Step 2 CK · Internal Medicine · Gastroenterology

GERD & Peptic Ulcer Disease

Name: GERD & Peptic Ulcer Disease
Creator: Veli Bakalov, MD

PPI trials, Barrett surveillance, H. pylori, and the ulcer that bleeds vs the one that perforates

Gastroenterology·Upper GI Disorders·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Typical heartburn/regurgitation without alarm features → empiric PPI trial; dysphagia, odynophagia, weight loss, GI bleeding or iron-deficiency anemia, recurrent vomiting, or new symptoms after 60 → endoscopy.
GERD management: weight loss, head-of-bed elevation, no late meals, and a PPI (more effective than H2 blockers); fundoplication for refractory or large-volume regurgitation.
Barrett esophagus = intestinal columnar metaplasia with goblet cells, the precursor of esophageal adenocarcinoma; no dysplasia → endoscopy every 3–5 years, low-grade → eradication or 6–12-month surveillance, high-grade → RFA/EMR.
Duodenal ulcer (H. pylori ~90%) pain improves with food and recurs 2–4 h later; gastric ulcer (H. pylori ~70%, NSAIDs) pain worsens with food, causes weight loss, and must be biopsied and followed to healing.
NSAIDs cause ulcers by inhibiting COX-1 prostaglandins; in high-risk patients add a PPI or misoprostol or use a COX-2 selective agent.
Diagnose and confirm cure of H. pylori with urea breath test or stool antigen after holding PPIs 1–2 weeks and antibiotics/bismuth 4 weeks; serology cannot confirm eradication.
Bismuth quadruple therapy (PPI + bismuth + tetracycline + metronidazole) is preferred; rifabutin triple or vonoprazan-amoxicillin dual therapy are alternatives (ACG 2024); clarithromycin triple therapy only when susceptibility is confirmed.
Posterior duodenal ulcer bleeds from the gastroduodenal artery; anterior duodenal ulcer perforates with free air under the diaphragm.
Zollinger-Ellison: multiple, refractory, or distal ulcers with diarrhea, fasting gastrin often over 1,000 pg/mL, and a paradoxical gastrin rise after secretin; screen for MEN1 with calcium.

GERD: diagnosis and management

Mechanism and symptoms. Gastroesophageal reflux disease (GERD) is driven mainly by transient relaxations of the lower esophageal sphincter. It presents with heartburn and regurgitation. With typical symptoms and no alarm features, GERD is a clinical diagnosis: start an empiric PPI trial (usually 8 weeks, taken 30–60 minutes before breakfast). Endoscopy is not needed first.

Alarm features that require endoscopy. These raise concern for malignancy, stricture, or severe esophagitis:

Dysphagia or odynophagia
Weight loss
GI bleeding or iron-deficiency anemia
Recurrent vomiting
New-onset symptoms after age 60

Treatment. Lifestyle measures are weight loss, elevating the head of the bed, and avoiding late meals and trigger foods. Add a proton pump inhibitor, which heals esophagitis more effectively than an H2 blocker. Reserve fundoplication for refractory disease or large-volume regurgitation.

Complications of untreated reflux.

Erosive esophagitis
Peptic stricture, which causes progressive dysphagia to solids
Barrett esophagus, which can progress to adenocarcinoma
Extraesophageal disease: chronic cough, laryngitis, asthma

Barrett esophagus

Definition. Chronic acid exposure converts the squamous epithelium of the distal esophagus to intestinal columnar epithelium with goblet cells. Barrett esophagus is the precursor lesion of esophageal adenocarcinoma. Screening endoscopy is considered in patients with chronic GERD and several risk factors, such as male sex, age over 50, White race, obesity, smoking, or a family history of Barrett esophagus or esophageal adenocarcinoma.

Barrett management by dysplasia grade

Biopsy finding	Management
No dysplasia	Surveillance endoscopy every 3–5 years
Low-grade dysplasia	Endoscopic eradication, or close surveillance every 6–12 months
High-grade dysplasia or intramucosal carcinoma	Endoscopic eradication: radiofrequency ablation, endoscopic mucosal resection

All patients with Barrett esophagus stay on a PPI.

Peptic ulcer disease

Two main causes. H. pylori and NSAIDs account for most ulcers. NSAIDs inhibit COX-1, which cuts the prostaglandins that maintain gastric mucus, bicarbonate secretion, and mucosal blood flow. NSAID ulcers are mostly gastric. In high-risk patients, add a PPI or misoprostol, or use a COX-2 selective agent to reduce GI toxicity. Misoprostol causes diarrhea and is contraindicated in pregnancy because it is an abortifacient.

Duodenal vs gastric ulcer

Feature	Duodenal ulcer	Gastric ulcer
Frequency	More common	Less common
Main cause	H. pylori in ~90%	H. pylori in ~70%; NSAIDs
Pain with meals	Improves with food, recurs 2–4 hours later	Worsens with food
Weight	Stable or gain	Weight loss
Malignant potential	Essentially none	Can be malignant: biopsy every one

Duodenal ulcer pain decreases with food; gastric ulcer pain is greater with food and comes with weight loss.

Gastric ulcers need biopsy and follow-up. Because gastric ulcers can be malignant, biopsy every one. Then document healing with repeat endoscopy. A gastric ulcer that persists or fails to heal needs re-biopsy to exclude gastric adenocarcinoma.

Helicobacter pylori: test, treat, confirm

Who to test. Patients with active or past peptic ulcer, uninvestigated dyspepsia, gastric MALT lymphoma, or a family history of gastric cancer.

Noninvasive tests. The urea breath test and the stool antigen test both diagnose infection and confirm eradication. Endoscopic biopsy with a rapid urease (CLO) test is the alternative when endoscopy is being done anyway.

Hold PPIs for 1–2 weeks and antibiotics or bismuth for 4 weeks before breath, stool, or urease testing. These drugs suppress the organism and cause false negatives.

Bismuth quadruple therapy (preferred)PPI + bismuth + tetracycline + metronidazole, usually for 14 days. Favored because clarithromycin resistance is rising.
Alternatives when susceptibility is unknownRifabutin triple therapy (PPI + amoxicillin + rifabutin) or vonoprazan + amoxicillin dual therapy, each for 14 days (ACG 2024).
Clarithromycin triple therapy (selected cases)PPI + amoxicillin + clarithromycin, only when testing shows clarithromycin susceptibility.
Confirm eradicationUrea breath test or stool antigen at least 4 weeks after therapy, off PPIs.

Serology stays positive after cure, so it cannot distinguish past from active infection and never confirms eradication.

Ulcer complications and Zollinger-Ellison syndrome

Ulcer complications

Complication	Typical ulcer	Presentation	Key point
Hemorrhage	Posterior duodenal ulcer eroding the gastroduodenal artery	Hematemesis, melena	The artery lies directly behind the duodenal bulb
Perforation	Anterior duodenal ulcer	Sudden severe pain, peritonitis, free air under the diaphragm	Emergency surgical repair with antibiotics
Gastric outlet obstruction	Chronic scarring near the pylorus	Early satiety, vomiting of undigested food, succussion splash	Vomiting causes hypochloremic, hypokalemic metabolic alkalosis

Free air under the diaphragm on an upright film means perforation until proven otherwise.

Zollinger-Ellison syndrome. A gastrin-secreting tumor (gastrinoma) of the duodenum or pancreas. Suspect it with multiple, refractory, or unusually distal ulcers (beyond the duodenal bulb), especially with diarrhea from acid inactivating pancreatic enzymes. Fasting gastrin is very high, often >1,000 pg/mL. Measure it off PPIs if possible, because acid suppression itself raises gastrin.

Secretin stimulation test. Secretin normally suppresses gastrin, but a gastrinoma responds with a paradoxical rise in gastrin. This confirms the diagnosis.

Gastrinoma can be part of MEN1 (parathyroid, pituitary, pancreas), so check serum calcium to screen for hyperparathyroidism.