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GI > Upper GI pharm > Flashcards

Upper GI pharm Flashcards

1
Q

misoprostol site of action

A

prostaglandin analog –> epithlial cell (mucus and bicarb), parietal cell (blocks cAMP –> blocked H secretion)

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2
Q

PPIs

A

omeprazole (prilosec), Lansoprazole (prevacid)

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3
Q

PPI mechanism of action

A

prodrug –> activated by H in parietal cells –> trapped in acidic secretory canniliculi –> irreversible inactivation of H/K ATPase

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4
Q

PPI absorption

A

rapid, highly protein-bound. bioavailability improved with enteric coating or NaHCO3.

give 1 hour before meals

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5
Q

PPI metabolism

A

first pass = CYP450

no accumulation in chronic renal failure

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6
Q

Indications for PPI

A

GERD, PUD, NSAID-induced ulcers, prevention of stress gastritis in ICU, Zollinger-Ellison syndrome

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7
Q

ADRs of PPIs

A

usually mild

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8
Q

DDIs of PPIs

A

omaprazole may inhibit conversion of antiplatelet agent clopidogrel to active form

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9
Q

H2 receptor antagonists

A

Ranitidine (Zantac), Cimetidine (Tagamet), Famotidine (Pepcid), Nizatidine (Axid)

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10
Q

H2 blocker use

A

best for blocking NOCTURNAL acid secretion

GERD, PUD, stress-related gastritis

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11
Q

H2 blocker absorption

A

rapid

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12
Q

H2 blocker metabolism

A

some hepatic metabolism, but no dosage adjustment for liver disease

renal excretion (dosage reduction if ipaired renal function)

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13
Q

H2 blocker side effects

A

generally well-tolerated. dizziness, diarrhea, constipation, headache

cimetidine can lead to mental status change and/or endocrine changes (gynecomastia, galactorrhea, decreased sperm count)

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14
Q

H2 blocker DDIs

A

cimetidine inhibits P450; all antisecretory agents –> increased gastric pH –> decreased ketoconazole absorption

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15
Q

Sucralfate mechanism of action

A

binds necrotic ulcer tissueand forms protective barrier –> blocked hydrolysis of mucosal proteins by pepsin

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16
Q

Sucralfate activation

A

pH less than 4 (don’t administer with antacids, H2 blockers)

17
Q

Sucralfate use

A

adjunct in ulcer tx

18
Q

Misoprostol absorption

A

rapid –> 30 minute onset

19
Q

Misoprostol half-life

A

30 min –> TID/QID dosing

20
Q

Misoprostol use

A

NSAID-induced GI ulceration

21
Q

Misoprostol side effects

A

diarrhea (promotes fluid secretion), uterine cramping

contraindicated in pregnancy

22
Q

Gastric antacids mechanism

A

rapidly raises pH of stomach to 4-5 (above pepsin optimum pH). pH 7 –> rebound acid secretion via increased gastrin release

23
Q

gastric antacids pharmacokinetics

A

absorption: NaHCO3 > Al, Mg, Ca antacids

24
Q

gastric antacid side effects

A

Ca and Al –> constipation

Mg –> diarrhea

25
Q

Prokinetic agent uses

A

bowel motility disorders (achalasia of esophagus, gastroparesis), symptom relief of esophagitis associated with GERD

26
Q

mechanisms of promotility drugs

A

direct/indirect agonists at smooth muscle M3 receptors

27
Q

Erythromycin mechanism

A

agonist at excitatory neural and smooth mucle motilin receptors

28
Q

Cisapride mechanism

A

agonist at excitatory neural 5-HT4 receptors on enteric nervous system cholinergic motor neurons

29
Q

Metoclopramide mechanism

A

antagonist at presynaptic D2 receptors –| Ach release

30
Q

Neostigmine mechanism

A

inhibits hydrolysis of Ach by AChE

31
Q

Bethanechol mechanism

A

agonist at excitatory M3 smooth muscle receptors

32
Q

Metoclopramide pharmacokinetics

A

rapid absorption –> peak effects in 1h

metabolized to sulfate and glucuronide conjugates –> urinary excretion

33
Q

Cisapride side effects

A

life-threatening arrythmias from prolonged QT

34
Q

metoclopramide side effects

A

D2 block –> somnolence, dystonic reactions, tardive dyskinesia

GI (19 decks)

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