Peptic ulcer disease and Gastritis in Adults

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 should raise suspicion of cancer; around 10% of gastric ulcers are malignant.

📖 Definitions

• Peptic Ulcer: A mucosal break ≥5 mm penetrating into the submucosa, most often in the stomach or duodenum.
• Gastritis: Inflammation of the gastric mucosa, which may be acute (erosive, haemorrhagic) or chronic (H. pylori-related, autoimmune, chemical).

⚙️ Pathophysiology

• Ulcers develop when there is an imbalance between aggressive factors (acid, pepsin, bile salts, H. pylori, NSAIDs) and defensive factors (mucus, bicarbonate, prostaglandins, blood flow, cell regeneration).
• H. pylori induces chronic gastritis → mucosal damage and increased acid (especially in the duodenum).
• NSAIDs block prostaglandin synthesis → reduced mucus and bicarbonate, impaired healing.
• Autoimmune gastritis causes parietal cell destruction → achlorhydria, pernicious anaemia, and ↑ risk of gastric cancer.

📊 Aetiology & Risk Factors

• 👨‍🦳 Older age, male sex (DU:M = 4:1).
• 🦠 H. pylori infection – present in ~95% of duodenal and ~80% of gastric ulcers.
• 💊 Medications – NSAIDs, aspirin, corticosteroids.
• 🔥 Severe physiological stress – burns, sepsis, trauma, major surgery (“stress ulcers”).
• ⚡ Zollinger–Ellison syndrome (gastrinoma → massive acid hypersecretion).
• 🧬 Genetic predisposition – DU more common in blood group O.
• 🦴 Hyperparathyroidism → hypercalcaemia stimulates gastrin and acid secretion.
• 🍷 Lifestyle factors – smoking, alcohol, diet play contributory roles.

📍 Common Sites

• Duodenum: ~80% (classically anterior wall of first part).
• Stomach: ~19% (lesser curvature).
• Both sites: ~5%.
• Oesophagus or Meckel’s diverticulum: <1%.

🔬 Types of Gastritis

• Acute erosive gastritis: Alcohol, NSAIDs, stress-related mucosal damage.
• Chronic H. pylori gastritis: Most common, associated with DU and gastric adenocarcinoma.
• Autoimmune (Type A) gastritis: Antibodies to parietal cells and intrinsic factor → B12 deficiency, ↑ risk of gastric carcinoma.
• Chemical gastritis: Reflux of bile salts after gastric surgery.

🩹 Clinical Presentation

• Epigastric pain: sharp, burning, or gnawing.
• GU: Pain worsens soon after eating.
• DU: Pain relieved by food, worsens at night or when fasting.
• Other: nausea, bloating, dyspepsia, haematemesis, melaena.
• Gastritis often presents with epigastric discomfort, nausea, vomiting; may be silent until bleeding occurs.

⚠️ Complications

• Haemorrhage: Most common. May cause haematemesis/melaena, shock, iron-deficiency anaemia.
• Perforation: Especially DU. Sudden severe pain, rigid “board-like” abdomen, free air under diaphragm.
• Gastric outlet obstruction: Vomiting, early satiety, metabolic alkalosis.
• Malignancy: 10% of GU are malignant; chronic H. pylori gastritis predisposes to gastric carcinoma and MALT lymphoma.

🧪 Investigations

• H. pylori detection: Urea breath test, stool antigen, rapid urease test (CLO), or histology.
• OGD (endoscopy): Gold standard. Biopsy required for all gastric ulcers to rule out malignancy.
• Follow-up OGD: At 6 weeks for gastric ulcers.
• Blood tests: FBC (anaemia), B12 (autoimmune gastritis), calcium (hyperparathyroidism).

💊 Management

• Lifestyle: Stop smoking, limit alcohol, avoid NSAIDs/aspirin.
• H. pylori-positive: Triple therapy (PPI + clarithromycin + amoxicillin/metronidazole) for 7–14 days.
• H. pylori-negative: PPI or H2 blocker for 4–8 weeks.
• Complications: Endoscopic therapy (adrenaline, clips) for bleeding. Omental patch repair for perforation. Stenting/surgery for obstruction.
• Gastritis: Remove offending cause (alcohol/NSAIDs), PPI for symptoms, treat H. pylori if present, B12 replacement in autoimmune gastritis.

Cases - Peptic Ulcer Disease & Gastritis in Adults

• Case 1 - Duodenal ulcer 🌙: A 40-year-old man presents with burning epigastric pain that improves after eating but returns at night, waking him from sleep. He takes NSAIDs for chronic back pain. OGD: duodenal ulcer. Diagnosis: PUD (duodenal, NSAID-related). Managed with H. pylori eradication (if positive), PPI, and stopping NSAIDs.
• Case 2 - Gastric ulcer ⚠️: A 65-year-old woman presents with epigastric pain and early satiety. Pain worsens with eating. She has weight loss and anaemia. OGD: gastric ulcer with irregular edges. Biopsy: negative for malignancy, H. pylori positive. Diagnosis: gastric ulcer due to H. pylori. Managed with eradication therapy and repeat endoscopy to confirm healing.
• Case 3 - H. pylori-associated gastritis 🦠: A 35-year-old woman reports bloating, nausea, and intermittent epigastric discomfort. She has no red-flag symptoms. Urea breath test: positive for H. pylori. Diagnosis: chronic gastritis due to H. pylori. Managed with triple therapy (PPI + clarithromycin + amoxicillin/metronidazole).
• Case 4 - Haemorrhagic gastritis (NSAID) 💊: A 58-year-old man presents with melaena and epigastric pain. He has been taking ibuprofen for osteoarthritis. Hb 8.6 g/dL, haemodynamically stable. OGD: diffuse erosive gastritis with multiple bleeding points. Diagnosis: NSAID-induced haemorrhagic gastritis. Managed with IV PPI, endoscopic haemostasis, and stopping NSAIDs.
• Case 5 - Stress-related erosive gastritis 🏥: A 46-year-old man in ITU after major trauma develops coffee-ground aspirates from his NG tube. Hb falls by 2 g/dL. OGD: multiple erosions in the gastric body. Diagnosis: stress-related erosive gastritis. Managed with IV PPI, sucralfate, and continued ITU supportive care.
• Case 6 - Perforated duodenal ulcer ⚡: A 48-year-old man with a history of untreated dyspepsia presents with sudden, severe epigastric pain radiating to the shoulder. Exam: rigid, board-like abdomen with absent bowel sounds. Erect CXR: free air under the diaphragm. Diagnosis: perforated duodenal ulcer. Managed with urgent resuscitation, IV antibiotics, and surgical repair (Graham patch).
• Case 7 - Gastric outlet obstruction (pyloric stenosis) 🚧: A 60-year-old man with long-standing PUD presents with persistent vomiting, early satiety, and weight loss. Exam: succussion splash in the epigastrium. Bloods: hypokalaemic, hypochloraemic metabolic alkalosis. OGD: scarred pyloric channel with narrowing. Diagnosis: pyloric stenosis secondary to chronic gastric ulcer. Managed with NG decompression, IV fluids/electrolyte correction, and surgical gastrojejunostomy after optimisation.

Teaching Point 🩺: Major complications of PUD include:

• 🔴 Haemorrhage - haematemesis, melaena, anaemia.
• ⚡ Perforation - peritonitis, free air under diaphragm.
• 🚧 Gastric outlet obstruction - persistent vomiting, metabolic alkalosis, succussion splash.
• 🎗️ Malignant transformation (gastric ulcers) - always biopsy and repeat endoscopy.