10.1 GI pharmacology Flashcards
why can NSAIDs cause gastric/duodenal ulceration?
inhibit protective prostaglandin mechanism, so cAMP increases, protein kinase activates more and proton pump works more
how do combination products like gavsicon work?
antacid- buffers stomach acid
alginate- increase stomach content viscosity and reduces reflux
so a foamy protective layer is formed in stomach
ADRs of the salts in gaviscon
magnesium salt- diarrhoea
aluminium salt- constipation
contraindications for alginates/antacids
high sucrose so caution in DM
NA and k so caution in renal failure
DDIs for alginates/antacids
separate drug doses as can reduce absorption of other drugs
increase aspirin excretion via urine alkalinity
how do PPIs work?
irreversibly inhibit H/K ATPase in gastric parietal cells at fin al stage of pathway so significantly reduce acid secretion
DDIs for PPIs
omeprazole inhibits CYP= reduced clopidogrel action as less converted to active metabolite
increase effects of warfarin, phenytoin
what’s often co prescribed with PPIs?
long term NSAID/ steroid due to risk of ulceration
how to H2 receptor antagonists work?
inhibit H2 receptors so less histamine release so less cAMP and proton pump action
but only partial effect as there are still other routes to proton pump
ADRs for H2 receptor antagonists
maybe diarrhoea, headache
contraindications for H2 receptor antagonists
mask symptoms of gastro-oesophageal cancer
renal impairment
current situation with ranitidine
recalled due to carcinogenic contaminant, give lansoprazole upon patient review
triple therapy options for H pylori
lansoprazole+ clarithromhcin+ amoxicillin
or If allergic to penicillins
metronidazole instead
first line treatment for UC
aminosalicylates e.g. mesalazine
how do aminosalicylates work?
release 5-aminosalicylic acid at colon
