I. Extrahepatic causes of liver failure include:
1. Hepatitis.
2. Cirrosis.
3. Gall bladder stones.
4. Inflammation of the bile ducts with cholestasis.
5. Heart failure.
6. Renal failure.
7. General hypoxia.
II. Hyperglycemia observed in liver failure may result from the following:
1. A decrease in hepatocellular mass.
2. Insulin receptor defect in hepatocytes.
3. Postreceptor insulin resistance in hepatocytes.
4. Hyperglucagonemia.
5. Hyperinsulinemia.
6. Impairment of gluconeogenesis.
7. Impairment of glycogenolysis.
III. Hypoglycemia in end-stage liver cirrhosis is caused by:
1. Decreased hepatic glycogen store.
2. Diminished glucagon responsiveness of the liver.
3. Decreased liver capacity to synthesize glycogen.
4. Decreased hepatic clearance of glucagon.
5. Impairment of glycolysis in hepatocytes.
6. Increased hepatic clearance of insulin.
IV. Severe liver damage may be accompanied by:
1. Aminoaciduria.
2. Decreased utilization of aromatic amino acids.
3. Reduction in blood urea nitrogen.
4. Accumulation of NH3 in the blood.
5. Hypoalbuminemia.
6. Hyperfibrinogenemia.
7. Hyperprothrombinemia.
8. Accumulation of phenol, indol and cadaverin in blood plasma.
V. Hemolytic jaundice is characterized by:
1. Increased serum unconjugated bilirubin.
2. Increased fecal stercobilinogen.
3. Increased urine stercobilinogen.
4. Normal level of bile salts in plasma.
5. Increased serum conjugated bilirubin.
6. Increased urine conjugated bilirubin.
7. Increased urine unconjugated bilirubin.
8. Increased activity of hepatic transaminases in blood plasma.
VI. Cholestatic jaundice is characterized by:.
1. Increased serum unconjugated bilirubin.
2. Decreased fecal urobilinogen.
3. Increased urine urobilinogen.