115b Clinical Viral Hepatitis Flashcards Preview

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Flashcards in 115b Clinical Viral Hepatitis Deck (16):
1

HBV vaccine is made of what antigen?

HBs

2

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

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

3

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

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)

4

which hep viruses are not cytopathic?

Hep A
Hep B
Hep E

5

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

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

6

HBsAg

Anti-HBs

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

7

HBeAg

from pre-core portion of gene
indicates active viral replication and transmissiblity

8

Chronic Hep B length and phases

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)

9

seroconversion

loss of HBeAg and gain of AHeAb --> carrier

10

Angi-HBc - IgM vs IgG

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

11

Acute HBV serum markers

+ HBsAg
+ HBeAg
IgM Anti-HBc

12

immunized HBV serum markers

Anti-HBs only

13

recovered HBV serum markers

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

14

Hep B treatment

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

15

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

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

16

what does Hep D need?

HBsAg for outside coat
oral antivirals won't stop Hep D virus from spreading b/c HBsAg still made