Articles on Medical Diseases and Conditions

Tag: Cirrhosis

  • Dilutional Syndromes

    Cirrhosis is frequently associated with hyponatremia and hypokalemia, either separately or concurrently. There are a variety of etiologies: ascitic fluid sequestration; attempts at diuresis, often superimposed on poor diet or sodium restriction; paracentesis therapy; and hemodilution. Electrolyte abnormalities are more likely to appear when ascites is present and are more severe if azotemia complicates liver disease. Hemodilution is a frequent finding in cirrhosis, especially with ascites; this may be due to increased activity of aldosterone, which is normally deactivated in the liver, or sometimes is attributable to inappropriate secretion of AVP (ADH).

    Congestive heart failure is frequently associated with hyponatremia and much less frequently with hypokalemia. The most frequent cause of hyponatremia is overtreatment with diuretic therapy, usually in the context of dietary sodium restriction. However, sometimes the hyponatremia may be dilutional, due to retention of water as the glomerular filtration rate is decreased by heart failure or by inappropriate secretion of AVP (ADH). If hypokalemia is present, it usually is a side effect of diuretics.

  • Cirrhosis

    The most common etiologies of portal cirrhosis are alcohol, hepatitis virus, or unknown (cryptogenic) cause. Less common causes are primary biliary cirrhosis and genetically related cirrhosis (Wilson’s disease, hemochromatosis, and alpha-1 antitrypsin deficiency). Cirrhosis exhibits a wide spectrum of test results, depending on whether the disease is active or inactive and on the degree of hepatocellular destruction. In patients with early or moderate degrees of inactive cirrhosis, there are usually no abnormalities in bilirubin or enzyme test results. Bile acid assay may be abnormal. In more pronounced degrees of inactive cirrhosis there may be minimal or mild elevations of AST, serum gamma-globulin, ALP, and serum bilirubin levels, although no definite pattern can be stated. In advanced cases the PT begins to rise, and mild abnormalities on other liver function tests are more frequent.

    In “active” cirrhosis (florid cirrhosis or alcoholic hepatitis), liver function tests show evidence of mild to moderate acute hepatocellular damage but occasionally there may be marked AST level elevation. The serum bilirubin level may be normal or elevated; if elevated, it is usually elevated only to a mild extent, but occasionally it may rise quite high. ALP levels are often less than 3 times normal, although occasionally they may be higher; and AST levels usually are less than 10 times normal. Active cirrhosis may have a clinical and chemical pattern simulating the minimal changes of advanced fatty liver, the moderate abnormalities of chronic hepatitis, occasionally the marked abnormalities of acute hepatitis with intrahepatic cholestasis, or infrequently the picture of obstruction with secondary liver damage. A history of chronic alcoholism, physical findings of spider angiomata and splenomegaly, AST level disproportionately elevated compared to ALT level, and GGT level disproportionately elevated compared to AST level help point toward alcohol-associated active cirrhosis. Liver biopsy is the best diagnostic test.

    In childhood cirrhosis, the possibility of Wilson’s disease (see Chapter 34) should be considered. Primary biliary cirrhosis would be likely in a 30- to 50-year-old woman with pruritus, slow onset of jaundice, protracted clinical course, liver biopsy showing bile duct destruction, and an abnormal antimitochondrial antibody test.