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Flashcards in FA Renal Deck (35):
1

Osmotic diuretic in the PCT, increased tubular fluid osmolarity, producing increased urine flow, decreased intracranial/ intraocular pressure.

Mannitol

2

Carbonic anhydrase inhibitor in PCT. Causes self­ limited NaHC03 diuresis and reduction in total-body HC03- stores.

Acetazolamide

3

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. Increased Ca2+ excretion.

Loop diuretic (furosemide)

4

Phenoxyacetic acid derivative (not a sulfonamide). Inhibits cotransport system (Na+, K+, 2 Cl-) of thick ascending limb of loop of Henle.

Ethacrynic acid

5

Inhibits NaCl reabsorption in early DCT, reducing diluting capacity of the nephron. Decreased Ca2+ excretion.

Hydrochlorothiazide

6

Competitive aldosterone receptor antagonists in the cortical collecting tubule.

Spironolactone
Eplerenone

7

Block Na+ channels in the CCT.

Amiloride
Triamterene

8

Mannitol clinical use

Drug overdose,
elevated intracranial/intraocular pressure.

9

Acetazolamide clinical use

Glaucoma,
urinary alkalinization,
metabolic alkalosis,
altitude sickness,
pseudotumor cerebri (idiopathic intracranial HTN)

10

Furosemide clinical use

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

11

Hydrochlorothiazide clinical use

Hypertension,
CHF,
idiopathic hypercalciuria,
nephrogenic diabetes insipidus.

12

K+-sparing diuretic clinical use

Hyperaldosteronism,
K+ depletion,
CHF.

13

Ethacrynic acid clinical use

Diuresis in patients allergic to sulfa drugs.

14

Pulmonary edema,
Dehydration.
Contraindicated in anuria, CHF.

Mannitol toxicity

15

Hyperchloremic metabolic acidosis,
Hypokalemia,
NH3 toxicity,
Neuropathy (paresthesias),
Sulfa allergy.

Acetazolamide toxicity

16

Ototoxicity,
Hypokalemia,
Hypocalcemia,
Hypomagnesemia
Dehydration,
Allergy (sulfa),
Nephritis (interstitial),
Gout.

Furosemide toxicity

17

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

Ethacrynic acid toxicity

18

Hypokalemic metabolic alkalosis,
hyponatremia,
hyperGlycemia,
hyperLipidemia,
hyperUricemia, and
hyperCalcemia.
Sulfa allergy.

Hydrochlorothiazide

19

Hyperkalemia (can lead to arrhythmias), gynecomastia, anti androgen effects,

Spironolactone

20

Which diuretics cause increased urine NaCl

All of them! (serum NaCl may decrease as a result)

21

Which diuretics cause increased urine K+?

All except K+ sparing (spironolactone, eplerenone, amiloride, triamterene)

22

which drugs cause acidemia?

Carbonic anhydrase inhibitors, K+ sparing

23

How do K+ sparing diuretics cause acidemia?

Aldosterone blockade prevents K+ secretion and H+ secretion. Additionally, hyperkalemia leads to K+ entering all cells (via H+fK+ exchanger) in exchange for H+ exiting cells.

24

Which diuretics cause alkalemia?

Loop and thiazides

25

How does volume contraction lead to alkalosis?

Increased AT II --> increased Na+/H+ exchange in PCT -> increased HC03- reabsorption ("contraction alkalosis")

26

What is the mechanism of "paradoxical acuduria?"

In low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule, leading
to alkalosis and "paradoxical aciduria"

27

How do loop and thiazide diuretics lead to alkalemia?

1. volume contraction.
2. K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells
3. In low K+ state, H+ exchanged for Na+ in cortical collecting tubule

28

Which diuretics cause high urine calcium?

Loop diuretics

29

How do loop diuretics cause high urine calcium?

Decreased paracellular Ca2+ reabsorption - hypocalcemia

30

Which diuretics cause low urine calcium?

Thiazides

31

How do thiazides cause low urine calcium?

Enhanced paracellular Ca2+ reabsorption in proximal tubule and loop of Henle.

32

Inhibit angiotensin-converting enzyme (ACE) --> decreased angiotensin II --> decreased GFR by preventing constriction of efferent arterioles. Levels
of renin increase as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator.

ACE inhibitors
Captopril
Enalapril
Lisinopril

33

Clinical use of ACE inhibitors

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

34

Cough, Angioedema, Teratogen (fetal renal malformations), Creatinine increase (decreased GFR), Hyperkalemia, and Hypotension.

ACE inhibitor toxicity (Captopril's CATCHH)

35

In what patients should you avoid the use of ACE inhibitors?

Avoid in bilateral renal artery stenosis, because ACE inhibitors will further decrease GFR --> renal failure.
Also avoid in pts with c1 esterase inhibitor deficiency.