Renal Drugs Flashcards Preview

USMLE Step 1 > Renal Drugs > Flashcards

Flashcards in Renal Drugs Deck (35):
1

Drugs that act on PCT

Mannitol, Acetazolamide

2

Mannitol: Mechanism

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

3

Mannitol: Clinical Use

Drug overdose, elevated intracranial/intraocular pressure

4

Mannitol: Toxicity

Pulmonary edema, dehydration.

5

Acetazolamide: Mechanism

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

6

Acetazolamide: Clinical Use

AGMAP

7

Acetazolamide: Toxicity

*ACID*azolamide caused *ACID*osis

8

Drug(s) that act on Loop of Henle

Furosemide, Ethracrynic Aid

9

Furosemide: Mechanism

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

10

How does furosemide affect prostaglandins?

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

11

How does furosemide affect Ca excretion?

It promotes Ca excretion.

12

Furosemide: Clinical Use

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

13

Furosemide: Toxicity

*OH DANG!

14

Ethacrynic Acid: Mechanism

Phenoxyacetic acid derivative (not a sulfonamide).

15

Ethacrynic Acid: Clinical Use

Diuresis in patients allergic to sulfa drugs

16

Ethacrynic Acid: Toxicity

Ototoxicity

17

Hydrochlorothiazide: Mechanism

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

18

Hydrochlorothiazide: Clinical Use

Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus

19

Hydrochlorothiazide: Toxicity

*Hypokalemic metabolic alkalosis*

20

K+ sparing diuretics

*S*pironolactone and eplerenone; *T*riametereme, *A*miloride

21

Spironolactone & Eplerenone

Competitive aldosterone receptor antagonists in the cortical collecting tubule

22

Triamterene & Amlioride

Block Na channels in the CCT

23

K+ sparing diuretics: Clinical Use

Hyperaldosteronism, K+ depletion, CHF

24

K+ sparing diuretics: Toxicity

Hyperkalemia (can lead to arrhythmias)

25

Spironolactone Toxicity.

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

26

After diuretic use: Urine NaCl

*Increases in all diuretics* . Serum NaCl may result

27

After diuretic use: Urine K

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

28

Diuretics that cause acidemia (decreased blood pH)

*Carbonic anhydrase inhibitors* --> decreased HCO3 reabsorption.

29

Diuretics that cause alkalosis (increased blood pH)

*LOOP DIURETICS & THIAZIDES* cause alkalemia via several mechanisms:

30

Diuretics increase urine Ca

Loop diuretics: Decreased paracellular Ca reabsorption --> hypcalcemia

31

Diuretics that decrease urine Ca

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

32

ACE Inhibitors

Captopril, Enalaprill, Lisinopril

33

ACE Inhibitors: Mechanism

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

34

ACE Inhibitors: Clinical Use

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

35

ACE Inhibitors: Toxicity

*CATCHH*