PATHO Chapter 38 Liver Disease

Steatohepatitis is caused by an accumulation of ________ in the liver cells. a. fat b. bile c. acetaminophen d. ferritin

ANS: A Alcoholic fatty liver (alcoholic steatohepatitis) is an accumulation of fat in the liver cells. It is caused by more fat being delivered to the hepatocyte than it can normally metabolize or by a defect in fat metabolism within the cell. An accumulation of bile does not contribute to steatohepatitis. Steatohepatitis is not related to an accumulation of acetaminophen levels. Serum ferritin levels are elevated in patients with hereditary hemochromatosis

A patient being treated for hepatic encephalopathy could be expected to receive a(n) ________ diet. a. low-protein and high-fiber b. high-protein and high-carbohydrate c. high-sodium d. unrestricted

ANS: A Restriction of protein is indicated for chronic encephalopathy, along with enhanced elimination of toxic nitrogenous substances. High fiber intake may help decrease constipation. As ammonia levels drop, protein is reintroduced into the diet. When protein is restricted, carbohydrate levels should be at least 400 g. Excessive levels of sodium in the diet are contraindicated with renal insufficiency. Dietary restrictions are utilized in patients with hepatic encephalopathy

Hepatitis with the presence of autoantibodies and positive antinuclear antibodies (ANA) is a. hepatitis D. b. autoimmune hepatitis. c. hepatitis A. d. hepatitis B.

ANS: B Autoimmune hepatitis is characterized by the presence of several autoantibodies as well as a polyclonal hypergammaglobulinemia. Antinuclear antibody (ANA) is generally positive at a high level. The diagnosis of hepatitis D is by anti-HDV IgM and IgG enzyme-linked immunosorbent assays. HAV infection is diagnosed through serologic testing. Presence of anti-HAV immune globulin G (IgG) indicates previous infection, and presence of immune globulin M (IgM) indicates acute infection. The serologic diagnosis for hepatitis B is complicated.

An increased urine bilirubin is associated with a. an increased indirect serum bilirubin. b. hemolytic reactions. c. Gilbert syndrome. d. hepatitis.

ANS: D In the presence of liver disease, the hepatic fraction of bilirubin decreases and the urinary fraction increases, thus accounting for a rise in urinary urobilinogen seen with liver dysfunction and hepatitis. An increase in indirect serum bilirubin is a sign of liver disease. Hemolytic reactions do not cause an increase in urine bilirubin. Disorders of the bile acid transport will cause an increase in serum bilirubin

A viral hepatitis screen with positive hepatitis B surface antigen (HBsAg) should be interpreted as ________ hepatitis B. a. recovered from b. immunity to c. chronic active d. acute

ANS: D With acute infection HBV core antigen (HBcAg) appears first, followed by seroconversion to core antibody (HBcAb). Presence of HBV surface antigen (HBsAg) indicates active infection. Conversion from surface antigen to surface antibody positivity can take as long as 1 year after acute infection. Development of surface antibody (HBsAb) points to resolution and immunity. In chronic infection, hepatitis B e antigen (HBeAg) is associated with viral replication and infectivity.

The most common causes of prehepatic jaundice are ________ and ineffective erythropoiesis. a. hemolysis b. metabolism c. fibrosis d. canalicular bilirubin transport

ANS:A The most common causes of prehepatic jaundice are hemolysis and ineffective erythropoiesis. The reabsorption of large hematomas in patients with mild liver disease is a frequent and harmless cause of mild jaundice. Dysfunction of each of the hepatic steps in bilirubin metabolism may cause jaundice. Increased resistance from fibrosis may cause jaundice in the cholestatic pathway. At the canalicular posthepatocytic level, jaundice may occur as a result of conjugated hyperbilirubinemia

Hepatic encephalopathy is associated with a. hyperbilirubinemia. b. hyperuricemia. c. toxic effects of alcohol on brain cells. d. increased blood ammonia levels.

ANS:D Hepatic encephalopathy is associated with liver failure or liver disease. It is positively correlated with elevated arterial ammonia levels. Hyperbilirubinemia is not related to hepatic encephalopathy but is associated with hypokalemia, hyponatremia, alkalosis, hypoxia, and hypercarbia. Hyperuricemia is not associated with hepatic encephalopathy. Hepatic encephalopathy is a complex neuropsychiatric syndrome characterized by symptoms ranging from mild confusion and lethargy to stupor and coma.

Liver transaminase elevations in which aspartate aminotransferase (AST) is markedly greater than alanine aminotransferase (ALT) is characteristic of a. viral hepatitis. b. alcohol-induced injury. c. cirrhosis. d. acetaminophen toxicity.

ANS: B Alcoholic and other toxic hepatitides virtually always show the aspartate aminotransferase (AST) markedly elevated in comparison with the alanine aminotransferase (ALT). In viral hepatitis, the alanine aminotransferase (ALT) is markedly higher than the aspartate aminotransferase (AST). Jaundice in patients with cirrhosis often shows elevations in all parameters, reflecting the widespread liver dysfunction and obstruction of the bile canals and small vessels because of scarring. Acetaminophen toxicity will cause signs of hepatic injury within 24 to 48 hours, including abnormal liver enzyme levels.

What form of viral hepatitis is likely to be transmitted sexually? a. Hepatitis A b. Hepatitis B c. Hepatitis C d. Hepatitis E

ANS: B Hepatitis B is spread by parenteral contact with infected blood or blood products, including contaminated needles, and by sexual contact. Hepatitis A virus (HAV) is usually spread by the fecal-oral route. The mode of transmission of hepatitis C closely resembles that of HBV, although sexual and perinatal transmission is much less likely. The majority of infections were acquired through IV drug abuse. Hepatitis E is an RNA virus spread via the fecal-oral route, especially through contaminated water

A patient admitted with bleeding related to esophageal varices could be expected to receive a continuous intravenous infusion of a. glucose. b. octreotide acetate. c. anticoagulants. d. proton pump inhibitors.

ANS: B Pharmacologic management is used to lower portal pressure by dilating collateral pathways and reducing splanchnic blood flow. Controlling bleeding is often accomplished using vasopressin, but side effects limit its use. Recently, octreotide acetate, a synthetic analog of the naturally occurring hormone somatostatin, has been effectively used as a replacement for vasopressin. Fluid resuscitation is carried out using normal saline. Anticoagulants are contraindicated in a patient with active bleeding. Intravenous proton pump inhibitors may be used, but not as a continuous infusion.

What laboratory data would support a diagnosis of hemochromatosis? a. Deficient protease inhibitor b. Elevated ferritin c. Elevated urine copper d. Positive antinuclear antibody

ANS: B Serum iron and ferritin studies are performed to diagnose hemochromatosis. Protease inhibitor is not used to diagnose hemochromatosis. Copper in the urine is not indicative of hemochromatosis. Antinuclear antibody is not diagnostic of hemochromatosis

________ disease is a rare autosomal recessive disorder in which excessive amounts of copper accumulate in the liver. a. Kayser-Fleischer b. Wilson c. Reye d. Byler

ANS: B Wilson disease, or hepatolenticular degeneration, is a rare autosomal recessive disorder in which excessive amounts of copper accumulate in the liver and other organs. As with hereditary hemochromatosis, it has now been linked to a specific abnormal protein, ATP7B, which results in retention of copper in the liver. Clinical signs and symptoms of Wilson disease include the presence of Kayser-Fleischer rings on the cornea. Reye syndrome is characterized by fatty infiltration of the liver with severe hepatic dysfunction, including encephalopathy, coagulopathy, and elevated levels of hepatocellular enzymes. Byler syndrome is caused by a single-gene mutation and traces back to an Amish kindred

Hepatitis B is usually transmitted by exposure to a. hepatitis vaccine. b. feces. c. blood or semen. d. contaminated food.

ANS: C Hepatitis B virus is highly prevalent worldwide. It is spread by parenteral contact with infected blood or blood products, including contaminated needles. HBV vaccine is a recombinant vaccine that is highly immunogenic. After the full course, the antibody response rate is 95% for normal hosts. Hepatitis A is spread by the fecal-oral route. Hepatitis E is spread through contaminated water.

Jaundice is a common manifestation of a. malabsorption syndromes. b. anemia. c. liver disease. d. cholecystitis.

ANS: C Jaundice results from impaired bilirubin metabolism and is one of the most characteristic signs of liver disease. Malabsorption syndromes are not manifested by jaundice. Anemia is not manifested by jaundice. Jaundice is not a common manifestation of cholecystitis

Brain injury secondary to high serum bilirubin is called a. hepatic encephalopathy. b. hepatic meningitis. c. kernicterus. d. encephalitis.

ANS: C Kernicterus refers to brain injury as a result of hyperbilirubinemia. It is a serious complication of the neonatal period, generally occurring in the setting of premature birth, neonatal jaundice, and especially hemolytic disease of the newborn. Hepatic encephalopathy is typically characterized by high ammonia levels in the blood. Meningitis is not associated with high serum bilirubin levels. Encephalitis may accompany viral hepatitis in children, but is not related to high serum bilirubin levels

An infusion of mannitol would be prescribed to treat a. varices. b. encephalopathy. c. peritonitis. d. cerebral edema.

ANS: D Cerebral edema is managed primarily by the intravenous infusion of mannitol, which by increasing serum osmolarity draws water from the brain and thus reduces the swelling. Octreotide acetate is used in the management of varices. Hepatic encephalopathy would be treated with lactulose. Peritonitis is managed with the use of antimicrobial agents.

Pathophysiologically, esophageal varices can be attributed to a. elevated bilirubin. b. diminished protein metabolism. c. fluid accumulation. d. portal hypertension.

ANS: D Esophageal varices result mainly from portal hypertension, which in Western society is generally the result of cirrhosis because of the chronic effects of alcoholism or viral hepatitis. Elevated bilirubin is not attributed to esophageal varices. Diminished protein metabolism does not contribute to esophageal varices. Increased vascular resistance in the liver plays a prominent role in the formation of variceal esophageal veins.

A patient with a history of alcoholism presents with hematemesis and profound anemia. The expected diagnosis is a. ascites. b. cerebral edema. c. hepatic encephalopathy. d. gastroesophageal varices.

ANS: D Esophageal varices primarily result from portal hypertension because of chronic alcoholism or hepatitis. Initial symptoms are bleeding, anemia, and shock. Ascites is an accumulation of fluid in the abdominal cavity. Cerebral edema is swelling of the brain related to hepatic encephalopathy. Hepatic encephalopathy does not cause symptoms related to bleeding.