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Hepatocirrhosis (cirrhosis) is the irreversible end result of the fibrous scarring and hepatocellualr regeneration that consti-tute the major responses of the liver to a variety of longstand-ing inflammatory, toxic, metabolic, and congestive insults. In cirrhosis, the normal hepatic lobular architecture is replaced by interconnecting bands of fibrous tissue surrounding nodules de. rived from loci of regenerating hepatocytes.
Regenerative nodules may be small (<3 ram, micronodu-lar cirrhosis), a typical feature of alcoholic cirrhosis, or large (>3 ram, macronodular cirrhosis). The latter, also termed postnecrotic cirrhosis, is more commonly seen as a sequel to chronic active hepatitis. The pathologic features of cirrhosis determine its natural history and clinical manifestations. Thus, fibrous scarring and disruption of the hepatic architec-ture distort the vascular bed and lead to portal hypertension and intrahepatic shunting. Normal hepatocyte function is dis-turbed by the resulting inadequacy of blood flow and ongoing direct toxic, inflammatory, and/or metabolic damage to hepa-tocytes.
