Hepatitis Flashcards by Ben Zielonka

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

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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

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How many people who are exposed to HepA become infected?

70-90%

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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

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HBV Epidemiology: Prevalence, transmission

5% world has HBV

Transmitted perinatally, blood products, sexually, IVDA

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How many people develop chronic infection?

5% adults

90% infants/children

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Describe the HepB serologies for the following: Acute HBV, chronic HBV, vaccinated

Know this

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What are treatments available for HepB?

Tenofovir, entecavir, interferon, lamivudine, adefovir

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What is treatment for infants born to HBsAg+ mothers?

Vaccine at birth
HBIG

Prevents perinatal HBV by 90%

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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

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HCV Epidemiology

5-7million americans infected
6 HCV genotypes
20% pts with chronic HCV have cirrhosis

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Describe global distribution of HCV genotypes

US: mostly 1 with some 2/3

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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

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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

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Describe epidemiology of Hepatitis E: Transmission, at-risk populations

Fecal-oral transmission

Immunosuppressed and pregnant women (higher risk of fulminant, especially during 3rd trimester)

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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