Makindo Medical Notes

Related Subjects: |Upper Gastrointestinal Bleed |Oesophageal Variceal Bleeding |Dieulafoy Lesion |Mallory-Weiss Tear |Gastric Cancer |Peptic Ulcer Disease |Oesophagogastroduodenoscopy (OGD/EGD) |Hereditary Haemorrhagic Telangiectasia |Hypovolaemic or Haemorrhagic Shock

Most patients with peptic ulcer disease have normal gastric acid secretion. Gastric ulcers (GU) with punched-out, heaped-up margins suggest cancer; indeed, about 10% of gastric ulcers are malignant.

About Peptic Ulcer Disease

• A peptic ulcer is defined as a break in the mucous membrane lining of the stomach or duodenum.

Physiology

• Acid Production: Parietal cells in the fundus and body of the stomach produce gastric acid.
• Gastrin: Produced by G cells in the antrum, it stimulates acid secretion. Gastrin release is triggered by gastric distension, protein, and calcium intake. Exists in two forms (G-34 and G-17), with G-17 being more abundant.

Aetiology

• Gastric Ulcers (GU): Result from mucosal breakdown.
• Duodenal Ulcers (DU): Associated with excess acid production.
• The exact mechanisms behind ulcer formation remain partially unclear.

Location of Peptic Ulcers

• Duodenum: 80%
• Stomach: 19%
• Both Duodenum and Stomach: 5%
• Meckel’s Diverticulum: <1%
• Oesophagus: <1%
• Multiple sites may indicate Zollinger-Ellison syndrome (ZES).

Risk Factors for Peptic Ulcer Disease

• Older age
• Males more affected than females (GU 3:1, DU 4:1)
• Helicobacter pylori (HP) infection
• Use of aspirin, NSAIDs, and corticosteroids (primarily GU)
• Zollinger-Ellison syndrome
• Severe stress, burns, major surgery, trauma
• Hyperparathyroidism
• Genetic predispositions (e.g., DU and blood group O)
• Gastric cell hyperplasia

Peptic Ulcer Disease Types

• Gastric Ulcer (GU): Associated with aspirin, NSAIDs, hyperparathyroidism, and Zollinger-Ellison syndrome. Commonly found along the lesser curvature of the stomach, with approximately 80% of cases HP-positive. Mean age of onset: 50-60 years.
• Duodenal Ulcer (DU): Approximately four times more common than GU. Predominantly affects men (95% HP-positive). Mean age of onset: 30-40 years.

Clinical Presentation

• Epigastric discomfort, often with specific "pointing" signs.
• DU may present with pain radiating to the back.
• GU pain often worsens immediately after eating, whereas DU pain is typically worse when hungry or at night.
• Associated symptoms: dyspepsia, nausea, haematemesis, and melaena.

Complications

• Haemorrhage: Refer to management of upper GI haemorrhage.
• Perforation: More common with DU, presenting with sudden localized pain that may become generalized, along with a rigid abdomen and free air under the diaphragm. Urgent laparotomy is typically required.
• Gastric Outlet Obstruction: Causes projectile vomiting, succussion splash, and hypochloraemic hypokalaemic metabolic alkalosis. Treatment includes fluid resuscitation, acid suppression, and possibly stenting or surgery.
• Recurrence: Risk of further ulcer development.

Investigations

• H. pylori Testing: Options include:
  • Urea Breath Test: Detects radioactive carbon from H. pylori urease activity.
  • IgG Serology: Indicates past infection; remains positive after eradication.
  • Stool Antigen Test: Non-invasive detection of H. pylori.
  • CLO Test (Endoscopy): Detects urease activity; color change from yellow to red indicates infection.
• OGD (Oesophagogastroduodenoscopy): Biopsies, especially in cases with suspected gastric ulcers or malignancy, are recommended. HP testing is also performed.
• Follow-Up OGD: For gastric ulcers, repeat at 6 weeks to rule out malignancy.
• HP Eradication Confirmation: Repeat testing at 6 weeks post-treatment.

Management

• Lifestyle Modifications: Stop smoking, reduce alcohol intake.
• HP-Positive: Eradication therapy achieves over 90% healing; continued PPI usually unnecessary.
• HP-Negative: Discontinue aspirin and NSAIDs if implicated; use proton pump inhibitors (PPIs) for acid suppression.
• Surgical Intervention: Now rare except in cases of uncontrolled bleeding or perforation. Surgical management includes underrunning bleeding vessels or using an omental patch for duodenal perforations.

Link to relevant diagram

Surgical intervention remains reserved for emergencies, such as uncontrolled haemorrhage. Persistent bleeding or spurting vessels that do not respond to adrenaline/epinephrine at endoscopy are indications for surgical intervention.