Renal Drugs

Question 1

mechanism of mannitol

Answer 1

• 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)

Question 2

clinical uses of mannitol

Answer 2

• drug overdose
• cerebral edema (increased ICP)
• acute glaucoma (increased IOP)
• oliguria in AKI

Question 3

SEs of mannitol

Answer 3

• pulmonary edema (contraindicated in CHF)
• dehydration, hypernatremia ultimately
• hyponatremia INITIALLY

Question 4

mechanism of acetazolamide

Answer 4

CA inhibitor in PCT –> H2CO3 builds up in lumen –> H+ does not get secreted, so HCO3- is not reabsorbed –> diuresis of NaHCO3

Question 5

clinical use of acetazolamide

Answer 5

• 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

Question 6

SEs of acetazolamide

Answer 6

• NAG met acidosis
• paresthesias
• NH3 toxicity
• sulfa allergy
• hypokalemia - more Na+ delivery to distal tubule

Question 7

ethacrynic acid

Answer 7

same as loop diuretics but no sulfa allergy

Question 8

mechanism of chlorthialidone, hydrochlororothiazide

Answer 8

• inhibition of NaCl reabsorption in early DCT

- increased Ca 2+ reabsorption

Question 9

clinical use of chlorthialidone, hydrochlororothiazide

Answer 9

• HTN
• HF
• idiopathic hypercalciuria causing renal stones
• nephrogenic DI - Na+ reabsorption stimulated in PCT –> decreased urine formation
• osteoporosis (increases Ca 2+)

Question 10

SEs of chlorthialidone, hydrochlororothiazide

Answer 10

• hyperglycemia
• hyperlipidemia
• hyperuricemia
• hypercalcemia
• sulfa allergy

hyperGLUCS + hyponatremia, hypokalemic met alkalosis

Question 11

mechanism of spironolactone, eplerenone

Answer 11

competitive aldosterone receptor antagonists in CCD

Question 12

mechanism of triamterene, amiloride

Answer 12

blocking of Na+ channels in CCD

Question 13

clinical use of K+ sparing diuretics

Answer 13

• hyperaldosteronism
• hypokalemia
• HF
• cirrhosis

Question 14

SEs of K+ sparing diuretics

Answer 14

• hyperkalemia

- spironolactone - gynecomastia (switch to eplerenone)

Question 15

mechanism of furosemide, bumetanide, torsemide

Answer 15

• 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+

Question 16

clinical use of furosemide, bumetanide, torsemide

Answer 16

• 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

Question 17

SEs of furosemide, bumetanide, torsemide

Answer 17

ototoxicity, hypokalemia (more Na+ delivery to distal tubule), dehydration, allergy (sulfa), interstitial nephritis, gout (hyperuricemia)

OH DANG!!