Flashcards in Hepatitis Deck (50):
What is the most common viral hepatitis worldwide?
What are risk factors for hepatitis A?
(1) contact with infected person
(3) IV drug use
(4) recent travel
(5) contaminated food or water
How is hepatitis A usually spread?
Fecal-to-oral. It is absorbed in the intestine, travels the portal vein, and enters and replicates within hepatocytes.
What is an indication that a hepatitis A patient is no longer contagious?
Jaundice has resolved.
Can hepatitis A lead to a chronic infection?
How is hepatitis A diagnosed?
Presence of HAV IgM antibodies.
When might you worry about a fulminant hepatitis A infection?
(1) >40 years
(2) chronic liver disease
Fulminant infections are rare.
How is hepatitis B usually spread?
(2) blood products
(4) IV drug use
Which are more likely to develop a chronic hepatitis B infection: adults or children?
Children (90% vs 5%).
What is the serology profile for acute HBV infection?
+: HBsAg, HBcAb (IgM or IgG), HBV DNA
What is the serology profile for chronic HBV infection?
+: HBsAg, HBcAb, HBV DNA
-: all else
What is the serology profile for a person vaccinated to HBV?
-: all else
What is the serology profile of a person with a cleared HBV infection?
+: HBsAb, HBcAb
-: all else
How is hepatitis B treated?
What is done for infants born to mothers that are HBsAg positive?
(1) vaccine at birth
How is hepatitis D spread?
Which virus requires HBV for infection?
Why is HBV infection necessary for HDV?
The HDV virions are coated using HBV products, allowing cell-to-cell spread.
What increases the risk of fulminant hepatitis from acute HBV infection?
Co-infection with HDV (34% vs 4%).
Is hepatitis C a DNA or RNA virus?
How is hepatitis C spread?
(1) IV drug use
(3) blood products
What is the probability of developing a chronic HCV infection once infected?
Which hepatitis infection has the strongest association with hepatocellular carcinoma?
How is HCV treated?
Is hepatitis E a DNA or RNA virus?
How is hepatitis E spread?
Which group has the greatest risk of fulminant hepatitis in an HEV infection?
How is hepatitis E treated?
Is hepatitis A a DNA or RNA virus?
Is hepatitis B a DNA or RNA virus?
What is the main difference between Type 1 and 2 autoimmune hepatitis?
(1) autoantibodies to ANA or SMA
(2) autoantibodies to LKM1
Which type of autoimmune hepatitis is more likely to have extrahepatic manifestations?
How is autoimmune hepatitis treated?
(2) prednisone & azathioprine
What is primary biliary cirrhosis?
An ongoing, auto-immune inflammatory destruction of the interlobular and septal bile ducts, leading to chronic cholestasis and biliary cirrhosis. (Not really cirrhosis.)
What is the trigger for primary biliary cirrhosis?
An immune-mediated response to a foreign or self antigen. Presence of AMA antibodies inevitably leads to PBC.
What is the LFT profile of primary biliary cirrhosis?
What are the histological features of primary biliary cirrhosis?
(1) damage to epithelial cells of small bile ducts
(3) non-caseating granulomas
How is primary biliary cirrhosis treated?
Ursodiol. Prednisone does not work.
What is primary sclerosing cholangitis?
A chronic cholestatic liver disease of unknown etiology characterized by inflammation and fibrosis of the biliary tree.
What is the primary worry with primary sclerosing cholangitis?
Development of cholangiocarcinoma.
What are the histological features of primary sclerosing cholangitis?
Onion skin fibrosis around bile ducts.
What other disorder is usually seen in patients with primary sclerosing cholangitis?
What is the primary cause of acute liver failure in the US?
Drug-induced liver disease (acetaminophen).
What profile is at increased risk of drug-induced liver disease?
An aging, obese, alcoholic female that has malnutrition and multiple prescriptions.
What are 2 drugs causing intrinsic DILI?
What are characteristics of hepatocellular DILI?
(1) elevated AST/ALT
(2) acute liver failure
(3) 10% mortality
What are characteristics of cholestatic DILI?
(1) elevated ALK
What is the reason for acetaminophen toxicity?
A buildup of the toxic metabolite, NAPQI, due to an exhaustion of glutathione stores.
How is acetaminophen-induced liver disease treated?
N-acetylcysteine, which is metabolized to glutathione in the body.