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

Lab: Anti-HAV IgM (positive by the time sx start, disappears at 14 weeks), Anti-HAV IgG (at 4 weeks, then forever)

- 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

Jaundice (at 2 weeks post-exposure)

Hepatomegaly

Elevated LFT's, bilirubin > 10, Alk.phos., GGT

No treatment available

99% get better

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.

All contacts need to get tx prophylactically.

Avoid ETOH, NSAIDS, acetaminophen.

Avoid fatigue.

Emphasize handwashing.

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

• 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

Same manifestations as Hep.A.

30% have no symptoms

10% will develop chronic hepatitis B

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.

chronic Hep.B. infection can lead to: 

- cirrhosis

- 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.

Percutaneous exposure (blood transfusion, IV drug use, HD, tatooing, body piercings, inh. cocaine, can be sexually).

10% no identified cause.

Most asymptomatic, found by elevated LFT's.

FATIGUE most common symptom.

RUQ discomfort, then cirrhosis when progresses.

Elevated ALT/AST

Then, check anti-HCV (ELISA assay)

**MOST SENSITIVE TEST** HCV RNA PCR measures actual amount of virus in blood

Pegylated interferon weekly SQ injections + Ribavirin PO

1 yr tx for genotype 1

6 mos tx for genotypes 2 & 3

No vaccine and no immunoglobulin.

Test HCV by PCR at 0, 4, 12 weeks.

If + at end of 12 weeks, begin therapy.

Cirrhosis = 80gms ETOH daily for 10-20years

80gms = 8 glasses of beer, 1/2 pint liquor, 1L wine.

• 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 in 20-40% of U.S.

7-9% with liver bx have NASH

Risk factors:

• - central obesity (large)
• - DMII
• - hyperlipidemia
• - metabolic syndrome

TPN, acute starvation, hypothyroidism

jejunal bypass, small bowel resection, biliopancreatic diversion

amiodarone, tamoxifen, tetracycline, minocycline

MAY BE NORMAL IN CIRRHOSIS, do not rely on LFT's.

WEIGHT LOSS (only approved therapy)

Possible:

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.

1. Alcohol

2. Chronic Hep.C.

3. NASH

jaundice, ascites, esoph.varices, hepatic encephal.

spider angiomas (nose, cheeks, upper trunk, neck, shoulders)

palmar erythema

Endocrine problems from liver's inability to metabolize hormones: testicular atrophy, gynecomastia, loss of axillary/pubic hair, loss of libido/impotence.