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Hepatitis A ("Infectious Hepatitis")
- - spread via fecal-oral route
- - never becomes chronic
- - may cause outbreaks from contaminated food/water
- - Causes 50% of all acute viral hepatitis in U.S.
- virus found in feces > or = 2 weeks before onset of symptoms, so greatest risk of transmission is before sx are even present
Diagnosis of Hepatitis A
Lab: Anti-HAV IgM (positive by the time sx start, disappears at 14 weeks), Anti-HAV IgG (at 4 weeks, then forever)
Hepatitis A symptoms
- start 4-6 weeks after exposure
- Many may be asymptomatic, but exposure causes Anti-HAV IgG positive result, GIVING PROTECTION.
- 1% will have fulminant hepatic failure
- - Decrease appetite
- - smokers lose taste for cigarettes
- Pre-icteric (prodromal) phase: up to 3 weeks, pt. most infectious.
- Icteric phase: lasts 2-4 weeks
- Post-icteric phase: avg 2-4 months
P.E. of Hepatitis A
Jaundice (at 2 weeks post-exposure)
Elevated LFT's, bilirubin > 10, Alk.phos., GGT
Treatment of Hepatitis A
No treatment available
99% get better
Prevention of Hepatitis A
Hep.A vaccine (protective after 4 weeks; give to chronic hepatitis pts. that are anti-HAV negative)
Immune globulin against hepatitis A (provides temporary passive immunity for 6-8 weeks; effective if given w/in 1-2 weeks after exposure) (Given to all close contacts who are Anti-HAV negative). Can be given prophylactically before travel.
Pt. education in Hepatitis A
All contacts need to get tx prophylactically.
Avoid ETOH, NSAIDS, acetaminophen.
Infection control precautions in hospital.
- - acute or chronic
- - spread percutaneously (IV drug use, needlestick injuries)
- - spread via permucosal exposure (sexual contact) (vaginal secretions, menstrual fluids, semen, saliva, respiratory secretions, gastric juice, synovial fluid and CSF)
- HBV can live on dry surfaces for seven days
Hepatitis B blood tests
- HBsAg - Hep.B surface antigen (present by the time symptoms arise)
- Anti-HBs/HBsAB - antibody to Hep.B surface antigen (IMMUNITY FROM HEP.B.)
- Anti-HBc (IgM, IgG) - antibodies to Hep.B core antigen
Symptoms of Hep.B.
Same manifestations as Hep.A.
30% have no symptoms
10% will develop chronic hepatitis B
Preventing Hep.B spread
HBIG: Hepatitis B immune globulin - given to anyone who is exposed including infants born to mothers positive for HBsAg.
Hepatitis B Vaccine - recommended for all newborns & adolescents, anyone at high risk for hep.B. (IV drug users, close contacts w/ hep.B carrier), postexposure prophylaxis, 3 injections, ALL HEALTHCARE WORKERS, HD pts.
Hepatitis B complications
chronic Hep.B. infection can lead to:
- hepatocellular carcinoma
Only for chronic Hep.B. (active virus for > 6 months)
Alpha interferon for 4 months effective in 30%.
Acute infection is usually asymptomatic.
85% of Hep.C. becomes chronic
- 20% of these will progress to cirrhosis
- 20% will develop liver fx &/or hepatocellular carcinoma
May take 20-30 years to progress to cirrhosis or cancer.
Hep.C. Mode of Transmission
Percutaneous exposure (blood transfusion, IV drug use, HD, tatooing, body piercings, inh. cocaine, can be sexually).
10% no identified cause.
Symptoms of Chronic Hep.C.
Most asymptomatic, found by elevated LFT's.
FATIGUE most common symptom.
RUQ discomfort, then cirrhosis when progresses.
Diagnosis of Hep.C.
Then, check anti-HCV (ELISA assay)
**MOST SENSITIVE TEST** HCV RNA PCR measures actual amount of virus in blood
Treatment of Hep. C.
Pegylated interferon weekly SQ injections + Ribavirin PO
1 yr tx for genotype 1
6 mos tx for genotypes 2 & 3
Post-exposure tx for Hep.C.
No vaccine and no immunoglobulin.
Test HCV by PCR at 0, 4, 12 weeks.
If + at end of 12 weeks, begin therapy.
Alcoholic liver disease
Cirrhosis = 80gms ETOH daily for 10-20years
80gms = 8 glasses of beer, 1/2 pint liquor, 1L wine.
NAFLD and NASH
- NAFLD (nonalcoholic fatty liver disease)
- NASH (nonalcoholic steatohepatitis)
NASH - dx by liver biopsy shows a fatty liver with inflammatory changes (cannot distinguish from alcoholic steatohepatitis - therefore must consume < 20gms ETOH /week)
NAFLD, risk factors
NAFLD in 20-40% of U.S.
7-9% with liver bx have NASH
- - central obesity (large)
- - DMII
- - hyperlipidemia
- - metabolic syndrome
TPN, acute starvation, hypothyroidism
jejunal bypass, small bowel resection, biliopancreatic diversion
amiodarone, tamoxifen, tetracycline, minocycline
NASH and LFT's
MAY BE NORMAL IN CIRRHOSIS, do not rely on LFT's.
Tx of NASH
WEIGHT LOSS (only approved therapy)
metformin, actos/avandia, losartan, orlistat, betaine
Late stage of progressive hepatic fibrosis characterized by distortion of hepatic structure & formation of regenerative nodules
Dx by liver bx, but may be dx w/o bx
Early cirrhosis: may be asymptomatic and good prognosis.
Advanced: jaundice, esophageal varices, ascites, hepatic encephalopathy - poor prognosis.
3 major causes of Cirrhosis
2. Chronic Hep.C.
Physical findings in advanced cirrhosis
jaundice, ascites, esoph.varices, hepatic encephal.
spider angiomas (nose, cheeks, upper trunk, neck, shoulders)
Endocrine problems from liver's inability to metabolize hormones: testicular atrophy, gynecomastia, loss of axillary/pubic hair, loss of libido/impotence.
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