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26 Cards in this Set
- Front
- Back
- 3rd side (hint)
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MOA of mannitol
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(osmotic diuretic); increases tubular fluid osmolarity, thereby increasing urine flow
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Clinical uses of mannitol
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shock, drug OD, to decrease intracranial/intraocular P
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MOA acetazolamide
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carbonic anhydrase inhibitor; causes self-limited NaHCO3 diuresis and reduction in total-body bicarb stores
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Clinical uses of acetazolamide
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glaucoma, urinary alkalinization, metabolis alkalosis, altitute sickness
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toxicities of acetazolamide
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hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
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MOA of ethacrynic acid
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(diuretic); phenoxyacetic acid derivative--NOT sulfonamide--that works like furosemide (loop diuretic)
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Clinical use of ethacrynic acid
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diuresis in pts with sulfa allergy (b/c NOT a sulfonamide)
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toxicity of ethacrynic acid
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similar to furosemide (OH DANG) but can be used in hyperuricemia and no sulfa allergy
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None
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MOA of furosemide
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sulfonamide loop diuretic; inhibits Na-K-2Cl contransporter of thick ascending limb; abolishes hypertonicity of medulla which prevents concentration of urine; increases Ca excretion
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toxicity of furosemide
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OH DANG! Ototoxicty, Hypokalemia, Dehydration, Allergy, Nephritis (interstitial), Gout
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MOA hydrochlorothiazide
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thiazide loop diuretic. Inhibits NaCl reabsorption in early distal tubule which reduces diluting capacity of nephron.
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thiazide diuretics vs. loop diuretics with respect to calcium?
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loop diuretics (furosemide, ethacrynic acid)--increase Ca excretion; thiazides DECREASE Ca excretion.
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4 K+ sparing diuretics
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spironolactone, triamterene, amiloride, eplereone
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MOA of spironolactone
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competitive aldosterone R antagonist in cortical collecting tubule
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MOA of triamterene
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(K+sparer) block Na channels in CCT (same as amiloride)
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MOA of amiloride
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(K+sparer) blocks Na channels in CCT (same as triameterene)
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Clinical use of K+ sparing diuretics
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hyperaldosteronism, K+ depletion, CHF
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toxicity of K+ sparing diuretics
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hyperkalemia, endocrine effects (eg. Spironolactone--gynecomastia, antiandrogenics)
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which diuretics decrease the blood pH (more acidic)
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carbonic anhydrase inhibitors (acetazolamide), K+ sparers (spironolactone, triamterene, amiloride, eplererone)
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which diuretics increase blood pH (make more basic)
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loop diuretics (furosemide, ethacrynic acid), thiazides
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3 AcE inhibitors
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captopril, enalapril, lisinopril
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MOA of ACE inhibitors
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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
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effect of ACE inhibitors on renin release?
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renin release increased due to loss of feedback inhibition
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Clinical uses of ACE inhibitors
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HTN, CHF, diabetic renal disease
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toxicities of ACE inhibitors
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CAPTOPRIL: cough, angioedema, proteinuria, taste changes, hypOtension, preggers problems, rash, increased renin, lower angiotension II. Also hyperkalemia.
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can ACE inhibitors be used in bilateral renal artery stenosis?
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no
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