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26 Cards in this Set
- Front
- Back
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1. What type of disease is Hepatitis A?
How is Hep A transmitted? What type of virus is it? Is there immunity for it? |
Benign, acute, self-limited disease
Feco-oral transmission (also shellfish) **shed in stool for 2-3 wks before and 1 wk after onset of jaundice RNA virus IgG persists for years conferring immunity |
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2. What is the incubation period of Hep B?
What is the transmission of Hep B? What type of virus is Hep B? |
Long incubation period (1-6 mos)
Exposure to blood and all body fluids and secretions except stool DNA virus with core, surface and e antigens **test for Hep by looking for three antigens (core, surface and e antigens) |
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3. What are the two phases of Hep B infection?
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1. Proliferative phase
2. Integrative phase |
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4. What happens during the proliferative phase?
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1. Formation of virions and antigens
2. T cell activation 3. Hepatocyte destruction |
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5. What happens during the integrative phase?
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1. Incorporation of viral DNA into host genome
2. Appearance of antibodies 3. Inflammation subsides 4. Risk of HCC persists |
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6. Which antigen appears first before the onset of symptoms?
What are markers of active replication? What makers the carrier state or chronic disease? |
HBsAg appears first
HBeAg, DNA and DNA polymerase are markers of active replication Persistence of HBaAg after 6 months |
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7. Which antibodies to Hep B appear first before the onset of symptoms?
What appears after the antigens disappear? What does this mark? What is present during the window period? Which may persist for life? |
Anti-HBc
Anti-HBa and Anti-HBe appear Imply the acute phase is over Only anti-HBc and anti-HBe Anti HBs **rises after the acute disease is over and may persist for life |
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8. What are the infection stages in Hep B infection and their time periods?
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1. Incubation (4-12 wks)
2. Acute infection (2-12 wks) 3. Recent Acute infection (2-16 wks) 4. Recovery (years) |
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9. What are the outcomes of Hep B acute infection?
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1. Subclinical disease
-can have recovery 2. Acute hepatitis -recovery or fulminant hep (death) 3. "Healthy" carrier 4. Persistent infection -recovery -chronic hepatitis **chronic hepatitis can lead to cirrhosis which can lead to HCC or death |
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10. What is the incubation period of Hep C?
What type of virus is it? How is transmission of Hep C? What else is likely to go along with Hep C? |
Incubation period of 2-26 wks
RNA virus Transmission through contaminated blood More likely to have chronic disease and cirrhosis |
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11. What are there fluctuating levels of in Hep C?
Is there immunity with Hep C? What is tested for with Hep C? |
Fluctuating levels of transaminases
Anti-HCV IgG does not confer immunity HCV-RNA (only serum marker) |
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12. What are the outcomes of Hep C?
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1. Resolution (15%)
-minority unlike with Hep B 2. Chronic Hepatitis (85%) -stable -cirrhosis 3. Fulminant hepatitis |
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13. What type of virus is Hep D?
How is Hep D transmitted? Does Hep D cause damage to liver? What does Hep D require? How is diagnosis made? |
RNA virus
Acquired by co-infection or super-infection Alone does no damage to liver Requires encapsulation by Hep B s Ag Detection of the HDV DNA and anti D IgM |
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14. What type of virus is Hep E?
How is transmission? Is there a risk of chronic disease? Who has a high mortality rate from Hep E? |
RNA virus
**self-limited Feco-oral transmission No risk of chronic disease Pregnant women |
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15. What clinicopathologic syndromes are associated with viral hepatitis?
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1. Asymptomatic infection (only serology)
2. Acute hepatitis (icteric & non-icteric) 3. Chronic hepatitis 4. Fulminant hepatitis |
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16. Which hepatotrophic viruses can cause acute hepatitis?
What are the symptoms of acute hepatitis? How is the liver? What can mimic the changes? |
All 5 hepatotropic viruses
Non-specific constitutional -pale stools -dark urine -pruritus Liver may be enlarged Changes may be mimicked by drugs |
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17. What micro changes can be seen with acute hepatitis?
Four things... |
1. Lobular inflammation
2. Portal inflammation 3. Cholestasis 4. Regeneration |
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18. What is chronic hepatitis?
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Symptomatic, biochemical or serological evidence of continuing or relapsing hepatic disease for at least 6 months with biopsy support
**symptoms may be non-specific |
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19. What can chronic hepatitis be due to?
Five things... |
1. Hep B, C and D
2. Drugs 3. Wilson's 4. A1AT 5. Autoimmunity |
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20. What is a carrier state?
What are the three types of carrier state? |
When individuals harbor the virus and can transmit the infection
1. Have virus but not clinical or histologic evidence of infection 2. Virus, asymptomatic, lab evidence of chronic disease 3. Virus, symptomatic, evidence of chronic disease |
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21. What is the carrier state defined as?
When will progressive liver damage occurs? |
Presence of HBsAg in the serum for 6 months or longer after initial detection
If in addition to HBsAg there is HBeAg, HBV DNA and antibodies |
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22. What is fulminant hepatitis?
What does it present with? (three things) |
When hepatic insufficiency progresses from onset of symptoms to hepatic encephalopathy in 2-3 wks
1. Jaundice 2. Encephalopathy 3. Fetor hepaticus |
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23. What are cause of fulminant hepatitis?
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1. Viral hepatitis (HAV, HBV)
2. Drugs and toxins 3. Wilson's disease 4. Acute fatty liver of pregnancy |
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24. What are there elevated levels of with autoimmune hepatitis?
What cell type is associated with autoimmune hepatitis? What will those with autoimmune hepatitis respond to? |
1. Elevated serum IgG levels
2. High titers of autoantibodies -ANA -ASMA -ALKMA Plasma cell infiltrate Dramatic response to steroids |
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25. What are three mechanisms of action for drug and toxin injury?
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1. Direct toxicity
2. Hepatic conversion of a xenobiotic to an active toxin 3. Through immune mechanisms of a drug or metabolite acting as a hapten to convert a cellular protein into an immunogen |
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26. What do predictable, expected drug reactions require?
Why do unpredictable, idiosyncratic drug reactions occur? |
Require accumulation of a certain dose
Occur due to... -idiosyncrasies of the host -different rates of metabolism of drugs -different rates of immune response |
