Peptic Ulcer Disease — Anti-ulcer Drugs, H. pylori & GERD

Peptic Ulcer Disease, Anti-ulcer Drugs, H. pylori & GERD

1. Definition, scope & central paradigm

• Acid-peptic disorders comprise gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD — gastric and duodenal ulcers), and stress-related mucosal injury; in all of them mucosal erosion/ulceration arises when aggressive factors (acid, pepsin, NSAIDs, Helicobacter pylori, bile) overwhelm defensive factors (mucus + bicarbonate secretion, prostaglandins, nitric oxide, mucosal blood flow, restitution/regeneration) (Katzung Ch.62, pp.1153–4; G&G 14e Ch.53, p.1073).
• Peptic ulcer = a break in the mucosa ≥5 mm extending through the muscularis mucosae, distinguishing it from the smaller, shallower erosions and gastritis; occurs in the part of the GI tract exposed to acid and pepsin — chiefly stomach and duodenum (DiPiro 12e Ch.51, p.479; KDT 8e Ch.47, p.695).
• Therapeutic logic is two-pronged: (a) decrease gastric acidity (antacids, H₂ antagonists, PPIs, potassium-competitive acid blockers) and (b) enhance mucosal defense (misoprostol, sucralfate, bismuth, rebamipide); for GERD a third lever exists — raising lower-esophageal-sphincter (LES) tone and improving esophageal/gastric motility (G&G 14e Ch.53, p.1073).
• The single most important conceptual shift in modern practice: recognition that an infectious agent, H. pylori, is central to the pathogenesis of most peptic ulcers — converting a chronically relapsing disease into a curable one through eradication (G&G 14e Ch.53, p.1073; KDT 8e Ch.47, p.695).
• Over 90% of peptic ulcers are caused by H. pylori infection or by NSAID/aspirin use; the remainder are stress-related (critically ill) or "idiopathic" (non-H. pylori, non-NSAID) (Katzung Ch.62, p.1153; DiPiro 12e Ch.51, p.479).

Epidemiology (PUD)

• Gastroduodenal ulcers occur in 0.1–0.3% of the general population annually; lifetime prevalence 5–10%; incidence has fallen with better drug therapy and the ambulatory shift, but 30-day readmissions for upper-GI haemorrhage have risen; mortality is higher in those ≥65 y and in males (DiPiro 12e Ch.51, pp.479–80).
• H. pylori prevalence is geography-, age-, ethnicity- and hygiene-dependent: ~30–40% in the USA (10–15% in children <12 y, 50–60% in adults >60 y), higher in resource-limited settings; KDT notes 20–70% commensal carriage in apparently normal individuals, with up to 90% of duodenal and gastric ulcer patients testing positive (DiPiro 12e Ch.51, pp.480; KDT 8e Ch.47, p.704).
• Endoscopic gastroduodenal lesions (erosions, petechiae, ulcers) are seen in 30–50% of chronic NSAID users; NSAIDs and low-dose aspirin raise relative risk of PUD ~2.7× and ~1.7× respectively (DiPiro 12e Ch.51, p.480).