Digestive Pathology – Hepatic Vocabulary

A comprehensive set of vocabulary flashcards covering key hepatic pathology concepts from the lecture notes.

Hepatic portal triad

The collective term for a branch of the portal vein, a branch of the hepatic artery, and an interlobular bile duct found in portal tracts.

Liver acinus Zone 1 (periportal)

Region nearest the portal triad; highest in oxygen and nutrients, thus most resistant to hypoxic injury.

Liver acinus Zone 3 (centrilobular)

Region around the central vein; most susceptible to hypoxia and toxic metabolites due to receiving blood last.

Limiting plate

A single layer of hepatocytes that immediately surrounds each portal tract in liver histology.

Primary liver diseases (major)

Viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, and hepatocellular carcinoma.

Jaundice

Yellow discoloration of skin and sclerae caused by impaired conjugation or excretion of bilirubin.

Conjugated hyperbilirubinemia

Water-soluble bilirubin excess leading to dark (tea-colored) urine in liver disease.

Hemosiderin

Iron-containing pigment that accumulates in hereditary hemochromatosis.

Reversible cellular swelling

Cell injury characterized by small clear cytoplasmic vacuoles of dilated ER or Golgi, causing pallor and nuclear displacement.

Fatty change (steatosis)

Abnormal accumulation of triglycerides within hepatocyte cytoplasm.

Microvesicular steatosis

Many tiny cytoplasmic fat vacuoles with a central nucleus in hepatocytes.

Macrovesicular steatosis

Single large fat vacuole displacing the hepatocyte nucleus to the periphery.

Councilman (acidophil) bodies

Eosinophilic apoptotic hepatocytes classically seen in viral hepatitis.

Focal (spotty) necrosis

Scattered individual hepatocyte necrosis within the lobule.

Centrilobular (Zone 3) necrosis

Necrosis around central veins, commonly due to hypoxia or drug toxicity (e.g., acetaminophen).

Mid-zonal (Zone 2) necrosis

Pattern of necrosis classically produced by yellow fever infection.

Bridging necrosis

Confluent hepatocyte death connecting vascular structures (portal-portal, portal-central, or central-central), predisposing to fibrosis and cirrhosis.

Massive (panlobular) hepatic necrosis

Widespread destruction of hepatocytes, often caused by fulminant viral hepatitis or severe drug injury such as acetaminophen overdose.

Interface hepatitis

Inflammation and hepatocyte injury at the portal–periportal junction with destruction of the limiting plate.

Chronic viral hepatitis with interface activity

Most frequently associated with hepatitis B and hepatitis C infections.

Hepatic stellate (Ito) cell

Perisinusoidal cell that transforms into a collagen-producing myofibroblast during fibrosis.

Fibrosis → cirrhosis progression

Periportal or perisinusoidal collagen deposition → bridging fibrosis → regenerative nodules within fibrous septa (cirrhosis).

Acute hepatitis (histology)

Lobular disarray with hepatocyte necrosis and apoptosis.

Chronic hepatitis (histology)

Portal-based chronic inflammation persisting longer than six months.

Hepatotropic viruses

Hepatitis A, B, C, D, and E viruses, which primarily infect the liver.

Hepatitis A transmission

Fecal–oral spread via contaminated food or water, especially in crowded or unsanitary settings.

Hepatitis A chronicity

HAV infection does not produce chronic liver disease or a carrier state in immunocompetent individuals.

Microscopic features of acute HAV

Periportal cholestasis, periportal plasma cells, ballooning degeneration, Councilman bodies, and relative sparing of centrilobular hepatocytes.

Ground-glass hepatocyte

HBsAg-laden hepatocyte with finely granular eosinophilic cytoplasm, characteristic of hepatitis B.

Chronicity rate of hepatitis C

Approximately 50–80 % of HCV infections progress to chronic liver disease.

Hepatitis C lymphoid aggregates

Portal-tract lymphoid follicles often surrounding damaged bile ducts; characteristic but only ~50 % sensitive for HCV.

Cirrhosis

Diffuse hepatic fibrosis forming regenerative nodules and distorting normal architecture.

Common causes of cirrhosis

Chronic HBV or HCV infection, alcoholic liver disease, and non-alcoholic fatty liver disease.

Micronodular vs. macronodular cirrhosis

Micronodular cirrhosis has uniformly small nodules (<3 mm); macronodular cirrhosis shows variable, larger nodules.

Histologic triad of cirrhosis

Bridging fibrosis, regenerative nodules, and loss of normal lobular architecture.

Mallory–Denk (Mallory) bodies

Aggregates of cytokeratin intermediate filaments in hepatocytes, classically associated with alcoholic liver disease.

Focal nodular hyperplasia (FNH)

Hyperplastic liver nodule in non-cirrhotic liver due to altered blood flow, grossly featuring a central stellate scar with radiating septa.

Hepatocellular adenoma risk factors

Benign tumor most common in women of reproductive age, strongly linked to long-term oral contraceptive use.

Histology of hepatocellular adenoma

Well-circumscribed lesion of benign hepatocytes lacking portal tracts and showing thin cell plates with minimal atypia.