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19 Cards in this Set
- Front
- Back
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Histamine
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causes inc in intracellular AC & cAMP -> activation of K+H+ATPase
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Cholinergic drugs
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cause influx of Ca2+ -> activates K+H+ATPase
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Gastrin
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cause influx of Ca2+ -> activates K+H+ATPase
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antacid therapy
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relieves pain, heals ulcers, high dose required
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anticholinergic agents
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dec HCL secretion, spasmolytic effect
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H2 receptor blockers
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inhibit 50-80% HCL secretion (basal & post-prandial)
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H+K+ATPase inhibitors (PPIs)
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sulfhydryl gp activated by acid -> noncompetative inhibition >90% HLC secretion (post-prandial only), pain relief
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bismuth salts
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forms crystals in acid enviro -> precipitate on ulcer crater ~lower recurrence than w/ H2 antagonists
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sucralfate
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aluminum hydroxide complex of sucrose, binds to ulcerated tissue in acidic enviro ~equal to H2 antagonists in healing & prevention
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PGD analogs
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inhibit cAMP by direct action on G protein but less effective than H2 antagonists but effective in NSAID use
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phenothiazine (neuroleptic class)
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suppresses chemoreceptor trigger zone
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metochlopramide (benzamide derivative)
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pro-motility and anti-emetic through CNS and peripheral dopaminergic receptor antagonism
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tetrahydro Cannabinol
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suppresses CRTZ by anticholinergic mech
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anticholinergic antidiarrheals
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relaxation of smooth muscle
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Loperamide
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increases rectal tone and disrupts peristalsis
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Diphenoxylate
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contraction of circular muscle segmentation
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codeine sulfate
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contraction of circular muscle segmentation
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colloids & pectins
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absorb water (do not prevent dehydration)
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anti-inflammatories for IBD
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use 5-amino-salicylic acid
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