Peptic ulcer disease

Break in the gastric or duodenal mucosa extending through the muscularis mucosa into deeper layers, typically due to acid–pepsin effects. Most commonly occurs in the stomach or first part of duodenum.

• Common cause of upper abdominal pain and GI bleeding. Can lead to serious complications (hemorrhage, perforation, obstruction). Understanding PUD is vital as H. pylori and NSAID management dramatically improved outcomes, and it's a frequent topic on exams.

• Gnawing, epigastric pain (dyspepsia) is typical. Duodenal ulcer pain often improves with meals (returns 2–3 hours later, may cause night waking), whereas gastric ulcer pain usually worsens with eating (patients may avoid food and lose weight).
• Key risk factors: H. pylori infection (cause of ~90% of duodenal and ~70% of gastric ulcers) and chronic NSAID/aspirin use. Others include severe physiological stress (e.g., ICU patients with burns or head injury can develop acute stress ulcers), Zollinger-Ellison syndrome (gastrinoma with excessive acid), smoking (impairs mucosal healing), and corticosteroids (especially with NSAIDs).
• Many ulcers are asymptomatic until a complication occurs. Signs of GI bleeding (e.g., melena or hematemesis, iron-deficiency anemia) may be the first presentation. Perforation presents with abrupt abdominal pain and peritonitis (rigid abdomen). Long-standing ulcer symptoms with weight loss or early satiety raise concern for ulcer-associated gastric cancer.

1. Always test for Helicobacter pylori in PUD. For confirmed ulcers, endoscopic biopsy can detect H. pylori (rapid urease test) and rule out malignancy (especially in gastric ulcers). Noninvasive tests (urea breath test or stool antigen) are used in initial dyspepsia without alarm signs.
2. Review medications and stop NSAIDs/aspirin if possible. If an NSAID must be continued, co-prescribe a PPI to protect the mucosa. Remember that removing the inciting factor heals most NSAID-related ulcers.
3. Use alarm features to guide management: patients with red flags (unintentional weight loss, progressive dysphagia, anemia, GI bleeding, or persistent vomiting) should undergo prompt endoscopy rather than empirical therapy.
4. Differentiate benign ulcer from cancer: Gastric ulcers generally require follow-up endoscopy (after ~8 weeks of therapy) to ensure healing and exclude gastric carcinoma. Duodenal ulcers have an extremely low malignancy risk, so routine biopsy/follow-up is not always needed if H. pylori is treated.

1. Acid suppression: Proton pump inhibitors (PPIs) are first-line to heal ulcers (much more effective than H2 blockers). Typical course is 4 weeks for duodenal ulcers and at least 8 weeks for large or gastric ulcers. Continue maintenance PPI if high-risk (e.g., require NSAIDs).
2. Eradicate H. pylori: If infection is present, use combination therapy. Standard triple therapy = PPI + clarithromycin + amoxicillin (or metronidazole if penicillin-allergic) for 14 days. In areas of high macrolide resistance or prior macrolide use, use bismuth quadruple therapy (PPI + bismuth + tetracycline + metronidazole). Always confirm H. pylori eradication (urea breath or stool test) after treatment.
3. Avoid ulcerogens: Discontinue NSAIDs/aspirin. If they are absolutely needed (e.g., cardiovascular stents), use the lowest dose and add daily PPI for prophylaxis. Advise smoking cessation and limiting alcohol, as these hinder ulcer healing.
4. Manage complications: For bleeding ulcers, perform endoscopic hemostasis (cautery, epinephrine injection, or clipping) plus high-dose IV PPI (to stabilize clots). Surgery or interventional radiology is reserved if bleeding cannot be controlled endoscopically. Perforated ulcers require urgent surgical repair after stabilizing the patient (IV fluids, antibiotics).
5. For gastric ulcers, repeat endoscopy ~6–8 weeks after therapy initiation to ensure healing and exclude malignancy (biopsy any persistent ulcer). Duodenal ulcers generally do not require routine follow-up endoscopy if symptoms resolve and H. pylori is eradicated.

• Pain Decreases with food for Duodenal ulcers (patients often gain weight or have night pain relieved by a snack), whereas pain Gets worse with food for Gastric ulcers (food aggravates pain, leading to weight loss).
• Ulcers that are recurrent, refractory, or in atypical locations (e.g., multiple duodenal/jejunal ulcers) → suspect Zollinger-Ellison syndrome (gastrinoma causing excessive acid secretion).
• H. pylori is a major culprit: it's present in most duodenal ulcers and many gastric ulcers—always confirm eradication after treatment, as this drops ulcer recurrence from ~50% to near zero.

• Hematemesis (vomiting blood or coffee-ground material) or melena (tarry black stools) → indicates GI bleeding; requires prompt endoscopic evaluation and treatment.
• Sudden severe abdominal pain with rigid abdomen → suspect perforation (peritonitis); this is a surgical emergency (confirm with free air on imaging).
• Unintended weight loss, progressive dysphagia, early satiety, or persistent vomiting in a patient with ulcer symptoms → alarm features suggesting possible gastric cancer or obstruction; urgent endoscopy indicated.

1. Evaluate dyspepsia or epigastric pain → check for alarm features (bleeding, anemia, weight loss, dysphagia, vomiting).
2. If any alarm feature or patient >60 years old → proceed directly to endoscopy (EGD) for diagnosis (visualize ulcer, biopsy).
3. If no alarm features and patient younger (<60) → do noninvasive H. pylori testing (urea breath test or stool antigen). If positive, treat with eradication therapy; if negative, empiric PPI therapy is often given.
4. If symptoms persist despite initial treatment or recur → perform endoscopy to confirm ulcer and rule out other pathology. Obtain biopsies (especially for gastric ulcers) for H. pylori and to exclude malignancy.
5. After treatment, ensure follow-up: confirm H. pylori clearance and, for gastric ulcers, repeat endoscopy to document healing.

• Middle-aged patient with burning epigastric pain that improves with eating and returns a few hours later (especially at night) → duodenal ulcer (likely H. pylori positive).
• Older patient on chronic NSAIDs with epigastric pain that worsens after meals, accompanied by weight loss and anemia → gastric ulcer (concern for NSAID injury or malignancy; endoscopy with biopsy needed).
• Patient with known PUD develops sudden, severe abdominal pain with guarding and rebound tenderness → ulcer perforation (emergency; expect free air under diaphragm on upright chest X-ray).