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26 Cards in this Set

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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.