Renal Drugs

Question 1

Drugs that act on PCT

Answer 1

Mannitol, Acetazolamide

Question 2

Mannitol: Mechanism

Answer 2

Can’t be reabsorbed. Osmotic diuretic. Increase tubular fluid osmolarity, producing increased urine flow, decrease intracranial/intraocular pressure

Question 3

Mannitol: Clinical Use

Answer 3

Drug overdose, elevated intracranial/intraocular pressure

Question 4

Mannitol: Toxicity

Answer 4

Pulmonary edema, dehydration.

Question 5

Acetazolamide: Mechanism

Answer 5

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

Question 6

Acetazolamide: Clinical Use

Answer 6

AGMAP

Question 7

Acetazolamide: Toxicity

Answer 7

ACIDazolamide caused ACIDosis

Question 8

Drug(s) that act on Loop of Henle

Answer 8

Furosemide, Ethracrynic Aid

Question 9

Furosemide: Mechanism

Answer 9

Sulfonamide loop diuretic. Inhibits co-transport system (Na, K, 2CL) of thick ascending limb of loop of Henle.

Question 10

How does furosemide affect prostaglandins?

Answer 10

Stimulates PGE release (vasoldilatory effect on afferent arteriole) –> decreased GFR

Question 11

How does furosemide affect Ca excretion?

Answer 11

It promotes Ca excretion.

Question 12

Furosemide: Clinical Use

Answer 12

Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema)

Question 13

Furosemide: Toxicity

Answer 13

*OH DANG!

Question 14

Ethacrynic Acid: Mechanism

Answer 14

Phenoxyacetic acid derivative (not a sulfonamide).

Question 15

Ethacrynic Acid: Clinical Use

Answer 15

Diuresis in patients allergic to sulfa drugs

Question 16

Ethacrynic Acid: Toxicity

Answer 16

Ototoxicity

Question 17

Hydrochlorothiazide: Mechanism

Answer 17

Thiazide diuretic. Inhibits NaCl reabsorption in early DCT, reducing diluting capacity of the neprhon.

Question 18

Hydrochlorothiazide: Clinical Use

Answer 18

Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus

Question 19

Hydrochlorothiazide: Toxicity

Answer 19

Hypokalemic metabolic alkalosis

Question 20

K+ sparing diuretics

Answer 20

Spironolactone and eplerenone; Triametereme, Amiloride

Question 21

Spironolactone & Eplerenone

Answer 21

Competitive aldosterone receptor antagonists in the cortical collecting tubule

Question 22

Triamterene & Amlioride

Answer 22

Block Na channels in the CCT

Question 23

K+ sparing diuretics: Clinical Use

Answer 23

Hyperaldosteronism, K+ depletion, CHF

Question 24

K+ sparing diuretics: Toxicity

Answer 24

Hyperkalemia (can lead to arrhythmias)

Question 25

Spironolactone Toxicity.

Answer 25

Aside from hyperkalemia (can lead to arrhythmias). It can cause endocrine effects (e.g. gynecomastia, antiandrogen effects)

Question 26

After diuretic use: Urine NaCl

Answer 26

Increases in all diuretics . Serum NaCl may result

Question 27

After diuretic use: Urine K

Answer 27

*Increase (all except K+ sparing diuretics). Serum K may decrease as a result

Question 28

Diuretics that cause acidemia (decreased blood pH)

Answer 28

Carbonic anhydrase inhibitors –> decreased HCO3 reabsorption.

Question 29

Diuretics that cause alkalosis (increased blood pH)

Answer 29

LOOP DIURETICS & THIAZIDES cause alkalemia via several mechanisms:

Question 30

Diuretics increase urine Ca

Answer 30

Loop diuretics: Decreased paracellular Ca reabsorption –> hypcalcemia

Question 31

Diuretics that decrease urine Ca

Answer 31

Thiazides: Enhanced paracellular Ca reabsorption in proximal tubule and loop of Henle

Question 32

ACE Inhibitors

Answer 32

Captopril, Enalaprill, Lisinopril

Question 33

ACE Inhibitors: Mechanism

Answer 33

Inhibit angiotensin-converting enzyme (ACE) –> decreased angiotensin –> decreased GFR by preventing constriction of efferent arterioles.

Question 34

ACE Inhibitors: Clinical Use

Answer 34

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

Question 35

ACE Inhibitors: Toxicity

Answer 35

CATCHH