Virology10 Flashcards

1
Q

T or F
HBc antigen can be found in blood
While Hbe i can’t detect it

A

False
We should look for the anti HBc
It’s not soluble
Hbe is soluble and we can detect it

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2
Q

Window period is :

A

The gap between the disappearance of the sAg and the formation of antibody

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3
Q

State the case of each of the following patients:

HbsAg         Anti-Hbs        Anti-HBc
Negative     Negative       Negative
Negative     Positive         Negative
Negative     Positive         Positive
Positive       Negative      IgM pos
Positive       Negative     IgG positive
A
Susceptible
Vaccinated
Past infection
Acute infection
Chronic infection
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4
Q

Stages of hepatitis B exacerbation:

A

Immune tolerant: viral load is high and we have HBe(soluble, indicator), normal LFTs
Inmune clearance: lowering of viral load and HBs become to disappear, increasing 5-fold of LFTs (not the case for HepC) , immunopathological damage
Immune control: seroconversion of HBe antigen, viral load is almost null

Immune active: high LFTs and high viral load.

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5
Q

Causes of reactivation of hepB (immune active):
1-
2-
3-

A

1- hepD
2- immunosuppresion(HIV)
3- stress

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6
Q

HepC
Fam:
Envelope:
Genome:

A

Flavivirus
Enveloped
+ ss RNA

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7
Q

Hep B risk of infection as an infant is to —— while as an adult ——-

A

Develop adulthood chronic disease
And to develop hepatocarcinoma
95% is the percentage to recover fully (good)

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8
Q

T or F

Hep B and C don’t have extra hepatic manifestations

A

False they have (rash , vasculitis, arthritis, glomerulo nephritis)

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9
Q

MOT of hepC:

A

Contaminated blood
Snorting (injury of nasal mucosa in drug dealers) (epistaxis)
Darb l haidar

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10
Q

Genotypes in hepatitis C are called—– and the most aggressive one is—–

A

Clades

1b

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11
Q

In religous rituals what infectious agents should be asked:

A
The ones transmitted by body fluids
HIV
B
C
Syphilis
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12
Q

Role of NS5A protein:

A

Inhibits apoptosis and this will lead to more cytokine release and consequently more damage (immune-mediated cytolysis)

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13
Q

Management of HCV infection:

A

Ask for serum test to look for Anti-HCV

HCV genotyping to know which genotype and treat upon the result

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14
Q

Characteristics of chronic HCV:

A

Not a very high LFTs (like in B)
80% byaamlu chronic
20% mn l acute hepatitis hene HCV

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15
Q

T or F

HepC causes hepatocarcinoma

A

True

It constitutes 25% of the hepatocarcinoma patients around the world

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16
Q

T or F

Cirrhosis will happen after 10 years of infection with hepC

A

False

After 20-30

17
Q
Highly predisposed to chronic hepC:
1-
2
3
4
5
6
A
Older than 40
Alcohol
HIV-HBV
Immunosuppresion
Diabetes or obesity
Schistosomiasis ( bilharzia) le met feha abd l halim hafez allah yrham ruhu
18
Q

All pateints should be treated(after hepC infection) except:

A

Pregnant
Liver transplant list
End of life ( baadelu 6 months la ymut)

19
Q

Sustained viral remission:

A

After 4 months of completing treatment we do pcr if it’s negative then i cleared the virus from the body

20
Q

Tx for hepC

A

1-Interferon alpha with PEG (polyethylene glycol) (provide long half life)
2-We can add ribavirin (as synergistic) (discontinued because of it’s side effects)
3- Direct acting antivirals
4- we should always take into consideration genotype- renal status and medications

21
Q

HepD

Genus:
Fam:
Envelope:
Genome:
Active or defective:
Surface antigen:
A
Deltavitus (D for Delta)
No fam
Enveloped
Ss- circular RNA
Defective ( as it's name D for defective)
HBsAg (mtl men ya helu?)
22
Q

T or F

Hepatitis D can’t infect unless it’s with B, and this will cause very severe hepatitis

A

True

23
Q

MOT of hep D

A

Same as B
Coinfection
Superinfection

24
Q

T or F

Hep E is same as A but it doesn’t cause fulminant hepatits

A

False

It causes fulminant hepatitis especially in pregos

25
Q

Varicella causes—– and can be severe in pregnant woman.

A

Pneumonia

26
Q

T or F

Both hep A and E don’t have vaccines

A

False

Hep A has while E doesn’t