Antacids and anti-ulcer Flashcards Preview

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Flashcards in Antacids and anti-ulcer Deck (57)
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1

indication for antacids

short-term, temporary relief of mild pain and symptoms associated with PUD/GERD

2

categories of antacids

low-systemic agents (aluminum, calcium, magnesium)
high systemic agents (sodium)
supplemental agents (simethicone)

3

low systemic antacids

aluminum
calcium
magnesium

4

high systemic antacids

sodium bicarbonate

5

MoA of antacids

combine chemically with hydrogen ions resulting in the generation of by-products - water, CO2, Cl

6

at higher doses of antacids, what happens to LES tone?

increases

7

T/F - antacids reduce acid secretion and production

no, dont reduce secretion or production

8

rapid onset antacids include

calcium and magnesium

9

slow onset antacids include

aluminum and sodium
S(low) A(ntacids)

10

long lasting antacids include

calcium and magnesium

11

best acid neutralizing capacity

calcium

12

surfactant that decreases surface tension and aids in the expulsion of gas

simethicone

13

aluminum adverse effects

constipation
hypophosphatemia ***
rare --> renal osteodystrophy, encephalopathy

14

magnesium adverse effects

diarrhea (stool-softening/laxative like activity)
hypermagnesemia

15

calcium adverse effects

contipation
hypercalcemia (milk-alkali syndrome resutling in nephrop)
hypophosphatemia (effective treatment for hyeprphosphatemia)
calcium based kidney stones

16

sodium adverse effects

gas/flatulence
hypernatremia
metabolic alkalosis

17

when prescribing antacids, what important information about TIMING should you educate them on

patients should take all antacids 1-2 hours BEFORE other medications or 2-4 hours AFTER
AVOID ANTACID AND MEDICATION CO-ADMINISTRATION

18

anti-ulcer drug families

h2 receptor antagonists (-tidine)
PPI (-prazole)
surface acting agent (sucralfate)
PGE1 analog (misoprostol)
bismuth compounds (bismuth subsalicylate)

19

nizatidine is unique of all the h2 blockers because

PO only
all others are IV/PO

20

MoA of H2 blockers

REVERSIBLY inhibit h2 recpetors on baso-lateral membrane of parietal cell
30min-2 hour onset (longer than antacids, shorter than PPIs)
ulcer healing occursin 4-8 weeks
inhibit 20-50% of acid production

21

H2 adverse effects

gi - nausea/diarrhea/constipatino
cns - headache
RARE - CEMETIDINE DECREASES TESTOSTERONE BINDING TO ANDROGEN RECPETOR -- GYNECOMASTIA IN MEN AND GALACTORRHEA IN WOMEN
blood dyscrasias such as neutropenia and thrombocytopenia

22

H2 drug interactions

primarily with cemetidine
CEMETIDINE INHIBITS CYP450 AND INTERACTS WITH A SHIT TON OF DRUGS
Ranitidine ~10% CYP450 inhibition and other in the family have no inhibition

23

CI for H2 blockers

pregnancy
if you have to - use ranitidine or famotidine

24

PPIs include

omeprazole
esomeprazole
lansoprazole
dexlansoprazole
pantoprazole
rabeprazole

25

PO ONLY PPIs

omeprazole
lansoprazole
dexlansoprazole
rabeprazole

26

PO/IV PPIs

esomeprazole
pantoprazole

27

MoA of PPIs

covalently bind to sulfhydryl groups of H+/K+ ATPase at parietal cell secretory sites, thereby inhibiting gastric acid secretion by IRREVERSIBLY INHIBITING functioning -ase pumps
takes several days to reach new steady state

28

PPIs are more effective than H2 blockers, reducing acid secretion by

50-90%, whereas H2 vblockers only reach 20-50%
however, H2 blockers have a more rapid onset than PPIs

29

PPIs adverse effects

GI- diarrhea/dyspepsia/nausea
*****CDAD - clostridium difficile-associated diarrhea *****
CNS - HA/dizziness
rare - generalized myalgias, fatigue, myopathies
increased risk for
kidney disease (AKI)
bone fractures
cardiovascular disease

30

PPI drug interactions

OMEPRAZOLE INHIBITS CYP450
many drug-drug interactions