FA Renal

Question 1

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

Answer 1

Mannitol

Question 2

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

Answer 2

Acetazolamide

Question 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.

Answer 3

Loop diuretic (furosemide)

Question 4

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

Answer 4

Ethacrynic acid

Question 5

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

Answer 5

Hydrochlorothiazide

Question 6

Competitive aldosterone receptor antagonists in the cortical collecting tubule.

Answer 6

Spironolactone

Eplerenone

Question 7

Block Na+ channels in the CCT.

Answer 7

Amiloride

Triamterene

Question 8

Mannitol clinical use

Answer 8

Drug overdose,

elevated intracranial/intraocular pressure.

Question 9

Acetazolamide clinical use

Answer 9

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

Question 10

Furosemide clinical use

Answer 10

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

Question 11

Hydrochlorothiazide clinical use

Answer 11

Hypertension,
CHF,
idiopathic hypercalciuria,
nephrogenic diabetes insipidus.

Question 12

K+-sparing diuretic clinical use

Answer 12

Hyperaldosteronism,
K+ depletion,
CHF.

Question 13

Ethacrynic acid clinical use

Answer 13

Diuresis in patients allergic to sulfa drugs.

Question 14

Pulmonary edema,
Dehydration.
Contraindicated in anuria, CHF.

Answer 14

Mannitol toxicity

Question 15

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

Answer 15

Acetazolamide toxicity

Question 16

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

Answer 16

Furosemide toxicity

Question 17

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

Answer 17

Ethacrynic acid toxicity

Question 18

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

Answer 18

Hydrochlorothiazide

Question 19

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

Answer 19

Spironolactone

Question 20

Which diuretics cause increased urine NaCl

Answer 20

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

Question 21

Which diuretics cause increased urine K+?

Answer 21

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

Question 22

which drugs cause acidemia?

Answer 22

Carbonic anhydrase inhibitors, K+ sparing

Question 23

How do K+ sparing diuretics cause acidemia?

Answer 23

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.

Question 24

Which diuretics cause alkalemia?

Answer 24

Loop and thiazides

Question 25

How does volume contraction lead to alkalosis?

Answer 25

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

Question 26

What is the mechanism of “paradoxical acuduria?”

Answer 26

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

Question 27

How do loop and thiazide diuretics lead to alkalemia?

Answer 27

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

Question 28

Which diuretics cause high urine calcium?

Answer 28

Loop diuretics

Question 29

How do loop diuretics cause high urine calcium?

Answer 29

Decreased paracellular Ca2+ reabsorption - hypocalcemia

Question 30

Which diuretics cause low urine calcium?

Answer 30

Thiazides

Question 31

How do thiazides cause low urine calcium?

Answer 31

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

Question 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.

Answer 32

ACE inhibitors
Captopril
Enalapril
Lisinopril

Question 33

Clinical use of ACE inhibitors

Answer 33

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

Question 34

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

Answer 34

ACE inhibitor toxicity (Captopril’s CATCHH)

Question 35

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

Answer 35

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