Gastric ulcers Flashcards
What is a H. pylori infection?
Gram-negative urease producing bacterium
Found in gastric antrum and gastric metaplasia in the duodenum
Found in greatest numbers under the mucous layers
Oral-oral or faeco-oral mainly in childhood
More common in older population
Cure of it stops duodenal ulcer disease
Why do people get duodenal ulcers?
Increased acid secretion (parietal cell mass and secretion)
Smoking impairs gastric mucosal healing
H. pylori produces toxins
Decreased inhibition of acid secretion possibly by H. pylori damaging somatostatin-producing cells in the antrum
More common in blood group O
What are gastric ulcers?
Associated with gastritis affecting the body as well as the antrum of the stomach
Parietal cell damage occurs so that acid production is normal or low
Local epithet damage by cytokines
What are the features of a duodenal ulcer?
Found in the duodenal cap
Surrounding mucosa is inflamed, haemorrhagic, friable
Pain classically occurs at night and is worse when hungry
Vomiting is infrequent but relieves pain
How is H. pylori diagnosed?
13C urea breath test
Serological tests detect IgG antibodies
Stool test
Endoscopy (rapid urease test, culture, histology)
What are the complications of a peptic ulcer?
Haemorrhage Perforation (DU more common, into peritoneal cavity) Pyloric stenosis or obstruction (projectile vomiting huge volumes)
What are other H. pylori associated diseases?
Gastric adenocarcinoma
Gastric B cell lymphoma
What causes gastropathy?
Epitheal/endothelial damage in the mucosa, little or no accompanying inflammation
Caused by aspirin, NSAIDs and alcohol use
Aetiology of peptic ulcer disease
Helicobacter Pylori infection (90% of duodenal, 70% of gastric)
NSAIDs (30%)
Zollinger-Ellison syndroms: non-insulin secreting islet cell tumour of pancreas secreting gastrin-like hormone –> excessive acid secretion
Smoking, coffee consumption, hepatic/renal failure
Peptic ulcer disease investigations
Urgent oesophago-gastro-duodenoscopy (OGD) if fit ALARMS55 criteria: biopsies (histology) & brushing (cytology)
If previous ulcer, assume H. Pylori infection + commence triple therapy
If not ALARMS55 + symptoms persist: H. Pylori investigation
13C Urea breath test: patient ingests 13C labelled urea –> H. Pylori urease enzyme metabolises to 13CO2 –> detected on breath
No antibiotics for 4w, no PPIs for 2w = false -ve
OR gastric biopsy added to urea solution + phenol red –> colour change with H. Pylori present
Differences between gastric and duodenal ulcers
Gastric: >55y, lesser curve of stomach, pain worse on eating, relieved by antacids
Duodenal: 4x more common than gastric, 90% <2cm from pylorus
Pain at night before meals, relieved by eating/drinking milk
Alcohol intake = risk factor
H. Pylori mechanism of association to peptic ulcers
Produces gastritis, mainly in gastric antrum, activation of inflammatory infiltrate
Increased acid secretion: increased gastrin, decreased somatostatin –> epithelial damage
Abnormal mucus production –> epithelial damage
Atrophic gastritis in body of stomach –> metaplasia (pre-malignant)
Causally associated with duodenal ulcers
Smoking mechanism of association to peptic ulcers
Impairs gastric mucosal healing
Nicotine increases acid secretion
NSAID mechanism of association to peptic ulcers
NSAIDs inhibit COX enzymes –> anti inflammatory as COX-2 isoform normally causes inflammatory prostaglandin synthesis
Adverse GI effects: inhibition of COX-1 in the stomach (responsible for production of prostaglandins that inhibit acid secretion and protect the mucosa)
Co-administration of PPIs or PG analogues (misoprostol) can diminish NSAID negative effects
Steroids = similar effect
