Renal Drugs

Question 1

Mechanism of mannitol

Answer 1

osmotic diuretic

increases tubular osmolarity –> increased urine flow, decreased intracranial/intraocular pressure

Question 2

Use of mannitol

Answer 2

drug overdose, elevated intracranial/intraocular pressure

Question 3

Toxicity of mannitol

Answer 3

pulmonary edema, dehydration

contraindicated in anuria, HF

Question 4

Mechanism of acetazolamide

Answer 4

carbonic anhydrase inhibitor - prevents brush border conversion of HCO3- + H+ to CO2 and H2O

causes a self-limited NaHCO3 diuresis and decrease total body HCO3- stores

Question 5

Use of acetazolamide

Answer 5

glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor

Question 6

Toxicity of acetazolamide

Answer 6

hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy

Question 7

Name the loops diuretics

Answer 7

furosemide, bumetanide, torsemide

Question 8

Mechanism of the loop diuretics

Answer 8

sulfonamide loop diruetics inhibit cotransport of Na/K/2Cl in thick ascending limb of loop of henle

abolish hypertonicity of medulla, preventing concentration of urine

stimulate PGE release (vasodilatory effect on afferent arteriole) - inhibited by NSAIDs

Question 9

Use of loop diuretics

Answer 9

edemtatous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia

Question 10

Toxicity of loop diurietics

Answer 10

hypercalciuria, ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout

Question 11

Mechanism of ethacrynic acid

Answer 11

phenoxyacetic acid derivative (not a sulfa drug) with same mech as furosemide

Question 12

Use of ethacrynic acid

Answer 12

as diuretic for pts with sulfa allergy

Question 13

Toxicity of ethacrynic acid

Answer 13

similar to furosemide; can cause hyperuricemia so never used to treat gout

Question 14

Name the thiazide diuretics

Answer 14

chlorthalidone, hydrochlorothiazide

Question 15

Mechanism of thiazide diruetics

Answer 15

inhibit NaCl reabsorption in DCT –> decreased diluting capacity of nephron

Question 16

Use of thiazide diruetics

Answer 16

hypertension, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis (bc increases calcium)

Question 17

Toxicity of thiazides

Answer 17

hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia

sulfa allergy

Question 18

Name the K+ sparing diruetics

Answer 18

spironolactone and eplerenone; trimaterene and amiloride

Question 19

Mechanism of spironolactone and eplerenone

Answer 19

competitive aldosterone antagonists in cortical collecting tubule

Question 20

Mechanism of triamterene and amiloride

Answer 20

act in cortical collecting tubule to inhibit ENAC channels

Question 21

Use of K+ sparing diuretics

Answer 21

hyperaldosteronism, K+ depletion, HF

Question 22

Toxicity of K+ sparing diuretics

Answer 22

hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (gynecomastia and antiandrogen effects)

Question 23

Urine NaCl changes

Answer 23

increases with all diuretics except acetazolamide

Question 24

Urine K+ changes

Answer 24

increases with loop and thiazides

Question 25

Blood pH

Answer 25

acidemia:

• carbonic anhydrase inhibitors
• K+ sparing

alkalemia:

• loops
• thiazides

Question 26

How do CA inhibitors cause acidemia?

Answer 26

decrease HCO3- reabsorption in the pCT

Question 27

How do K+ sparing cause acidemia?

Answer 27

aldosterone blockade prevents K+ secretion and H+ secretion

hyperkalemia –> K+ entering the cells in exchange for H+ leaving the calls contributing further to the acidemia

Question 28

How do loops and thiazides cause alkalosis?

Answer 28

1. volume contraction –> increased AT II –> increased Na+/H+ exchange in PT –> increased HCO3- reabsorption (“contraction alkalosis”)
2. K+ loss leading to K+ exiting the cells and H+ entering the cells
3. in low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule –> alkalosis and “paradoxical aciduria”

Question 29

Name the ACE inhibitors

Answer 29

captopril, enalapril, lisinopril, ramipril

Question 30

Mechanism of ACE inhibitors

Answer 30

inhibit ACE –> decreased AT II –> decreased GFR by preventing constriction of efferent arteriole
increase renin levels
inhibition of ACE also leads to decreased bradykinin breakdown –> vasodilation

Question 31

Use of ACE inhibitors

Answer 31

hypertension, HF, proteinuria, diabetic nephropathy

prevent unfavorable heart remodeling in chronic hypertension

Question 32

How do ACE inhibitors work in diabetic nephropathy?

Answer 32

decrease intraglomerular pressure, slowing GBM thickening

Question 33

Toxicity of ACE inhibitors

Answer 33

dry cough, angioedema, teratogen, increased creatinine, hyperkalemia, and hypotension

Question 34

Contraindications to ACE inhibitors

Answer 34

C1 esterase inhibitor deficiency

bilateral renal artery stenosis because will further decrease GFR –> renal failure

Question 35

Name the angiotensin II receptor blockers

Answer 35

losartan, candesartan, valsartan

Question 36

Mechanism of ARBs

Answer 36

selectively block binding of angiotensin II to AT1 receptors

effects similar to ACE inhibitors, but no bradykinin increase

Question 37

Use of ARBs

Answer 37

hypertension, HF, proteinuria, or diabetic nephropathy with intolerance to ACE inhibitors (e.g. cough, angioedema)

Question 38

Toxicity of ARBs

Answer 38

hyperkalemia, decreased renal function, hypotension; teratogen

Question 39

Mechanism of aliskiren

Answer 39

direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I

Question 40

Use of aliskiren

Answer 40

hypertension

Question 41

Toxicity of aliskiren

Answer 41

hyperkalemia, decreased renal function, hypotension

Question 42

Contraindication of aliskiren

Answer 42

diabetics taking ACE inhibitors or ARBs