PA24.1-9 | Hepatobiliary System — Glossary

Mnemonic for major cholesterol gallstone risk factors: Female, Fat, Forty, Fertile, Fair — each reflecting oestrogen excess, obesity, advancing age, multiparity, or genetic predisposition.

Acute gallbladder inflammation without gallstones, occurring in critically ill patients due to biliary stasis and ischaemia; associated with higher perforation risk than calculous cholecystitis.

Acute inflammation of the gallbladder secondary to cystic duct or Hartmann's pouch obstruction by a gallstone, triggering chemical mucosal injury, ischaemia, and often secondary bacterial infection.

Acute deterioration of stable chronic liver disease, triggered by an identifiable precipitant such as infection, variceal bleeding, or alcohol binge, carrying a high short-term mortality.

A mycotoxin produced by Aspergillus flavus/parasiticus contaminating stored grain and groundnuts; a potent hepatocarcinogen that induces a specific TP53 codon-249 (R249S) mutation, synergistic with HBV.

An acute inflammatory injury pattern in the liver characterised by hepatocyte ballooning, Mallory-Denk bodies, and neutrophilic infiltrate, occurring in the setting of chronic heavy alcohol use.

Enzyme synthesised by biliary epithelium, bone, placenta, and small intestine; elevated in cholestasis and bone disease; confirm biliary origin with concurrent GGT elevation.

An oncofetal glycoprotein normally produced by the fetal liver and yolk sac; elevated in ~70% of HCC cases; a serum level > 400 ng/mL in a cirrhotic patient with a liver mass is diagnostic of HCC.

Morphologically enlarged astrocytes with prominent nuclei and swollen cytoplasm, found in the basal ganglia and cortex in hepatic encephalopathy due to ammonia-induced osmotic stress.

IgM antibody to hepatitis B core antigen; the sole serological marker detectable during the window period (after HBsAg clears, before anti-HBs appears).

An autoantibody directed against F-actin; a serological marker of autoimmune hepatitis type 1, together with ANA and elevated IgG.

Bacterial infection ascending through an obstructed biliary tree; classically presents as Charcot's triad (fever, jaundice, right upper quadrant pain); may progress to Reynolds' pentad with septic shock.

Abnormal accumulation of free fluid in the peritoneal cavity; in portal hypertension, caused by raised sinusoidal hydrostatic pressure, hypoalbuminaemia, and secondary RAAS activation.

A flapping tremor of outstretched hands caused by brief lapses in sustained posture; a clinical sign of metabolic encephalopathy, seen in hepatic, renal, and respiratory failure.

Swelling of hepatocytes due to impaired membrane ion transport; the most common histological change in acute hepatitis; cytoplasm appears pale and granular.

Green deposit of inspissated bile within a dilated bile canaliculus between tumour cells in hepatocellular carcinoma; a pathognomonic marker of hepatocellular (rather than biliary or metastatic) differentiation.

The presence of greenish bile within tumour cell cytoplasm or canalicular spaces in HCC; pathognomonic of hepatocellular differentiation and used to distinguish HCC from cholangiocarcinoma and metastatic adenocarcinoma.

Yellow pigment formed from haem catabolism; the end-product of red blood cell breakdown, metabolised by the liver and excreted in bile.

Gallstones composed predominantly of calcium bilirubinate polymer, forming in sterile supersaturated bile from excess unconjugated bilirubin; seen in haemolytic disorders and cirrhosis.

Fibrous bands connecting portal tracts to each other and to central veins, the histological precursor to cirrhosis; represents irreversible stellate cell activation.

Necrosis forming continuous bands linking portal tracts to central veins (portal-central bridges) or portal-portal; indicates severe acute or active chronic hepatitis.

Soft, laminated gallstones composed of calcium bilirubinate and fatty acid soaps, formed in infected bile through bacterial β-glucuronidase action; may form primarily in bile ducts.

Obstruction of hepatic venous outflow due to thrombosis of one or more hepatic veins, causing posthepatic portal hypertension with painful hepatomegaly, ascites, and centrizonal hepatic necrosis.

Dilated para-umbilical veins visible on the anterior abdominal wall, radiating from the umbilicus, resulting from recanalization of the umbilical vein as a porto-systemic shunt.

Persistence of HBsAg for >6 months with normal or near-normal liver function tests and minimal hepatic inflammation; viral DNA may integrate, conferring HCC risk even without cirrhosis.

Clinical triad of fever with rigors, jaundice, and right upper quadrant pain, indicating ascending cholangitis from biliary obstruction; requires prompt biliary decompression.

A five-parameter clinical scoring system (bilirubin, albumin, PT/INR, ascites, encephalopathy) that classifies cirrhosis severity into Classes A, B, and C and predicts short-term prognosis.

Presence of stones within the common bile duct; may cause obstructive jaundice, ascending cholangitis, or acute pancreatitis depending on the level and degree of obstruction.

Presence of calculi (gallstones) within the gallbladder or biliary tree; most common biliary disorder in adults.

Impairment of bile flow, either within hepatocytes (intrahepatic cholestasis) or in the bile ducts (extrahepatic cholestasis), causing accumulation of conjugated bilirubin.

State in which bile contains more cholesterol than can be solubilised by available bile salts and lecithin, promoting cholesterol monohydrate crystal nucleation.

The irreversible end-stage of chronic liver disease defined by diffuse bridging fibrosis and regenerative nodule formation that distorts the normal hepatic lobular architecture.

A bleeding diathesis resulting from reduced hepatic synthesis of coagulation factors II, V, VII, IX, X; manifested as prolonged PT/INR; Factor VII falls first due to its short half-life.

Water-soluble form of bilirubin produced by UGT1A1-catalysed attachment of glucuronic acid in hepatocytes; filterable by the kidney and detectable in urine.

A shrunken, round, eosinophilic apoptotic hepatocyte (also called apoptotic body); a hallmark of acute hepatitis; may be extruded into the sinusoidal space.

Palpable, non-tender gallbladder in a jaundiced patient, indicating malignant biliary obstruction (typically carcinoma of the head of the pancreas); uncommon with gallstone obstruction.

Rare severe unconjugated hyperbilirubinaemia from complete (Type I) or near-complete (Type II) UGT1A1 deficiency; Type I requires liver transplantation to prevent kernicterus.

Cytochrome P450 2E1; the enzyme responsible for metabolising paracetamol to NAPQI; concentrated in zone 3 (centrilobular) hepatocytes; explains the centrilobular pattern of paracetamol necrosis.

Ratio of AST to ALT; >2:1 is characteristic of alcoholic hepatitis (mitochondrial AST release + relative pyridoxine deficiency); ≈1:1 in viral hepatitis.

A pathognomonic molecular alteration of fibrolamellar HCC created by a somatic deletion on chromosome 19, fusing a heat-shock protein chaperone gene to the catalytic subunit of protein kinase A.

Autosomal recessive conjugated hyperbilirubinaemia caused by MRP2 deficiency; characterised by black liver pigment on biopsy; benign prognosis.

Collection of frank pus within the distended gallbladder lumen resulting from complete cystic duct obstruction with secondary bacterial infection; a surgical emergency.

A distinct variant of HCC occurring in young adults without cirrhosis, characterised by large eosinophilic hepatocytes separated by lamellar fibrous bands and driven by the DNAJB1–PRKACA fusion gene.

A 5-point scale (F0–F4) used to quantify hepatic fibrosis on biopsy: F0=none, F1=portal, F2=periportal, F3=bridging, F4=cirrhosis; guides antiviral treatment decisions.

Massive hepatocyte necrosis resulting in rapid-onset hepatic failure (within 8 weeks of symptom onset) in a patient with no prior liver disease.

Hepatic encephalopathy and coagulopathy (INR >1.5) within 8 weeks of jaundice onset in a patient without pre-existing liver disease; associated with massive hepatic necrosis.

Malignant tumour (usually adenocarcinoma) of the gallbladder, associated with chronic gallstones and cholecystitis; India has among the highest global incidence; prognosis is poor due to late clinical presentation.

Mechanical small bowel obstruction (typically at the ileocaecal junction) caused by a large gallstone entering the gut lumen via a cholecystoenteric fistula; associated with Rigler's triad on plain X-ray.

Liver-specific enzyme elevated in biliary obstruction, alcohol use, and by enzyme-inducing drugs; used to confirm hepatic origin of an isolated ALP elevation.

Benign, common hereditary unconjugated hyperbilirubinaemia caused by a UGT1A1 promoter polymorphism reducing enzyme activity to ~30%; precipitated by fasting and stress.

Hepatocyte with pale, finely granular cytoplasm resulting from smooth-ER proliferation packed with hepatitis B surface antigen (HBsAg); confirmed by orcein or Victoria blue special stains.

Hepatocytes with pale, finely granular eosinophilic cytoplasm due to massive HBsAg accumulation in smooth ER; specific to chronic HBV infection; confirmed by orcein or Victoria blue stain.

Vomiting of blood, often bright red and in large volume when caused by ruptured oesophageal or gastric varices; the most lethal acute complication of portal hypertension.

The nucleocapsid protein of HBV; not detectable in serum but anti-HBc IgM marks acute infection and anti-HBc IgG marks past exposure.

Envelope protein of hepatitis B virus; its presence in serum for >6 months defines chronic hepatitis B infection.

A defective RNA virus that cannot replicate independently; requires HBsAg as its envelope protein; transmitted only in HBV-infected individuals (co-infection or superinfection).

A neuropsychiatric syndrome in liver failure caused by accumulation of neurotoxins — principally ammonia — due to failed hepatic detoxification and porto-systemic shunting.

Accumulation of triglyceride-rich lipid vacuoles within hepatocytes due to impaired fatty acid oxidation or increased synthesis; the earliest, reversible stage of alcoholic liver disease.

Perisinusoidal cells that normally store vitamin A; activated by TGF-β during liver injury to become myofibroblasts that synthesise excess collagen, driving fibrosis.

The commonest primary malignant tumour of the liver, arising from hepatocytes, almost always associated with chronic liver injury (HBV, HCV, cirrhosis, aflatoxin).

Swelling and pallor of hepatocytes due to cytoskeletal disruption by acetaldehyde-protein adducts; a hallmark of alcoholic and non-alcoholic steatohepatitis.

Intrapulmonary vascular dilatation in cirrhosis causing arteriovenous shunting, hypoxaemia, and the clinical signs of platypnoea and orthodeoxia.

Functional acute renal failure in severe liver disease caused by splanchnic vasodilatation leading to compensatory renal vasoconstriction; kidneys are structurally normal.

A virus that preferentially infects hepatocytes; the five classical hepatotropic viruses are HAV, HBV, HCV, HDV, and HEV.

Immunohistochemical marker (hepatocyte paraffin antigen 1) that stains normal hepatocytes and most hepatocellular carcinomas; used alongside Arginase-1 and GPC3 to confirm hepatocellular origin in difficult liver tumours.

The haemodynamic state in portal hypertension characterised by splanchnic vasodilation (mediated by nitric oxide), increased cardiac output, and reduced peripheral vascular resistance, which sustains and amplifies portal hypertension.

Excessive destruction of all blood cell lines (pancytopenia) by an enlarged, congested spleen, commonly occurring in portal hypertension with congestive splenomegaly.

Reduced serum albumin (<35 g/L) due to impaired hepatic synthesis in chronic liver disease; reduces plasma oncotic pressure and contributes to oedema and ascites.

Drug-induced liver injury occurring unpredictably in a small minority of exposed individuals; not dose-dependent; may be metabolic (aberrant CYP450) or immune (hapten-mediated).

Lymphocyte-mediated destruction of periportal hepatocytes at the junction of the portal tract and the hepatic parenchyma (limiting plate); formerly called piecemeal necrosis; the key histological marker of chronic hepatitis activity.

Erosion of the hepatocyte limiting plate at the portal–lobular interface by lymphocytes; the histological hallmark of active chronic hepatitis; used to grade activity.

Yellow discolouration of skin, sclerae, and mucous membranes caused by elevated serum bilirubin (>2.5 mg/dL clinically visible).

Bilirubin-induced brain damage caused by deposition of unconjugated bilirubin in basal ganglia and brainstem nuclei, seen in neonates with severe unconjugated hyperbilirubinaemia.

Proliferation and enlargement of resident hepatic macrophages in response to hepatocyte injury; the enlarged cells contain ceroid/lipofuscin pigment from phagocytosed debris; a feature of acute hepatitis.

The layer of hepatocytes immediately surrounding portal tracts; disrupted in interface hepatitis (piecemeal necrosis) in chronic hepatitis.

Ratio expressing cholesterol saturation of bile relative to its micellar and vesicular solubilising capacity; values >1 indicate supersaturation favouring crystallisation.

Loss of the normal radial cord-and-sinusoid arrangement of hepatocytes due to hepatocyte swelling and dropout in acute hepatitis.

A pattern of cirrhosis with irregular regenerative nodules larger than 3 mm, typical of post-viral hepatitis cirrhosis; carries a higher risk of hepatocellular carcinoma.

Large, single fat vacuoles that displace the hepatocyte nucleus to the cell periphery, seen in alcoholic fatty liver and NAFLD.

Irregular eosinophilic cytoplasmic inclusions in hepatocytes, composed of aggregated misfolded cytokeratin 8 and 18 intermediate filaments; characteristic of alcoholic hepatitis and NASH.

Irregular, rope-like, eosinophilic cytoplasmic inclusion within ballooned hepatocytes, composed of ubiquitinated and misfolded cytokeratin 8/18 intermediate filaments; characteristic of alcoholic hepatitis but also seen in NASH, Wilson disease, and primary biliary cholangitis.

Panacinar destruction of hepatocytes with collapse of the reticulin framework; the macroscopic correlate of fulminant hepatic failure; the liver appears shrunken, yellow-green, and soft.

Special stain that colours collagen blue-green; indispensable for grading liver fibrosis and visualising the fibrous septa surrounding nodules in cirrhosis.

Standardised histological scoring system for chronic hepatitis biopsies consisting of an Activity score (A0-A3, based on interface and lobular hepatitis) and a Fibrosis score (F0-F4, from no fibrosis to cirrhosis).

A pattern of cirrhosis with uniform regenerative nodules smaller than 3 mm, typical of alcoholic, haemochromatotic, and cardiac cirrhosis.

External compression of the common hepatic duct by a large stone impacted in Hartmann's pouch or the cystic duct, causing obstructive jaundice without a stone in the common bile duct itself.

Canalicular membrane transporter that actively secretes conjugated bilirubin into bile; deficient in Dubin-Johnson syndrome.

Chronic distension of the gallbladder with clear mucus secretion resulting from complete cystic duct obstruction in the absence of infection; wall thin and translucent on imaging.

Arrest of inspiration during deep palpation at the right costal margin as the inflamed gallbladder contacts the examiner's hand; positive in acute cholecystitis.

A glutathione precursor used as antidote in paracetamol overdose; replenishes intracellular GSH stores, enabling continued NAPQI detoxification; most effective within 8–10 hours of ingestion.

Non-alcoholic fatty liver disease and its inflammatory variant (non-alcoholic steatohepatitis), histologically identical to alcoholic liver disease but occurring in metabolic syndrome without significant alcohol use.

N-acetyl-p-benzoquinone imine; the reactive electrophilic metabolite of paracetamol generated by CYP2E1; hepatotoxic when glutathione stores are exhausted.

Clustering of neutrophils around Mallory-Denk body-containing hepatocytes; a distinguishing feature of alcoholic hepatitis that differentiates it from the lymphocyte-dominant infiltrate of viral hepatitis.

An Indian-specific entity characterised by idiopathic obliterative portal venopathy causing presinusoidal portal hypertension and massive splenomegaly without hepatic nodule formation or significant hepatocellular dysfunction.

Precipitation of cholesterol monohydrate crystals from supersaturated bile, accelerated by pronucleating factors (mucin, calcium) and retarded by antinucleating apolipoproteins.

Sinusoidal uptake transporters that import conjugated bilirubin and other organic anions from portal blood into hepatocytes; deficient in Rotor syndrome.

Dilated, tortuous submucosal veins in the lower oesophagus formed when the left gastric (coronary) vein shunts blood into the azygos system; rupture causes potentially fatal haematemesis.

Fibrosis radiating from the central vein (zone 3) into the surrounding sinusoids in a pericellular 'chicken-wire' pattern; a direct toxic effect of alcohol on hepatocytes in zone 3, the region of lowest oxygen tension.

Dystrophic mural calcification of the gallbladder on a background of chronic cholecystitis; patchy (selective) calcification carries higher associated risk of gallbladder carcinoma than diffuse calcification.

Sustained elevation of portal venous pressure above 12 mmHg, caused by increased resistance or increased blood flow in the portal circulation, leading to porto-systemic collateral formation and multiple complications.

Invasion of the portal vein lumen by HCC tumour cells; it exacerbates portal hypertension, spreads tumour intraheptically, and is a major adverse prognostic factor.

Pre-existing vascular connections between portal tributaries and systemic veins that dilate and carry blood when portal pressure is elevated, forming varices at clinically important sites.

Jaundice caused by excess bilirubin production (typically haemolysis) that exceeds hepatic conjugation capacity, resulting in predominantly unconjugated hyperbilirubinaemia.

Cluster of hepatocytes enclosed by fibrous septa in cirrhosis, lacking a normally positioned central vein; forms as a proliferative response to hepatocyte loss and represents the hallmark structural unit of cirrhosis.

Silver impregnation stain that highlights the delicate type-III collagen scaffold (reticulin fibres) of the liver plate; collapse of the reticulin network in a nodule indicates loss of normal plate architecture, distinguishing cirrhosis from nodular hyperplasia.

Charcot's triad plus altered sensorium and hypotension, indicating septic shock from ascending cholangitis; a biliary surgical emergency requiring urgent decompression and ICU support.

Radiological triad diagnostic of gallstone ileus: pneumobilia (air in the biliary tree), small bowel obstruction, and ectopic calcific opacity (the obstructing gallstone) visible on plain abdominal X-ray.

Epithelial invaginations of the gallbladder mucosa penetrating through the muscularis propria into the perimuscular connective tissue, arising from chronic elevation of intraluminal pressure in chronic cholecystitis.

Autosomal recessive conjugated hyperbilirubinaemia from OATP1B1/1B3 deficiency; no liver pigment (distinguishes from Dubin-Johnson); benign.

Calculated as serum albumin minus ascites albumin; a value ≥ 1.1 g/dL indicates portal hypertension as the cause of ascites with high specificity.

The histological appearance of neutrophils surrounding and invading ballooned or necrotic hepatocytes; characteristic of alcoholic hepatitis.

Infection of ascitic fluid without a surgically treatable cause, occurring in cirrhotic patients due to bacterial translocation from the gut and impaired hepatic immune clearance.

Focal death of individual or small groups of hepatocytes scattered within the hepatic lobule; associated with lymphocytic infiltration; seen in both acute and chronic hepatitis.

Oxidised form of urobilinogen responsible for the normal brown colour of faeces; absent in complete biliary obstruction, producing pale/clay-coloured stools.

The characteristic pattern of periportal fibrosis in hepatic schistosomiasis (S. mansoni/japonicum), where granulomatous inflammation around embolised eggs causes dense portal tract fibrosis resembling the cross-section of a pipe stem.

The commonest somatic mutation in conventional HCC (~60%); reactivates telomerase, conferring replicative immortality on malignant hepatocytes by preventing telomere shortening.

The commonest histological growth pattern in HCC; tumour cells form plates ≥ 3 cells thick separated by sinusoid-like vascular channels, compared to the 1–2-cell-thick plates of normal liver.

Growth pattern of hepatocellular carcinoma in which tumour cells form plates 2-20 cells thick, separated by endothelial-lined sinusoidal spaces; the most common HCC pattern, seen in over 80% of cases.

Hepatic enzyme that catalyses the conjugation of bilirubin with glucuronic acid, converting it from fat-soluble unconjugated to water-soluble conjugated form.

Lipid-soluble form of bilirubin that is albumin-bound in plasma, insoluble in water, and requires hepatic conjugation before excretion.

Colourless compound formed by bacterial reduction of conjugated bilirubin in the colon; partially reabsorbed and excreted in urine as a normal trace finding.

Presence of tumour cells within vascular channels (portal veins, hepatic veins) in HCC; associated with satellite nodule formation, intrahepatic spread, and adverse prognosis.

Interval during acute hepatitis B recovery when HBsAg has cleared but anti-HBs has not yet appeared; anti-HBc IgM is the only positive marker.

Bacterial enzyme (produced by E. coli, Clostridium spp.) that deconjugates bilirubin glucuronide in bile, releasing insoluble unconjugated bilirubin — the key step in brown pigment stone formation.