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71 Cards in this Set

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