Peptic Ulcer Disease and H. pylori

• Audio chapter
  Single-voice audio, 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 6.1: H. pylori biology, diagnosis, and test of cure

  Helicobacter pylori is a spiral, gram-negative, microaerophilic bacterium that lives in a niche no other organism reliably occupies, the layer of mucus that coats the gastric epithelium, and everything about diagnosis and treatment flows from how the organism survives there.

• Section 6.2: First-line eradication regimens

  The first-line landscape has shifted because clarithromycin resistance has risen above the threshold at which clarithromycin-based regimens can be given empirically with confidence.

• Section 6.3: Salvage therapy after failed eradication

  Failure of first-line eradication shifts management onto a second axis, treatment-experienced rather than treatment-naive, and the 2024 ACG guideline made this distinction explicit because the data and the choices are different.

• Section 6.4: NSAID and aspirin ulcers

  NSAIDs and aspirin damage the gastroduodenal mucosa by a dual mechanism, and the systemic mechanism explains why parenteral, rectal, and topical NSAIDs all cause ulcer disease while the topical mechanism explains why a tablet swallowed without water injures the mucosa it touches.

• Section 6.5: Refractory and idiopathic ulcers

  A non-healing ulcer at follow-up endoscopy is a differential expansion problem, because the standard explanations (H. pylori and NSAIDs) have either been excluded or addressed, and the task is to systematically exclude what was missed.

• Section 6.6: Perforation and penetration

  Perforation is the surgical emergency of peptic ulcer disease, and management depends on whether the perforation is free into the peritoneum or contained against an adjacent structure, and on whether the patient is hemodynamically stable.

Podcast episodes

1. 01

   H. pylori: Biology, Eradication, and Salvage

   H. pylori from biology through eradication and salvage, driven by a handful of load-bearing mechanisms. Urease survival explains both diagnosis and why acid suppression causes false negatives, infection location decides gastric versus duodenal disease, and rising clarithromycin resistance has reshaped first-line therapy toward optimized bismuth quadruple and vonoprazan-based regimens.

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2. 02

   NSAID Ulcers, Refractory Disease, and Perforation

   Episode two of the Peptic Ulcer Disease and H. pylori chapter covers the ulcers that are not driven by H. pylori. It works through NSAID and aspirin injury and its prevention, the sequential exclusion behind refractory and idiopathic ulcers, and the perforation and penetration emergencies that split on whether the leak is free or contained.

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Key topics

• ·Urease biology and diagnostic tests
• ·Infection location and ulcer physiology
• ·Suppression rule and false negatives
• ·Serology limits and test of cure
• ·Expanded testing indications
• ·Clarithromycin resistance and first-line therapy
• ·Vonoprazan-based regimens
• ·Salvage and susceptibility testing
• ·NSAID and aspirin ulcer mechanism
• ·Multiplicative NSAID risk factors and tiers
• ·Acid-blocker co-prescription and misoprostol
• ·Celecoxib, the aspirin trap, and dual antiplatelet therapy
• ·Refractory ulcer sequential exclusion
• ·Gastric cancer and repeat biopsy rule
• ·Zollinger-Ellison and fasting gastrin pitfalls
• ·Free perforation versus contained penetration