Liver· Chapter 18

Viral Hepatitis

HBV serology phases and the entecavir versus tenofovir choice, reactivation prophylaxis around rituximab and other immunosuppression, HBV in pregnancy with TDF for high viral load, HCV pan-genotypic DAAs in 8 versus 12 weeks, HDV bulevirtide, and the HEV mortality risk in pregnancy.

44 MCQs
  • Audio chapter
    Attending-narrated, listen on the commute.
  • ABIM-format MCQs
    5-option vignettes with full wrong-answer teaching.
  • Study guide
    Tables, decision trees, primary sources.
  • AI tutor
    Chapter-grounded, answers the question you're stuck on.

What this chapter covers

  • Section 18.1: Acute viral hepatitis phases and differential

    Acute viral hepatitis has the same clinical envelope regardless of the offending virus, which is why the candidate must learn to read the serologic panel rather than the symptoms.

  • Section 18.2: HBV serology

    HBV serology is the question type in hepatology that gets memorized as a grid because the grid maps directly onto management.

  • Section 18.3: HBV treatment and reactivation prevention

    The decision to treat chronic HBV is a multifactorial integration of HBV DNA, ALT, fibrosis stage, and clinical context, and the candidate who tries to memorize a single threshold will miss vignettes.

  • Section 18.4: HBV in pregnancy and vertical transmission

    Vertical transmission of HBV is the dominant route by which chronic HBV is acquired worldwide because perinatal infection produces the highest chronicity rate of any age window: 90 percent of neonates infected at birth become chronic carriers, compared with 30 percent of children infected between ages 1 and 5 and only 1 to 5 percent of immunocompetent adults.

  • Section 18.5: HCV diagnosis and DAA regimens

    Chronic HCV is now a curable disease, which is the single most consequential change in hepatology over the past decade and the orientation point for every board question on HCV.

  • Section 18.6: HCV special populations and post-SVR

    Special populations modify DAA selection because protease inhibitors are hepatically cleared and unsafe in decompensated liver disease, while nucleotide and NS5A inhibitors have distinct renal and drug-interaction profiles.

  • Section 18.7: HDV and bulevirtide

    Hepatitis D is a defective negative-stranded RNA virus that requires HBsAg from HBV as its envelope protein, which is why HDV exists only in patients who are also infected with HBV.

  • Section 18.8: HAV and HEV

    Hepatitis A is a fecal-orally transmitted picornavirus that produces an acute self-limited illness with an incubation period averaging 28 days, and the boards reward candidates who recognize both the canonical acute presentation and the few atypical presentations.

Podcast episodes

  1. 01

    Oral Viruses

    The acute hepatitis framework and the two fecal-oral viruses: the phases of acute infection, the serologic panel that reads the virus, hepatitis A as a post-exposure prophylaxis decision, and hepatitis E with its high mortality in pregnancy and chronic infection in the immunocompromised.

  2. 02

    Hepatitis B and D

    Hepatitis B by phase: the serology that names the phase, nucleoside-analog treatment, the bundle that prevents vertical transmission, and the screen-and-prophylax rule for reactivation around immunosuppression. Then hepatitis D and its new entry inhibitor.

  3. 03

    Hepatitis C

    The reflex antibody-then-RNA diagnosis, the pangenotypic direct-acting antiviral regimens by fibrosis stage and renal function, the special populations including decompensated cirrhosis and kidney disease, and the post-cure hepatocellular carcinoma surveillance question.