Flashcards in Renal Drugs Deck (17):
1
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)
2
clinical uses of mannitol
- drug overdose
- cerebral edema (increased ICP)
- acute glaucoma (increased IOP)
- oliguria in AKI
3
SEs of mannitol
- pulmonary edema (contraindicated in CHF)
- dehydration, hypernatremia ultimately
- hyponatremia INITIALLY
4
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
5
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
6
SEs of acetazolamide
- NAG met acidosis
- paresthesias
- NH3 toxicity
- sulfa allergy
- hypokalemia - more Na+ delivery to distal tubule
7
ethacrynic acid
same as loop diuretics but no sulfa allergy
8
mechanism of chlorthialidone, hydrochlororothiazide
- inhibition of NaCl reabsorption in early DCT
- increased Ca 2+ reabsorption
9
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+)
10
SEs of chlorthialidone, hydrochlororothiazide
- hyperglycemia
- hyperlipidemia
- hyperuricemia
- hypercalcemia
- sulfa allergy
hyperGLUCS + hyponatremia, hypokalemic met alkalosis
11
mechanism of spironolactone, eplerenone
competitive aldosterone receptor antagonists in CCD
12
mechanism of triamterene, amiloride
blocking of Na+ channels in CCD
13
clinical use of K+ sparing diuretics
- hyperaldosteronism
- hypokalemia
- HF
- cirrhosis
14
SEs of K+ sparing diuretics
- hyperkalemia
- spironolactone - gynecomastia (switch to eplerenone)
15
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+
16
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
17