Mucosal break >5 mm in the stomach or duodenum, most often due to H. pylori or NSAIDs.
Also known as: PUD, peptic ulcer, gastric ulcer, duodenal ulcer
Overview
Mucosal defect of the stomach or duodenum extending through the muscularis mucosae, typically ≥5 mm in diameter. Caused by an imbalance between mucosal aggressors (acid, pepsin, H. pylori, NSAIDs) and protective factors (mucus, bicarbonate, prostaglandins, blood flow).
Epidemiology
Lifetime prevalence 5-10%. Duodenal ulcers outnumber gastric ulcers ~4:1 historically, declining with H. pylori eradication. Incidence falling in developed countries; NSAID-related ulcers rising in elderly.
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Glucocorticoids — risk amplifier when combined with NSAIDs (independent risk weak)
Pathophysiology
H. pylori produces urease, ammonia, cytotoxin-associated antigen (CagA), and vacuolating toxin (VacA), inducing chronic gastritis. Antral-predominant infection increases acid secretion → duodenal ulcer. Corpus-predominant atrophic gastritis decreases acid → gastric ulcer and cancer risk. NSAIDs inhibit COX-1, reducing prostaglandin-mediated mucus, bicarbonate, and mucosal blood flow.
Clinical presentation
Symptoms
Epigastric pain — burning, gnawing, or hunger-like
Duodenal ulcer: pain 2-3 h after meals, relieved by food or antacids, nocturnal awakening
Gastric ulcer: pain worsened by food, weight loss
Nausea, early satiety, bloating, belching
Hematemesis, melena, or hematochezia if bleeding
Signs / physical exam
Epigastric tenderness on palpation
Signs of GI bleeding: pallor, tachycardia, orthostasis
Peritoneal signs (rigid abdomen, rebound) if perforated — surgical emergency
Succussion splash if gastric outlet obstruction
Classic findings
Duodenal: pain relieved by eating. Gastric: pain provoked by eating.
Differential diagnosis
GERD — Retrosternal burning rather than epigastric pain; relieved by antacids; normal mucosa or esophagitis on EGD
Functional dyspepsia — Symptoms identical to PUD but normal EGD; Rome IV criteria; treat with PPI ± prokinetic
Gastric cancer — Weight loss, anemia, persistent ulcer despite therapy, age >55; biopsy all gastric ulcers
Acute pancreatitis — Epigastric pain radiating to back, lipase >3× ULN; alcohol or gallstones
Cholelithiasis / biliary colic — RUQ or epigastric pain after fatty meals, lasting hours; gallstones on ultrasound
Mesenteric ischemia — Postprandial pain out of proportion, weight loss, atherosclerotic risk factors; CT angiography
Acute coronary syndrome (inferior MI) — Epigastric pain with diaphoresis, dyspnea; ECG and troponin in older patients or with cardiac risk factors
Zollinger-Ellison syndrome — Multiple, refractory, or distal ulcers; diarrhea; fasting gastrin >1000 pg/mL with elevated gastric pH
Diagnostic workup
Labs
CBC (anemia from chronic blood loss)
BMP, LFTs
Type and screen / crossmatch if acute bleed
H. pylori testing: urea breath test or stool antigen (preferred non-invasive); biopsy-based rapid urease test or histology if EGD performed
Fasting gastrin level if Zollinger-Ellison suspected
Imaging
Upper endoscopy (EGD) — gold standard; visualizes ulcer, allows biopsy and therapeutic intervention; biopsy ALL gastric ulcers to exclude malignancy
Upright CXR — free air under diaphragm in perforation
CT abdomen with contrast if perforation or complication suspected
Other studies
Withhold PPI 2 weeks and antibiotics 4 weeks before H. pylori testing to avoid false negatives
Repeat EGD in 8-12 weeks to confirm gastric ulcer healing and re-biopsy if not healed
Diagnostic algorithm
Feature
Duodenal Ulcer
Gastric Ulcer
Pain timing
2-3 h after meals, nocturnal
Soon after eating
Effect of food
Relieved
Worsened
Typical age
30-55
55-70
Acid secretion
Increased or normal
Normal or decreased
H. pylori prevalence
~70%
~40%
Malignancy risk
Negligible
4% — biopsy all
Bleeding risk
Higher (posterior — gastroduodenal artery)
Lower
Repeat EGD
Not routine
8-12 weeks to confirm healing
Duodenal vs gastric ulcer — distinguishing features.
Treatment
First-line
PPI — omeprazole, pantoprazole, esomeprazole — 4-8 weeks (8-12 weeks for gastric ulcer)
H. pylori eradication if positive (see by_subtype)
Discontinue NSAIDs and aspirin if possible; switch to acetaminophen
Lifestyle: smoking cessation, limit alcohol
H. pylori positive — first-line if local clarithromycin resistance <15%
Bismuth quadruple therapy (PREFERRED in most US regions): PPI BID + bismuth subsalicylate QID + tetracycline QID + metronidazole QID × 14 days
Or clarithromycin triple therapy: PPI BID + clarithromycin BID + amoxicillin BID (or metronidazole if PCN-allergic) × 14 days — only if no prior macrolide exposure and local resistance low
H. pylori — second-line / salvage
Levofloxacin triple: PPI BID + levofloxacin daily + amoxicillin BID × 14 days
Rifabutin triple (PPI + rifabutin + amoxicillin) for refractory cases
Confirm eradication 4 weeks after therapy with urea breath test or stool antigen
NSAID-induced
Stop NSAID; if continuation necessary, use lowest dose plus PPI co-therapy
Misoprostol QID as alternative gastroprotective agent (contraindicated in pregnancy)
Consider COX-2 selective inhibitor (celecoxib) with PPI in high-risk patients balanced against CV risk
Bleeding ulcer (Forrest classification)
IV PPI bolus + infusion (or intermittent high-dose IV PPI)
Endoscopic hemostasis for active bleeding, visible vessel, or adherent clot (combination injection plus thermal or clip)
Transfuse to Hgb ≥7 (≥8 if cardiovascular disease)
IR embolization or surgery if endoscopic failure
Complications
Upper GI bleeding (most common complication)
Perforation — sudden severe epigastric pain, peritonitis, free air on imaging; surgical repair (Graham patch)
Penetration — into pancreas, biliary tree, or adjacent organ
Gastric outlet obstruction — early satiety, vomiting of undigested food, succussion splash
Gastric malignancy — especially long-standing H. pylori; MALT lymphoma can regress with eradication
PANCE pearls
Biopsy ALL gastric ulcers — 4% harbor malignancy; duodenal ulcers virtually never malignant.
Confirm H. pylori eradication 4 weeks post-treatment in all patients (especially complicated PUD, MALT lymphoma, refractory dyspepsia).
Withhold PPI 2 weeks before urea breath test or stool antigen; serology unaffected but cannot confirm active infection.
Forrest IIc (flat pigmented spot) and III (clean base) do not require endoscopic therapy — early PPI and feeding.
Recurrent or refractory ulcer, multiple ulcers, or ulcers distal to duodenal bulb — check fasting gastrin for Zollinger-Ellison.
Curling ulcer (burn patient) and Cushing ulcer (head injury) are stress ulcers — prophylax high-risk ICU patients with PPI or H2RA.
References
ACG 2017 — Chey WD et al. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol 2017;112:212-239
ACG 2021 — Laine L et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol 2021;116:899-917
Maastricht VI/Florence — Malfertheiner P et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence Consensus Report. Gut 2022;71:1724-1762
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