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.  
π Definitions
- Peptic Ulcer: A mucosal break β₯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).
βοΈ 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 β mucosal damage and increased acid (especially in the duodenum).
- NSAIDs block prostaglandin synthesis β reduced mucus and bicarbonate, impaired healing.
- Autoimmune gastritis causes parietal cell destruction β achlorhydria, pernicious anaemia, and β risk of gastric cancer.
π Aetiology & Risk Factors
- π¨β𦳠Older age, male sex (DU:M = 4:1).
- π¦  H. pylori infection β present in ~95% of duodenal and ~80% of gastric ulcers.
- π Medications β NSAIDs, aspirin, corticosteroids.
- π₯ Severe physiological stress β burns, sepsis, trauma, major surgery (βstress ulcersβ).
- β‘ ZollingerβEllison syndrome (gastrinoma β massive acid hypersecretion).
- 𧬠Genetic predisposition β DU more common in blood group O.
- 𦴠Hyperparathyroidism β hypercalcaemia stimulates gastrin and acid secretion.
- π· Lifestyle factors β smoking, alcohol, diet play contributory roles.
π Common Sites
- Duodenum: ~80% (classically anterior wall of first part).
- Stomach: ~19% (lesser curvature).
- Both sites: ~5%.
- Oesophagus or Meckelβs diverticulum: <1%.
π¬ 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 β B12 deficiency, β risk of gastric carcinoma.
- Chemical gastritis: Reflux of bile salts after gastric surgery.
π©Ή 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.
β οΈ Complications
- Haemorrhage: Most common. May cause haematemesis/melaena, shock, iron-deficiency anaemia.
- Perforation: Especially DU. Sudden severe pain, rigid βboard-likeβ 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.
π§ͺ 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).
π Management
- Lifestyle: Stop smoking, limit alcohol, avoid NSAIDs/aspirin.
- H. pylori-positive: Triple therapy (PPI + clarithromycin + amoxicillin/metronidazole) for 7β14 days.
- H. pylori-negative: PPI or H2 blocker for 4β8 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 β Peptic Ulcer Disease & Gastritis in Adults
- Case 1 β Duodenal ulcer π: 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 β Gastric ulcer β οΈ: 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 β H. pylori-associated gastritis π¦ : 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 β Haemorrhagic gastritis (NSAID) π: 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 β Stress-related erosive gastritis π₯: 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 β Perforated duodenal ulcer β‘: 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 β Gastric outlet obstruction (pyloric stenosis) π§: 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 π©Ί: Major complications of PUD include:
- π΄ Haemorrhage β haematemesis, melaena, anaemia.
- β‘ Perforation β peritonitis, free air under diaphragm.
- π§ Gastric outlet obstruction β persistent vomiting, metabolic alkalosis, succussion splash.
- ποΈ Malignant transformation (gastric ulcers) β always biopsy and repeat endoscopy.
Management ranges from PPI and eradication β endoscopy β surgery depending on severity and complication.