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26 Cards in this Set

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MOA of mannitol
(osmotic diuretic); increases tubular fluid osmolarity, thereby increasing urine flow
Clinical uses of mannitol
shock, drug OD, to decrease intracranial/intraocular P
MOA acetazolamide
carbonic anhydrase inhibitor; causes self-limited NaHCO3 diuresis and reduction in total-body bicarb stores
Clinical uses of acetazolamide
glaucoma, urinary alkalinization, metabolis alkalosis, altitute sickness
toxicities of acetazolamide
hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
MOA of ethacrynic acid
(diuretic); phenoxyacetic acid derivative--NOT sulfonamide--that works like furosemide (loop diuretic)
Clinical use of ethacrynic acid
diuresis in pts with sulfa allergy (b/c NOT a sulfonamide)
toxicity of ethacrynic acid
similar to furosemide (OH DANG) but can be used in hyperuricemia and no sulfa allergy
MOA of furosemide
sulfonamide loop diuretic; inhibits Na-K-2Cl contransporter of thick ascending limb; abolishes hypertonicity of medulla which prevents concentration of urine; increases Ca excretion
toxicity of furosemide
OH DANG! Ototoxicty, Hypokalemia, Dehydration, Allergy, Nephritis (interstitial), Gout
MOA hydrochlorothiazide
thiazide loop diuretic. Inhibits NaCl reabsorption in early distal tubule which reduces diluting capacity of nephron.
thiazide diuretics vs. loop diuretics with respect to calcium?
loop diuretics (furosemide, ethacrynic acid)--increase Ca excretion; thiazides DECREASE Ca excretion.
4 K+ sparing diuretics
spironolactone, triamterene, amiloride, eplereone
MOA of spironolactone
competitive aldosterone R antagonist in cortical collecting tubule
MOA of triamterene
(K+sparer) block Na channels in CCT (same as amiloride)
MOA of amiloride
(K+sparer) blocks Na channels in CCT (same as triameterene)
Clinical use of K+ sparing diuretics
hyperaldosteronism, K+ depletion, CHF
toxicity of K+ sparing diuretics
hyperkalemia, endocrine effects (eg. Spironolactone--gynecomastia, antiandrogenics)
which diuretics decrease the blood pH (more acidic)
carbonic anhydrase inhibitors (acetazolamide), K+ sparers (spironolactone, triamterene, amiloride, eplererone)
which diuretics increase blood pH (make more basic)
loop diuretics (furosemide, ethacrynic acid), thiazides
3 AcE inhibitors
captopril, enalapril, lisinopril
MOA of ACE inhibitors
inhibit angiotensin converting enzyme which reduces levels of angiotensin II and prevents inacitvation of bradykinin (potent vasodilator); renin release increased b/c of lack of feedback inhibition
effect of ACE inhibitors on renin release?
renin release increased due to loss of feedback inhibition
Clinical uses of ACE inhibitors
HTN, CHF, diabetic renal disease
toxicities of ACE inhibitors
CAPTOPRIL: cough, angioedema, proteinuria, taste changes, hypOtension, preggers problems, rash, increased renin, lower angiotension II. Also hyperkalemia.
can ACE inhibitors be used in bilateral renal artery stenosis?