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71 Cards in this Set
- Front
- Back
a. How is Hep A transmitted? Who most commonly contracts it?
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i. Fecal-oral
ii. Travelers |
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b. What is the disease state of Hep A?
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i. Acute only
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c. What markers signal an active Hep A and Hep E infection?
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i. Anti-virus IgM
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d. What does anti-virus IgG indicate in a Hep A and Hep E infection?
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i. Protection
ii. Presence indicates prior infection or immunization |
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e. What does a Hep E infection in a pregnant woman indicate?
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i. Fulminant hepatitis→ liver failure with massive liver necrosis
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a. How is Hep B transmitted?
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i. Parenteral transmission
ii. Childbirth, unprotected intercourse, IV drug abuse, needle stick |
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b. What is the disease state of Hep B?
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i. Acute
ii. Rarely goes chronic |
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a. How is Hep C transmitted?
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i. IVDA
ii. Unprotected intercourse |
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b. What is the disease state of Hep C?
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i. Acute
ii. Chronic in most cases |
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c. What test confirms a Hep C infection?
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i. HCV-RNA test
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a. What does Hep D depend upon for infection?
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i. Hep B
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a. What is the first serologic marker to rise in Hep B?
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i. HBsAG
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b. What indicates chronic Hep B?
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i. HBsAG for more than 6 months
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c. What indicates that a chronic Hep B infection is contagious?
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i. HBeAg or HBV DNA
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d. What immunoglobulin is present in the acute phase of HBV infection?
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i. IgM
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e. What immunoglobulin is present in the window phase of HBV infection?
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i. IgM
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f. What immunoglobulin is present in a resolved HBV infection?
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i. IgG
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g. What immunoglobulin is present in a chronic HBV infection?
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i. IgG
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a. What is viral hepatitis?
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i. Inflammation of liver parenchyma
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b. How does viral hepatitis present?
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i. Jaundice
ii. Dark urine→ CB iii. Fever iv. Malaise v. Nausea vi. Elevated liver enzymes |
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c. What is histological evidence of viral hepatitis?
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i. Apoptosis of hepatocytes in lobules of liver
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d. How long does acute viral hepatitis last?
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i. < 6 mos.
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e. How long does chronic viral hepatitis last?
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i. > 6 mos.
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f. Where is the inflammation generally found in chronic viral hepatitis?
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i. Portal tract
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g. What are some histological hallmarks of acute hepatitis?
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i. Ballooning degeneration
ii. Cholestasis iii. Macrophage aggregates iv. Apoptosis v. Kupffer cell hyperplasia |
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h. How do you dx acute viral hepatitis?
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i. Serological markers
ii. No need for bx |
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a. What is the serological indicator for a dx of viral hepatitis?
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i. Serological markers are negative
ii. Highs serum titers of autoantibodies→ iii. ANA iv. SMA v. Anti-LKM1 |
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a. What is cirrhosis?
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i. End-stage liver damage characterized by disruption of the normal hepatic parenchyma
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b. What is the histological hallmark of cirrhosis?
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i. Bands of fibrosis
ii. Regenerative nodules of hepatocytes |
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c. What is the key mediator of fibrosis in cirrhosis?
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i. TGF-β from stellate cells
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d. How will a patient with cirrhosis present?
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i. Portal hypertension (principal symptoms, causes all others)
ii. Ascites iii. Congestive splenomegaly iv. Portosystemic shunts v. Decreased liver function |
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e. How will decreased hepatic detoxification due to cirrhosis present?
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i. Mental status changes
ii. Asterixis iii. Eventual coma iv. Hyperesterinism v. Jaundice |
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f. What will decreased protein synthesis due to cirrhosis lead to?
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i. Hypoalbuminemia
ii. Coagulopathy |
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a. What is fatty liver?
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i. Accumulation of fat in hepatocytes
ii. Results in heavy, greasy liver |
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b. How can you cure alcoholic fatty liver?
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i. Abstinence from alcohol
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c. What is alcoholic hepatitis?
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i. Chemical injury to hepatocytes
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d. What mediates the damage in alcoholic hepatitis?
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i. Acetaldehyde
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e. What are the histological signs of alcoholic hepatitis?
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i. Swelling of hepatocytes
ii. Formation of Mallory bodies |
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f. What are found within Mallory bodies?
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i. Damaged intermediate filaments
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g. What are the symptoms of alcoholic hepatitis?
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i. Painful hepatomegaly
ii. Elevated liver enzymes |
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a. What is nonalcoholic fatty liver disease?
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i. Fatty change, hepatitis, and/or cirrhosis that develop without exposure to alcohol
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b. What condition is associated with nonalcoholic fatty liver disease?
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i. Obesity
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c. How can you dx nonalcoholic fatty liver disease?
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i. Dx of exclusion
ii. Elevated liver enzymes |
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a. What is hemochromatosis
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i. Excess body iron leading to deposition in tissues and organ damage
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b. What mediates tissue damage in hemochromatosis?
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i. Free radicals
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c. What causes primary hemochromatosis?
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i. Defect in iron absorption in hepatocytes
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d. What causes secondary hemochromatosis?
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i. Chronic blood transfusions
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e. What is the classic triad of presentation for hemochromatosis?
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i. Cirrhosis
ii. Secondary diabetes mellitus iii. Bronze skin |
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f. What will a liver biopsy of hemochromatosis show?
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i. Prussian blue positive for iron
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a. What causes Wilson disease?
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i. Lack of copper transport into bile
ii. Lack of copper incorporation into ceruloplasmin |
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b. What causes tissue damage in Wilson disease?
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i. Hydroxyl free radicals
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c. When does Wilson disease present? How?
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i. Cirrhosis
ii. Neurologic manifestations iii. Kayser-Fleisher rings in cornea |
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a. What is primary biliary cirrhosis?
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i. Autoimmune granulomatous destruction of intrahepatic bile ducts
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b. What antibody is present in primary biliary cirrhosis?
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i. Antimitochondrial antibody
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c. What is the presentation of primary biliary cirrhosis?
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i. Obstructive jaundice
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a. What is primary sclerosing cholangitis?
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i. Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts
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b. What is the histological appearance of primary sclerosing cholangitis?
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i. Periductal fibrosis with an onion-skin appearance
ii. Uninvolved regions are dilated resulting in a bedaded appearance on contrast imaging |
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c. With what disorders is primary sclerosing cholangitis associated?
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i. UC
ii. p-ANCA positive |
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d. How does primary sclerosing cholangitis present?
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i. Obstructive jaundice
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a. What is secondary biliary cirrhosis?
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i. Prolonged obstruction of the extrahepatic bile duct from biliary atresia, gallstones, carcinoma, and strictures
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b. What can cause ascending cholangitis in secondary biliary cirrhosis?
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i. Enteric bacilli and enterococci
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c. What are the symptoms of secondary biliary cirrhosis?
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i. Pruritis
ii. Jaundice iii. Malaise iv. Dark stools v. Hepatosplenomegaly |
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d. What is the histologic appearance of secondary biliary cirrhosis?
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i. Liver is hard with a finely granular appearance
ii. Hepatic fibrous septa in jigsaw pattern |
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a. What is acute cholecystitis?
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i. Inflammation of the gallbladder wall
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b. What are some complications associated with acute cholecystitis?
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i. Impacted stone in cystic duct results in dilatation with pressure ischemia, bacterial overgrowth and inflammation
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c. What are the signs of acute cholecystitis?
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i. RUQ pain radiating to right scapula
ii. Fever iii. Elevated WBC count iv. Nausea, vomiting v. Increased serum alkaline phosphatase |
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a. What is chronic cholecystitis?
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i. Chronic inflammation of the gallbladder
ii. Due to chemical irritation from longstanding cholelithiasis |
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b. What are the signs of chronic cholecystitis?
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i. Herniation of gallbladder mucosa into muscular wall
ii. Vague RUQ pain iii. Porcelain gallbladder |
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c. What is the histological presentation of cholesterolosis?
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i. Yellow streaks on gross examination
ii. Lipid-laden macrophages in lamina propria iii. May occasionally form cholesterol polyps |
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a. What is α1 antitrypsin deficiency?
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i. Autosomal recessive disorder involving chromosome 14
ii. α1-antitrypsin inhibits proteases |
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b. What are the symptoms of α1 antitrypsin deficiency?
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i. Emphysema
ii. Chronic liver disease |