Define Peptic Ulcer Disease. Describe its aetiology, clinical features, investigations and management.

The Concept — a Balance Tipped

A peptic ulcer is a breach in the mucosa of the stomach or duodenum that penetrates the muscularis mucosae, occurring wherever mucosa is exposed to acid and pepsin. The unifying idea is an imbalance between aggressive and defensive factors: aggression from acid, pepsin, Helicobacter pylori and NSAIDs, versus defence from mucus, bicarbonate, mucosal blood flow and prostaglandins. Anything that increases aggression or weakens defence produces an ulcer, and this framework explains both the causes and the treatment.

Aetiology

• Helicobacter pylori — the dominant cause: a Gram-negative spiral bacterium found in the great majority of duodenal (~95%) and gastric (~70%) ulcers. It damages the mucosa directly and disturbs acid regulation.
• NSAIDs — inhibit cyclo-oxygenase and hence prostaglandins, removing a key mucosal defence.
• Others — smoking, severe physiological stress (Cushing's ulcer after head injury, Curling's ulcer after burns), steroids, and the rare gastrin-secreting tumour of Zollinger-Ellison syndrome.

Duodenal VS Gastric Ulcer

Clinical Features

The typical symptom is epigastric pain — burning or gnawing — with a characteristic relationship to food (relieved by eating in duodenal ulcers, worsened in gastric ulcers), along with nausea and dyspepsia. Sometimes a complication (bleeding or perforation) is the first presentation, which is why dyspepsia with alarm features is investigated.

Investigation

Upper GI endoscopy is the key investigation — it visualises the ulcer, and importantly every gastric ulcer is biopsied to exclude malignancy and tested for H. Pylori (rapid urease/CLO test, histology). Non-invasive H. Pylori tests include the urea breath test and stool antigen. A fasting serum gastrin is measured if Zollinger-Ellison syndrome is suspected.

Management

• Eradicate H. Pylori — triple therapy: a PPI plus two antibiotics (e.g. Amoxicillin and clarithromycin) for 1–2 weeks — which cures most ulcers and prevents recurrence.
• Acid suppression — a PPI to heal the ulcer.
• Remove precipitants — stop NSAIDs and smoking; use gastroprotection if NSAIDs are essential.
• Surgery — now rare, reserved for complications or truly refractory disease (historically vagotomy and antrectomy).

How H. Pylori Causes Ulcers

Understanding the organism's mechanism ties the topic together. H. Pylori survives in the hostile acid of the stomach by producing urease, which splits urea to release ammonia and neutralise the acid around it. It colonises the gastric antrum, causing inflammation that increases gastrin and thus acid output; the excess acid damages the duodenum, where gastric metaplasia then allows the organism to colonise and ulcerate — explaining duodenal ulcers. In the body of the stomach it can instead cause atrophic gastritis, predisposing to gastric ulcers and cancer. This dual behaviour explains why the same organism causes different diseases.

Alarm Features & Follow-up

Dyspepsia is extremely common and mostly benign, so 'alarm features' select who needs urgent endoscopy: age over ~55 with new symptoms, weight loss, dysphagia, persistent vomiting, gastrointestinal bleeding (haematemesis/melaena) or iron-deficiency anaemia. After treatment, gastric ulcers are re-scoped to confirm healing and exclude an underlying cancer, and H. Pylori eradication is confirmed (e.g. By urea breath test) — steps not needed for a straightforward healed duodenal ulcer.

Surgery & its Historical Context

Although drugs have made ulcer surgery rare, the classic operations are worth knowing for context: truncal or highly selective vagotomy (reducing acid by cutting the vagal supply, historically with a drainage procedure), and partial gastrectomy (Billroth I/II). These are now reserved almost entirely for complications — a perforation, uncontrolled bleeding, or obstruction not relieved endoscopically — reflecting the shift from elective acid-reducing surgery to emergency, complication-driven surgery in the H. Pylori era.

• Triple therapy = PPI + amoxicillin + clarithromycin for 1–2 weeks (H. Pylori eradication).
• Every gastric ulcer is biopsied to exclude malignancy; confirm healing/eradication.
• Duodenal pain relieved by food; gastric pain worsened by food.

Eradication of H. Pylori prevents recurrence.

• Peptic ulcer = mucosal breach from imbalance of aggressive (acid, pepsin, H. Pylori, NSAIDs) vs defensive (mucus, bicarbonate, blood flow, prostaglandins) factors.
• Main causes: H. Pylori (most DU/GU) and NSAIDs; also stress (Cushing's/Curling's), Zollinger-Ellison.
• Duodenal (younger, pain relieved by food, not malignant) vs gastric (older, pain worse with food, biopsy for cancer).
• Endoscopy is key — biopsy every gastric ulcer + test for H. Pylori (urease/breath/stool).
• Treat by H. Pylori eradication (triple therapy) + PPI, stop NSAIDs/smoking; surgery only for complications.