Renal Drugs Flashcards
mechanism of mannitol
- osmotic diuretic - pulls water into ECF compartment by preventing H2O reabsorption in PCT, tdLH, and CD
- increases urine flow, decreases time in tubules (less reabsorption)
clinical uses of mannitol
- drug overdose
- cerebral edema (increased ICP)
- acute glaucoma (increased IOP)
- oliguria in AKI
SEs of mannitol
- pulmonary edema (contraindicated in CHF)
- dehydration, hypernatremia ultimately
- hyponatremia INITIALLY
mechanism of acetazolamide
CA inhibitor in PCT –> H2CO3 builds up in lumen –> H+ does not get secreted, so HCO3- is not reabsorbed –> diuresis of NaHCO3
clinical use of acetazolamide
- glaucoma - decreases aqueous humor production
- urinary alkalinization - uric acid and cysteine stones more soluble
- metabolic alkalosis - HCO3- is secreted
- altitude sickness - induces NAG met. acidosis –> hyperventilation
- pseudotumor cerebri
SEs of acetazolamide
- NAG met acidosis
- paresthesias
- NH3 toxicity
- sulfa allergy
- hypokalemia - more Na+ delivery to distal tubule
ethacrynic acid
same as loop diuretics but no sulfa allergy
mechanism of chlorthialidone, hydrochlororothiazide
- inhibition of NaCl reabsorption in early DCT
- increased Ca 2+ reabsorption
clinical use of chlorthialidone, hydrochlororothiazide
- HTN
- HF
- idiopathic hypercalciuria causing renal stones
- nephrogenic DI - Na+ reabsorption stimulated in PCT –> decreased urine formation
- osteoporosis (increases Ca 2+)
SEs of chlorthialidone, hydrochlororothiazide
- hyperglycemia
- hyperlipidemia
- hyperuricemia
- hypercalcemia
- sulfa allergy
hyperGLUCS + hyponatremia, hypokalemic met alkalosis
mechanism of spironolactone, eplerenone
competitive aldosterone receptor antagonists in CCD
mechanism of triamterene, amiloride
blocking of Na+ channels in CCD
clinical use of K+ sparing diuretics
- hyperaldosteronism
- hypokalemia
- HF
- cirrhosis
SEs of K+ sparing diuretics
- hyperkalemia
- spironolactone - gynecomastia (switch to eplerenone)
mechanism of furosemide, bumetanide, torsemide
- loop diuretic - inhibits Na+/K+/Cl- cotransporter of TaLH
- abolishes hypertonicity of medulla and prevents concentration of urine
- stimulates prostaglanding (PGE) release –> RBF increases
- increased excretion of Ca 2+ and Mg 2+
clinical use of furosemide, bumetanide, torsemide
- edematous states - HF, cirrhosis, nephrotic syndrome, pulmonary edema
- severe HTN
- hypercalcemia
- hyperkalemia
- SIADH - since medullary concentration gradient is abolished, ADH won’t be useful since there is no drive for water reabsorption once aquaporins have been stimulated
SEs of furosemide, bumetanide, torsemide
ototoxicity, hypokalemia (more Na+ delivery to distal tubule), dehydration, allergy (sulfa), interstitial nephritis, gout (hyperuricemia)
OH DANG!!
