Peptic Ulcers



Peptic ulcers involve ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum (duodenal ulcer). Duodenal ulcers are more common.

Pathophysiology

The stomach mucosa is prone to ulceration from:

  • Breakdown of the protective layer of the stomach and duodenum
  • Increase in stomach acid

There is a protective layer in the stomach comprised of mucus and bicarbonate secreted by the stomach mucosa. This protective layer can be broken down by:

  • Medications (e.g. steroids or NSAIDs)
  • Helicobacter pylori

Increased acid can result from:

  • Stress
  • Alcohol
  • Caffeine
  • Smoking
  • Spicy foods

Presentation

  • Epigastric discomfort or pain
  • Nausea and vomiting
  • Dyspepsia
  • Bleeding causing haematemesis, “coffee ground” vomiting and melaena
  • Iron deficiency anaemia (due to constant bleeding)

TOM TIP: In your MCQ exams, eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.

Management

Peptic ulcers are diagnosed by endoscopy. During endoscopy a rapid urease test (CLO test) can be performed to check for H. pylori. Biopsy should be considered during endoscopy to exclude malignancy as cancers can look similar to ulcers during the procedure.

Medical treatment is the same as with GORD, usually with high dose proton pump inhibitors. Endoscopy can be used to monitoring the ulcer to ensure it heals and to assess for further ulcers.

 

Complications

Bleeding from the ulcer is a common and potentially life threatening complication.

Perforation resulting in an “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic).

Scarring and strictures of the muscle and mucosa. This can lead to a narrowing of the pylorus (the exit of the stomach) causing difficulty in emptying the stomach contents. This is known as pyloric stenosis. This presents with upper abdominal pain, distention, nausea and vomiting, particularly after eating.

Last updated April 2019
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