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Gastro > Viral hepatitis RPA > Flashcards

Viral hepatitis RPA Flashcards

1
Q

Who is at risk of hep C?

A 
IVDU
Migrants from high prevalence areas - egypt, pakistan, miditerranean, eastern europe, africa, asia
ATSI - mother to baby 
Sex workers
Other blood bourne viruses
Children with positive mothers
needle stick injury
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2
Q

Risk of acute hep C progressing to chronic hep C

A

75% will go to HCV

Another 30% will progress to liver cancer, liver failure, cirrhosis

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3
Q

Risk Factors associated with increased rate of progression to cirrhosis in HCV

A

Metabolic risk factors especially

Diabetes, obesity, MAFLD, ETOH, genetic factors, post-menopause in women, age at infection, HCV genotype 3, HIV co-infective

Even if HCV is treated, can still develop cirrhosis later on. Will require ongoing monitoring after HCV treatment if above risk factors present.

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4
Q

How do we assess fibrosis?

A

1)
APRI score (AST platelet ratio index)
<1: unlikely to have fibrosis. Can be DC from follow up if HCV is treated and no risk factors i.e. metabolic risk factors

Also Hepascore
<0.8: unlikely

Others
Fibrogene (not used much at the moment)

2) Fibroscan (transient elastography)
- More specific than APRI but equally sensitive
- High NPV
- Cirrhosis likely if MLS ≥12.5
- Unlikely if MLS <12.5

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5
Q

How do we assess fibrosis?

A

1)
APRI score (AST platelet ratio index)
<1: unlikely to have fibrosis. Can be DC from follow up if HCV is treated and no risk factors i.e. metabolic risk factors

Also Hepascore
<0.8: unlikely

Others
Fibrogene (not used much at the moment)

2) Fibroscan (transient elastography)
- More specific than APRI but equally sensitive
- High NPV
- Cirrhosis likely if MLS ≥12.5
- Unlikely if MLS <12.5

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6
Q

Benefits of HCV cure

A

12 weeks after treatment can impede fibrosis progression, can reverse liver decompensation, prevent liver decompensated, reduce risk of HCC and transplant

Reduce mortality

Reduce extrahepatic complications
- Reduce liver associated NHL, CV disease, renal disease, neurocognitive dysfunction, improve QOL

Reduces HCV transmission

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7
Q

DAA treatment for HCV

A

Standard treatment

  • All oral treatments
  • 98-100% efficacy in both fibrosis and non-fibrosis
  • All pan-genotypic

SOF-VEL (epclusa)
- 12 weeks

GLE-PIB (Maviret)
- 8 weeks

Resistant treatment 
SOF-VEL-VOX (vosevi)
- Salvage regimen
- high effective for those who have failed standard therapy due to resistance 
- Has protease inhibitor
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8
Q

Does HIV coinfection, actively drinking ETOH, reinfection of HCV, cirrhosis reduce the chance of cure?

A

No

Nothing reduces the risk of cure

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9
Q

Challenges with DAA treatments

A

Drug drug interactions (PPI reduce absorption of DAA, statins can cause rhabdo, OCP, amiodarone can cause CHB)

Protease inhibitors are CI in decompensated cirrhosis

Accurate pre-treatment assessment of fibrosis status so that cirrhotic patients get appropriate regimen and duration, and are enrolled in long-term follow up with liver ca surveillance regatrdless of SVR

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10
Q

Can you use DAAs in dialysis/CKD?

A

yes

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11
Q

Can you use DAAs in children >12 years

A

yes

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12
Q

can you use DAAs in preganncy?

A

No

Small risk of mother to baby transmission (2-5%)

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13
Q

Can you get reinfected post HCV curte?

A

Yes
There is no immunity to HCV
Need to do RNA test to check reinfection (can’t do antibody)

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14
Q

Resistance is almost always towards …

A

NS5A inhibitors and protease inhibitor

WE don’t check for these

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15
Q

HCV and HBV coinfection

How should we manage this?

A

HBV DNA is low or undetectable
HCV is usually driver of hepatic inflammation

Potential risk of HBV reactivation after/during HCV clearance with DAA therapy

Hep B should be checked before DAA treatment and be treated at the same time

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16
Q

HCV and COVID19 is it worse?

A

No increased mortality or ICU admission

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17
Q

Cirrhosis and COVID19 is it worse?

A

Increased mortality from lung disease and decompensated liver disease

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18
Q

Mother to baby transmission

How likely is this?

A

Mother to baby

- If baby doesn’t receive prophylaxis, 95% of chronic HBV infection

19
Q

Should we check HBV genotype?

A

No

However
Asia - B (less active disease, low HCC, less progression), C (high HCC, cirrhosis)
A and B respond better to IFN than C and D
F is fulminant disease but rare

20
Q

How

A

Mother to mother
IVDU
MSM

21
Q

When to check hep B?

A 
At risk populations e.g. SE asians, africa, middle east
IVDU
MSM
Pregnant women
Before immunosuppression/chemotherapy
22
Q

Factors associated with increased risk of cirrhosis and HCC in hep B?

A

Persistent high HBV DNA or presence of HBeAg
HBV phenotype C>B
Core promotor mutations
Coinfection with HCV, HDV, HIV

Male
Metabolic risk factors
FHx HCC
Cirrhosis
Heavy ETOH
23
Q

Models for prediction of HCC in HBV

A

REACH-B

Age, gender, HBV DNA< ALT, HBeAg

24
Q

Tests to do in confirmed Hep B

A

HBeAg
Anti-HBe
HBV DNA
ALT

Fibrosis assessment

25
Q

4 phases of hep B

A

1) Immune tolerance
- Positive HBeAg
- high HBV DNA
- Low ALT

2) Immune clearance
- ALT flare
- HBV DNA drop
- At some point, seroconvert from HBeAg to Anti-HBe (ab)

3) Immune control
- Low HBV DNA
- Low ALT
- Anti-HBe (ab) positive

4) Immune escape
- High ALT and HBV DNA
- Low anti-HBe (ab)

26
Q

Which phase do we treat hep B?

A

we target therapy in immune clearance and immune escape

However, no such thing as a healthy carrier. We need to monitor annually no matter what phase they are in.

27
Q

Can we cure hep B?

A

No

We just suppress it

28
Q

Treatment of chronic hep B

A 
Entecavir - preferred; no effect on bone or kidney
Tenofovir disaporxil (TDF) - associated with bone and kidney dysfunction
Tenofovir alafenamide (TAF) - TGA approved but not PBS reimbursed. Less toxicity compared to TDF.
29
Q

When to treat hep B?

A

ALT >2 ULN

HBV DNA elevated

30
Q

Can we stop hep B treatment?

A

Can stop after HBeAg negative but significant risk of relapse

31
Q

Risk of HBV in chemotherapy patients

A

Can be fatal

Reactivation can result in elevated liver enzymes, jaundice, acute hepatic failure and death

Can occur up to 2/3 of HBsAg positive patients undergoing chemotherapy especially B cell depleting therapies (in lymphoma/leukemia, RA)

Can also occur in anyone under immunosuppression in solid tumours, rheumatology, IBD, transplant settings

32
Q

Babies born to mothers who are HBsAg positive are given …

A

HBIG and HB Vax x3

33
Q

Pregnant women on antiviral therapy for Hep B

A

Can stop or continue tenofovir

34
Q

How to get hep D hepatitis?

How to treat it?

A

Need hep B surface antigen to replicate

Nucleoside and nucleotide therapy not impact hep D viraemia or outcomes

Only rx available is Peg-interferon - 25% response rate only
Bulevirtide - inhibitor of HbsAg entry via binding to the NTCP receptor hepatocytes - approved in europe

35
Q

Hep E

A

RNA virus
Small
Found in humans, pigs, cows, rodents, deer, moose, camels, boars

36
Q

Transmission of hep E

A

Can be food acquired - pork in Europe
Most outbreaks associated with faecally contaminated drinking water (Subcontinent north africa, asia, russia)
Can also be transmitted through blood

37
Q

Hep E and pregnancy

A

High rates of acute liver failure and death

genotypes 1 and 2

38
Q

CAn you get chronic hep E?

A

Not in immunocompetent

Only in immunocompromised especially HEV infected organ transplants

39
Q

Diagnosis Hep E infection

A

Detection of anti-HEV antibodies

40
Q

Rx acute hep E infection

A

No treatment required. Infection will just clear.

But in immunosuppression, may not clear and will need ribavirin. However can get treatment failure associated with resistance.

41
Q

Vaccine hep E?

A

Yes
100% efficacy after 3 doses
But only licensed in China and not accessible to the rest of the world

42
Q

Most common cause of acute hepatitis?

A

Hep E

43
Q

Cirrhosis and chronic hep B

How long to treat?

A

Treat indefinitely with tenofivir or entecovir even if low viral load

44
Q

Which agent is safe in pregnancy?

A

Tenofivir

Gastro (9 decks)

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