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Abstract Cirrhosis is defined anatomically as diffuse process with fibrosis and nodular formation ending in disruption of the normal lobular architecture of the liver following hepato— cellular necrosis C Anthony et al., 1977 Functionally the disorder is characterised by disturba— nce of hepatic hemodynamics associated with a reduced functioning liver mass and with secondary alteration of extra— hepatic circulation. The disturbance of hemodynamics is reflected in portal hypertension and reduced effective hepatic blood flow ( Popper, 1977 ). Fibrosis may be centrizpnal as in heart failure or peripheral as in bile duct obstruction and congenital hepatic fibrosis or interlobular in granulomatous liver disease, but without true cirrhosis. Nodule formation without fibrosis, as in Felty’s syndrome, or partial nodular tranformation, is not cirrhosis ( Sherlock, 1989 ). PATHOGENESIS Cirrhosis is initiated by injury and necrosis to hepatocytes. The transition to the characteristic architectural disfigurement depends on processes common to many aetiologic factors there is passive developement of fibrous septa from collapse of the connective tissue framework due to death and loss of liver cells. |