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Viral hepatitis flashcards

19 high-yield MRCP Part 1 cards from the Intellect Medicos Gastroenterology & Hepatology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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  1. Which serological marker confirms ACUTE hepatitis A infection?

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    IgM anti-HAV.

    Why? IgG anti-HAV indicates past infection or vaccination. Hepatitis A is a faeco-oral picornavirus with no chronic or carrier state.

  2. A kidney transplant recipient on tacrolimus has a persistently raised ALT. He often eats undercooked pork sausages. HEV RNA remains positive after 3 months. Which antiviral is used for chronic hepatitis E?

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    Ribavirin (for about 3 months), alongside reducing immunosuppression where possible.

    Why? HEV is usually self-limiting, but immunosuppressed patients can develop chronic infection and cirrhosis.

  3. Which serological result defines CHRONIC hepatitis B infection?

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    HBsAg positive for more than 6 months.

    Why? HBsAg is the hallmark of active infection. In recovery it disappears and anti-HBs appears.

  4. During the 'window period' of acute hepatitis B, which marker may be the only positive one?

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    IgM anti-HBc.

    Why? HBsAg has cleared but anti-HBs has not yet appeared, so only core antibody shows the infection.

  5. Hepatitis B serology: vaccinated only = ______; past infection now cleared = anti-HBc positive, HBsAg negative (usually with anti-HBs).

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    anti-HBs positive, anti-HBc negative

    Why? The vaccine contains only surface antigen, so vaccinated people never make anti-HBc.

  6. Hepatitis B serology: vaccinated only = anti-HBs positive, anti-HBc negative; past infection now cleared = ______ (usually with anti-HBs).

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    anti-HBc positive, HBsAg negative

    Why? The vaccine contains only surface antigen, so vaccinated people never make anti-HBc.

  7. Under NICE guidance, what is first-line antiviral treatment for an adult with chronic hepatitis B and COMPENSATED liver disease?

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    A 48-week course of peginterferon alfa-2a.

    Why? A finite course can achieve lasting HBeAg seroconversion. Second line: tenofovir disoproxil if HBeAg-positive; entecavir or tenofovir disoproxil if HBeAg-negative.

  8. What is first-line antiviral treatment for chronic hepatitis B with DECOMPENSATED liver disease?

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    Entecavir (tenofovir disoproxil if there is lamivudine resistance).

    Why? Peginterferon must NOT be given in decompensated disease because it can precipitate liver failure.

  9. NICE CG165: pregnant women with hepatitis B are offered ______ if HBV DNA is above 10⁷ IU/mL in the third trimester.

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    tenofovir disoproxil

    Why? This reduces transmission to the baby, alongside vaccine and immunoglobulin at birth.

  10. NICE CG165: pregnant women with hepatitis B are offered tenofovir disoproxil if HBV DNA is above ______ in the third trimester.

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    10⁷ IU/mL

    Why? This reduces transmission to the baby, alongside vaccine and immunoglobulin at birth.

  11. What is the main renal adverse effect of tenofovir disoproxil?

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    Nephrotoxicity – proximal tubular damage (Fanconi-type syndrome) – so renal function and phosphate are monitored.

    Why? Tenofovir is cleared by the proximal tubule. It can also reduce bone mineral density.

  12. After a full hepatitis B vaccine course, a healthcare worker's anti-HBs is below 10 mIU/mL. What is done?

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    Treat as a non-responder: repeat the full vaccine course and recheck; if still a non-responder, give HBIG after any exposure.

    Why? Anti-HBs of 100 or more indicates a good response; 10–99 is a suboptimal response needing a booster dose.

  13. Hepatitis C: screen with ______, then confirm active infection with HCV RNA (PCR).

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    anti-HCV antibody

    Why? Antibody stays positive after clearance or cure, so RNA is needed to show current infection. Test RNA directly if immunocompromised or acute infection is suspected.

  14. Hepatitis C: screen with anti-HCV antibody, then confirm active infection with ______.

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    HCV RNA (PCR)

    Why? Antibody stays positive after clearance or cure, so RNA is needed to show current infection. Test RNA directly if immunocompromised or acute infection is suspected.

  15. What is the modern treatment for chronic hepatitis C, and how is cure defined?

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    A pangenotypic direct-acting antiviral combination (e.g. sofosbuvir/velpatasvir for 12 weeks or glecaprevir/pibrentasvir for 8 weeks); cure = SVR12, undetectable HCV RNA 12 weeks after finishing.

    Why? DAAs cure about 95% of patients; interferon and ribavirin are now rarely used.

  16. Sofosbuvir is a nucleotide inhibitor of the HCV ______; velpatasvir and ledipasvir inhibit NS5A.

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    NS5B RNA-dependent RNA polymerase

    Why? Combining drugs that hit different viral proteins prevents resistance. NS3/4A protease inhibitors (e.g. grazoprevir, glecaprevir) are a third class.

  17. Sofosbuvir is a nucleotide inhibitor of the HCV NS5B RNA-dependent RNA polymerase; velpatasvir and ledipasvir inhibit ______.

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    NS5A

    Why? Combining drugs that hit different viral proteins prevents resistance. NS3/4A protease inhibitors (e.g. grazoprevir, glecaprevir) are a third class.

  18. Which antiarrhythmic must not be combined with sofosbuvir-containing regimens, and why?

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    Amiodarone – risk of severe, sometimes fatal, bradycardia and heart block.

    Why? The mechanism is not fully understood. If unavoidable, it needs specialist advice and close cardiac monitoring.

  19. Which renal lesion is classically associated with hepatitis C infection?

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    Membranoproliferative glomerulonephritis (often with mixed cryoglobulinaemia).

    Why? Immune complexes and cryoglobulins deposit in glomeruli. Other extrahepatic links: porphyria cutanea tarda, lichen planus, Sjögren's, insulin resistance.

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