Peptic Ulcer Disease (PUD)
PUD Definition
  • Peptic Ulcer Disease (PUD) refers to mucosal erosions extending through the muscularis mucosae, occurring most commonly in the stomach (gastric ulcers) and duodenum (duodenal ulcers). It results from an imbalance between mucosal protective factors (e.g., mucus, bicarbonate, prostaglandins) and aggressive factors (e.g., gastric acid, pepsin, Helicobacter pylori infection, NSAIDs).
PUD Epidemiology, Risk Factors & Prevention
  • Peptic Ulcer Disease Clinical Epidemiology
  • Risk Factors: Helicobacter pylori infection is the primary risk factor, implicated in over 90% of duodenal ulcers and 70% of gastric ulcers. Long-term NSAID use, including aspirin, increases ulcer risk by inhibiting prostaglandin synthesis, reducing gastric mucosal protection. Other risk factors include smoking (which impairs mucosal healing), excessive alcohol consumption, chronic stress, Zollinger-Ellison syndrome (gastric acid hypersecretion), and a family history of ulcers.
  • Prevention: Reducing NSAID use or co-prescribing proton pump inhibitors (PPIs) for high-risk patients can lower ulcer risk. Eradicating H. pylori in infected individuals reduces recurrence. Smoking cessation and moderating alcohol intake contribute to mucosal protection. Stress management and avoiding excessive caffeine consumption may also help prevent ulcer formation.
PUD Pathophysiology
  • The development of PUD is a result of the imbalance between mucosal defence and damaging agents. Key factors include:
    • H. pylori infection: This bacterium colonises the gastric mucosa, causing inflammation and weakening the protective mucus layer, allowing gastric acid to damage the tissue.
    • NSAIDs: These medications inhibit cyclooxygenase (COX) enzymes, decreasing the production of prostaglandins, which are essential for maintaining the gastric mucosal barrier.
    • Gastric acid hypersecretion: Conditions like Zollinger-Ellison syndrome cause excessive acid production, overwhelming the mucosal defences.
    • Other factors: Smoking, alcohol use, and stress have been linked to increased risk by impairing mucosal defences.
PUD Time Course
  • Initial phase: Symptoms may develop gradually over weeks to months, with periods of symptomatic relief between episodes of pain.
  • Chronic phase: Long-term, intermittent symptoms may continue if underlying factors (e.g., H. pylori or NSAID use) are not addressed. Complications like bleeding or perforation can occur at any stage.
  • Acute exacerbation: Sudden complications such as bleeding, perforation, or obstruction can occur, especially in untreated or poorly managed cases.
PUD Symptoms
  • Epigastric pain: This is the most common symptom, often described as a burning or gnawing pain, which may improve with food (duodenal ulcer) or worsen with food (gastric ulcer). The pain results from acid exposure to the damaged mucosa.
  • Bloating and fullness: Due to impaired gastric emptying and irritation of the stomach lining.
  • Nausea and vomiting: These symptoms occur due to irritation and inflammation of the gastric mucosa, especially in gastric ulcers.
  • Haematemesis or melaena: Occurs in cases with ulcer bleeding. The blood arises from erosion into gastric vessels.
  • Asymptomatic: Up to 20% of patients, particularly the elderly or those taking NSAIDs, may have ulcers without noticeable symptoms until complications arise.
PUD Signs
  • Epigastric tenderness: Localised pain on palpation due to inflammation or ulceration of the stomach or duodenal wall.
  • Pallor: May indicate anaemia from chronic blood loss in ulcer bleeding.
  • Hypotension or tachycardia: Suggestive of significant bleeding or perforation.
  • Rebound tenderness/guarding: These are signs of peritonitis, often indicating perforation of the ulcer.
PUD Red Flag Features
  • Haematemesis (vomiting blood): Suggests active ulcer bleeding, potentially leading to haemorrhagic shock if untreated.
  • Melaena (black, tarry stools): Indicates digested blood from an upper GI bleed.
  • Sudden severe abdominal pain with rigidity: May indicate perforation, causing peritonitis and requiring urgent surgical intervention.
  • Unexplained weight loss: May indicate malignancy or chronic disease-related malnutrition.
PUD Atypical Presentations
  • Silent PUD: Common in older adults or patients on NSAIDs, who may not experience typical pain but present with complications like bleeding or perforation.
  • Chest pain: Occasionally, PUD can mimic cardiac pain, leading to misdiagnosis as angina or myocardial infarction.
PUD Diagnostic Tests
  • Upper GI endoscopy: The gold standard for diagnosing PUD, allowing direct visualisation of ulcers and biopsies for H. pylori or malignancy. Ulcers appear as mucosal breaks with inflamed margins.
  • H. pylori testing: Non-invasive tests include urea breath test or stool antigen test, both detecting active infection.
  • FBC (Full Blood Count): May show anaemia due to chronic blood loss from ulceration.
  • Faecal occult blood test: May be positive in cases of chronic bleeding ulcers.
PUD Problem Representation
  • A 45-year-old male presents with a 3-month history of epigastric pain, worsened by meals, associated with bloating and occasional nausea. He has a history of NSAID use for chronic knee pain. On examination, epigastric tenderness is noted.
PUD Differential Diagnosis
  • Gastro-oesophageal reflux disease (GORD): GORD is characterised by heartburn and regurgitation, whereas PUD presents more commonly with localised epigastric pain and may not respond to acid suppression therapy as dramatically as GORD.
  • Gastric cancer: Weight loss and early satiety are more prominent, and endoscopy will reveal a mass or irregular ulcer rather than a smooth ulcer base as seen in PUD.
  • Chronic pancreatitis: Pain radiates to the back, worsens after meals, and is associated with malabsorption and steatorrhoea.
  • Biliary colic: The pain is more likely to be right upper quadrant, colicky, and associated with fatty food intake, without the epigastric burning characteristic of PUD.
PUD Treatment
  • Proton pump inhibitors (PPIs): First-line treatment to reduce gastric acid production (e.g., omeprazole 20-40 mg daily).
  • H. pylori eradication: Triple therapy (PPI + clarithromycin + amoxicillin or metronidazole) for 7-14 days if H. pylori positive.
  • Discontinuation of NSAIDs: Essential if NSAIDs are the underlying cause. Consider alternative analgesics like paracetamol.
  • Endoscopic therapy: For actively bleeding ulcers, endoscopy may be used for haemostasis via clips, coagulation, or injection therapy.
PUD Complications
  • Bleeding: Occurs in 15-20% of ulcers. Chronic blood loss may lead to anaemia, while acute bleeding can cause haemorrhagic shock.
  • Perforation: Occurs in about 5% of ulcers, leading to peritonitis. Surgical intervention is often required.
  • Gastric outlet obstruction: Scarring from chronic ulcers may lead to obstruction, causing persistent vomiting and weight loss.
  • Malignancy: Gastric ulcers, but not duodenal ulcers, carry a small risk of malignant transformation, particularly if non-healing despite treatment.

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