GI Week and Toby (Old Case maybe need to know drugs)

Question 1

Apomorphine drug class

Answer 1

D-2 Dopamine receptor agonist

Question 2

Apomorphine mechanism of action

Answer 2

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

Question 3

bismuth subsalicylate drug class

Answer 3

(aka pepto bismol) Drug class: None Given

Question 4

bismuth subsalicylate mechanism of action

Answer 4

bismuth: absorbs bacterial enterotoxins and endotoxins and has GI protective effect salicylate: has anti prostaglandin and anti secretory activity in intestine

Question 5

butorphanol drug class

Answer 5

(Aka torbugesic) Drug Class: Synthetic Opiod agonist-antagonist analgesic

Question 6

cimetidine drug class

Answer 6

H2-histamine receptor antagonist

Question 7

cimetidine mechanism of action

Answer 7

-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

Question 8

lactulose drug class

Answer 8

synthetic sugar

Question 9

lactulose mechanism of action

Answer 9

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

Question 10

loperamide drug class

Answer 10

(aka as immodium) opiod

Question 11

loperamide mechanism of action

Answer 11

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

Question 12

metaclopramide drug class

Answer 12

D-2 dopamine receptor antagonist

Question 13

metaclopramide mechanism of action

Answer 13

inhibits D2 dopamine receptors in CTZ which normally-> relays info of stimulation to emetic center ->stimulation V+ so inhibit them inhibit V+

Question 14

butorphanol mechanism of action

Answer 14

competitive mu receptor antagonist, exerts analgesic effects by acting as agonist at kappa receptor

Question 15

midazolam drug class

Answer 15

short acting hypnotic-sedative benzodiazepine drug with anxiolytic and amnestic properties

Question 16

midazolam mechanism of action

Answer 16

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

Question 17

omeprazole drug class

Answer 17

proton pump inhibitor

Question 18

omeprazole mechanism of action

Answer 18

-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

Question 19

PEG 3350 drug class

Answer 19

(aka miralax) Drug Class: Osmotic laxative

Question 20

PEG 3350 mechanism of action

Answer 20

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

Question 21

Propofol drug class

Answer 21

ultra-short acting parenteral anesthetic in the US

Question 22

Propofol mechanism of action

Answer 22

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

Question 23

sucralfate drug class

Answer 23

mucosal protectant

Question 24

sucralfate mechanism of action

Answer 24

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)