Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
26 Cards in this Set
- Front
- Back
OTC antacids and H2RAs are only indicated for
|
symptomatic treatment of acid indigestion, heartburn, or sour stomach
|
|
prilosec otc is only indicated for
|
frequent heartburn (symptoms atleast 2d/ week)
|
|
prilosec otc is not indicated for
|
bleeding, diarrhea, severe pain, vomiting, or if wght. loss are present.
-not to be used for longer than 2 weeks w/o physician approval |
|
GERD or peptic ulcer disease cannot be safely treated without physicain supervision
|
true
|
|
GERD symptoms can be mistaken for anginal pain
|
true
|
|
mech. of action for antacids
neutralize acid in stomach |
(to pH ~4-5)
-do not affect rate of acid secretion -affect pH in s.i. more than gastic pH -dec. activation of pepsin -INC. LES TONE |
|
mech. of action for antacids
cytoprotective effects (help protect the lining of the stomach and the upper small intestine (duodenum) to allow ulcer healing to occur) |
-stimulate mucus/bicarb secretion
-stimulate mucosal blood flow -stimulate mucosal cell regeneration -bind bile salts |
|
mech. of action for antacids
simethicone |
-added to some antacid products as antiflatulent
-DEC. the surface tension of gas bubbles in the stomach, promoting bursting and elimination by belching or flatus |
|
mech. of action for antacids
alginic acid |
-added to some antacid products for SYMPTOMATIC RELIEF OF GERD-reacts with NaHCO3 in saliva to form a viscous solution that floats on the surface of gastric contents; if reflux occurs sodium alginate is refluxed rather than gastric contents
-works better if the pt. drinks a full glass of water and remains upright (should not lie down for atleast 1h after taking each dose) |
|
AE of antacids:
sodium bicarb. -->metabolic alkalosis -milk-alkali syndrome -sodium overload |
antacid (exogenous NaHCO3) and gastric acid (HCl) irreversibly form NaCl, H20, and CO2
-NaCl does not react with endogenous NaHCO3, which is absorbed systemically -bicarb accumalates systemically in pts. with renal dysfx |
|
AE of antacids:
sodium bicarb. -metabolic alkalosis -->milk-alkali syndrome (NaHCO3 administered with high doses of calcium) [symtoms and patients at risk] -sodium overload |
symptoms: metabolic alkalosis, hypercalcemia, n/v, myalgias, and renal dysfunction
|
|
AE of antacids:
sodium bicarb. -metabolic alkalosis -milk-alkali syndrome -->sodium overload (deliver 12mEq Na per gram NaHCO3)[symptoms and contraindications] |
-fluid retention and weight gain
-htn, renal failure, CHF, cirrhosis, salt-restricted diets |
|
AE of antacids:
Calcium carbonate -->hypercalcemia [symptoms and pts at risk] -acid rebound -milk-alkali syndrome |
-10% of dose is absorbed systemically as CaCl2; prolonged administration can cause hypercalcemia
symptoms: renal dysfuntion and stones, dec. neurologic function. pts. at risk- preexisting renal dysfx |
|
Calcium carbonate
hypercalcemia -->acid rebound -milk-alkali syndrome |
-acid secretion inc. ~2h after antacid is emptied from the stomach, cont. for 3-5h
-may be due to stimulation of gastrin release by calcium |
|
Calcium carbonate
-hypercalcemia -acid rebound -->milk-alkali syndrome [risk factors] |
-risk is lower than with NaHCO3 because systemic alkalosis is rare with CaCO3
-renal dysfunction, dehydration, prolonged administration, concomitant administration of vit. D |
|
Aluminum (hydroxide, carbonate, phosphate, and aminoacetate)
-->constipation (most common)[risk factors, offset of use] -hyperaluminemia -hypophosphotemia |
fluid restriction, dehydration, dec. GI motility
offset by use of combo aluminu/mag antacid products |
|
Aluminum (hydroxide, carbonate, phosphate, and aminoacetate)
-constipation (most common) -->hyperaluminemia-hypophosphotemia |
-17-30% of dose is absorbed as AlCl3; can accumalate in pts w/ renal dysf(x)
-Al may be neurotoxic |
|
Aluminum (hydroxide, carbonate, phosphate, and aminoacetate)
-constipation (most common) -hyperaluminemia -->hypophosphotemia |
-Al binds phosphate in the gut, preventing systemic absorbtion
-used to control hyperphosphatemia in CRF -can cause clinical hypophosphatemia in pts. with normal renal fx: osteomalacia, osteoporosis, bone fractures |
|
pts. at risk of hypophosphatemia
|
elderly, alcoholics, malabsorption syndromes, inadequate dietary phosphorus, prolonged intake of high Al(OH)3 doses
|
|
Magnesium (hydroxide or chloride)
-->diarrhea (most common) -hypermagnesemia |
excess mg in gut converted to insoluble salts which cause osmotic diarrhea
incidence is related to daily dose |
|
Magnesium (hydroxide or chloride)
-diarrhea (most common) -->hypermagnesemia [symptoms] |
5-10% of a dose is absorbed as MgCl2; can accumalate in pts. with renal dysfunction
symptoms; dec. muscle reflexes, n/v, hotn, resp. depression, bradycardia |
|
drug interactions of antacids
binding of drugs in gut=dec. oral absorption esp. with |
divalent or trivalent cations (ca2+, mg2+, and al3+)
|
|
binding interactions of antacids clinically significant with
|
tetracycline or quinolone antibiotics, H2RAs
(sep. dose by atleast 2h with antacid taken last) |
|
binding of drugs in gut (esp. with ca2+, mg2+, al3+)
|
dec. oral absorption of ketoconazole, inc. absorption of salicylates, dec. efficacy of enteric coatings
|
|
drug interactions: (esp. with sodium bicarbonate) changes in urinary pH
|
-dec. urinary elimination of weak bases
-inc. urinary elimination of weak acids |
|
recommended OTC dose of antacid is 40-80 mEq ANC (acid neutralizing capacity)
|
-no more than 2 weeks
-no more than 500-600mEq ANC per day -tablets should be chewed thoroughly -neutralize acid for up to 3h if taken 1h after eating. |