gastric acid secretion - disorders Flashcards
what is the mechanism of peptic ulcer formation
breakage of mucosal barriers
tissues exposed to erosion by Hcl and pepsin
factors responsible for acid secretion
histamine ach gastrin alcohol, smoking, caffeine NSAIDs H pylori
risk factors for peptic ulceration
gastric/duodenal H. pylori infection
how is h pylori acquired
childhood - distribution and colonisation determined by environmental and host factors
factors that prevent infection of gastric mucosa
mucus production peristalsis seamless epithelium - tight junctions fast cell turnover IgA secretion at mucosal surfaces
what prevents autodigestion of the stomach
secretion of alkaline mucus and HCO3
protein in food
tight cell junctions
prostaglandins E and I - inhibit acid secretion, enhance blood flow
how does h. pylori cause ulcers
penetrates ;) gastric mucosa, highly pathogenic with many virulence factors
increases gastrin secretion
virulence factors of H pylori
motility - moves close to epithelium
produces urease
what does urease do
converts urea to ammonia - buffers acid to allow survival of h pylori and produces CO2
what does gastrin do
stimulate HCl release
what does h pylori infection do to cell numbers
increases no of G cells, reduced number of antral D cells
what does the virulence factor CagA do
disrupt cell junctions
affects proliferation and differentiation
induces inflammation
tends to cause more severe gastritis
what does virulence factor VacA do
induces apoptosis
disrupts cell pathways
induces inflammation
modulates immune system eg allows h pylori to live in macrophages
what causes mucosal breakdown
increased gastric secretions - HCl and pepsin
what can aggravate peptic ulcers
regurgitated bile acids NSAIDs genetics smoking, alcohol, curry h pylori
where are some common locations of peptic ulcers
duodenal cap
junction of stomach antrum and body
distal oes
what are some diagnostic tests for suspected gastric ulcer
endoscopy histological exam test for h pylori stool antigen test urea breath test test for virulence factors
symptoms of peptic ulcer
anaemia nausea dyspepsia (indigestion) vomiting, incl blood epigastric pain
RFs for chronic peptic ulcer
hyperacidity duodenal refluc h pylori nsaids genes being male
causes of acute peptic ulcer
develops from areas of corrosive gastritis, sever stress or shock, or acute hypoxia of surface epithelium
outcomes of acute peptic ulcer
severe bleeding
healing w/o scarring
chronic peptic ulcerw
peptic ulcer complications
GI haemorrhage
peritonitis
narrowing of pyloric canal
what type of drugs are anti-secretory agents
h2 receptor antagonists
clinical uses of H2 receptor antagonists
peptic ulcer, reflex oesophagitis
mechanism of action for h2 receptor antagonists
inhibit histamine action at h2 receptors on PARIETAL cells
reduce secretion of gastrin and therefore pepsin
unwanted side effects of H2 receptor antagonists
diarrhoea, muscle cramps, transient rashes, hypergastrinaemia
side effects of cimetidine
gynaecomsatia in men - rare
inhibits P450 enzymes - decreased metabolism of anticoagulants and tricyclic antidepressants.
examples of PPIs used to treat gastric ulcers
omeprazole, lanzoprazole
clinical uses of PPIs
peptic ulcer, reflux oesophagitis
mechanism of PPIs
weak bases - inactive at neutral pH and irreversibly inhibit the H+/K+ATPase pump
decreases basal and food stimulated gastric acid secretion
drugs that protect the gastric mucosa
prostaglandins PGE2 and PGI2
what is misoprostol
a stable analogue of PGE1
what is the mechanism for misoprostol
inhibits basal and food-stimulated gastric acid secretion
inhibits histamine and caffeine induced secretion
increases mucosal blood flow and can augment the secretion of HCO3 and mucus