Renal Drugs Flashcards

1
Q

Drugs that act on PCT

A

Mannitol, Acetazolamide

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2
Q

Mannitol: Mechanism

A

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

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3
Q

Mannitol: Clinical Use

A

Drug overdose, elevated intracranial/intraocular pressure

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4
Q

Mannitol: Toxicity

A

Pulmonary edema, dehydration.

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5
Q

Acetazolamide: Mechanism

A

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

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6
Q

Acetazolamide: Clinical Use

A

AGMAP

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7
Q

Acetazolamide: Toxicity

A

ACIDazolamide caused ACIDosis

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8
Q

Drug(s) that act on Loop of Henle

A

Furosemide, Ethracrynic Aid

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9
Q

Furosemide: Mechanism

A

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

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10
Q

How does furosemide affect prostaglandins?

A

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

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11
Q

How does furosemide affect Ca excretion?

A

It promotes Ca excretion.

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12
Q

Furosemide: Clinical Use

A

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

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13
Q

Furosemide: Toxicity

A

*OH DANG!

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14
Q

Ethacrynic Acid: Mechanism

A

Phenoxyacetic acid derivative (not a sulfonamide).

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15
Q

Ethacrynic Acid: Clinical Use

A

Diuresis in patients allergic to sulfa drugs

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16
Q

Ethacrynic Acid: Toxicity

A

Ototoxicity

17
Q

Hydrochlorothiazide: Mechanism

A

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

18
Q

Hydrochlorothiazide: Clinical Use

A

Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus

19
Q

Hydrochlorothiazide: Toxicity

A

Hypokalemic metabolic alkalosis

20
Q

K+ sparing diuretics

A

Spironolactone and eplerenone; Triametereme, Amiloride

21
Q

Spironolactone & Eplerenone

A

Competitive aldosterone receptor antagonists in the cortical collecting tubule

22
Q

Triamterene & Amlioride

A

Block Na channels in the CCT

23
Q

K+ sparing diuretics: Clinical Use

A

Hyperaldosteronism, K+ depletion, CHF

24
Q

K+ sparing diuretics: Toxicity

A

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*