Flashcards in Pharm Deck (50):
H2 blockers MOA
reversibly inhibit H2 receptors of gastric parietal cells (decrease acid secretion)
mild and intermittent GERD first line tx
OTC PPI, H2RA, antacid
you should consider rx strength PPI if GERD lasts longer than how long?
how long do they take it initially?
increase pH of stomach (neutralize existing acid); decreased activation of pepsinogen
can calcium carbonate be used in preggers?
you might not want to give sodium bicarb to patients with heart failure. why?
can cause Na overload, fluid retention
which antacid has the longest duration but slightly slower onset
H2 receptor antagonist place in therapy
mild/moderate and FREQUENT sxs
what H2 receptor blocker should you NEVER use d/t drug-drug interactions
cimetidine (CYP inhibitor)
do you need to adjust H2 receptors for renal function
irreversibly inhibit H+/K+ ATPase pump in parietal cells
what should you use for frequent GERD and erosive disease?
PPIs are enteric coated. what pt education relates to this?
do NOT crush tablets
what risks are associated with PPIs (newer data)
2. c.diff infections
what's a big drug-drug interaction with omeprazole & esomeprazole?
antacids, H2RA, PPI ... which class is associated with constipation & diarrhea
if patient has ESRD, what should you be worried about with antacids?
your pt is on daily PPI, but he is having sxs at night. what can you tell him?
take it BID
1st line for PUD?
x 14 days
if positive h.pylori dx, do you have to treat?
your pt is being treated for heliobacter and has dark tongue and stool. what med is responsible?
pt education for metronidazole?
avoid ETOH during and 72 hours AFTER (disulfiram rxn)
pt takes nsaids chronically. are they more at risk for duodenal or gastric ulcers?
when should you consider adding a PPI for pts taking NSAIDs?
moderate risk (age >65, high dose of NSAID, hx ulcer, concurrent ASA, steroids, anticoags)
high risk: hx of ulcer and multiple risk factors, steroids, anticoags
sucralfate (carafate) MOA and indication
forms complex that covers ulcer; indicated ONLY for duodenal ulcers
main ppx drug for stress ulcer prophylaxis (esp in ICU)
heart AE of clarithromycin
what meds can cause constipation?
can saline laxatives be used on a daily basis?
no (can cause dependency, esp. if enema route)
what might occur if mineral oil is routinely used (especially in elderly or children <6)?
aspiration and lipoid pneumonia risk
emollient laxative: mush or push?
only a mush (ie, prevent constipation, but doesn't move poo along)
bulk laxatives MOA
1. increase stool bulk
2. decrease transit time
3. increase motility
saline/osmotic laxatives MOA
pulls water into intestines along osmotic gradient
stimulant laxatives MOA
surfactant action; secretion
antimotility agents should not be used for what type of diarrhea?
acute bacterial due to toxic megacolon risk
what is the MOA of loperamide, diphenoxylate/atropine, paregoric
works like an opioid; slows intestinal transit
what is the MOA of dicyclomine and hycoscyamine?
anti-cholinergic/ antimuscarinic; blocks activity
with N/V, what types of meds are good for motion sickness?
block D2 receptors
is IV preferred with phenothiazines? why or why not?
severe tissue damage risk
extrapyramindal sxs, sedation, anticholinergic effects, QTc prolongation, neuroepiletic malignant syndrome, seizure
what are 4 5HT3 receptor antagonists?
granisteron (PO), ondansetron (PO), palonosteron (IV),
what N/V treatment is SOC for CINV, PONV, RINV?
5HT3 receptor antagonists
what is useful in delayed CINV (3)
2. neurokinin-1 antagonists
3. serotonin inhibitors
what N/V drug is best in gastroparesis?
what N/V drugs are good for anticipatory N/V?
how does famotidine work?
reversibly inhibit H2
what does clopidogrel interact with?