Renal

Question 1

Mannitol (MOA)

Answer 1

Osmotic diuretic, increases tubular fluid osmolarity, producing increased urine flow, decreased intracranial/intraocular pressure

Question 2

Mannitol (CU)

Answer 2

Drug overdose, increased intracranial/intraocular pressure

Question 3

Mannitol (T)

Answer 3

Pulmonary edema, dehydration, Contraindicated in anuria, CHF

Question 4

Acetazolamide (MOA)

Answer 4

Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and decreases total body HCO3 stores

Question 5

Acetazolamide (CU)

Answer 5

Glaucome, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudo tumor cerebri

Question 6

Acetazolamide (T)

Answer 6

Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy

Question 7

Furosemide (MOA)

Answer 7

Sulfonamide loop diuretic, Inhibits cotransport system (Na/K/2Cl) 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. Increases Ca excretion.

Question 8

Furosemide (CU)

Answer 8

Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, Hypercalcemia

Question 9

Furosemide (T)

Answer 9

Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout

Question 10

Ethacrynic Acid (MOA)

Answer 10

Same mechanism as furosemide. Not a sulfonamide.

Question 11

Ethacrynic Acid (CU)

Answer 11

Diuresis in pts allergic to sulfa drugs

Question 12

Ethacrynic Acid (T)

Answer 12

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

Question 13

Hydrochlorothiazide (MOA)

Answer 13

Inhibits NaCl reabsorption in early distal tubule, decreases diluting capacity of the nephron. Decreases Ca excretion.

Question 14

Hydrochlorothiazide (CU)

Answer 14

HTN, CHF, idopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis

Question 15

Hydrochlorothiazide (T)

Answer 15

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

Question 16

Spironolactone (MOA)

Answer 16

Competitive aldosterone receptor antagonists in the cortical collecting tubule.

Question 17

Spironolactone (CU)

Answer 17

Hyperaldosteronism, K+ depletion, CHF

Question 18

Spironolactone (T)

Answer 18

Hyperkalemia (can lead to arrhythmias), Gynecomastia, anti androgen effects.

Question 19

Eplerenone (MOA)

Answer 19

Competitive aldosterone receptor antagonists in the cortical collecting tubule.

Question 20

Eplerenone (CU)

Answer 20

Hyperaldosteronism, K+ depletion, CHF

Question 21

Eplerenone (T)

Answer 21

Hyperkalemia (can lead to arrhythmias)

Question 22

Triamterene (MOA)

Answer 22

Block Na+ channels in CCT

Question 23

Triamterene (CU)

Answer 23

Hyperaldosteronism, K+ depletion, CHF

Question 24

Triamterene (T)

Answer 24

Hyperkalemia (can lead to arrhythmias)

Question 25

Amiloride (MOA)

Answer 25

Block Na+ channels in CCT

Question 26

Amiloride (CU)

Answer 26

Hyperaldosteronism, K+ depletion, CHF

Question 27

Amiloride (T)

Answer 27

Hyperkalemia (can lead to arrhythmias)

Question 28

Captopril, Enalapril, Lisinopril (MOA)

Answer 28

Inhibit ACE -> decreases ATII -> decreased GFR by preventing constriction of efferent arterioles. Level of renin increases as a loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator.

Question 29

Captopril, Enalapril, Lisinopril (CU)

Answer 29

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

Question 30

Captopril, Enalapril, Lisinopril (T)

Answer 30

Cough, angioedema, teratogen, elevated creatinine and decreased GFR, hyperkalemia and hypotension. Avoid in bilateral renal artery stenosis because ACE inhibitors will further decrease GFR-> renal failure.