module 13 hepatitis Flashcards
hepatitis s/s
sequence
- incubation
- prodromal (preicteric) phase
- variety of s/s ending with jaundice
- icteric phase: hepatocellular destruction and bile stasis, phase of illness
- recovery phase
Hepatitis A
RNA
fecal-oral transmission (enteric)
2-7 week incubation
immunity via IgG
Hep A risk factors
crowded, unsanitary conditions
food and water contamination
Hep A s/s
anicteric: no s/s or mild without jaundice Majority - jaundice - malaise - anorexia - nausea - low fever - RUQ pain
Hep B
Double stranded DNA
incubation 2-6 months
parental transmission: infected blood, body fluids, or contaminated needles
3 types of viral particles
prodromal period longer with immune-complex related s/s
Hep B s/s
urticaria rashes arthralgia arthritis angioedema serum sickness glomerulonephritis jaundice
Hep B infection to recovery/death
acute infection
- 60-65% sublinical disease -> 100% recovery
- 20-25% acute hepatitis -> 99% recovery, 1% fulminant hepatitis -> death
- 4% chronic hepatitis -> 20-30% cirrhosis -> hepatocellular carcinoma/death
fulminant hepatitis
liver coma
Hep C
RNA
Parental transmission, though less through sex or perinatal
- drug use, blood transfusion, needle stick
Hep C infection to recovery/death
acute infection
- 85% chronic hepatitis -> 80% stable disease, 20% cirrhosis -> 50% stable, 50% death
- 15% resolution
- rare: fulminant hepatitis
Hep D
co-infection
- depends on Hep B for replication
Parental transmission
Hep A and Hep E similar
typically self-limiting
2-8 wk incubation
does not cause chronic hepatitis or cancer
oral transmission
Hep B, Hep C, and Hep D similar
cause carrier state
cause chronic hepatitis and cancer
parenteral transmission
Hep E
RNA
transmission: fecal- oral
parental may occur
incubation: 2-9wks
chronic hepatitis
inflammation of liver > 6mo.
chronic persistant
chronic active
autoimmune
chronic persistant
triaditis, transaminitis
- chronic, low-grade inflammation
- portal triads w/out destruction of liver structures
- inc. serum transaminase
- not progressive
chronic acute
progressive, destructive
extends beyond portal triad to hepatic lobule
could spontaneously arrest or progress to cirrhosis
chronic acute s/s
fatigue malaise nause anorexia ascites hepatomegaly abdominal pain jaundice
autoimmune hepatitis
progressive inflammation characterized by autoantibodies and polyclonal hypergamaglobulinemia
cirrhosis
irreversible end stage of many different hepatic injuries
- acute hepatitis
- chronic hepatits
- toxic hepatitis
- metal storage diseases
- alcoholism
nodule regeneration and fibrosis -> dec. hepatic function
Biliary channels obstructed -> portal HTN
-> blood shunting away from liver, hypoxic necrosis
alcoholic cirrhosis
more fat delivered to hepatocyte than it can metabolize; defect in fat metabolism fatty infiltration (hepatic steatosis) - inc. lipogenesis and dec. fatty acid oxidation Alcohol -> acetaldehyde -> lipid peroxidation -> disruption of cellular function, damage, and inflammation
alcoholic cirrhosis s/s
usually mild and asymptomatic enlarged liver abdominal discomfort portal HTN multisystem disease r/t alcohol intake
Biliary cirrhosis
end result of continuous inflammation of bile ducts r/t biliary obstruction and backup of bile in the liver
-> inflammation and scarring of liver with obliteration of bile ductules, diffuse, widespread fibrosis, and nodule formation
Portal HTN
Biliary autoimmue (1st degree)
unknown etiology
destruction of intrahepatic ducts
portal inflammation
fibrosis