Acute/Chronic Liver Disease Flashcards Preview

MODHIII - Unit 3 > Acute/Chronic Liver Disease > Flashcards

Flashcards in Acute/Chronic Liver Disease Deck (34)
1

Signs of chronic hepatitis

- often asymptomatic
- liver enzymes may be normal or minimally elevated
- abnormalities persist > 6 months

2

Consequences of acute and chronic hepatitis

- acute: none, resolves, fulminant hepatitis-recovery/death
- chronic: none, liver disease-cirrhosis, hepatocellular cancer

3

Viruses that may cause hepatitis

- epstein barr virus
- HIV
- herpes simplex virus
- adenovirus

4

Enterically transmitted hepatitis

- A and E
- no chronic hepatitis

5

Parenterally transmitted hepatitis

- C, D, and B
- can develop chronic hepatitis

6

HAV

- RNA virus, picornaviridae
- symptomatic infection (& fulminant) more common in adults
- no specific treatment

7

Lab values: HAV

- IgM anti-HAV: diagnostic of acute HAV infection
- IgG anti-HAV: indicated prior HAV infection

8

HEV

- RNA virus
- endemic in many developing countries
- high mortality (fulminant hepatitis) in pregnant women

9

HBV

- DNA virus, hepadnaviridae
- parenteral spread
- important effect of age at infection on natural history

10

HBV: age matters

- infant/children: asymptomatic, chronic, high risk of HCC (25%)
- adults: more symptomatic, rarely fulminant, less likely to develop chronic HBV

11

HBV and HCC

- 80% of all HCC cases attributable to HBV infection
- HBV can cause HCC in absence of cirrhosis

12

HBV vaccine

- first "ANTI CANCER" vaccine

13

Acute HBV infection lab values

- HBsAg: piece of the virus-if present have HBV
- will deplete and anti HBs will develop

14

Chronic HBV infection lab values

- HBsAg chronically elevated b/c virus is always there

15

Treatment of HBV

- 7 drugs approved
- NONE ARE CURATIVE
- oral meds suppress HBV replication

16

Prevention of HBV infection

- vaccines use recombinant HBsAg effective
- included in routine childhood immunizations

17

HDV

- RNA virus
- occur only in PRESENCE of HBV
- spread by parenteral route
- "defective virus": HDV RNA encodes only the delta antigen, requires HBsAg to provide outer coat

18

HCV

- RNA virus, flaviviridae
- spread by parenteral route
- most common form of chronic viral hepatitis in US

19

HCV serologies

- anti HCV antibody: first line test-persists even after infection is cleared
- PCR + HCV RNA confirms active infection
- HCV genotype used in decision making for treatment

20

Treatment of HCV

- rapidly evolving
- IFN old, IFN vairable (75%), other oral regimens without IFN (90%)
- access limited by expense

21

Prevention of HCV

- prevention of exposure
- post exposure IG ineffective
- vaccine development ongoing

22

Vaccines for hepatitis

- A and B: YES
- C, D, and E: NO

23

Classical histologic findings of chronic viral hepatitis

- portal inflammation with interface damage
- lobular inflammation
- kupffer cell clusters
- acidophil bodies

24

Histologic findings of HCV vs. HBV

HCV: rounded portal lymphoid aggregates
HBV: ground glass hepatocytes

25

Alcoholic liver disease

- steatosis, hepatitis, cirrhosis
- MINORITY of heavy drinkers develop serious liver pathology (10-20%)
- genetic factors important
- excess EtOH factor in progression of HCV

26

Alcohol related live pathology

- steatosis: common after heavy EtOH intake, reversible
- hepatitis: can be life threatening, precursor to cirrhosis
- cirrhosis: abstinence can lead to clinical improvement

27

Thresholds for alcohol induced liver damage

- male: 60 g/d
- female: 40 g/d

28

Lab clues to ALD

- AST:ALT > 2
- elevations in MCV and gamma-glutamyl transpeptidase activity
- urinary ethyl glucuronide useful to confirm RECENT heavy intake

29

Alcoholic hepatitis

- jaundice, ascites, muscle wasting
- fever, tender hepatomegaly, vomiting, malaise
- discriminant function (DH) > 32 predicts hight mortality risk
- treatment: abstinence, nutritional support, steroids if DF > 32

30

ALD diagnosis

- history
- exclude other potential causes
- liver biopsy sometimes helpful

31

Nonalcoholic fatty liver (NAFLD)

- histology: steatosis w/ or w/out inflammation, signs of hepatocellular injury, and fibrosis
- associated with obesity, diabetes, hypertriglyceridemia
- insulin resistance may be common denominator

32

NAFLD vs. NASH

NAFLD................................................................................NASH
Fat, fat + inflammation, fat + hepatocyte damage, fat + fibrosis

33

NAFLD/NASH diagnosis and treatment

- diagnosis: requires liver biopsy, not all pts w/ presumed fatty liver require biopsy
- treatment: none proven; weight loss, treatment of diabetes, hyperlipidemia

34

Signs of acute hepatitis

- jaundice, liver enlargement, & tenderness classical signs of hepatitis
- ALT/AST > 10X normal
- clinical and lab abnormalities resolve within 6 months