Viral Hepatitis Flashcards

1
Q

What questions do you ask to screen for viral hepatitis?

A
  • Any recent travel, contact history, sexual history?
  • Any illicit drug use? Exposure to needles?
  • Any blood donations?
  • Any tattoos?
  • Eaten any undercooked meat, shellfish, canned food?
  • Have you been Vaccinated against Hep A & B?
  • Are you a chronic Hep B carrier?
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2
Q

Acute vs chronic presentation

  • Hep A
  • Hep B
  • Hep C
  • Hep D
  • Hep E
A

Hep A- always acute

Hep B: acute / chronic presentation

  • ADULT-acquired: majority (95%) do NOT get CHB
  • PERINATAL infection: majority (90%) get CHB

Hep C: usually chronic presentation

  • 80% of acute Hep C is SUBCLINICAL; >85% dev CHC
  • Hence Hep C most commonly p/w chronic hep

Hep D: always chronic, against B/G of CHB infection

Hep E: always acute unless immunocompromised

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3
Q

Phase 1: Length of incubation period

  • Hep A
  • Hep B
  • Hep C
  • Hep D
  • Hep E
A

Hep A: 2-6 weeks
Hep B/D: 2-6 months
Hep C: 1-5 months
Hep E: 2-8 weeks

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4
Q

What are the symptoms during the prodromal phase of hepatitis (Phase 2)?

A

Usually precedes jaundice by 1-2 weeks, lasts 3-5 days

Flu-like symptoms

  • Anorexia, Lethargy
  • N&V, arthralgia, myalgia, headache
  • pharyngitis, cough
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5
Q

What are the symptoms during the icteric phase of hepatitis (Phase 3)?

A

Fever, Tender Hepatomegaly

N&V, +/- Change in bowel habits

Splenomegaly & Tender Cervical Lymphadenopathy (10-20%)

If severe – features of liver impairment
- Clinical Jaundice only in 1/3 of pt!

Pale stools, Dark urine
If fulminant: signs of ALF. Pt p/w encephalopathy

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6
Q

Phase 4: Length of recovery phase

  • Hep A
  • Hep B
  • Hep C
  • Hep E
A

Hep A/E: 2-12 weeks

Self-limiting Hep B/C: 3-4 months

Chronic hepatitis B/C: >6 months

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7
Q

Hepatitis A

  • route of transmission
  • Clinical presentation
  • investigations
  • Management
A

A/W poor water quality 🡪 F/O route (sewage)

Acute illness common in children (c/f 50% of adults). Rarely Fulminant, more common in elderly or Hep B/C pt

Dx: anti-HAV IgM (IgG used for vaccine response/past exposure)

Mx: supportive

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8
Q

Hepatitis E

  • route of transmission
  • Clinical presentation
  • investigations
  • Management
A

Spread via F/O route: uncooked meat/shellfish

Incubation: 2-8 weeks

Presentation:

  • Acute illness common in children (c/f 50% of adults).
  • Rarely Fulminant, more common in elderly or Hep B/C pt
  • May have Neuro involvement: Bell’s palsy, GBS (Guillian-Barre), meningoencephalitis or other neuropathies
  • Pancreatitis
  • Arthritis
  • High mortality if pregnant / immunoC 🡪 can become chronic in these pt

Dx: anti-HEV IgM, HEV RNA

Tx:

  • Supportive (usually self-clearing)
  • If serious: KIV ribavirin
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9
Q

Hepatitis B

  • route of transmission
  • investigations
  • Management
A

Spread via blood or sexual contact

Dx: HDV-IgM

Tx: PEG-IFN

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10
Q

Hep C

  • route of transmission
  • clinical presentation
  • investigations
  • Management
A

RFs: IVDU (sexual/vertical transmission less common than Hep B)

Acute infection

  • Of the acute infections, 80% of pt are subclinical: they may p/w simply flu-like S&S
  • 10-20% of acute HCV infection presents with icteric acute hepatitis

Chronic Infection
- 50-85% of acutely Hep C become chronic carriers 🡪 Risk of Cirrhosis and HCC

Dx:

  • Anti-HCV ELISA 🡪 RIBA (recombinant immunoblot assay) / EIA
  • Consider PCR for HCV RNA (for HIV pt with negative EIA)

How to treat Hep C

  • Old therapy: Ribavirin + Peg-INF (aka a form of INF-a)
  • New: NS3/4A protease inhibitors (boceprevir, simeprevir, telaprevir), NS5B polymerase inhibitors (sofosbuvir)
  • Cure is possible! – up to 95% cure 😊
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11
Q

Natural history of hepatitis B:

Acute infection: majority of SUBCLINICAL

  • Of the acute infections, 70% of pt are Subclinical 🡪 aka they present with ______________ (hence Dx of Acute Hep B is missed)
  • 30% of acute HBV infection presents with _____________
  • 1% presents with __________________

Chronic infection
- ______ of adult-acquired acute Hep B becomes chronic
- _______ of perinatal (aka vertical) Hep B becomes chronic
- Hence chronic Hep B most commonly occurs in children
Its better to contract Hep B as adult than as child via vertical transmission

Of all chronic HBV 🡪 ________ leads to cirrhosis

  • Usually HCC develops after cirrhosis
  • However, there is ↑ HCC risk even BEFORE cirrhosis in chronic HBV infection
  • HENCE: despite majority of Hep B attacks are ACUTE, most people present with CHRONIC Hep B infection instead, since majority of acute infection is subclinical
A

flu like symptoms;

Icteric Acute Hepatitis;

fulminant Hepatitis!

<5%;

> 90%;

20%

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12
Q

How is Hep B spread?

A

Blood, Sexual contact, IVDU, Vertical Transmission (MOST COMMON!)

Hence, highest risk of chronic status in children (>90%, c/f 20-30% in adults)

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13
Q

What does the window period of acute hepatitis mean?

What are the HBsAg, anti- HBs, HBcAg results

A

Interpretation:

  • Could be from early infection before HBsAg appears
  • OR Could be between disappearance of HBsAg & synthesis of Anti-HBs Ab

HBsAg -ve; Anti-HBs Ab -ve; HBcAg +ve 🡪 This means: even though pt does not have HBsAg, pt is still having infection as virus has not been cleared (no HBsAb; HBV DNA is still present in blood

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14
Q

What is the interpretation of this results in this patient with chronic HBV infection?

  • ALT normal
  • HBsAg high
  • HBV DNA >10^7 IU/ mL
  • HBeAg positive
  • Anti Hbe Ab -ve
  • none/ minimal liver disease
A

IMMUNE TOLERANT

Immune system tolerates infection virus multiples w no immune reaction hence no illness symptoms + no damage to liver.

This is seen exclusively in children who are infected via vertical transmission.

This is due to their weak immune system which cannot mount IR. Transits into immune active phase after decades

No reliable treatment at this stage.

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15
Q

What is the interpretation of this results in this patient with chronic hep B?

  • HBsAg high/ immediate
  • ALT elevated
  • HBV DNA 10^4 IU/ mL - 10^7 IU/ mL
  • HBeAg positive
  • Anti Hbe Ab negate
  • Moderate/ severe liver disease
A

Immune reactive HBeAg positive.

10-20% of these patients convert to HBeAg -ve every year.

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16
Q

What is the interpretation of this results in this patient with chronic HBV infection?

  • HBsAg low
  • ALT normal
  • HBV DNA <2000 IU/mL
  • HBeAg negative
  • Anti Hbe Ab positive
  • no liver disease
A

Inactive carrier

Seroconversion is a/w lower rates of disease progression to cirrhosis and hcc, and improved survival rates.

1-3% of spontaneous disease remission per year (i.e. spontaneous loss of HBsAg).

Prognosis is good! need not treat

17
Q

What is the interpretation of this results in this patient with chronic hep B?

  • ALT elevated
  • HBV DNA >2000 IU/ mL
  • HBeAg negative
  • Anti Hbe antibody positive
  • Fibrosis moderate/ severe
A

HbeAg negative chronic hepatitis

Treatment is appropriate

18
Q

What are the indications of treatment for hepatitis B?

A

ACUTE HEP B: Decompensated acute hep B

CHRONIC HEP B:

1) Chronic HBV pt p/w acute flare / active dz (i.e. HBeAg +ve / -ve Chronic Hepatitis B)
- Treat regardless of compensation (icteric or anicteric) b/c the window of deterioration is very narrow and pt can get sick very quickly
- Active HBV is defined by an elevated HBV DNA greater than >2000-20000 IU/ml (depending on HBeAg status) with either an elevated in serum liver transaminases or evidence of liver fibrosis
2) Chronic HBV (HBsAg +ve) and cirrhosis regardless of active / inactive dz
3) HBeAg +ve pregnant women in T3 with high viral load >6log b/c this grp has highest risk of transmission to child via vertical transmission

19
Q

In what groups of patients are Hep B treated?

A

ACUTE HEP B: When patient is fully compensated e.g: no jaundice w/ Acute Hep B infection

CHRONIC HEP B: Pt w/ no cirrhosis and no acute flares (i.e. HBeAg +ve / -ve Chronic HBV Infection)

20
Q

How do we manage hepatitis B

A

Oral nucleoside analogues MONOTHERAPY

  • Tenofovir: high barrier to resistance hence 1st line
  • Entecavri: high barrier to resistance hence 1st line
  • Adefovir: rarely used today, due to renal impairment risk + high resistance risk
  • Telbivudine: rarely used today

PEG INF: rarely given today due to S/E

HBV/HIV co-infection: 2 of Lamivudine, Tenofovir, Emtricitabine

Need to screen all pt for HIV (risk of HIV resistance with HBV monotherapy)

21
Q

What is the follow up required for patients with inactive hep B?

A

6-Monthly Follow up with:

  • ALT, Bilirubin, Albumin for INFLAMMATION & function
  • AFP For HCC
  • U/S HBS 6-12 Monthly For CIRRHOSIS
  • HBeAg annually

If any feature is ABNORMAL: may suggest active HEPATITIS (not just CHB, b/c there is inflammation) 🡪 Refer gastroenterologist

  • EITHER Clinical signs of Jaundice / Decompensated Liver Failure
  • OR Abnormal lab Values: ALT / AST persistently raised over 3 months
  • AFP raised OR rising trend OR HBe Ag +ve at age 40 and above
  • Low albumin, raised bilirubin level, Low platelet level
  • OR U/S HBS suspicious for cirrhosis
22
Q

What do you need to counsel patients with HBV about?

A

Notifiable Disease – Both Hep B and Hep C

Prevent transmission

  • Avoid sharing toothbrushes/dental/shaving equipment
  • Cover any bleeding wound
  • Avoid donating blood
  • Stop illicit drugs
  • Barrier protection

Prevent further liver insult

  • Alcohol cessation, weight loss
  • Hep A Immunisation

Clinical course of disease

  • Risk of Cirrhosis and HCC (applies to Hep C as well!)
  • Need for further follow up