates of HBsAg-positive mothers (0.5 mL IM at birth, simultaneously with the HBV birth dose vaccine); provides immediate but short-term (3–6 months) protection.

A pattern of liver function test abnormalities characterised by predominantly elevated ALT and AST (>3× ULN) with relatively preserved ALP; indicates hepatocyte injury or necrosis; causes include viral hepatitis, alcoholic hepatitis, NAFLD, drug-induced hepatocellular injury, and autoimmune hepatitis.

Functional renal failure complicating advanced cirrhosis with ascites; caused by splanchnic vasodilatation-driven renal vasoconstriction; Type 1 (HRS-AKI) is rapid (creatinine doubling within 2 weeks); Type 2 is gradual; treated with terlipressin plus albumin.

Elevation of serum bilirubin above 1.2 mg/dL; clinically visible as jaundice when bilirubin exceeds approximately 2.5–3 mg/dL; classified as pre-hepatic (unconjugated dominant), hepatic (mixed), intrahepatic cholestatic (conjugated dominant), or extrahepatic obstructive (conjugated dominant).

Golden-brown deposits of copper in Descemet's membrane at the peripheral cornea, best visualised by slit-lamp examination; pathognomonic for Wilson disease when present in the context of hepatic or neuropsychiatric disease; may be visible to the naked eye in advanced cases.

Clinical criteria for identifying patients with acute liver failure (paracetamol or non-paracetamol induced) unlikely to survive without liver transplantation; paracetamol ALF: pH <7.3 OR (INR >6.5 + creatinine >3.4 mg/dL + grade III–IV encephalopathy); non-paracetamol ALF: INR >6.5 OR three of five specified variables including age extremes, aetiology, jaundice-to-encephalopathy interval, bilirubin, INR.

A non-absorbable disaccharide used in hepatic encephalopathy management; fermented by colonic bacteria to short-chain organic acids that acidify the colon and convert ammonia (NH₃) to ammonium (NH₄⁺) — ionised form that cannot cross the gut epithelium; also acts as a laxative to clear nitrogenous substrate; dose titrated to 2–3 soft stools per day.

White discolouration of the nails; in the context of liver disease, caused by hypoalbuminaemia altering the nail bed vascular supply; Terry's nails (distal pink/brown band with proximal white) is a variant specifically associated with cirrhosis.

Liver transplantation using a portion (typically the right lobe) of the liver from a living donor, usually a first-degree relative; the remaining donor liver regenerates over weeks; particularly important in India where deceased donor organ availability is severely limited; donor mortality approximately 0.1–0.5% at experienced centres.

Eosinophilic intracytoplasmic inclusions in hepatocytes composed of aggregated ubiquitinated cytokeratin 8 and 18 filaments; a histological hallmark of alcoholic liver disease (also seen in NASH, Wilson disease, and other conditions); associated with hepatocyte ballooning injury.

A mortality prediction score for cirrhosis calculated from three objective laboratory values: serum bilirubin, serum creatinine, and INR. Used for liver transplant allocation. A score ≥15 generally indicates transplant benefit. Does NOT include albumin or clinical parameters.

The internationally accepted criteria for liver transplantation in hepatocellular carcinoma: single tumour ≤5 cm OR up to 3 tumours each ≤3 cm, with no macrovascular invasion and no extrahepatic metastases; 5-year post-transplant survival >70%; HCC outside Milan criteria generally not considered for transplant without downstaging.

Non-invasive MRI-based imaging of the biliary and pancreatic ductal system using heavily T2-weighted sequences; the diagnostic investigation of choice for biliary obstruction when ERCP intervention is not immediately planned; images the entire biliary tree without radiation or endoscopy; cannot provide therapeutic intervention.

The antidote for paracetamol hepatotoxicity; replenishes hepatocyte glutathione stores (by providing cysteine precursor), neutralising NAPQI before it binds mitochondrial proteins; most effective when given early (within 8–10 hours of ingestion); evidence also supports its use in non-paracetamol acute liver failure.

The reactive electrophilic metabolite of paracetamol produced by CYP2E1 and CYP3A4; normally detoxified by hepatocyte glutathione; accumulates in paracetamol overdose and causes centrilobular (zone 3) hepatocyte necrosis; counteracted by N-acetylcysteine therapy.

Reddening of the thenar and hypothenar eminences of the palms, sparing the central palm; caused by hyperoestrogenaemia and increased cutaneous blood flow; a sign of chronic liver disease and occasionally hyperthyroidism or pregnancy.

Ascitic fluid polymorphonuclear leucocyte count ≥250 cells/mm³ is the diagnostic criterion for SBP and triggers immediate empirical antibiotic treatment; this threshold is used even when culture is negative because culture sensitivity in SBP is low (40–50%).

Elevation of portal venous pressure above 12 mmHg (HVPG ≥12 mmHg); drives the major complications of cirrhosis including oesophageal varices, ascites, SBP, and hepatorenal syndrome; sinusoidal type is the most common (due to cirrhosis).

A haemodynamic complication of large-volume paracentesis (>5 litres) in which rapid reduction of intra-abdominal pressure worsens splanchnic vasodilatation, reducing effective circulating volume and potentially triggering hepatorenal syndrome; prevented by IV albumin infusion (6–8 g per litre of ascites removed).

An autoimmune chronic progressive cholestatic liver disease characterised by immune-mediated destruction of small intrahepatic bile ducts; predominantly affects middle-aged women; presents with pruritus, fatigue, and elevated ALP; anti-mitochondrial antibody (AMA) is present in >95%; treated with ursodeoxycholic acid.

A non-absorbable oral antibiotic active against gram-positive, gram-negative, and anaerobic gut bacteria; reduces intestinal ammonia production; combined with lactulose for recurrent or refractory hepatic encephalopathy; very few systemic side effects due to negligible absorption; dose 550 mg twice daily.

A graph plotting serum paracetamol concentration versus time since ingestion; used to predict risk of hepatotoxicity after acute paracetamol overdose and to guide N-acetylcysteine administration; serum paracetamol must be drawn at ≥4 hours post-ingestion for accurate interpretation.

Calculated as serum albumin minus ascites albumin (in g/dL); SAAG ≥ 1.1 g/dL indicates portal hypertension as the driving mechanism; SAAG < 1.1 g/dL indicates a non-portal aetiology such as TB peritonitis, malignant ascites, or pancreatitis.

Bacterial infection of ascitic fluid in cirrhotic patients; diagnosed when ascitic PMN count ≥250 cells/mm³; treated empirically with third-generation cephalosporins without waiting for culture results; bedside inoculation into blood culture bottles increases culture sensitivity from ~40% to ~80%.

A clinical examination finding for ascites; dullness in the flank on percussion shifts to the dependent flank when the patient rolls to the opposite side, because the ascitic fluid redistributes by gravity; requires approximately 500 mL of ascitic fluid to be clinically detectable.

Cutaneous vascular lesions with a central arteriole from which fine vessels radiate like spider legs; found on the chest wall, face, and arms above the nipple line; caused by hyperoestrogenaemia due to impaired hepatic oestrogen catabolism; >5 is considered clinically significant for chronic liver disease.

An aldosterone receptor antagonist (potassium-sparing diuretic); first-line diuretic for cirrhotic ascites because it targets the RAAS-driven sodium retention that underlies ascites formation; combined with furosemide in a 100:40 ratio to prevent hyperkalaemia; maximum dose 400 mg/day.

Bacterial infection of ascitic fluid in cirrhotic patients, usually by gram-negative enteric organisms via bacterial translocation; diagnosed when ascitic PMN count ≥ 250 cells/mm³; treated empirically with third-generation cephalosporins before culture results.

HCV RNA undetectable 12 weeks after completing antiviral treatment; the definition of cure in hepatitis C; associated with regression of liver fibrosis, reduction in HCC risk, and improved survival; achieved in >95% of patients with current pan-genotypic DAA regimens.

A nucleotide analogue reverse transcriptase inhibitor; first-line antiviral treatment for chronic hepatitis B; high potency, very high resistance barrier, inexpensive as generic; safe in pregnancy (FDA category B); used in pregnant women with high HBV DNA to prevent perinatal transmission.

A synthetic vasopressin analogue that causes splanchnic vasoconstriction; first-line pharmacological treatment for hepatorenal syndrome (combined with albumin infusion) and an adjunct in acute variceal haemorrhage; mechanism: reduces splanchnic blood flow and portal pressure, redirecting blood to the kidneys.

An interventional radiology procedure placing an expandable metal stent between the portal vein and hepatic vein via the internal jugular vein, creating a low-resistance intrahepatic shunt that reduces portal pressure; used for refractory ascites, refractory variceal haemorrhage, and Budd-Chiari syndrome; main complication is worsening hepatic encephalopathy.

Water-insoluble bilirubin bound to albumin in plasma; not filtered by the kidney; elevated in pre-hepatic (haemolytic) jaundice and hereditary conjugation defects such as Gilbert syndrome and Crigler-Najjar syndrome.

Grading system for HE severity: Grade I = subtle personality change, impaired attention; Grade II = obvious confusion, disorientation, asterixis; Grade III = somnolence, gross confusion, incoherent speech — still arousable; Grade IV = coma, not arousable.

An autosomal recessive disorder of copper metabolism caused by mutations in the ATP7B gene, impairing hepatic copper excretion; copper accumulates in liver, brain, cornea (Kayser-Fleischer rings), and kidneys; presents in young adults with hepatitis/cirrhosis + neuropsychiatric features + haemolytic anaemia; treated with copper chelation (d-penicillamine or trientine) or zinc.

The period in acute HBV infection when HBsAg has declined to undetectable levels but anti-HBs has not yet appeared; the only serological marker reliably positive during this period is anti-HBc IgM; missing this diagnosis is prevented by including anti-HBc IgM in the acute hepatitis serology panel.

Yellow lipid deposits at the medial eyelid margins (not specific to the eyelid but typical); associated with prolonged cholestasis and elevated serum cholesterol; common in primary biliary cholangitis.