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Hepatitis Flashcards

1
Q

Hepatitis A: Epidemiology

A

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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2
Q

How is HepA spread and how does it reach liver?

A

Virus shed in feces and is generally spread through oral route…. absorbed in intestine==>portal vein==>liver==>hepatocyte replication

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3
Q

How many people who are exposed to HepA become infected?

A

70-90%

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4
Q

Describe clinical presentation of HepA:

Describe diagnosis

A

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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5
Q

HBV Epidemiology: Prevalence, transmission

A

5% world has HBV

Transmitted perinatally, blood products, sexually, IVDA

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6
Q

How many people develop chronic infection?

A

5% adults

90% infants/children

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7
Q

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

A

Know this

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8
Q

What are treatments available for HepB?

A

Tenofovir, entecavir, interferon, lamivudine, adefovir

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9
Q

What is treatment for infants born to HBsAg+ mothers?

A

Vaccine at birth
HBIG

Prevents perinatal HBV by 90%

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10
Q

What is Hepatitis D?

A

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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11
Q

HCV Epidemiology

A

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

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12
Q

Describe global distribution of HCV genotypes

A

US: mostly 1 with some 2/3

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13
Q

Describe course of HCV Infection

A

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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14
Q

What are some of the HCV treatments?

A 
Old: IFN, Ribavirin, telaprevir/bocoprevir
New:
Sofosbuvir: NS5B polymerase inhibitor
Previr: NS3/4A protease inhibitors
Ledipasvir: NS5A polymerase inhibitor
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15
Q

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

A

Fecal-oral transmission

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

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16
Q

What is the typical serological course of Hep E?

A

Can lose IgM some time after exposure

17
Q

What are features of autoimmune hepatitis? (5)

A 
Hepatocellular necroinflammation 
Autoantibodies
Hypergammaglobulinemia
Non-pathognomic histopathology
Responsive to immunosuppressive medications (i.e prednisone)
18
Q

Describe Epidemiology of AIH

A

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

19
Q

What is the clinical spectrum for AIH?

A

Acute hepatitis: 25-30%; younger
Asymptomatic: 15-20%
Fulminant hepatic failure: 5%; get OLT

20
Q

What is the classification for AIH?

A

Type 1 (95-97%): Autoabs to ANA/SMA

Type 2: 93-5%): Autoab for LKM1

21
Q

What are characteristic histological features of autoimmune hepatitis? (2)

A

Lymphocyte/plasma cell inflammation

Interface hepatitis

22
Q

What is treatment course for AIH?

A

Prednisone…. then add azathioprine and start to taper prednisone

23
Q

What is primary biliary cirrhosis?

A

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

24
Q

Describe epidemiology of PBC:

sex, age, sympomatic

A

Female»>M
Age of onset ~50
25% pts are asymptomatic at time of diagnosis

25
Q

What is the presentation of primary biliary cirrhosis?

A

Fatigue, pruritis, jaundice, hyperpigmentation, hepatomegaly, splenomegaly, xanthelasma

26
Q

What is diagnostic criteria for PBC? (3)

A

Positive AMA
Elevated Alk phos
Liver biopsy shows damage to epithelial cells or small bile ducts and ductopenia

Imaging is normal

27
Q

What is treatment/management for PBC? (4)

A

Treat with ursodiol
Check fat soluble vitamins
Assess for osteoporosis
Manage hypercholesterolemia

28
Q

Describe epidemiology for Primary sclerosing cholangitis:

Age, sex, prevalence, RF, autoantibody prevalence

A 
Age of onset: 40yr
M>F
Annual incidence=1/100k
80% pts have IBD (especially UC)
80% have p-ANCA
29
Q

What is a characteristic histological feature of primary sclerosing cholangitis?

A

Onion skin fibrosis around bile duct

30
Q

What is prognosis for PSC?

A

8-30% risk of cholangiocarcinoma
Symptomatic at diagnosis: mean survival~12 yr
Asymptomatic at dx: survival much longer

31
Q

What is the leading cause of acute liver failure in the US?

A

Drug induced liver disease

32
Q

What are RFs for drug-induced liver disease?

A

Age>50, gender (female), obesity, chronic alcohol use, malnutrtion, history of DILI, polypharmacy

33
Q

Describe features of intrinsic DILI

A

Intrinsic is dose dependent, predictable
Involves a hepatocellular reaction due to a toxic metabolite

Examples: acetaminophen and MTX

34
Q

Describe features of idiosyncratic DILI

A

Genetic association, not dose dependent or predictable

Involves a cholestatic/mixed run due to hypersensitivity

Example: Augmentin, statins

35
Q

What is the biochemical pattern for hepatocellular rxn in DILI?

A

Elevated AST/ALT
Acute liver failure
Mortality~10%

36
Q

What is the biochemical pattern for cholestatic rxn in DILI?

A

Elevated Alk Phos
Jaundice and pruritis
Low acute liver failure and extremely low failure rate

37
Q

Describe Acetaminophen metabolism

A

Acetaminophen overwhelms livers ability to metabolize and becomes toxic NAPQI.

38
Q

Treatment for acetaminophen acetaminophen DILI

A

Give N-acetylcystein, a precursor of glutathione to increase metabolism of NAPQI

39
Q

Prognosis for DILI

A

If ALF, poor prognosis: 30% death for acetaminophen, 75% death for idiosyncratic

If hepatocellular with jaundice: 10% mortality

GI (41 decks)

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