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PH-GI02

Peptic ulcer disease

How Helicobacter pylori and NSAIDs tip the balance between acid and mucosal defence, what makes an ulcer deeper than an erosion, and why ulcers bleed, perforate or block the gastric outlet.

By the end, you can

  • Describe how the gastric and duodenal mucosa defends itself against acid and pepsin.
  • Explain how Helicobacter pylori and NSAIDs each weaken that defence, and how antral infection raises acid.
  • Distinguish an erosion from an ulcer by the layers of the wall it breaches.
  • Relate the site and depth of an ulcer to bleeding, perforation, penetration and outlet obstruction.
  • Recognise the classic appearance and layers of a chronic ulcer, its classifications and tests, and explain how each main treatment acts on the mechanism.

What it is

A peptic ulcer is a break in the lining of the stomach or duodenum that extends through the muscularis mucosae into the submucosa or deeper, caused when acid and pepsin overcome mucosal defence. Most are due to Helicobacter pylori infection or NSAID use; a shallower defect confined to the mucosa is an erosion.

3 types to tell apart
Duodenal ulcer
Usually in the first part of the duodenum. Typically linked to H. pylori infection of the antrum, which raises acid output.
Gastric ulcer
Often on the lesser curvature. Linked to NSAIDs or to H. pylori gastritis spreading through the body of the stomach; acid output is normal or low, so weakened defence is the main problem.
Erosion
A defect that stays within the mucosa, above the muscularis mucosae. It heals within days without a scar and rarely bleeds heavily.

Normal function

Acid, pepsin and the mucosal defence

The stomach makes a fluid strong enough to digest meat. Parietal cells in the glands of the and secrete hydrochloric acid; chief cells secrete pepsinogen, which acid converts to the protein-digesting enzyme pepsin. Gastrin from G cells in the , histamine and acetylcholine drive acid secretion; somatostatin brakes it.

The protects itself in layers. Surface cells secrete a gel of mucus with bicarbonate trapped beneath it, so the pH at the cell surface stays near neutral. Tight junctions stop acid passing between cells, damaged cells are replaced within days, and a rich blood flow removes acid that gets in. Prostaglandins, made by the enzyme cyclo-oxygenase (COX), sustain mucus, bicarbonate and blood flow.

The receives this acid. Bicarbonate from its own glands and from the pancreas neutralises it; the first part, the duodenal cap, meets the most acid.

Point to it on the model