115b Clinical Viral Hepatitis Flashcards

1
Q

HBV vaccine is made of what antigen?

A

HBs

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2
Q

which hep viruses have vaccines? should we vaccinate in shit holes?

A

A and B –> dramatic decrease in US.
Hep A still big in south america, africa, india - don’t vaccinate in these areas b/c everyone gets it when young and is thus low risk

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3
Q

Hep A

1) Genetic material and virus type
2) transmission
3) carriers?
4) incubation
5) HCC risk?
6) symptoms
7) treatment
8) Notes

A
1) Genetic material and virus type
SS+ RNA; picornavirus
2) transmission
Fecal-oral (like Hep E) --> resilient b/c no membrane
3) carriers?
No
4) incubation
Short - weeks
5) HCC risk?
No
6) Symptoms
Jaundice, fever, fatigue, 
7) Treatment
supportive
8) Notes (4 A's)
Asymptomatic (children usually; adults get sick)
Acute (IgM for acute infection, IgG previous/vaccine)
Alone (no carriers)
Ain't going to hurt (not cytopathic by itself)
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4
Q

which hep viruses are not cytopathic?

A

Hep A
Hep B
Hep E

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5
Q

Hep B

1) Genetic material and virus type
2) transmission
3) carriers?
4) incubation
5) HCC risk?
6) symptoms
7) treatment
8) Notes

A
1) Genetic material and virus type
DNA; hepadnavirus 
2) transmission
parenteral, sexual, maternal-fetal
3) carriers?
Yes (kids)
4) incubation
long (months)
5) HCC risk?
Yes - integrates into genome (oncogene)
6) symptoms
7) treatment - oral antivirals or interferon 
8) Notes
-Babies become carriers; adults with acute hepatitis are clearing virus so don't usually treat
-own dna poly to finish d/s dna then uses host rna poly
-overlapping reading frame genome
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6
Q

HBsAg

Anti-HBs

A

Surface antigen - indicates Hep B infection (acute and chronic); may be negative during window period; doesn’t indicate active replication

indicates immunitiy

**both negative during window period so check Anti-HBc

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7
Q

HBeAg

A

from pre-core portion of gene

indicates active viral replication and transmissiblity

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8
Q

Chronic Hep B length and phases

A

Occurs over decades
1- immune tolerance - virus replicates (high DNA); ignored by immune system (normal LFTs)
2- Immune reactive/clearance - hepatitis presentation due to immune system; seroconversion may occur –> carrier
3- Inactive carrier - low DNA, normal LFTs; some may lose HBsAg with gain of HBsAb (recovery)

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9
Q

seroconversion

A

loss of HBeAg and gain of AHeAb –> carrier

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10
Q

Angi-HBc - IgM vs IgG

A

IgM - acute infection
IgG - chronic/prior exposure
+ during windown period

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11
Q

Acute HBV serum markers

A

+ HBsAg
+ HBeAg
IgM Anti-HBc

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12
Q

immunized HBV serum markers

A

Anti-HBs only

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13
Q

recovered HBV serum markers

A

+Anti-HBs
+Anti-HBe
+Anti-HBc IgG

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14
Q

Hep B treatment

A

1) oral antivirals (“_vir”) - won’t clear but limits replication
2) interferon - helps stimulate immune system so can clear but not tolerated; can worse liver damage

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15
Q

Hep C

1) Genetic material and virus type
2) transmission
3) carriers?
4) incubation
5) HCC risk?
6) symptoms
7) treatment
8) Notes

A
Hep C
1) Genetic material and virus type
\+SS RNA; flavivirus
2) transmission
Blood, IVDU, transfusion
3) carriers?
Yes
4) incubation
long
5) HCC risk?
yes - chronic inflammation
6) symptoms
Hep C
7) treatment
protease inhibitors ("_vir")
RdRp inhibiros/NS5A inhbiitors 
8) Notes
Chronic
Cirrhosis
Carcinoma
Carrier
Can't vaccinate (RNA poly error prone)
Continuos polyprotein
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16
Q

what does Hep D need?

A

HBsAg for outside coat

oral antivirals won’t stop Hep D virus from spreading b/c HBsAg still made