Acute/Chronic Liver Disease Flashcards
Signs of chronic hepatitis
- often asymptomatic
- liver enzymes may be normal or minimally elevated
- abnormalities persist > 6 months
Consequences of acute and chronic hepatitis
- acute: none, resolves, fulminant hepatitis-recovery/death
- chronic: none, liver disease-cirrhosis, hepatocellular cancer
Viruses that may cause hepatitis
- epstein barr virus
- HIV
- herpes simplex virus
- adenovirus
Enterically transmitted hepatitis
- A and E
- no chronic hepatitis
Parenterally transmitted hepatitis
- C, D, and B
- can develop chronic hepatitis
HAV
- RNA virus, picornaviridae
- symptomatic infection (& fulminant) more common in adults
- no specific treatment
Lab values: HAV
- IgM anti-HAV: diagnostic of acute HAV infection
- IgG anti-HAV: indicated prior HAV infection
HEV
- RNA virus
- endemic in many developing countries
- high mortality (fulminant hepatitis) in pregnant women
HBV
- DNA virus, hepadnaviridae
- parenteral spread
- important effect of age at infection on natural history
HBV: age matters
- infant/children: asymptomatic, chronic, high risk of HCC (25%)
- adults: more symptomatic, rarely fulminant, less likely to develop chronic HBV
HBV and HCC
- 80% of all HCC cases attributable to HBV infection
- HBV can cause HCC in absence of cirrhosis
HBV vaccine
- first “ANTI CANCER” vaccine
Acute HBV infection lab values
- HBsAg: piece of the virus-if present have HBV
- will deplete and anti HBs will develop
Chronic HBV infection lab values
- HBsAg chronically elevated b/c virus is always there
Treatment of HBV
- 7 drugs approved
- NONE ARE CURATIVE
- oral meds suppress HBV replication
Prevention of HBV infection
- vaccines use recombinant HBsAg effective
- included in routine childhood immunizations
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
HCV
- RNA virus, flaviviridae
- spread by parenteral route
- most common form of chronic viral hepatitis in US
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
Treatment of HCV
- rapidly evolving
- IFN old, IFN vairable (75%), other oral regimens without IFN (90%)
- access limited by expense
Prevention of HCV
- prevention of exposure
- post exposure IG ineffective
- vaccine development ongoing
Vaccines for hepatitis
- A and B: YES
- C, D, and E: NO
Classical histologic findings of chronic viral hepatitis
- portal inflammation with interface damage
- lobular inflammation
- kupffer cell clusters
- acidophil bodies
Histologic findings of HCV vs. HBV
HCV: rounded portal lymphoid aggregates
HBV: ground glass hepatocytes
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
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
Thresholds for alcohol induced liver damage
- male: 60 g/d
- female: 40 g/d
Lab clues to ALD
- AST:ALT > 2
- elevations in MCV and gamma-glutamyl transpeptidase activity
- urinary ethyl glucuronide useful to confirm RECENT heavy intake
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
ALD diagnosis
- history
- exclude other potential causes
- liver biopsy sometimes helpful
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
NAFLD vs. NASH
NAFLD……………………………………………………………………..NASH
Fat, fat + inflammation, fat + hepatocyte damage, fat + fibrosis
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
Signs of acute hepatitis
- jaundice, liver enlargement, & tenderness classical signs of hepatitis
- ALT/AST > 10X normal
- clinical and lab abnormalities resolve within 6 months
