Hepatitis Flashcards
Hepatitis A: Epidemiology
Most common cause of viral hepatitis worldwide
Incidence is 9.1 per 100k
RFs: contact with infected person, daycare, IV drug use, recent travel
How is HepA spread and how does it reach liver?
Virus shed in feces and is generally spread through oral route…. absorbed in intestine==>portal vein==>liver==>hepatocyte replication
How many people who are exposed to HepA become infected?
70-90%
Describe clinical presentation of HepA:
Describe diagnosis
Acute infection only… in rare cases fulminant infection (more common in older pts, those with chronic hepatitis). Disease is self limiting
Dx: HAV IgM
HBV Epidemiology: Prevalence, transmission
5% world has HBV
Transmitted perinatally, blood products, sexually, IVDA
How many people develop chronic infection?
5% adults
90% infants/children
Describe the HepB serologies for the following: Acute HBV, chronic HBV, vaccinated
Know this
What are treatments available for HepB?
Tenofovir, entecavir, interferon, lamivudine, adefovir
What is treatment for infants born to HBsAg+ mothers?
Vaccine at birth
HBIG
Prevents perinatal HBV by 90%
What is Hepatitis D?
Delta agent that is spread by percutaneous exposure and causes coinfection with HBV and is associated with higher risk of severe/fulminant liver
HCV Epidemiology
5-7million americans infected
6 HCV genotypes
20% pts with chronic HCV have cirrhosis
Describe global distribution of HCV genotypes
US: mostly 1 with some 2/3
Describe course of HCV Infection
Acute infection==>Most (75-85%) develop persistent chronic infection==>Either non progressive (25%), slowly progressive (35%), severe progressive hepatitis (20%)==>Antiviral treatment (majority are responsive)….if treatment fails then cirrhosis and either HCC or decompensation
What are some of the HCV treatments?
Old: IFN, Ribavirin, telaprevir/bocoprevir New: Sofosbuvir: NS5B polymerase inhibitor Previr: NS3/4A protease inhibitors Ledipasvir: NS5A polymerase inhibitor
Describe epidemiology of Hepatitis E: Transmission, at-risk populations
Fecal-oral transmission
Immunosuppressed and pregnant women (higher risk of fulminant, especially during 3rd trimester)
What is the typical serological course of Hep E?
Can lose IgM some time after exposure
What are features of autoimmune hepatitis? (5)
Hepatocellular necroinflammation Autoantibodies Hypergammaglobulinemia Non-pathognomic histopathology Responsive to immunosuppressive medications (i.e prednisone)
Describe Epidemiology of AIH
Prevalence: 16.9 per 100k
F»M
Bimodal age distribution (10-20 and 45-75)
High association with other autoimmune diseases
6% liver tx in US
40% mortality in symptomatic patients
What is the clinical spectrum for AIH?
Acute hepatitis: 25-30%; younger
Asymptomatic: 15-20%
Fulminant hepatic failure: 5%; get OLT
What is the classification for AIH?
Type 1 (95-97%): Autoabs to ANA/SMA
Type 2: 93-5%): Autoab for LKM1
What are characteristic histological features of autoimmune hepatitis? (2)
Lymphocyte/plasma cell inflammation
Interface hepatitis
What is treatment course for AIH?
Prednisone…. then add azathioprine and start to taper prednisone
What is primary biliary cirrhosis?
Ongoing inflammatory destructino of interlobular and septal bile ducts that leads to chronic cholestasis and biliary cirrhosis
Triggered by immune-mediated response to auto antigen AMA
Describe epidemiology of PBC:
sex, age, sympomatic
Female»>M
Age of onset ~50
25% pts are asymptomatic at time of diagnosis
What is the presentation of primary biliary cirrhosis?
Fatigue, pruritis, jaundice, hyperpigmentation, hepatomegaly, splenomegaly, xanthelasma
What is diagnostic criteria for PBC? (3)
Positive AMA
Elevated Alk phos
Liver biopsy shows damage to epithelial cells or small bile ducts and ductopenia
Imaging is normal
What is treatment/management for PBC? (4)
Treat with ursodiol
Check fat soluble vitamins
Assess for osteoporosis
Manage hypercholesterolemia
Describe epidemiology for Primary sclerosing cholangitis:
Age, sex, prevalence, RF, autoantibody prevalence
Age of onset: 40yr M>F Annual incidence=1/100k 80% pts have IBD (especially UC) 80% have p-ANCA
What is a characteristic histological feature of primary sclerosing cholangitis?
Onion skin fibrosis around bile duct
What is prognosis for PSC?
8-30% risk of cholangiocarcinoma
Symptomatic at diagnosis: mean survival~12 yr
Asymptomatic at dx: survival much longer
What is the leading cause of acute liver failure in the US?
Drug induced liver disease
What are RFs for drug-induced liver disease?
Age>50, gender (female), obesity, chronic alcohol use, malnutrtion, history of DILI, polypharmacy
Describe features of intrinsic DILI
Intrinsic is dose dependent, predictable
Involves a hepatocellular reaction due to a toxic metabolite
Examples: acetaminophen and MTX
Describe features of idiosyncratic DILI
Genetic association, not dose dependent or predictable
Involves a cholestatic/mixed run due to hypersensitivity
Example: Augmentin, statins
What is the biochemical pattern for hepatocellular rxn in DILI?
Elevated AST/ALT
Acute liver failure
Mortality~10%
What is the biochemical pattern for cholestatic rxn in DILI?
Elevated Alk Phos
Jaundice and pruritis
Low acute liver failure and extremely low failure rate
Describe Acetaminophen metabolism
Acetaminophen overwhelms livers ability to metabolize and becomes toxic NAPQI.
Treatment for acetaminophen acetaminophen DILI
Give N-acetylcystein, a precursor of glutathione to increase metabolism of NAPQI
Prognosis for DILI
If ALF, poor prognosis: 30% death for acetaminophen, 75% death for idiosyncratic
If hepatocellular with jaundice: 10% mortality
