Drugs Employed in GI Disease 1 Flashcards
the 2 causes for ulcers
increased acid production and decreased mucosal resistance
3 interventions for ulcers
- neutralize acid
- decrease acid production
- increase mucosal resistance
calcium carbonate
antacid. reacts w/ HCl to make calcium chloride and carbonic acid. side effect is constipation. use in combo with magnesium compounds
sodium bicarbonate
antacid. rarely used because of systemic alkalosis. high sodium content
magnesium hydroxide/magnesium carbonate
antacid. may cause magnesium toxicity in presence of renal disease. adverse effects include diarrhea. can cause bradycardia with renal problems.
aluminum hydroxide
antacid. combines with HCl to make aluminum chloride and water. aluminum Cl -> aluminum phosphate which cant be absorbed. doesnt disturb serum electrolyte or pH. useful in renal failure patients. may have protective effect on mucosa. causes constipation
simethicone
defoaming agent in antacids. decreases gas bubbles/bloating
sodium
used with antacids. small amounts, but can cause concern in patients with edema and hypertension.
anticholinergic agents effect
vagotomy type of effect. reduction of HCl secretion, spasmolytic effect. adverse effects include dry mouth, blurry vision, atony of bladder, constipation, drowsiness, confusion.
anticholinergic drugs + when you take them
atropine, propantheline, dicyclomine. administered 30 minutes before meals and at bedtime.
blockade of histamine H2 receptor
lower acid secretion by blocking H2 histamine receptors on parietal cells. decrease basal and food stimulated acid secretion. dont need to be given in relationship to meals
H2 receptor antagonists list
cimetidine, ranitidine, famotidine, nizatidine. inhibi 50-80% of 24 hour acid secretion.
other use for H2 receptor antagonists
can be used prophylactically to decrease stress ulcers in ICU and burn patients.
what happens if you abruptly stop h2 blockers?
hyperproduction of acid! ween off slowly
H2 blocker adverse effects
messes with p450 so can interfere with metabolism of other drugs. headache, lethargy, confusion, depression. severe side effects uncommon
list the 6 H/K ATPase inhibitors (proton pump inhibitors)
omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole, dexlansoprazole
which proton pump inhibitors can be given IV
pantoprazole. doesn’t mess with p450.
proton pump inhibitor mechanism of action
accumulate selectively in the highly acid environment of the canniliculus. protonated to a reactive thiophillic sulfenamide that binds to cysteine 813 in the alpha subunit of the enzyme. non competitive inhibitors. better pain relief and faster ulcer healing rates than with H2 antagonists. will heal H2 refractory ulcers
adverse effects of PPIs
headache, gynecomastia, inhibition of P450, gastric hyperplasia possible in long term stuff.
factors impairing mucosal resistance to acid
smoking, genetics, stress, NSAIDs, H. pylori
bismuth salts
in acid environment it forms crystals that precipitate on the ulcer crater. lower ulcer recurrence rate than with h2 antagonists
sucralfate
aluminum hydroxide complex, activates in acid environment, binds to ulcerated tissue. as effective as H2 antagonists.
what type of ulcers are prostaglandin E2 analogs
used in people with NSAID ulcers, because duodenal ulcer patients already hyperproduce E2 prostaglandins
misoprostol
prostaglandin E2 analog. decrease acid production, increase mucous and bicarb secretion. less effective than H2 blockers when used solo. approved for prevention of NSAID ulcers. can cause diarrhea, dont use in pregnant bitches!
