GI Week and Toby (Old Case maybe need to know drugs) Flashcards
Apomorphine drug class
D-2 Dopamine receptor agonist
Apomorphine mechanism of action
stimulates D2 dopamine receptors in CTZ -> relays info to emetic center ->stimulation V+ - will have depressant effect on emetic center so don’t give multiple doses if first doesn’t work
bismuth subsalicylate drug class
(aka pepto bismol) Drug class: None Given
bismuth subsalicylate mechanism of action
bismuth: absorbs bacterial enterotoxins and endotoxins and has GI protective effect salicylate: has anti prostaglandin and anti secretory activity in intestine
butorphanol drug class
(Aka torbugesic) Drug Class: Synthetic Opiod agonist-antagonist analgesic
cimetidine drug class
H2-histamine receptor antagonist
cimetidine mechanism of action
-Competitive antagonist of H2 receptors that inhibit gastric acid secretion so inhibits basal and food stimulated acid secretion and promote healing of gastric and duodenal ulcers - Normally histamine released by ECL cells b/c gastrin or acetylcholine and histamine directly stimulates acid secretion by binding H2 receptors on parietal cells - by decreasing amount of gastric juice produced H2-blockers reduce amount of pepsin secreted
lactulose drug class
synthetic sugar
lactulose mechanism of action
synthetic disaccharide metabolized by bacteria in LI producing acetic, lactic, and formic acids which have osmotic effect drawing fluid into intestine by osmosis -> increase fluid content of feces -> intestinal distention and promotion of peristalsis
loperamide drug class
(aka as immodium) opiod
loperamide mechanism of action
synthetic opiate specifically targets GI tract w/o causing other effects act on mu and game receptors decreasing propulsive intestinal contractions increasing segmentation and increase GI sphincter tone; stimulate absorption of fluids, electrolytes, and glucose
metaclopramide drug class
D-2 dopamine receptor antagonist
metaclopramide mechanism of action
inhibits D2 dopamine receptors in CTZ which normally-> relays info of stimulation to emetic center ->stimulation V+ so inhibit them inhibit V+
butorphanol mechanism of action
competitive mu receptor antagonist, exerts analgesic effects by acting as agonist at kappa receptor
midazolam drug class
short acting hypnotic-sedative benzodiazepine drug with anxiolytic and amnestic properties
midazolam mechanism of action
bind and activate benzodiazepine receptor bidding site on game subunit of GABAa -> increase frequency of opening of Cl- ion channels -> decreased GABA required to open channels and hyperpolarization of postsynaptic neuron and decreased neuronal transmission -> CNS depression Also possible mechanisms: - antagonism of serotonin - diminished release or turnover of acetylcholine in CNS
omeprazole drug class
proton pump inhibitor
omeprazole mechanism of action
-prodrug activated in acid environment - gains access to parietal cell via systemic circulation -> accumulates in acidic canaliculi as weak base -> protein-catalyzed conversion to sulfenamide -> drug activation and prevents diffusion of drug across canalicular membrane -> activated drug binds H+-K+-ATPase irreversibly inactivating it (acid secretion will return to normal after new pump proteins are synthesized and inserted into luminal membrane) Role of parietal cell proton pump in molecular mechanism of acid secretion: - pump uses ATP hydrolysis to drive extrusion of H+ into lumen of gastric gland in exchange for K+; K+ recycled into lumen through symporter that caciltations secretion of Cl- into gastric lumen -> net increase HCl and increase of parietal cell pH -> passive uptake H2O and CO2 which = converted to HCO3- and H+ by carbonic anhydrase -> HCO3- leaves cell via CL- HCO3- exchanger in basalt membrane which replensihes intracell Cl- -> fuels net movement HCl (gastric acid) onto apical membrane
PEG 3350 drug class
(aka miralax) Drug Class: Osmotic laxative
PEG 3350 mechanism of action
Large molecular weight water-soluble polymer that forms hydrogen bonds with 100 molecules of H2O per molecule -> high osmotic pressures and preventing absorption of H2O out of lumen
Propofol drug class
ultra-short acting parenteral anesthetic in the US
Propofol mechanism of action
not well understood: - decreases rate of GABA dissociation from receptors -> increase opening of chloride channels -> hyperpolarization of postsynaptic cell membranes and inhibition of postsynatpci neurons -> hypnosis and amnesia
sucralfate drug class
mucosal protectant
sucralfate mechanism of action
Undergoes extensies cross-linking in acidic environment (pH <4) -> forms sticky polymer that adheres to epithelial cells and ulcer craters -> promotes ulcer healing and limits proton diffusion - also cytoprotective effects (local production prostaglandins and epidermal growth factor)
