GI pharm Flashcards

1
Q

Antacids: which are absorbable and adverse affects? non absorbable? characteristics?

A

Mg (diarrhea), Al (constipation), Ca (constipation) based.
NaHCO3 (alkalosis) based.
Rapid onset and short duration

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2
Q

H-2RAs: suffix? mechanism? when should they be taken?

A

-tidine. competitive inhibition. Taken before bedtime (NO EATING afterwards b/c food signal can overcome blockade)

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3
Q

H2RA drug interactions

A

cimetidine inhibits CYP450 (relevant for phenytoin, warfarin, theophylline b/c of narrow therapeutic window)

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4
Q

PPIs: suffix? mechanism? side effects?

A

-prazole. Taken up by parietal cell, protonated, excreted, covalent bond with H/K ATPase (body must make new pump to regain secretion).
Slight risk of C. diff

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5
Q

PPI: drug interactions

A

Omeprazole weakly interacts with phenytoin, warfarin, diazepam, CLOPIDOGREL

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6
Q

What do you use PPIs for?

A

GERD, as part of H. pylori triple therapy (PPI, clarithromycin, amoxicillin), peptic ulcers (idiopathic, NSAID related), bleeding ulcer

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7
Q

sucralfate: complications

A

problematic in pts with renal insufficiency due to Al. Works at acidic pH (don’t give with PPI, H2RA)

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8
Q

Alosetron: what is it? what do you use it for? why was it withdrawn?

A

5-HT3 antagonist. Used to tx women with SEVERE IBS-D.

Ischemic colitis, constipation, death

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9
Q

Drugs that cause constipation

A

verapamil, sucralfate, Ca or Al based antacids

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10
Q

Linaclotide: who not to give it to

A

Children under 6.

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11
Q

How to treat opioid constipation

A

peripheral mu antagonists: methylnaltrexone, alvimopan

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12
Q

Sulfasalazine: mechanism of activation and action. Used to treat?

A

split by colonic bacteria into sulfapyridine (toxic) and 5-ASA which has local anti-inflamm effects for ulcerative colitis

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