What is Peptic Ulcer Disease?
Peptic ulcer disease (PUD) refers to a break in the mucosal lining of the stomach or duodenum that extends through the muscularis mucosae, creating a craterlike lesion. Ulcers are classified according to location:
- Gastric ulcer occurs in the stomach.
- Duodenal ulcer occurs in the first part of the small intestine.
- Esophageal ulcer rare, usually related to severe reflux.
Epidemiology
Worldwide, an estimated 410% of the adult population will develop a peptic ulcer at some point in life. The prevalence is slightly higher in men than women, and the incidence peaks between ages 4060. While the overall mortality has declined because of better diagnostics and therapy, complications such as bleeding or perforation still cause significant morbidity.
Pathophysiology
The gastric mucosa is constantly exposed to aggressive factors (hydrochloric acid, pepsin, bile). Under normal conditions, a protective barrier of mucus, bicarbonate, prostaglandins, and adequate blood flow neutralises these agents. Ulcer formation results when this balance is disturbed:
- Increased acidpepsin secretion hypersecretion overwhelms the mucosal defenses.
- Compromised mucosal protection decreased mucus, reduced prostaglandin synthesis, or impaired blood flow.
Two major etiologic agents are recognized:
- Helicobacter pylori infection a gramnegative bacterium that damages epithelium, causes inflammation, and alters acid regulation.
- Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit cyclooxygenase1, reducing protective prostaglandins.
Other contributors include smoking, alcohol excess, stressrelated hypersecretion, and rare conditions such as ZollingerEllison syndrome.
Risk Factors
| Factor | How it Increases Risk |
|---|---|
| H. pylori infection | Chronic gastritis, altered gastric acidity |
| Regular NSAID use | Reduced prostaglandin synthesis |
| Smoking | Impaired mucosal blood flow, increased acid |
| Alcohol excess | Irritates mucosa and potentiates acid secretion |
| Stress (severe physiological stress) | Elevated cortisol and catecholamines increase acid |
| Age >60 years | Decreased mucosal repair capacity |
Clinical Presentation
Classic symptoms are often described as a burning epigastric pain:
- Pain that improves with food or antacids (duodenal ulcer) or worsens after meals (gastric ulcer).
- Nocturnal pain that may awaken the patient.
- Nausea, occasional vomiting.
- Bloating, early satiety, or loss of appetite.
Complications present with more alarming signs:
- Upper gastrointestinal bleeding coffeeground emesis, melena, or hematemesis.
- Perforation sudden severe abdominal pain, rigid abdomen, signs of peritonitis.
- Gastric outlet obstruction persistent vomiting, weight loss.
Diagnostic Approach
Diagnosis rests on a combination of clinical suspicion, endoscopic evaluation, and testing for H. pylori.
Endoscopy (EGD)
Upper gastrointestinal endoscopy is the gold standard. It allows direct visualization, size measurement, and biopsy for histology or H. pylori detection.
Noninvasive H. pylori testing
- Urea breath test highly sensitive and specific.
- Stool antigen test.
- Serology useful only for initial screening; antibodies persist after eradication.
Radiographic studies
Upper GI series with barium may reveal ulcer crater but is less sensitive than endoscopy and is rarely used today.
Management
Therapy aims to eradicate H. pylori (if present), suppress gastric acid, protect the mucosa, and eliminate risk factors.
Eradication Regimens (H. pyloripositive)
- Triple therapy (1014days): PPI + clarithromycin + amoxicillin (or metronidazole).
- Quadruple therapy: PPI + bismuth subsalicylate + tetracycline + metronidazole.
- In areas with high resistance, a concomitant or sequential regimen may be preferred.
Acid Suppression
- Protonpump inhibitors (omeprazole, esomeprazole, lansoprazole) 48weeks.
- Histamine2 receptor blockers less effective for ulcer healing.
- Potassiumcompetitive acid blockers (e.g., vonoprazan) emerging alternatives.
Mucosal Protection
Sucralfate or misoprostol can be added, especially when NSAIDs must continue.
NSAID Management
Discontinue nonessential NSAIDs. If continued use is unavoidable, prescribe a COX2 selective agent plus a PPI.
Followup
Repeat endoscopy is recommended for highrisk lesions (e.g., size >2cm, ulcer with suspicion of malignancy) after 812weeks of therapy.
Key point: A successful eradication test (urea breath or stool antigen) should be performed at least 4weeks after completing therapy to confirm H. pylori clearance.
Prevention Strategies
- Screen and treat H. pylori infection, especially in highprevalence regions.
- Use the lowest effective NSAID dose; consider gastroprotective agents.
- Quit smoking and limit alcohol intake.
- Adopt a balanced diet rich in fruits, vegetables, and fiber.
- Manage stress through regular exercise, adequate sleep, and relaxation techniques.
Frequently Asked Questions
Can stress alone cause a peptic ulcer?
Stress can increase gastric acid secretion, but on its own it is rarely sufficient to cause an ulcer without a preexisting mucosal defect or other risk factors.
Is it safe to take antacids while on ulcer medication?
Yes, antacids can provide symptomatic relief and are safe to use alongside PPIs. However, they should not replace prescribed acidsuppressive therapy.
How long does it take for an ulcer to heal?
Most uncomplicated ulcers show significant healing after 46weeks of appropriate therapy, with complete closure usually evident by 8weeks.
Can ulcer disease recur?
Recurrence is possible, especially if H. pylori infection persists or NSAID use continues. Eradication of H. pylori and avoidance of harmful habits greatly reduce relapse rates.
