FA Renal

Question 1

Mannitol Mechanism

Answer 1

Osmotic diuretic, ↑ tubular fluid osmolarity, producing ↑ urine flow, ↓ intracranial/intraocular pressure.

Question 2

Mannitol Use

Answer 2

Drug overdose, ↑ intracranial/intraocular pressure.

Question 3

Mannitol Toxicity

Answer 3

Pulmonary edema, dehydration. Contraindicated in anuria, CHF.

Question 4

Acetazolamide Mechanism

Answer 4

Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and ↓ total-body HCO3- stores. Acts at PCT.

Question 5

Acetazolamide Use

Answer 5

Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri.

Question 6

Acetazolamide Toxicity

Answer 6

Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy.

Question 7

Loop Diuretics

Answer 7

Furosemide, ethcrynic acid

Question 8

Furosemide Mechanism

Answer 8

Sulfonamide loop diuretic. Inhibits cotransport system (Na+/K+/2 Cl-) of thick ascending limb of loop of Henle. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs. ↑ Ca2+ excretion.

Question 9

Furosemide Use

Answer 9

Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia.

Question 10

Furosemide Toxicity

Answer 10

OH DANG: Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout

Question 11

Ethacrynic Acid Mechanism

Answer 11

Phenoxyacetic acid derivative (not a sulfonamide). Essentially same action as furosemide.

Question 12

Ethacrynic Acid Use

Answer 12

Diuresis in patients allergic to sulfa drugs.

Question 13

Ethacrynic Acid Toxicity

Answer 13

Similar to furosemide; can cause hyperuricemia; never use to treat gout.

Question 14

Hydrochlorothiazide (HCTZ) Mechanism

Answer 14

Thiazide diuretic. Inhibits NaCl reabsorption in early distal tubule, ↓ diluting capacity of the nephron. ↓ Ca2+ excretion.

Question 15

Hydrochlorothiazide (HCTZ) Use

Answer 15

Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis.

Question 16

Hydrochlorothiazide (HCTZ) Toxicity

Answer 16

Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia. Sulfa allergy.

Question 17

Potassium-Sparing Diuretics

Answer 17

Spironolactone and eplerenone; triamterene and amiloride

Question 18

Spironolactone, Eplerenone Mechanism

Answer 18

Competitive aldosterone receptor antagonists in the cortical collecting tubule.

Question 19

Triamterene, Amiloride Mechanism

Answer 19

Block Na+ channels in the cortical collecting tubule.

Question 20

Spironolactone, Eplerenone Use

Answer 20

Hyperaldosteronism, K+ depletion, CHF.

Question 21

Triamterene, Amiloride Use

Answer 21

Hyperaldosteronism, K+ depletion, CHF.

Question 22

Spironolactone, Eplerenone Toxicity

Answer 22

Hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (e.g., gynecomastia, antiandrogen effects).

Question 23

Triamterene, Amiloride Toxicity

Answer 23

Hyperkalemia (can lead to arrhythmias)

Question 24

ACE Inhibitors

Answer 24

Captopril, enalapril, lisinopril

Question 25

ACE Inhibitor Mechanism

Answer 25

Inhibit ACE → ↓ angiontensin II → ↓ GFR by preventing constriciton of efferent arterioles. Levels of renin ↑ as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator.

Angiotensin II receptor blockers (Losartan, -sartans) have effects similar to ACE inhibitors but do not ↑ bradykinin → ↓ risk of cough or angioedema.

Question 26

ACE Inhibitor Use

Answer 26

Hypertension, CHF, proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a result of chronic hypertension.

Question 27

ACE Inhibitor Toxicity

Answer 27

Captopril’s CATCHH: Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), ↑ Creatinine (↓ GFR), Hyperkalemia, and Hypotension. Avoid in bilateral renal artery stenosis, because ACE inhibitors with further ↓ GFR → renal failure.