Gastro-Hepatitis B

Front 1

What is the mode of transmission of hepatitis B?

Back 1

vertical transmission (common worldwide but uncommon in Africa)
- related to the HBV replicative
state of the mother (90% HbeAg+, 30% HbeAg−ve)

horizontal transmission(common in africa)

IV route-transfusion, IVDU.

Sexual contacts.

Front 2

Can you transmit hep B from breastfeeding?

Back 2

No

Front 3

what is the hep B virus?

Back 3

A DNA virus-partially double stranded.

Front 4

Is the virus itself cytopathic?

Back 4

No.HBV is not directly cytopathic.The liver damage produced is by the cellular immune response of the host.

Front 5

Which genotype has the worse outcome.

Back 5

Genotype C.

Front 6

which genotype is more responsive to interferon?

Back 6

Genotype A and B.

Front 7

What happens in a precore mutation of Hepatitis B?

Back 7

No production of HBeAg
HBsAg non affected.

To detect infectivity, HBV DNA must always be measured.

Front 8

What did the REVEAL study show?

Back 8

The study showed that the risk of HCC was related to levels of HBV DNA rather than a raised ALT.

Front 9

What is the body's immune response to Hep b infection?

Back 9

Th1 response clears the virus
Th2 response is responsible for the chronicity of the disease.

Front 10

What are the phases of chronic HBV infection?

Back 10

Replicative phase
Integrated phase

Front 11

what happens in the replicative phase?

Back 11

Active viral replication
HBeAg and HBV DNA positive.

patient is highly infectious.

Front 12

what happens in the integrated phase?

Back 12

the viral genome integrates with host DNA.

HBeAg negative.
HBV DNA low
HBeAb positive.

Front 13

What is the significance of viral markers in Hep B

Back 13

As per table 7.7.

Front 14

What is the marker of acute hep B infection?

Back 14

Presence of anti-HBc IgM.

Front 15

Which marker is the most sensitive index of viral replication?

Back 15

HBV DNA

Front 16

Interpret the following graft.

Back 16

Antigens:
HBsAg appears in the blood from about 6 weeks to 3
months after an acute infection and then disappears.

HBeAg rises early and usually declines rapidly.

Antibodies:
Anti-HBc is the first antibody to appear and high titres of IgM anti-HBc suggest an acute and continuing viral
replication. It persists for many months. IgM anti-HBc may
be the only serological indicator of recent HBV infection in a period when HBsAg has disappeared and anti-HBs is not
detectable in the serum.

Anti-HBe appears after the anti-HBc and its appearance
relates to a decreased infectivity, i.e. a low risk.

Anti-HBs appears late and indicates immunity.

Front 17

Interpret the following graft.

Back 17

(b) Development of chronic hepatitis followed by
seroconversion

HBsAg persists and indicates a chronic infection (or carrier
state).

HBeAg persists and correlates with increased severity and
infectivity and the development of chronic liver disease.
When anti-HBe develops (seroconversion) the Ag
disappears and there is a rise in ALT.

HBV DNA suggests continual viral replication.

Front 18

What is the treatment for acute hepatitis?

Back 18

Mainly symptomatic.1-10% progress to inactive chronic HBV infection.

Front 19

what are the viral markers of inactive chronic HBV infection?

Back 19

HBsAg positive
HBeAg negative
HBe Ab positive
HBV DNA in low levels.
normal or slightly raised ALT,AST.

Front 20

what are the viral markers of active chronic HBV infection?

Back 20

HBs Ag positive
HBe Ag positive**
HBV DNA positive.
Raised AST,ALT
Liver biopsy shows chronic hepatitis.

** unless a mutant virus is involved.

Front 21

Interpret these HBV panels

Back 21

Main features:

1) Active Hep B infection-Must be HBsAg positive and IgM HBcAb positive.

2) Chronic Hep B infection-Must be HBsAg positive and IgM HBcAb negative.

3) Past Hep B infection
Must have HBsAg negative, HBeAb positive, IgG HBcAb positive.

4) Previous Hep B vaccination:
Must have HBsAg negative, IgG HBcAb negative.

HINT:
First look at HBsAg.

Secondly look at:
IgM HBcAb, if HBsAg +ve.

IgG HBcAb, if HBsAg -ve.

Front 22

Who to treat?

Back 22

Front 23

what is the aim of treatment?

Back 23

Seroconversion of HBeAg
Reduction of HBV DNA to undetectable levels by PCR.

Front 24

Name the antiviral agents for treatment of Hep B?

Back 24

Pegylated Interferon
Lamivudine
Adefovir
Tenofovir
Entecavir

(PILATE)

Front 25

which patients should not receive interferon?

Back 25

Patients with cirrhosis.(Child-Pugh category C status)

Front 26

what are the side effects of interferon?

Back 26

flu-like illness
malaise
headache
myalgia
depression
reversible hair loss
bone marrow depression

Front 27

what factors predicts good response to treatment?

Back 27

short duration of disease
high ALT,AST
Active liver disease on histology
Low HBV DNA levels
Absence of immunosuppression
Female
Adult acquired
Delta virus negative
Rapidity of response to oral therapy.

Front 28

If a patient responds poorly to interferon,(ie: HBeAg negative disease) what is the next option?

Back 28

Lamivudine
-But by 4 years 80% develop viral resistance due to YMDD mutant.

Entecavir more effective than lamivudine.

Tenofovir is effective against lamivudine resistant virus.

Front 29

how long is the duration of treatment with interferon?

Back 29

1 year.

Front 30

What is the reason for viral resistance?

Back 30

Monotherapy.

Front 31

What is the reason for not responding to Lamivudine by 4 years of treatment?

Back 31

80% develop resistance due to YMDD mutant.

Front 32

How to confirm a co-infection of HDV and HBV?

Back 32

Confirmed by finding serum IgM anti-HDV in the presence of IgM anti-HBc.

Front 33

What is the early marker of HDV infection?

Back 33

HDV RNA

Front 34

what type of virus is the Hepatitis D virus?

Back 34

RNA virus.

Front 35

what is the significance of Hep D virus co-infection with Hep B?

Back 35

Acute HBV and HDV co-infection tends to be more severe than acute HBV infection alone.

Likely to result in fulminant hepatitis.

treatment is with interferon for 12 months.but response is poor.

Front 36

In cell injury, what type of immune response is stimulated?

Back 36

T cell response.

Front 37

What are the extrahepatic manifestations of Hep B infection?

Back 37

Serum sickness like syndrome
Polyarteritis nodosa
Glomerular disease

Front 38

What is the percentage of patients with chronic hep b that will progress to cirrhosis?

Back 38

20% will develop cirrhosis.

Front 39

A patient receives vaccination for Hep B with 6 doses but is still HBs Ab negative.

Now comes in contact with a patient with active Hep B.

What should be the next step?

Back 39

Assume non protected.

Treat with HB immunoglobulin.

Front 40

A patient has had 3 doses of Hep B vaccine and is found to be HBs Ab negative.

What should be the next step?

Back 40

Give added doses.
(95-99% achieve titre anti-HBs >10mlU/ml after 3 doses.)

50% will respond to added doses.
(Up to 6 doses)

Front 41

A patient received 3 doses of Hep B vaccine 10 years ago and was found to be HBs Ab positive.

Repeat testing the following year reveals he is now HBs Ab negative.

What should happen next?

Back 41

No action required.

Anti-HBs titre falls with time

60% of responders will have no antibodies at 12 months

They are still immune.No need for boosters.