peptic ulcers - aetiology, pathophysiology + clinical features

what are the two types of peptic ulcers?

gastric and duodenal

what is the definition of an erosion?

superficial/partial break within epithelium or mucosal surface

what is the defintion of an ulcer?

deep break through full thickness of epithelium or mucosal surface

what is the estimated lifetime prevalence of peptic ulcers?

5-10%

what are the 2 main causes of peptic ulcers?

- H. pylori
- medications

what medications can cause peptic ulcers? (3)

- NSAIDs
- corticosteroids
- alcohol

what are other causes of peptic ulcers? (4)

- Zollinger-Ellsion syndrome
- acute stress
- malignancy
- inflammatory (e.g. Crohn's)

what is Zollinger-Ellison syndrome?

cancer of G cells which causes an increase in gastrin release

what is H. pylori?

helicobacter pylori - gram negative curved bacilli

what percentage of peptic ulcers is H. pylori associated with?

95% - duodenal ulcers
70-80% - gastric ulcers

how is H.pylori successful at replicating in the stomach? (3)

- contains enzyme urease which converts urea into ammonia and water
- ammonia acts as a buffer to H⁺ ions in stomach acid
- this raises the pH of stomach and allows bacterium to survive

how else does H.pylori disrupt stomach? (3)

releases cytokine CagA:
- which inhibits mucous production
- so less protection of stomach epithelium
destroys D-cells:
- less somatostatin released
- less inhibtion of HCl production
increases pH in area surrounding infection:
- G-cells detect increase in pH and stimulate parietal cells to release more HCl

how do NSAIDs cause peptic ulcers?

inhibit COX-1 (and COX-2) which reduces the production of prostaglandins

what do COX-1 and COX-2 usually do in the stomach?

acts as enzymes to catalyse production of mediators like prostaglandins from arachidonic acid

what do prostaglandins usually do in the stomach?

- stimulate epithelial cells to secrete mucous and bicarbonate
- cause inflammation
- inhibit gastric acid production
- inhibit and stimulate gastric motility

therefore what happens when NSAIDs inhibit COX-1 (and 2)? (3)

- causes decreases mucous production so less protection of stomach epithelium
- decreased bicarbonate production so less available to neutralise stomach acid
- reduced inflammation when erosion/damage occurs

what are the symptoms of peptic ulcers? (5)

- epigastric pain
- dyspepsia (e.g. distension + bloating)
- heartburn
- nausea
- vomiting

what are the signs of peptic ulcers?

epigastric tenderness

how could a patient present acutely with peptic ulcers?

- upper GI bleed
- perforation

what would be the signs of an upper GI bleed from peptic ulcer? (2)

- haematemesis +/- melaena
- features of shock

what is malaena?

black coloured stools from GI bleeding

what would be the signs of perforation of peptic ulcer? (4)

- acute, severe abdominal pain + tenderness
- localised or generalised guarding
- features of shock
- free air under diaphragm

what are some differences between gastric and duodenal ulcers?

G - not relieved/worsened by eating (weight loss)
D - relieved temporarily after eating (weight gain)
G - more likely to be associated with vomiting
D - more likely associated with eosinophil aggregation

where are gastric ulcers most likely found?

on the lesser curvature between antrum and fundus