Acute and Chronic Hepatitis Flashcards
Most common cause of viral hepatitis
Hep A
Transmission of hepA
fecal-oral –> intestine –> PV –> liver –> hepatocyte replication
T/F hepA is highly resistant to degradation by environmental factors
T
How long does hepA last?
acute only –> no chronic disease, rare fulminant infection, benign, self-limited
Dx of hepA
HAV IgM (acute)
Transmission of hepB
sexual, blood, IVA, perinatally
Chronicity of hepB
5% get chronic infection among adults, 90% of children get chronic infection
+ HBsAg, + HBcAb IgM or IgG
acute HBV
+ HBsAG, + HBcAb IgG
chronic HBV
+HBsAb
vaccinated
+HBsAb, +HBcAb
cleared infection
Contemporary Tx of hepatitis B
tenofovir, entecavir, vaccine at birth, HBIG in neonates
Where does hepD replication take place?
only liver –> HepB is necessary for coating HDV virions for spreading cell to cell
Transmission of HDV/delta agent
percutaneous exposure
Transmission of HCV
mostly IVDA, some sexually, some transfusion
What is the significance of anti-hcv antibody
not immunity like in the case of HBV…just implies you’ve had or have it
How many HCV become chronic?
most (75-85%)…30% leading to cirrhosis
Hepatitis E transmission
enteric –> fecal-oral –> pregnant women at high risk
Markers of HEV
IgM anti-HEV during symptomatic course w/elevated ALT, IgG kicks in soon after
Features of autoimmune hepatitis
hepatocellular necroinflammation, autoantibodies, hypergammaglobulinemia, responsiveness to steroids
M/F autoimmune hepatitis
F>M w/biomodal distribution
Prognosis of autoimmune hepatitis
40% mortality in symptomatic patients
Spectrum of autoimmune hepatitis
acute hepatitis (25-30%, young, icteric acute viral-like picture), asymptomatic (15-20%), fulminant failure (potentially reversible, 5%)
Antibodies in type 1 autoimmune hepatitis
ANA/SMA, SLA/LP, pANCA, ASPGR
Antibodies in type 2 autoimmune hepatitis
LKM1, SLA/LP
Which is more common among autoimmune hepatitis, Type 1 or 2?
2
Histologic finding in autoimmune hepatitis
lymphoplasmacytic interface hepatitis
Tx of autoimmune hepatitis
prednisone +/- azathiporine
PBC
primary biliary cholestasis –> ongoing inflammatory destruction of interlobular and septal bile ducts leading to chronic cholestasis and BILIARY cirrhosis (most patients dont have liver cirrhosis)
Antibody in PBC
AMA
M/F PBC and other features of patient
F >M, 50 years old…elevated alk phos, possible asymptomatic, fatigue, pruritis, xanthelasma, hepatosplenomegaly, hyperpigmentaiton, jaundice
Dx of PBC
AMA, elevated Alkphos, damage to epithelia of small bile ducts, ductopenia, noncaseating granulomas
Tx of PBC
ursodiol, vitamins, cholesterol
PSC
primary sclerosing cholangitis –> chronic disease of unknown etiology with inflammation and fibrosis of biliary tree
M/F PSC
M>F
antibody in PSC
pANCA
Histologic finding in PSC
onion skin fibrosis around bile duct
What disease do most people with PSC start off with?
IBD
PSC Cancer risk
cholangiocarcinoma…up to 30%
Risk factors for DILD
age, gender (f), obesity, alcohol, history, polypharmacy
2 classifications of DILD
intrinsic (dose dependent, predictable, non-genetic, hepatocellular injury by toxic metabolite)
vs.
idiosyncratic (not dose dependent or predictable, gene link, cholestatic/mixed effect, hypersensitivity type)
Most common cause of acute liver failure in US
acetaminophen –> metabolite NAPQI is directly toxic (intrinsic)
Tx of acetominophen toxicity
N-acetylcysteine to increase metabolism of NAPQI
Prognosis of DILI +ALF
poor –> depends on drug
Hy’s Law
in DILI with ALF, hepatocellular injury + jaundice leads to 10% mortality
