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antacids Flashcards

1. Describe the syndromes involving gastric acid production and the pharmacological approaches used to modulate gastric acidity 2. List the prototype proton pump inhibitors, H2 antagonists, anti-muscarinics, antacids and mucosal protective agents, describe their mechanism of action, pharmacokinetics, clinical uses, and significant side effects 3. Define peptic ulcers, describe the role that Helicobacter pylori play in inducing peptic ulcers, list the two therapeutic approaches for treatment of

1
Q

how stomach acid is formed

A

1) meal, or anticipation of a meal relases gastrin
2) gastrin induces the release of histamin from ECL cells
3) histamine deffuses to paritel cells and acts on H2 receptors to produce cAMP
4) cAMP actiavtes the proton pump to secrete H+

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2
Q

acid protective factor released by epithelial cells

A

prostaglandin

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3
Q

recurrence rate of h pylori caused ulcers if the bug is not eliminated

A

100%

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4
Q

PPIs

A

-prazole

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5
Q

MOA of PPI

A

suicide inhibitor of H+/K+ pase

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6
Q

long acting antiacids

A

PPI

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7
Q

reason PPIs are long active

A

recovery requires sythethis of new enzyme and instertion into the cell membrane

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8
Q

requires an acidic environment for activation

A

PPI

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9
Q

cleared by hepatic metabolism

A

PPI

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10
Q

best taken before meals

A

PPI

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11
Q

inhibits CYP2C19 the least

A

pantoprazole

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12
Q

uses for PPI

A

1st line for GERD, best for peptic ulcers, ZOllinger-ellison

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13
Q

best drug for peptic ulcers

A

PPI

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14
Q

DOC for zollinger-ellison

A

PPI

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15
Q

potential serious side effect of PPI

A

bacterial bloom

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16
Q

drug intereaction with PPI

A

clopidogrel, ketoconazole, ampiclillin esters

17
Q

drug regimen for H pylori

A

PPI+amoxicillin + clarithromycin (PAC)

18
Q

H2 receptor antagonists

A

-tidine

19
Q

uses for H2 receptor agonists

A

non-ulcer indigestion, duodenal ulcer, gastric ulcer, GERD

20
Q

more effective antiacid

A

PPI

21
Q

MOA of H2 RAs

A

inhibits secretion by gastrin and muscaric agonists. Inhibits basal and meal-induced gastric HCL secretion

22
Q

decreases intrinsic factor production

A

H2 RA

23
Q

absorbed by the SI

A

H2 RA

24
Q

excreted unchanged by the kidney

A

H2 RA

25
Q

requires reduction in H2 RA dose

A

H2 RA

26
Q

has anti-nadrogenic effect

A

cimetdine

27
Q

bismuth subcitrate/nitrate/salicylate

A

mucosal protocive agents

28
Q

MOA of mucosal protocive agents

A

increase mucosal secretion, coats ulcer, detaches H pylori from gastric epithelium

29
Q

sucralfate MOA

A

binds to and coats ulcer

30
Q

SE of sucralfate

A

dry mouth, constipation

31
Q

sucralafate decreases bioavailabllity of

A

tetracyline, phenytoin, digoxin, cimetidine

32
Q

analog of PGE1

A

misoprostol

33
Q

approved for NSAID induced ulcer

A

misoprostol

34
Q

SE of misoprostol

A

smooth muscle exication (abdominal.uterine contraction)

35
Q

SE of OTC antacids

A

kidney stones
hypernatremia
many drug interactions

36
Q

Do NOT use sodium bicarb for

A

GERD, peptic ulcers

37
Q

sometimes recommended to pregnant women

A

tums (CaCO3)

38
Q

can cause diarrhea

A

milk of magnesia

39
Q

can be constipating

A

Al compounds

GI (22 decks)

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