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Gastroenterology > Hepatitis > Flashcards

Hepatitis Flashcards

1
Q

Features of Hep A

  • Virus type
  • Transmission
  • Incubation period
  • Symptoms
  • Progression to chronicity
  • Immunisation
  • Diagnosis
  • Treatment + prognosis
A 
HEP A 
- Virus type: RNA 
- Transmission: fecal-oral
- Incubation period: 2-6 weeks
- Symptoms: Symptoms
of acute HAV are jaundice, fatigue, mild abdominal pain,
fever, and diarrhoea.
- Progression to chronicity: never, typically resolves without sequeale 
- Immunisation: yes

Diagnosis: Hep A IgM
Treatment: supportive
Prognosis: full recovery within 3 months

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2
Q

Features of Hep B

  • Virus type
  • Transmission
  • Incubation period
  • Symptoms
  • Progression to chronicity
  • Immunisation
  • Brief treatment
A
  • Virus type: DNA
  • Transmission: sexual, parenteral, perinatal
  • Incubation period: 1-6 months
  • Progression to chronicity: Yes
  • Immunisation: yes

Has associated extrahepatic manifestations

  • Polyarteritis nodosa
  • Membranous GN
  • Aplastic anaemia

Treatment normally involves:
tenofovir, entecavir, pegylated interferon alfa

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3
Q

How many genotypes of Hep B are there?

A

10 HBV genotypes: A-J

  • B is associated with less active disease, slower progression and lower incidence of HCC than C
  • C has higher risk of HCC and cirrhosis
  • A + B respond better to IFN than C + D
  • F is associated with fulminant liver disease, rare
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4
Q

Hep B progression of disease

A
  1. Acute Infection
  2. Chronic Infection
    - From chronic infection, 5-10% can develop HCC WITHOUT CIRRHOSIS
    - >30% develop cirrhosis which can then lead to HCC + liver failure (decompensation)
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5
Q

Can chronic HBV patients have liver cancer without cirrhosis

A

Yes

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6
Q

Hep B Serology and which ones do you need to make a diagnosis?

A

Hepatitis B surface antigen (HBsAg) - infected or not

  • Indicated current infection
  • Chronic Hep B defined as HBsAg > 6months
  • Appearance of HBsAb equates with seroconversion

HBeAg = e antigen - replication or not

  • Correlates with infectivity (active viral replication) and thus high transmissibility
  • Marker of active viral replication in patients with chronic Hep B

Hepatitis B Core Antibody (anti-HBc) - expsure or not

  • Antibody to a core protein, marker of past infection
  • Indicates exposure to the virus
  • IgM anti-HBc (acute hepatitis B)
  • IgG anti-HBc (chronic hepatitis B)

Antibody to surface antigen (Anti-Hbs)
- Marker of immunity

Hep B DNA

  • Correlates with infectivity (active viral replication)
  • Only replication marker in HBeAg negative hepatitis B
  • Covalently closed ciruclar (CCC) DNA is the template for ongoing infection

HBsAg (surface antigen)
HbcAb (core antibody)
HbsAb (surface antibody)

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7
Q

Interpretation of HBV Serology

HBsAg -
anti-HBc -
anti-Hbs -

HBsAg -
anti-HBc +
anti-Hbs +

HBsAg -
anti-HBc -
anti-Hbs +

HBsAg +
anti-HBc +
IgM anti-HBc +
anti-Hbs -

HBsAg +
anti-HBc +
anti-Hbs -

HBsAg -
anti-HBc +
anti-Hbs -

A

HBsAg -
anti-HBc -
anti-Hbs -
Susceptible

HBsAg -
anti-HBc +
anti-Hbs +
Previous/resolved infection - risk of reactivation with immunosuppresion

HBsAg -
anti-HBc -
anti-Hbs +
Immune through vaccination

HBsAg +
anti-HBc +
IgM anti-HBc +
anti-Hbs -
Acute infection

HBsAg +
anti-HBc +
anti-Hbs -
Chronic infection

HBsAg -
anti-HBc +
anti-Hbs -
Occult hep B or resolved hep B - risk of reactivation

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8
Q

What are the natural history of chronic HBV: 4 phases

A
  1. IMMUNE TOLERANCE = NO TREATMENT
    - High HBV DNA, normal LFTs, HBeAg positive
  2. IMMUNE CLEARANCE = ASSESS FOR TREATMENT
    - High HBV DNA >20,000, abnormal LFTs (elevated ALT), HBeAg positive
    - At risk of progression to cirrhosis + HCC
  3. IMMUNE CONTROL = NO TREATMENT
    - Inactive carrier status
    - Low HBV DNA, normal LFTs, HBeAg negative, anti-HBe positive
  4. IMMUNE ESCAPE = TREATMENT , REACTIVATION
    - High HBV DNA > 2000, abnormal LFTs, HBeAg neg, anti-HBe positive
    - At risk of progression to cirrhosis + HCC
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9
Q

Treatment for Hep B

A

For Hep B - there is NO cure, only VIRAL SUPPRESSION
- Current treatments failure to eradicate cccDNA, template for HBsAg and RNA production

  1. Nucleoside Analogue: Tenofovir disoproxil, entecavir - INDEFINITE
    - Suppression of HBV DNA
    - HBeAg seroconversion
    SE: renal toxicity, bone disease
    - Indefinite, oral tablet
    - High rate of DNA suppression
    - Potential of drug resistance
    - Tenofovir alafenamide - less KIDNEY + BONE toxicity
  2. Pegylated Interferon
    - Defined 1 year duration of therapy, subcut injection, no resistance
    - May lead to HbeAg loss, may reduce HbsAg levels
    - Higher rate of HBeAg loss in 1 year

Multiple SE

  • Flu like symptoms
  • Arthralgia, myalgia
  • Leukopenia, thrombocytopenia
  • Neuropsychiatric disorders, major depressive disorder
  • Hair loss, dry mouth, weight loss

Contraindications

  • decompensated liver disease, cirrhosis
  • Pregnancy, acute hep B, immunosuppressed, psychiatric instability

If patient has Hep B + cirrhosis = antiviral is indefinite

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10
Q

When do you treat for

  • HBeAg + patients
  • HBeAg - patients
A

HBeAg + patients
- If ALT >2x ULN + HBV > 20,000

HBeAg - patients
- If ALT >2x ULN + HBV >2000

Treatment can stop in HBeAg pateitents 12 months after HbeAg to anti-HBeAg seroconverstion but often reactivate

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11
Q

How do you monitor for HCC in patient’s with cirrhosis

A

US + AFP every 6

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12
Q

Hep B and pregnancy

A
  • Tenofovir 300mg/day in 3rd trimester - together with timely vaccination and HBIG associated with significantly lower mother-to-child transmission of HBV than vaccination and HBIG alone
  • 3rd trimester is highly viremic especially HBeAg + who carry >10% risk of vertical HBV transmission despite HBIg and vaccination
  • Mother to infant transmission high as 90% if the baby does not receive Hep B immune globulin within 12 hours and vaccination at birth (within 24 hours) and then 3 doses at 2/4/6 months.
  • Risk of transmission increases in eAg +
  • Breastfeeding not contraindicated, even if on tenofovir
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13
Q

Which virus normally co-exists with Hep B?

A

Hep D

Hep D - requires HepB surface antigen +

  • HDV is a defective RNA virus requiring the simultaneous presence of hepatitis B to full express is pathogenicity
  • HDV always occurs in the presence of HBV - needs HBVsAg to replicate
  • HBV nucleotide treatment does NOT treat HDV as sAg remains
  • Infection varies from benign acute hepatitis to fulminant hepatitis

Diagnosis:

  • HDVsAG and sAb
  • HDV viral load

Tx: Pegylated interferon alpha

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14
Q

The risk of patients having Hep B reactivation

A

High Risk

  • Rituximab for sAG + and sAg -
  • Anthracycline derivatives, eg: doxorubicin
  • Mod/High dose steroids > 4 weeks

Medium Risk

  • TNF inhibitors
  • TK inhibitors
  • Leflunomide, methotrexate, cyclophosphamide

Low

  • Calcineurin inhibitors,
  • Azathioprine
  • Thiopurines (mercaptopurine)

Nil

  • Low dose steroids (<7.5mg/day)
  • Sulfasalazine
  • Hydroxochloroquine
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15
Q

When do you start treatment for patients on immunosuppression for haematological and solid organ malignancy and when to stop the antivirals

A
  • HbsAg positive = HBV antivirals

HbsAg negative
- If anti-HBc positive and high risk chemo = HBV antiviral
- If anti-HBC positive and low risk chemo = no antiviral
- If anti-HBc negative = no antiviral
Essentially if you are HbsAg negative but anti-HBc positive and on high risk chemo, eg: ritux, you need antiviral therapy

When to stop anti-viral therapy

  • 18-24 months after cessation of B cell depleting or haematopoietic stem cell therapy
  • 6-12 months after cessation of other cancer therapy (that is not B cell depleting/HSCT)
  • If they fulfil treatment for chronic hep B will need to remain on tx
  • ALT and HBV DNA should be used to monitor patients receiving antiviral prophylaxis
  • ## Should consider Hep B infection if there is an unexplained elevation of ALT for any patients receiving cancer tx
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16
Q

Fibroscan results

A
  • Normal <6 kPa

* Cirrhosis > 12 kPa

17
Q

Features of Hep C

  • Virus type
  • Transmission
  • Incubation period
  • Symptoms
  • Progression to chronicity
  • Immunisation
  • Brief treatment
A
  • Virus type: RNA
  • Transmission: parenteral
  • Incubation period: 2 weeks - 6 months
  • Progression to chronicity: up to 85% if untreated
  • Immunisation: No
  • Diagnosis:
    Anti-HCV IgM
    HCV RNA PCR

Has extrahepatic manifestations

  • Vasculitis
  • Cryoglobulinemia
  • Membranoproliferative type 1 GN

Brief Treatment
▪ Acute and chronic: always multidrug approach, depends on viral genotype
- Ledipasvir + sofosbuvir (genotype 1)
- Sofosbuvir + Velpatasvir (all 6 genotypes)
- Interferon + Ribavirin (for all genotypes in case of treatment failure)
Last resort: liver transplant

18
Q

Features of Hep C

  • Virus type
  • Transmission
  • Incubation period
  • Symptoms
  • Progression to chronicity
  • Immunisation
  • Brief treatment
A
  • Virus type: RNA
  • Transmission: parenteral
  • Incubation period: 2 weeks - 6 months
  • Progression to chronicity: up to 85% if untreated
  • Immunisation: No
  • Diagnosis:
    Anti-HCV IgM
    HCV RNA PCR

Has extrahepatic manifestations

  • Vasculitis
  • Cryoglobulinemia
  • Membranoproliferative type 1 GN

Brief Treatment
▪ Acute and chronic: always multidrug approach, depends on viral genotype
- Ledipasvir + sofosbuvir (genotype 1)
- Sofosbuvir + Velpatasvir (all 6 genotypes)
- Interferon + Ribavirin (for all genotypes in case of treatment failure)
Last resort: liver transplant

19
Q

Which hepatitis virus have a vaccine

A

Hep A and B

20
Q

What extra-hepatic manifestations are associated with Hep C?

A
  • Membranoproliferative GN: immune complex deposition
  • Porphyria cutanea tarda - bullous skin lesions
  • Cryoglobulinaemia
21
Q

Hep C treatment

  • Aims of treatment
  • Different drug classes
A
  • Hep C can be cured!
  • Direct acting antivirals - relies on combinations of medications from different classes to avoid resistance and optimise efficacy.
  • Provide cure for most patients

Aim:

  • Complete cure
  • Eradication of HCV RNA in serum as defined by sustained virologic response (SVR) - defined by PCR negative 12 weeks AFTER COMPLETION DATE of Hepatitis C therapy

NS3/4A protease inhibitors: inhibit viral protein production (“-previr”)

  • Paritaprevir
  • Grazoprevir
  • Glecaprevir
  • Voxilaprevir

NS5A Inhibitors (“-svir”): prevent HCV assembly and release

  • Daclatasvir
  • Ledipasvir
  • Ombitasivir
  • Elbasvir
  • Velpatasvir
  • Pibrentasvir

NS5B polymerase inhibitors (“-buvir”): inhibit HCV replication

  • Nucleoside: Sofosbuvir
  • Non-nucleoside: Dasabuvir

+/- Ribavirin - combined with DAAs to increase antiviral activity.

Treatment Regimes for treatment naive pts with compensated cirrhosis/no cirrhosis in 2021:

  • Sofosbuvir (NS5B) + Velpatasvir (NS5A) for 12 weeks = all 6 genotypes
  • Glecaprevir (NS3/4A) + pibrentasvir (NS5A) for 8 weeks = all 6 genotypes

Sofosbuvir (NS5B) + Velpatasvir (NS5A) + Voxilaprevir (NS3/4A protease) = salvage for DAA failure

DAAs are well tolerated

  • Nausea
  • Fatigue
  • Headache
  • Ribavirin: anaemia, rash, insomnia
22
Q

Managing a patient on DAA treatment

A

• Monitoring on treatment: usually not required

  • Hep B: risk of reactivation of Hep B during treatment for Hep C
  • Hep BsAg positive: check PCR at baseline and treat if meet criteria
  • Hep BcAb positive: check LFT week 4-8 and test PCR if increase
• Adherence counselling
• Avoidance of pregnancy
• Drug interactions
○ Cytochrome P450 involved in metabolism of many drugs. Particular concerns:
-PPIs
-Statins
-Amiodarone
- Anti-epileptics
• Harm minimization
• Vaccination opportunities
• Cirrhosis: usual screening
• Check SVR: sustained virological response
23
Q

Resistance to DAA in Hep C

A
  • Genetic sequence polymorphisms which are naturally produced during the HCV life cycle may result in amino acid changes that confer resistance to DAAs
  • Detectable in the majority of patients with treatment failure to NS3 protease inhibitor-or NS5A inhibitor-based antiviral therapy.
  • The most clinically significant of these is Y93H, which is associated with decreased response to common DAA regimes
  • New DAA regimen (Vosevi) effective - SOF-VEL-VOX

RESISTANCE: lmost always to NS3 and NS5A inhibitors

24
Q

Complications of Hep C

A

· Rarely fulminant hepatitis (liver failure)
· Liver cirrhosis
· HCC
· Secondary haemochromatosis

25
Q

What medications are their potential drug-drug interactions with DAA

A

PPI
Statin
OCP
Amiodarone

26
Q

Which DAA is contraindicated in decompensated cirrhosis?

A

Protease inhibitors

Protease inhibitors - cause worsening liver function, so in decompensated use SOF+VEL and often added ribavirin.

27
Q

What coinfection can occur with Hep C

A

Hep B

  • In HCV-HBV coinfection, HBV DNA is low or undetectable
  • Hep C usually driver of hepatic inflammation.
  • Potential risk of HBV reactivation during or after HCV clearance with DAA therapy
  • Recommended that all pts are tested for HBsAg, anti-HBc and anti-HBs prior to DAA therapy
  • If HBsAg + = should be considered for concurrent HBV antiviral therapy until at least 12 weeks post anti- HCV therapy
28
Q

Features of Hep E

  • Virus type
  • Transmission
  • Incubation period
  • Symptoms
  • Progression to chronicity
  • Immunisation
  • Diagnosis
A
  • Virus type: RNA
  • Transmission: fecal-oral
  • Incubation period: 2-8 weeks
  • Progression to chronicity: rare, possible in immunsuppresion
  • Immunisation: No
  • Increased risk of fulminant hep in pregnancy
  • Diagnosis:
    Anti-HEV IgM: active infection
    Anti-HEV IgG: past detection
    HEV RNA PCR
29
Q

Which Hep viruses are RNA vs DNA

A

RNA: Hep A, C, D, E
DNA: Hep B

30
Q

how many genotypes of Hep E are there?

A

8

  • Genotype 1 and 2: spread through dirty water
  • Genotype 3/4: spread through pork and sometimes blood products, 3 (main one in AUS) and 4 are mostly foodborne
31
Q

Hep E chronic infection

A
  • No chronic HEV in IMMUNOCOMPETENT patients
  • IMMUNOSUPPRESSED patients can fail to clear HEV infection - progression to chronic hep with extrahepatic manifestations

Immunosuppressed groups

  • Solid organ transplant
  • Patients with haem disorders
  • HIV
  • Rheumatic disorders receiving heavy immunosuppression
32
Q

How do you treat Hep E?

A
  • Acute HEV infection does not usually require antiviral therapy and most cases are spontaneously cleared
  • Ribavirin may be considered in severe acute hepatitis or acute on chronic liver failure
  • Ribavirin is effective treatment for chronic HEV (immunosuppressed pts) however treatment failure is associated with HEV mutations
33
Q

Assessment of Fibrosis

A
  1. Non Invasive Serum Markers:
    - APRI: AST to platelet ratio oindex
    APRI <1: can exclude cirrhosis
    APRI >1 cirrhosis
  2. Fibroscan
    - Negative predictive value for excluding cirrhosis
    - >12.5 kPA: cirrhosis
    - <12.5: unlikely cirrhosis
    F4 - cirrhosis
    F3 - advanced fibrosis
    <7 - normal
    >13 - cirrhosis
  3. Liver Biopsy
34
Q

What cancer is associated with Hep C?

A

Non hodgkin lymphoma

35
Q

What medications does sofosbuvir interact with?

A

PPI

Amiodarone - can cause heart block

36
Q

Features of DAAs

A
  • Safe for use in CKD
  • Not recommended in breastfeeding + pregnancy
  • There is NO immunity to HCV - can occur multiple times
  • Check viral load
37
Q

Immunosuppression and Hep B treatment

A
  • If sAg negative, cAb positive (previously cleared): monitor only
  • If sAg positive (active infection), antiviral therapy for duration of treatment + 6-12 months after
  • If rituximab, antiviral therapy regardless sAg status for duration of Rx + 1 year post
38
Q

What is given to reduce vertical transmission of Hep B?

A
  • Hep B vaccine is given to all newborns
  • Hep B immunoglobulin to all newborns of mothers who are HBsAg detected
  • Antiviral treatment only started at approx 30 weeks if mother’s viral load > 10^7IU/mL

Gastroenterology (11 decks)

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