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.

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.

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 worsens immediately after eating, DU pain is 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