Flashcards in Liver Lecture 2 Deck (21):
1
A transmission
fecal-oral
incubation 3-6 weeks
no chronic state
mild or asymptomatic
50% of people over 50 show previous exposure
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B transmission
perinatal, sexual
-incubation period 4-26 weeks
1. Acute or chronic
-fulminant .1-.5%
-chronic hepatitis
Histology: ground glass
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C transmission
Source:
IV drug use 60%
Sexual 15%
Transfusion 10% (before screening)
Occupational (4%)
incubation period 2-26 weeks
85% of patients with acute infection
Fulminant -rare
chronic 80-85%- 20-30% progress to cirrhosis
-increased risk of hepatocellular cancer
RNA
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D transmission
-incubation period 4-26 weeks (same as in B)
Fulminant 3-4%*
Chronic
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E transmission
Fecal-oral -contaminated water
incubation 6 weeks
fulminant .2-.3%
***20% in pregnancy
no carrier state
-unlikely risk of hepatocellular carcinoma
Endemic in tropical and subtropical countries
6
Histological difference between acute and chronic hepatitis
acute:
1. ballooning degeneration
2. macrophage aggregates
3. apoptosis
4. sometimes necrosis
5. portal inflammation
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sAG
eAG
cAB
sAB
surface AG: active infection
-if greater than 6 months chronic
eAG-infectivity
cAB-way to tell chronic or acute, won't have if you were vaccinated without disease
sAB-victory
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Stage 3 fibrosis is..
bridging fibrosis
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What causes fulminant hepatitis?
1. viral hepatitis
-usually B or A
-rarely C, HSV, or dengue virus
2. drugs and chemical toxicity
3. autoimmune hepatitis
4. wilson's disease
5. budd chiari
6. rare (ischemia, malignancy
7. unknown (15%)
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fulminant
B
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Chronic
C
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Acetaminophen-related liver injury
-leading cause of acute liver failure
-dose related toxin exceed 10gm/day
-very high aminotransferase levels
low t. bilirubin?
Build up of NAPQI
GIve NAC
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What do you see in autoimmune hepatitis histology ?
Plasma cell
Interface Hepatitis
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Hepatic Steatosis
-Reversible
short term ingestion of 80gm of alcohol
-6 beers or 8 oz of 80 proof
-10-15% of alcoholics develop fibrosis
macrovasicualr
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Alcoholic hepatitis
fatty liver
inflammation
hepatocellular injury (hepatocyte swelling, apoptotic bodies), mallory hyaline often associated with neutrophils (proteinaceous debri)
-balloon and chicken wire fibrosis
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How does alcohol cause Alcoholic Hepatitis
1. acetaldehyde
-metabolite of Etoh
-disrupts the cytoskeleton membrane function
2. induction of cytochrome p450 and generation of reactive species
-damages membranes and hepatocyte function
3. decrease glutathione levels
4. malnutrition and vitamin deficiencies
5. bacterial endotoxins from gut inducing inflammatory responses
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alcoholic cirrhosis
fibrosis
hyperplastic nodule
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Non alcoholic fatty liver disease
Histology: identical to ETOH
Obesity and metabolic syndrome: dyslipidemia, hyperinsulinemia, and insulin resistance
*most common cause of chronic liver disease and cryptogenic cirrhosis
70% of obese individuals
hepatic steatosis
-minor nonspecific inflammation
non alcoholic steatohepatitis NASH
-hepatocyte injury
-can progress to fibrosis s
-can be asymptomatic or RUQ discomfort
-associated with cardiovascular disease and metabolic syndrome
-elevated transaminases
(simple steatosis does not progress to cirrhosis)
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Hemochromatosis
Disease of iron overload
Hereditary: recessive (HFE gene chromosome 6)
-excessive absorption of dietary iron
Secondary: transfusions or hemolysis
-iron deposition in parenchymal tissue
Treatment: phlebotomy or chelation
******SIGNIFICANT risk of hepatocellular carcinoma 200x risk
Diagnosis:
elevated serum iron
elevated ferritin
test for HFE gene
liver biopsy for quantitative iron studies and histological examination
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wilsons disease
copper accumulation
-liver and brain
-recessive
-impaired copper excretion
-symptoms start 6-20 years
-neuropsychiatric
-kayser fleischer ring
-liver failure
-hemolytic anemia
Treatment: copper chelation
chameleon on biopsy?
Diagnosis:
-low ceruloplasmin
-increased urinary copper
-liver biopsy for quantitative copper analysis
-kayser-fleischer rings
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