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Flashcards in Renal Drugs Deck (42)
1

Mechanism of mannitol

osmotic diuretic

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

2

Use of mannitol

drug overdose, elevated intracranial/intraocular pressure

3

Toxicity of mannitol

pulmonary edema, dehydration
contraindicated in anuria, HF

4

Mechanism of acetazolamide

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

5

Use of acetazolamide

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

6

Toxicity of acetazolamide

hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy

7

Name the loops diuretics

furosemide, bumetanide, torsemide

8

Mechanism of the loop diuretics

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

9

Use of loop diuretics

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

10

Toxicity of loop diurietics

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

11

Mechanism of ethacrynic acid

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

12

Use of ethacrynic acid

as diuretic for pts with sulfa allergy

13

Toxicity of ethacrynic acid

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

14

Name the thiazide diuretics

chlorthalidone, hydrochlorothiazide

15

Mechanism of thiazide diruetics

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

16

Use of thiazide diruetics

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

17

Toxicity of thiazides

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

sulfa allergy

18

Name the K+ sparing diruetics

spironolactone and eplerenone; trimaterene and amiloride

19

Mechanism of spironolactone and eplerenone

competitive aldosterone antagonists in cortical collecting tubule

20

Mechanism of triamterene and amiloride

act in cortical collecting tubule to inhibit ENAC channels

21

Use of K+ sparing diuretics

hyperaldosteronism, K+ depletion, HF

22

Toxicity of K+ sparing diuretics

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

23

Urine NaCl changes

increases with all diuretics except acetazolamide

24

Urine K+ changes

increases with loop and thiazides

25

Blood pH

acidemia:
- carbonic anhydrase inhibitors
- K+ sparing

alkalemia:
- loops
- thiazides

26

How do CA inhibitors cause acidemia?

decrease HCO3- reabsorption in the pCT

27

How do K+ sparing cause acidemia?

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

28

How do loops and thiazides cause alkalosis?

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"

29

Name the ACE inhibitors

captopril, enalapril, lisinopril, ramipril

30

Mechanism of ACE inhibitors

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

31

Use of ACE inhibitors

hypertension, HF, proteinuria, diabetic nephropathy

prevent unfavorable heart remodeling in chronic hypertension

32

How do ACE inhibitors work in diabetic nephropathy?

decrease intraglomerular pressure, slowing GBM thickening

33

Toxicity of ACE inhibitors

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

34

Contraindications to ACE inhibitors

C1 esterase inhibitor deficiency
bilateral renal artery stenosis because will further decrease GFR --> renal failure

35

Name the angiotensin II receptor blockers

losartan, candesartan, valsartan

36

Mechanism of ARBs

selectively block binding of angiotensin II to AT1 receptors
effects similar to ACE inhibitors, but no bradykinin increase

37

Use of ARBs

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

38

Toxicity of ARBs

hyperkalemia, decreased renal function, hypotension; teratogen

39

Mechanism of aliskiren

direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I

40

Use of aliskiren

hypertension

41

Toxicity of aliskiren

hyperkalemia, decreased renal function, hypotension

42

Contraindication of aliskiren

diabetics taking ACE inhibitors or ARBs