Internal Diseases and Therapy · MU Sofia

92. Peptic ulcer

Covers gastritis first, distinguishing acute transient mucosal inflammation from chronic gastritis, mainly driven by H. pylori, and how the stomach's protective mechanisms fail. It then moves to peptic ulcers, their causes and risk factors, typical pain patterns for gastric versus duodenal ulcers, investigation by gastroscopy, and medical and surgical management. A table summarises NHS guidance on gastritis types and treatments, and another gives NICE referral criteria for dyspepsia alongside a note on H. pylori testing. The note closes with a summary of acute bleeding ulcer management, including PPI dosing and scoring.

Inside: 3 sections · 4 labelled pictures · 2 tables · 14 flashcards · 6 min

Topic 93 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 3 sections, about 682 words (6 min of reading), with 14 flashcards.

In this note

  1. Gastritis
  2. Peptic ulcer
  3. Treatment of peptic diseases of the gastrointestinal tract

Gastritis

Acute gastritis

This is transient mucous inflammation that may be asymptomatic or cause epigastric pain, nausea and vomiting.

The stomach is a highly acidic environment, gastritis can occur when either the protective mechanisms of the stomach fail, or there is an increase in acid production. Protection mechanisms include:

  • Foveolar cells produce Mucin which prevents direct contact with the epithelium
  • Bicarbonate ion secretion by epithelial cells create neutral layer
  • Rich vascular supply delivers oxygen, bicarbonates and nutrients, while removing acid that has diffused into the lamina propria

Disruption to any of these elements (e.g. reduced mucin synthesis due to age) increases susceptibility, as do drugs such as NSAIDs which reduce bicarbonate availability, and ingestion of harsh chemical elements.

Chronic gastritis

Signs and symptoms typically less severe but more persistent than acute form. Nausea and upper abdominal pain can present. Most common cause is infection of H.pylori (see below) with atrophic gastritis due to autoimmune causes making up the remainder of cases.

H. Pylori increase the acid secretion and weaken defences in the stomach and as such increase risk of gastritis and ulcers. H. Pylori create urease, elevating local gastric pH and therefore allows it to survive, while simultaneously releasing toxins which increase gastric secretions.

Over time chronic gastritis can become pangastritis with multifocal atrophic gastritis and increased risk of adenocarcinoma.

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