Renal Pharm

Question 1

Osmotic diuretic, increased tubular fluid osmolarity, producing increased urine flow. Primary site of action at proximal convoluted tubule.

Answer 1

Mannitol mechanism of action?

Question 2

Shock, drug overdose, decreases intracranial/intraocular pressure (glaucoma), decreases cyclosporine toxicity, oligouric states (statin induced rhabdomyolysis).

Answer 2

Mannitol uses?

Question 3

Pulmonary edema, dehydration, headache, nausea, and vomiting.
- Contraindicated in anuria, and CHF.

Answer 3

Mannitol side effects?

Question 4

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

Answer 4

Acetazolamide, dorzolamide mechanism of action?

Question 5

Glaucoma (dorzolamide), urinary alkalinization, metabolic alkalosis, altitude sickness.

Answer 5

Acetazolamide, dorzolamide uses?

Question 6

Hyperchloremic metabolic acidosis, paresthesia, NH3 toxicity, sulfa allergy, hypokalemia, renal stones (struvite, due to increased urine pH).

Answer 6

Acetazolamide, dorzolamide (“ACID”azolamide causes ACIDosis)

Question 7

Inhibits NaKCC of the TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilation of afferent arteriole); inhibited by NSAIDs.

Answer 7

Furosemide, torsemide mechanism of action?

Question 8

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

Answer 8

Furosemide, torsemide uses?

Question 9

Reversible Ototoxicity, Hypokalemic metabolic alkalosis, Dehydration, sulfa Allergy, interstitial Nephritis, hyperuricemia (Gout), hypocalcemia/hypomagnesemia. Increased toxicity with aminoglycosides, lithium, and digoxin.

Answer 9

Furosemide, torsemide (OH DANG!)

Question 10

Inhibits NaKCC of the TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilation of afferent arteriole); inhibited by NSAIDs.

Answer 10

Ethacrynic acid mechanism of action?

Question 11

Diuresis in patients allergic to sulfa drugs.

Answer 11

Ethacrynic acid uses?

Question 12

NO SULFA ALLERGY, can be used with gout. Irreversible otoxoticity (higher than furosemide), hypokalemic metabolic alkalosis, dehydration, nephritis, hypocalcemia/hypomagnesemia. Increased toxicity with aminoglycosides, lithium, an digoxin.

Answer 12

Ethacrynic acid side effects?

Question 13

Inhibits NaCl reabsorption in the early distal tubule. Opens ATP-dependent K+ channel (beta islet cells, arterioles).

Answer 13

Hydrochlorothiazide, indapamide, metolazone mechanism of action?

Question 14

Hypertension, CHF, idiopathic hypercalcinuria (nephrolithiasis), nephrogenic diabetes insipidus. DON’T USE IN PATIENTS WITH DIABETES MELLITUS TYPE 2.

Answer 14

Hydrochlorothiazide, indapamide, metolazone uses?

Question 15

Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia (inhibits insulin release), hyperLipidemia (LDL, cholesterol), hyperUricemia, and hyperCalcemia. Sulfa allergy. Increased toxicity with digoxin.

Answer 15

Hydrochlorothiazide, indapamide, metolazone (HyperGLUC)

Question 16

Aldosterone antagonist on principle cells of the cortical collecting tubule. Potassium sparing diuretic.

Answer 16

Spironlactone mechanism of action?

Question 17

Hyperaldosteronism (Conn’s syndrome), reverses hypokalemia, CHF. Slows cardiac remodeling. Anti-androgen (for acne, hirsutism).

Answer 17

Spironlactone uses?

Question 18

Hyperkalemic metabolic acidosis. Gynectomastia (anti-androgen effects).

Answer 18

Spironlactone side effects?

Question 19

Selective aldosterone antagonist on principle cells of the cortical collecting tubule. Potassium sparing diuretic.

Answer 19

Eplerenone mechanism of action?

Question 20

Hyperaldosteronism (Conn’s syndrome), reverses hypokalemia, CHF. Slows cardiac remodeling.

Answer 20

Eplerenone uses?

Question 21

Hyperkalemic metabolic acidosis. No anti-androgen effects.

Answer 21

Eplerenone side effects?

Question 22

Block sodium channels in the cortical collecting tubule. Potassium sparing diuretic.

Answer 22

Triamterene mechanism of action?

Question 23

Reverses hypokalemia, CHF, lithium-induced nephrogenic diabetes insipidus.

Answer 23

Triamterene uses?

Question 24

Hyperkalemic metabolic acidosis.

Answer 24

Triamterene side effects?

Question 25

Block sodium channels in the cortical collecting tubule. Potassium sparing diuretic.

Answer 25

Amiloride mechanism of action?

Question 26

Reverses hypokalemia, CHF, lithium-induced nephrogenic diabetes insipidus.

Answer 26

Amiloride uses?

Question 27

Hyperkalemic metabolic acidosis.

Answer 27

Amiloride side effects?

Question 28

Mech: Inhibit angiotensin-converting enzyme (ACE) –> decreased angiotensin II –> decreased GFR by preventing efferent arteriole constriction.

• Renin increases.
• Inactivation of bradykinin (potent vasodilator)

Answer 28

Ace Inhibitors (PRILs)
- Captopril, enalapril, lisinopril

Question 29

Similar to ACE inhibitors but do not increase bradykinin –> no cough or angioedema.

Answer 29

Angiotensin II Receptor Blockers

Question 30

Used for: Hypertension, CHF, proteinuria, diabetic renal disease.
- Also prevents unfavorable heart remodeling from chronic hypertension.

Answer 30

Ace Inhibitors (PRILs)
- Captopril, enalapril, lisinopril

Question 31

SE: Cough, Angioedema, Teratogen (fetal renal malformation), Creatinine increase (decreased GFR), Hyperkalemia, and Hypotension.
- Avoid in bilat renal artery stenosis because they will further decrease GFR –> renal failure.

Answer 31

Ace Inhibitors (PRILs)

• Captopril, enalapril, lisinopril
• Captopril’s CATCHH.