Patterns of Hepatic Injury
Degeneration & Intracellular AccumulationDegeneration
mild to moderate hepatocyte swelling reversible
severe damage ballooning degeneration irregularly clumped organelles and large clear spaces
Accumulations in Viable Hepatocytes
iron and copper
triglyceride fat deposits STEATOSIS
microvesicular – multiple, tiny (e.g. acute fatty liver of pregnancy, alcoholic fatty liver
macrovesicular – single large deposit displacing the nucleus (e.g. obesity, diabetes, alcoholism)
Macrovesicular steatosis
Iron stain using the Prussian Blue Reaction (x400). Hemosiderin granules stain as dark blue, coarse granules.Patterns of Hepatic Injury
Necrosis and ApoptosisTypes:
Ischemic coagulative necrosis – “mummified” liver cells with lysed nuclei
Apoptotic cell death – shrunken, pyknotic & intensely eosinophilic cells with fragmented nuclei
Lytic necrosis – outcome of ballooning degeneration (+) shards of cellular debris
Liquefactive necrosis - abscesses
Necrosis (left lower) is around the centrilobular area. The periportal area is viable.
Ischemia of centrilobular area resulting in coagulative necrosis of hepatic cords. (Preservation of cellular contour with disappearance of nucleus) Some viable hepatocytes with nucleus are seen in the upper middle and upper right areas.Bridging confluent lytic necrosis in severe chronic viral hepatitis B. Inflamed portal tract ‘bridged’ through area of necrosis with centrilobular area (lower left). The upper right part corresponds to an area of extensive lytic necrosis.
Patterns of Hepatic Injury
Necrosis and ApoptosisDistribution:
Centrilobular – most common; immediately around terminal hepatic vein
Mid-zonal and periportal – rare
Degree of involvement:
Focal or spotty – limited to scattered cells within hepatic lobules
Interface hepatitis – between periportal parenchyma & inflamed portal tracts
Bridging necrosis – span adjacent lobules
Submassive necrosis – entire lobules
Massive – most of the liver
Interface hepatitis
Patterns of Hepatic Injury
InflammationHepatitis
Influx of acute and chronic inflammatory cells
Regeneration
Occurs in all but the most fulminant hepatic diseases
Features:
Mitosis
Thickening of hepatic cords
Disorganization of parenchymal structure
Patterns of Hepatic Injury
FibrosisConsequence of inflammation or direct toxic insult to liver
Irreversible
May eventually subdivide liver into nodules of proliferating hepatocytes surrounded by scar tissue CIRRHOSIS