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MHD > Liver Lecture 2 > Flashcards

Liver Lecture 2 Flashcards

1
Q

A transmission

A 
fecal-oral 
incubation 3-6 weeks 
no chronic state 
mild or asymptomatic 
50% of people over 50 show previous exposure
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2
Q

B transmission

A

perinatal, sexual

  • incubation period 4-26 weeks
    1. Acute or chronic
  • fulminant .1-.5%
  • chronic hepatitis

Histology: ground glass

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3
Q

C transmission

A 
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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4
Q

D transmission

A

-incubation period 4-26 weeks (same as in B)
Fulminant 3-4%*
Chronic

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5
Q

E transmission

A

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

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6
Q

Histological difference between acute and chronic hepatitis

A

acute:

  1. ballooning degeneration
  2. macrophage aggregates
  3. apoptosis
  4. sometimes necrosis
  5. portal inflammation
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7
Q

sAG
eAG
cAB
sAB

A 
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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8
Q

Stage 3 fibrosis is..

A

bridging fibrosis

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9
Q

What causes fulminant hepatitis?

A
  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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10
Q

fulminant

A

B

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11
Q

Chronic

A

C

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12
Q

Acetaminophen-related liver injury

A

-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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13
Q

What do you see in autoimmune hepatitis histology ?

A

Plasma cell

Interface Hepatitis

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14
Q

Hepatic Steatosis

A

-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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15
Q

Alcoholic hepatitis

A

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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16
Q

How does alcohol cause Alcoholic Hepatitis

A
  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
17
Q

alcoholic cirrhosis

A

fibrosis

hyperplastic nodule

18
Q

Non alcoholic fatty liver disease

A

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)

19
Q

Hemochromatosis

A

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
20
Q

wilsons disease

A 
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
21
Q

Alpha 1 antitrypsin deficiency

A
  • defective production of a1at in liver
  • errors in coding sequence prevent export
  • accumulation results in cell death, inflammation, fibrosis and cirrhosis
  • pulmonary emphysema
  • autosomal recessive chromosome 14
  • PiZZ has only 10% of normal circulating levels

Can use PAS stain in histology

MHD (81 decks)

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