GUT- Gastric Acid Secretion: Disorders Flashcards
what is the mechanism of peptic ulcer formation
breakage of the mucosal barrier - possibly due to an imbalance between protective and damaging factors
exposure of the tissues to erosive effects on HCl and pepsin
what sites are affected by peptic ulcer formation
oesophagus, stomach, duodenum
what factors predispose to peptic ulceration
gastric and duodenal infection with H.Pylori
what factors prevent infection with H pylori
mucus production peristalasis and fluid movement seamless epitherlium with tight junctions fast cell turnover IgA secretion at mucosal surfaces Peyers Patches
what protective factors prevent autodigestion of the stomach
secretion of alkaline mucus and bicarbonate
protein content of food
presence of tight junctions
replacement of damaged cells
prostaglandins (E2 and I2) - these inhibit acid secretion and enhance blood flow (vasodilation)
how do NSAIDS contribute to gastric acid disorders
Aspirin inhibits cyclooxygenase - important for making prostaglandins
impairs the barrier properties of mucosa
supresses the gastric prostaglandin synthesis
decreases gastric blood flow
interferes with the repair of superficial injury
inhibits platelet aggregation
what is H.Pylori
gram negative, spiral shaped aerobic bacterium
penetrates the gastric mucosa (this is how it is able to survive under the harsh conditions of the stomach
what are the virulence factors of H. Pylori
motility - moves close to the epithelium
mucinase activity - produces urease (CagA) - inserts pathogenicity islands and confers ulcer forming potential
vacuolating toxin - alters the trafficking of intracellular protein in gastric cells
where are peptic ulcers common
duodenal cap stomach distal oesophagus Meckel's diverticulum after gastroenterostomy
what are the investigations for peptic ulcers
low does PPI
endoscopy
histological examination and staining of EGD biopsy
test for presence of H.Pylori (stool sample, urea breath test)
what are the clinical presentations of peptic ulcers
nausea vomiting (blood) - haematemesis epigastric pain - chest discomfort, weight loss melena (black tarry stools) anaemia
what are the complications of peptic ulcers
haemorrhage (GI bleeding)
perforation (peritonitis)
penetration (liver and pancreas may be affected) - causing leakage of luminal contents
narrowing of pyloric canal
malignant change is more likely with H.Pylori infection
what are examples of H2 receptor antagonists
cimetidine, ranitidine, famotidine, nizatidine
what are the clinical uses of H2 receptor antagonists
peptic ulcer, reflex oesophagitis
what is the mechanism of action of the H2 receptor antagonists
inhibit histamine action and the H2 receptor on parietal cells
reduce gastric acid secretion and as a consequence reduce pepsin secretion (the conversion of pepsin to pepsinogen needs hyperacidity)
inhibit histamine, ACh and gastrin stimulated acid secretion
decrease basal and food stimulated secretion by 90%
