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DipHIV > Hepatitis (BHIVA 2013) > Flashcards

Hepatitis (BHIVA 2013) Flashcards

1
Q

Why should all PLW HIV be screened for HEPATITIS A?

A

Vaccine-preventable disease

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2
Q

What complications occur in people with persistent HEPATITIS B?

A 
chronic progressive liver disease
hepatocellular carcinoma (HCC)
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3
Q

How many GENOTYPES of HEPATITIS B are there?

A

TEN (10)

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4
Q

What value does HEPATITIS B genotype testing offer?

A

helps predict outcome with PEGYLATED INTERFERON

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5
Q

What is the definition of ‘chronic persistence’ of HEPATITIS B?

A

HB surface antigen DETECTABLE

>6 months

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6
Q

What proportion of PLW HIV have detectable HBsAg?

A

7%

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7
Q

What factors were associated with detectable HBsAg in PLW HIV?

A

Black person
IDU
MSM

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8
Q

What might explain an isolated HBcAb in the absence of HBsAg or evidence of immunity in PLW HIV?

A 
FALSE positive
or
loss of HBsAb due to IMMUNE DYSFUNCTION
or
loss of HBsAg before HBsAb (less likely)
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9
Q

What proportion of people with isolated HBcAb will eventually develop HBsAb over time?

A

20-40%

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10
Q

What proportion of people with isolated HBcAb will develop SURFACE antigen?

A

2-4%

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11
Q

In a person with previous isolated HBcAb who develops HBsAg, what does this indicate?

A

REACTIVATION
or
NEW infection

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12
Q

Which group of people are at highest risk of HEPATITIS C?

A

IDU

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13
Q

What is the prevalence of HEPATITIS C in PLW HIV?

A

9%

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14
Q

What risk factors increase a PLW HIV of acquiring HEPATITIS C?

A 
MSM
\+
multiple partners
STI
insertive anal sex
douches/enemas
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15
Q

What is the re-infection rate for HEPATITIS C in PLW HIV?

A

8-25%

UK vs Dutch cohort

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16
Q

At what clinical stage is PEG-IFN and ribavirin more successful in treatment for HEPATITIS C?

A

ACUTE infection

note - old treatment

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17
Q

What impact does HIV infection have on HEPATITIS C seroconversion?

A

DELAYS

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18
Q

What factors are associated with DELAYED seroconversion of HEPATITIS C in PLW HIV?

A

low ALT

low CD4

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19
Q

What molecular aspects of HEPATITIS C virus are associated SPONTANEOUS CLEARANCE?

A 
Single nucleotide polymorphisms
in
IL28B locus
on
Chromosome 19
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20
Q

What was the past ‘gold standard’ for staging and grading liver disease?

A

Liver BIOPSY

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21
Q

What is the modern day choice of investigation to assess for liver fibrosis?

A

Hepatic Transient Elastography (TE)

Fibroscan

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22
Q

At what level of kPa is cirrhosis diagnosed on fibroscan in HEPATITIS B?

A

> 11kPa

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23
Q

At what level of kPa is cirrhosis diagnosed on fibroscan in HEPATITIS C?

A

> 14.5kPa

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24
Q

What is the limitation of hepatic transient elastography (ie Fibroscan)?

A

less accurately differentiates between lower levels of fibrosis

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25
Q

If there is uncertainty of level of fibrosis on hepatic transient elastography what alternative investigation can be performed?

A

Liver BIOPSY

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26
Q

What is the vaccination schedule for HEPATITIS B in PLW HIV?

A

DOUBLE dose
40 microgram
0, 1, 2 and 6 months

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27
Q

When can an accelerated hepatitis B vaccination schedule be used in PLW HIV?

A

need for RAPID completion
AND
CD4 >500 cells

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28
Q

When should HBsAb levels be checked following hepatitis B vaccination?

A

4-8 weeks after last dose

check - is this old guidance

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29
Q

If HBsAB titre is less than 10IU/L after vaccination course, what is the recommended action?

A

RE-VACCINATE 3 doses
40microgram
MONTHLY

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30
Q

If HBsAB titre is between 10IU/L to 100IU/L after vaccination course, what is the recommended action?

A

ONE further vaccine
40 microgram
re-check HBsAb 4-8 weeks

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31
Q

When is a BOOSTER dose of vaccine indicated for HEPATITIS B?

A

HBsAB <10IU/L

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32
Q

What is the dose of hepatitis B booster dose?

A

40microgram

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33
Q

How many weeks post vaccination is the presence or not of HBsAb predictive of durability of immunity?

A

28 weeks

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34
Q

What is the incidence of ART related severe HEPATOTOXICITY?

A

10%

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35
Q

What increases the risk of ART related hepatotoxicity?

A

Hepatitis + HIV co-infection

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36
Q

What modifiable lifestyle factors in particular may increase the risk of ART related hepatotoxicity?

A

ALCOHOL

COCAINE

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37
Q

Which ART can induce a hypersensitivity reaction which includes hepatotoxicity?

A 
NEVIRAPINE
DARUNAVIR
FOSAMPRENAVIR
DIDANOSINE
TIPRANAVIR
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38
Q

What liver condition is didanosine specifically associated with?

A

Non-cirrhotic portal hypertension

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39
Q

Which ART may reduce the efficacy of PEG-IFN/RBV treatment for HCV?

A

ABACAVIR

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40
Q

What dose adjustment is required for RIBAVIRIN if a person is taking ABACAVIR?

A

Increase ribavirin

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41
Q

Why might a person have high HBV DNA but surface antigen negative?

A

Drug selective pressure
Often on lamivudine
mutations in the surface gene

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42
Q

What impact does HIV have on hepatitis B outcomes [name 4 things]?

A

1) more likely to progress to chronic HBV
2) Lower clearance of eAg
3) Higher viral load than HBV alone
4) more rapid progression to cirrhosis/HCC

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43
Q

Presence of HBsAg after what time period is diagnostic of chronic infection?

A

6 months

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44
Q

In what circumstance might HBcAb IgG not develop in HBV + HIV co-infection?

A

Advanced immunosuppression

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45
Q

Hepatitis B infection - describe IMMUNE TOLERANT stage.

A 
HBsAg POSITIVE
HBeAg POSITIVE
HBV DNA HIGH
ALT/AST NORMAL
BIOPSY - little or no fibrosis
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46
Q

In what population is HBV immune tolerant stage most likely to occur?

A

those infected in EARLY CHILDHOOD or VERTICAL transmission

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47
Q

Hepatitis B infection - describe IMMUNE ACTIVE stage.

A 
HBsAg POSITIVE
HBeAg POSITIVE
HBV DNA HIGH
ALT/AST RAISED
BIOPSY - inflammation/fibrosis
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48
Q

In what population is HBV immune active stage most likely to occur?

A

those infection in OLDER CHILDHOOD or ADULT

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49
Q

Hepatitis B infection - describe IMMUNE CONTROL stage.

A 
Inactive
HBsAg POSITIVE
HBeAg NEGATIVE
HBV DNA VERY LOW
ALT/AST NORMAL
BIOPSY - not required
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50
Q

Hepatitis B infection - describe eAg NEGATIVE CHRONIC ACTIVE stage.

A 
HBsAg POSITIVE
HBeAg NEGATIVE
HBV DNA FLUCTUATING
ALT/AST FLUCTUATING
BIOPSY - inflammation/fibrosis
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51
Q

What is the GENETIC BARRIER to resistance for lamivudine, emtricitibine, telbivudine for HBV?

A

LOW

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52
Q

What is the GENETIC BARRIER to resistance for adefovir for HBV?

A

LOW to MEDIUM

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53
Q

What is the GENETIC BARRIER to resistance for entecavir or tenofovir for HBV?

A

HIGH

54
Q

What impact does previous exposure to lamivudine have on the utility of ENETECAVIR for HBV?

A

genetic barrier LOWERED for entecavir

55
Q

What is the most common GENOTYPE of HBV in the UK?

A

D

56
Q

What is the definition of VIROLOGICAL RESPONSE to antiviral therapy for HEPATITIS B?

A

UNDETECTABLE HBV DNA at 24 weeks

57
Q

In what THREE situations should HBV be treated in HBV/HIV co-infection?

A

1) HBV DNA >2000
2) Fibrosis F2 or more
3) CD4 <500 cells

58
Q

Through what mechanism might HIV have a direct effect on fibrogenic process in liver in hepatitis/HIV co-infection?

A

binding of gp120 to CCR5 on hepatic cells triggers increased COLLAGEN and inflammatory CHEMOKINES

59
Q

What is the ‘NORMAL’ levels of ALT for women with HBV?

A

19IU/L

60
Q

What is the ‘NORMAL’ levels of ALT for men with HBV?

A

30IU/L

61
Q

Which FOUR drugs used for HBV also have activity against HIV?

A

lamivudine
emtricitibine
tenofovir
entecavir

62
Q

What consideration may be made when planning HBV treatment if PLW HIV is not on ART?

A

Use drug with HBV activity but NOT HIV activity

63
Q

What treatment options are available if treating HBV but not HIV?

A

PEG-IFN

Adefovir

64
Q

What is the FIRST line treatment for HBV MONOINFECTION?

A

ENTECAVIR
or
TENOFOVIR

65
Q

What is the criteria for use of PEG-IFN to treat HBV infection?

A

HbsAg POSITIVE
RAISED ALT
low DNA <2x10to6
minimal fibrosis

66
Q

What complication may occur if PEG-IFN is given to a person with cirrhosis?

A

DECOMPENSATED liver failure

67
Q

Why can adefovir be used for treatment for HBV despite no ART for HIV?

A

low dose has no effect on HIV replication therefore does not select out HIV resistance mutations

68
Q

Which is more effective treatment of HBV - adefovir or tenofovir?

A

TENOFOVIR

69
Q

Which measurement does tenofovir have more of an effect on that adefovir?

A

HBV DNA (more likely undetectable)
no significant difference on
ALT, seroconversion eAg, sAg loss

70
Q

What is an unsuppressed HBV DNA on adefovir associated with?

A

higher BASELINE HBV DNA

71
Q

What ART should be used to cover both HBV and HIV?

A

Tenofovir disoproxil
+/-
lamivudine or emtricitabine

72
Q

Which if preferred additional NRTI for HBV+HIV infection - lamivudine or emtricitabine?

A

Emtricitabine
(longer half life, more potent, resistance less rapid)
however either 3TC or FTC is sufficient

73
Q

What proportion of people with acute hepatitis B will lose sAg and develop sAb?

A

60-80%

74
Q

What proportion of people with acute hepatitis B will develop severe or fulminant liver disease?

A

<0.1%

75
Q

How should severe or fulminant HBV infection be initially managed?

A

TDF + 3TC or FTC
+/as
ART (if HIV co-infection)

76
Q

How long should treatment for severe or fulminant HBV infection continue?

A

continue until sAg lost or indefinitely if chronic HBV

note - old guideline, now if HIV+HBV, continue ART with HBV cover

77
Q

Which hepatitis C genotypes predominate in UK?

A

ONE (1)
&
THREE (3)

78
Q

What is the prevalence of hepatitis C in the UK?

A

0.4%

79
Q

In MSM who experience acute hepatitis C infection what is the main mode of transmission?

A

PerMUCOSAL

traumatic sex practice + mucosa admin of drugs + concurrent STI

80
Q

What impact does hepatitis C infection have on HIV?

A

chronic immune ACTIVATION

  • immune dysfunction
  • cytokine production
  • enhanced viral replication
  • CD4 apoptosis
81
Q

What is the increased risk of CIRRHOSIS in HCV + HIV co-infection?

A

TWO-fold higher

82
Q

How does HIV accelerate FIBROSIS in HCV + HIV co-infection?

A
  • HIV virus enters HEPATIC cells
  • immune ACTIVATION inducing CYTOKINE release and increase liver INFLAMMATION
  • increase TNF induced APOPTOSIS
83
Q

What impact does HCV + HIV co-infection have on the risk of HCC?

A

INCREASED
younger age
shorter time period

84
Q

What is the investigation of choice for hepatitis C infection?

A

HCV Ab (if not past infection)
+
HCV PCR

85
Q

Within what time frame is HCV PCR positive after initial infection?

A

ONE (1) month

86
Q

What proportion of patients with acute hepatitis C infection will have abnormal transaminases?

A

88% within 3 months

87
Q

What proportion of people with HCV infection will have a negative antibody test still at ONE year after infection?

A

5%

88
Q

How often should HCV Ab be tested in MSM with high risk of exposure?

A

3-6 monthly

89
Q

What high risk practices increase risk of exposure to HCV infection in MSM?

A

UPSI
Recreational drug use
Sharing paraphernalia

90
Q

For whom should ART be started in HCV+HIV co-infection?

A

ALL (regardless CD4)

91
Q

What is the benefit of starting ART in HCV+HIV co-infection?

A

improved IMMUNE function

reduced HIV-immune activation

92
Q

What impact does CD4 cell count have on treatment outcome with PEG-IFN + RBV in HCV+HIV co-infection?

A

REDUCED treatment SUCCESS

as CD4 cell count DECLINE

93
Q

Through what mechanism does HIV contribute to the FIBROGENIC process within liver in HCV/HIV co-infection?

A

DIRECT binding of gp120 to CCR5 receptor on hepatic STELLATE cells

94
Q

If DAA BOCEPREVIR is to be is to be used what is the recommended first line ART?

A

TDF/FTC + RALTEGRAVIR

95
Q

If DAA TELAPREVIR is to be is to be used what is the recommended first line ART?

A

TDF/FTC + RALTEGRAVIR

96
Q

What is a suitable alternative ART if DAA TELAPREVIR is to be is to be used?

A

TDF/FTC
+
boosted ATAZANAVIR

97
Q

Which THREE ART are specifically contraindicated in conjunction with HCV treatment?

A

Thymidine analogues

  • DIDANOSINE
  • STAVUDINE
  • ZIDOVUDINE
98
Q

For which HCV GENOTYPE are BOCEPREVIR and TELAPREVIR licenced?

A

ONE (1)

99
Q

What is the definition of sustained virological response (SVR) for HCV treatment?

A

negative HCV PCR

24 weeks after treatment

100
Q

What FOUR factors should be considered prior to HCV treatment?

A

1) PATIENT
2) VIRAL
3) HEPATIC
4) GENETIC

101
Q

What ‘PATIENT’ factors should be considered prior to HCV treatment?

A 
preference
risk of transmission
risk of re-infection
adherence
age
co-morbidities
DDI
102
Q

What ‘VIRAL’ factors should be considered prior to HCV treatment?

A

genotype
HCV viral load
IFN responsiveness

103
Q

What ‘HEPATIC’ factors should be considered prior to HCV treatment?

A

fibrosis

risk of decompensation

104
Q

What ‘GENETIC’ factors should be considered prior to HCV treatment?

A

IL28B status

105
Q

What is the disadvantage of DAAs BOCEPREVIR and TELAPREVIR?

A

co-prescription with PEG-IFN & RBV
dosing schedule (TDS)
TOXICITY
DDI

106
Q

What is the TOXICITY profile of BOCEPREVIR?

A

anaemia
neutropenia
dysgeusia (taste dysfunction)

107
Q

What is the TOXICITY profile of TELAPREVIR?

A

anaemia
rash
anal discomfort

108
Q

What is the recommended treatment for HCV GENOTYPE 1?

A 
PEG-IFN + RIBAVARIN
\+
TELAPREVIR
or
BOCEPREVIR
109
Q

What is the recommended treatment for HCV GENOTYPE 2 or 3?

A

PEG-IFN
+
RIBAVARIN

110
Q

How long should PEG-IFN + RBV be give for HCV infection?

A

48 weeks

111
Q

Which group of patients with HCV infection can have treatment duration reduced to 24 weeks?

A

NON-CIRRHOTIC
+
rapid response (undetectable at 4 weeks)

112
Q

Which pegylated interferon is more effective in HCV treatment?

A

pegylated a-interferon 2b

113
Q

Which HCV genotypes respond best to PEG-IFN + RBV?

A

TWO (2) & THREE (3)

114
Q

How can bone marrow toxicity from IFN or RBV in HCV treatment be managed/supported?

A

GROWTH factors

  • erythropoietin
  • granulocyte colony stimulating (GCSF)
115
Q

What is the recommended treatment for HCV GENOTYPE 4?

A

DEFER until newer treatment

PEG-IFN + RBV

116
Q

What assessment of virological response should be made if treating HCV GENOTYPE 4?

A

Check HCV RNA at 12 weeks

if detectable stop treatment

117
Q

If HCV RNA is DETECTABLE at 12 weeks of treatment for HCV GENOTYPE 4, what should be done?

A

consider STOP treatment

low rates of success

118
Q

What is the impact of treatment with PEG-IFN + RBV on HCV genotype 4?

A

Low response
May need longer >48 weeks if virological response by 12 weeks
Need to stop if no virological response at 12 weeks

119
Q

When should treatment be offered following acute HCV infection?

A

less than 2 log drop in HCV RNA 4 weeks
or
HCV RNA positive 12 weeks

120
Q

What monitoring should occur if a person has undetectable HCV RNA without treatment?

A

Test at
4, 12, 24 and 48 weeks
ensure clearance

121
Q

What is the recommended timing of treatment for ACUTE HCV with HIV co-infection?

A

EARLY treatment

higher chance of treatment success in acute infection

122
Q

Is the incidence in the UK higher for hepatitis A or E?

A

E

123
Q

Who is at risk of severe liver disease from hepatitis E?

A

PREGNANT women

pre-existing LIVER DISEASE

124
Q

Hepatitis E infection is associated with the consumption of what meat?

A

wild BOAR

125
Q

What is the limitation of the measurement of HEV antibody in PLW HIV and low CD4 count?

A

low CD4 count may not develop HEV antibody

126
Q

When is hepatitis E testing recommended for PLW HIV?

A

elevated transaminases or cirrhosis
+
no other cause found

127
Q

What is the recommended treatment for hepatitis E + HIV co-infection?

A

optimise ART

128
Q

What is the median survival following first liver decompensation in PLW HIV + HCV vs HCV mono-infection?

A

13 months
vs
5 years

129
Q

Which hepatitis virus can cause HCC without cirrhosis?

A

HEPATITIS B (directly carcinogenic)

130
Q

What is the recommended HCC surveillance?

A

6 monthly liver US and AFP

131
Q

What are potential INDICATIONS for liver TRANSPLANT in PLW HIV?

A

viral hepatitis CIRRHOSIS +/- HCC
HIV drug induced liver injury
HIV related liver disease (NCPH)
non-HIV liver disease

132
Q

Which group of viral hepatitis has best post-transplant outcomes?

A

B

DipHIV (14 decks)

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