Acute viral hepatitis There is disruption of lobular architecture, inflammatory cells in the portal tracts & sinusoids, and hepatocellular apoptosis (arrow).

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Acute viral hepatitis There is disruption of lobular architecture, inflammatory cells in the portal tracts & sinusoids, and hepatocellular apoptosis (arrow).

Portal inflammation with interface hepatitis (arrow) Acute viral hepatitis Portal inflammation with interface hepatitis (arrow)

Acute viral hepatitis B Acute viral hepatitis B. Centrolobular area of liver lobule, characterized by ballooning of hepatocytes, and mononuclear (mainly lymphocytic) inflammatory infiltration. (H&E)

Acute viral hepatitis: Acidophilic (apoptotic) bodies Hepatocytes shrink, become intensely eosinophilic, and have fragmented or absent nuclei. Apoptotic cells are phagocytosed within hours by macrophages and hence may be difficult to find despite extensive apoptosis.

Acute viral hepatitis B with confluent necrosis Severe necrotizing acute viral hepatitis B. Overview of liver lobule; mild to moderate mononuclear cell infiltration in portal tracts (lower left, top, and lower right). Bridging portal-central confluent lytic necrosis, creating a "star-shaped" area of necrosis with a centri-lobular vein at its center (arrow) and peripheral points reaching portal tracts. Inflammatory cells are scattered throughout the lobule. (H&E)

Chronic hepatitis showing interface hepatitis (formerly piecemeal necrosis) Interface hepatitis. Lymphocytic infiltrates extend from the portal tracts into acinar tissue with destruction of the limiting plate. Findings are consistent with autoimmune hepatitis, drug reaction, or viral infection.

Interface hepatitis (piecemeal necrosis) Note inflamed portal tract (upper right) and wedge-like extension of necro-inflammation (towards lower left) and irregular interface between portal periphery and adjacent parenchyma.

Chronic hepatitis with hepatocytes regeneration (hepatitic-type liver cell rosettes) Severe chronic viral hepatitis B. Area of multilobular lytic necrosis in phase of postnecrotic collapse and early fibrosis, with several small islands of surviving hepatocytes, appearing swollen and pale, and sometimes arranged in tubular fashion (”hepatitic-type liver cell rosettes”). (H&E)

Chronic viral hepatitis B showing ground glass hepatocytes Ground glass hepatocytes, characterized by more pale, eosinophilic, and homogeneous cytoplasm than surrounding normal (more granular) hepatocytes. Note (artifactual) cleft between "ground glass" cytoplasm and hepatocellular cell membrane. The change corresponds to extensive endoplasmic reticulum hyperplasia and massive accumulation of HBsAg. (H&E)

Chronic viral hepatitis C Portal lymphoid aggregates and minimal steatosis. The findings are consistent with a chronic hepatitis C infection.

Chronic viral hepatitis C progressing to cirrhosis This is a case of viral hepatitis C with extensive fibrosis and progression to macronodular cirrhosis, as evidenced by the large regenerative nodule at the center right.

Posthepatitic cirrhosis Cirrhosis resulting from chronic viral hepatitis. Note the irregular nodularity of the liver surface resulting in a macronodular pattern of cirrhosis.