CLINICAL AMD LABORATORY FEATURES



The presence of cirrhosis may remain unde­tected until autopsy. Individuals with cirrhosis who experience no symptoms and show little clinical evidence of hepatocellular dysfunction are often said to have well-compensated cirrhosis. As evidence of complications develops, particu­larly signs implying disturbed hepatocellular function, the clinical condition is referred to as decompensated cirrhosis. Where the disease pro­cess leading to cirrhosis primarily affects the he­patocytes, e.g., alcohol (parenchymal liver dis­ease), evidence of failing hepatocellular function may be prominent in the clinical presentation. On the other hand, if the biliary system is primarily affected, as occurs in primary or secondary biliary - cirrhosis, the clinical features of cholestasis pre­dominate and hepatocellular function is often well-preserved until late in the course of the dis­ease.
It is convenient to divide the main clinical and laboratory features of cirrhosis into four categories :
1. Size and consistency of the liver.
2. Features attributable to hepatocellular dys­function. These result from both intrinsically “sick” hepatocytes and the shunting of portal blood away from hepatocytes with consequent failure to extract toxins and metabolites.
3. Features attributable to portal hypertension.
4. Extrahepatic features related to specific dis­eases causing cirrhosis.
Liver size depends upon the underlying path­ological process. In end-stage hepatitis B virus liver disease, the liver is often small, scarred, and shrunken. In alcoholic cirrhosis, fat infiltration may lead to marked enlargement of the liver. Im­paired hepatic detoxification of estrogens, as well as disturbed hypothalamic-pituitary function,produces several cutaneous signs (often called “stigmata” of cirrhosis, e.g., spider angiomata, palmar erythema). Marked jaundice in the ab­sence of complete bile duct obstruction is often a grave prognostic sign implying advanced hepa­tocellular dysfunction. Impaired hepatocellular protein synthesis leads to hypoalbuminemia and hypoprothrombinemia.