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FA Active Learning > FA - Renal Pharmacology > Flashcards

FA - Renal Pharmacology Flashcards

1
Q

What is the osmolarity in Bowman’s capsule?

A

290 mOsm (isotonic)

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2
Q

What is the osmolarity in PCT?

A

290 mOsm (isotonic)

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3
Q

What diuretics act on the PCT?

A

Acetazolamide (CA inhibitor)

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4
Q

What is the osmolarity in the proximal straight tubule?

A

600 mOsm

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5
Q

What diuretics act on the proximal straight tubule?

A

Mannitol

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6
Q

What is the osmolarity in the thin descending limb of Henle?

A

800 mOsm

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7
Q

What is the osmolarity at the bottom of the loop of Henle?

A

1200 mOsm

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8
Q

What is the osmolarity in the TAL?

A

600 mOsm

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9
Q

What diuretics act on the TAL?

A

Loop diuretics (furosemide, torsemide), ethacrynic acid

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10
Q

What is the osmolarity in the DCT?

A

80-100 mOsm

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11
Q

What diuretics act on the DCT?

A

Thiazides

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12
Q

What is the osmolarity in the CD?

A

50 - 1200 mOsm (depends on action of ADH)

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13
Q

What diuretics act on the CD?

A

Potassium-sparing diuretics (spironolactone, eplerenone, amiloride, triamterene)

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14
Q

What is the MOA of mannitol?

A

Osmotic diuretic –>increases tubular fluid osmolarity producing increased urine flow, decreased ICP/IOP

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15
Q

What are the clinical uses of mannitol?

A

Drug overdose, elevated ICP/IOP

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16
Q

What are the AEs of mannitol?

A

Pulmonary edema, dehydration, dilutional hyponatremia, hyperkalemia, metabolic acidosis

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17
Q

What are the contraindications for mannitol use?

A

Anuria, CHF

18
Q

What is the MOA of acetazolamide?

A

CA inhibitor; causes self-limited NaHCO3 diuresis and reduction in total-body HCO3- stores

19
Q

What are clinical uses of acetazolamide?

A

Glaucoma (decreased aqueous humor production), urinary alkalinization, altitude sickness, pseudotumor cerebri, drug-induced edema, CHF

20
Q

What are the AEs of acetazolamide?

A

Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy, hypokalemia

21
Q

What is the MOA of loop diuretics?

A

Inhibits co-transport system (Na+, K+, 2Cl-) of TAL. Abolishes hypertonicity of medulla, preventing concentration of urine.
Stimulates PGE release –>aff arteriole dilation (effect also inhibited by NSAIDs)
Increases Ca++ excretion

22
Q

What are the clinical uses of loop diuretics?

A

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

23
Q

What are the AEs of loop diuretics?

A

Ototoxicity, hypokalemia, dehydration, allergy, nephritis, gout (OH DANG)
Hyperuricemia, hypocalcemia, hypomagnesemia, and metabolic (contraction) alkalosis

24
Q

What is the MOA of ethacrynic acid?

A

Phenoxyacetic acid derivative; works similarly to furosemide

25
Q

What is the clinical use of ethacrynic acid?

A

Diuresis in patients allergic to sulfa drugs

26
Q

What are the AEs of ethacrynic acid?

A

Similar to furosemide; can cause hyperuricemia so do not use to treat gout. Also may generate PVCs if given with digoxin.

27
Q

What is the MOA of thiazide drugs?

A

Inhibits NaCl reabsorption in the early distal tubule, reducing diluting capacity of the nephron –>decreased Ca++ excretion

28
Q

What are the clinical uses of thiazides?

A

HTN (including isolated systolic HTN), CHF, idiopathic hypocalciuria, nephrogenic DI

29
Q

What are the AEs of thiazides?

A

Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy

30
Q

What is the MOA of K+ sparing diuretics?

A

Spiro and eplerenone: competitive MR antagonists

Amiloride and triamterene: block Na+ channels in CCTs

31
Q

What are the clinical uses of K+ sparing diuretics?

A

Hyperaldosteronism, K+ depletion, CHF (spiro used to prevent aldosterone-mediated adverse remodeling in stage III/IV HF)

32
Q

What are the AEs of K+ sparing diuretics?

A

Hyperkalemia, endocrine effects with spironolactone (gynecomastia, antiandrogenic effects)

33
Q

How is urine NaCl affected with diuretic use?

A

Increased, may also see decreased serum NaCl

34
Q

How is urine K+ affected with diuretic use?

A

Increased (except for K+ sparing), serum K+ may decreased as a result

35
Q

How is blood pH affected by diuretic use?

A

Acidemia with CA inhibitors and K+ sparing diuretics, alkalemia with loop diuretics and thiazides

36
Q

How is urine Ca++ affected by diuretic use?

A

Increases with loop diuretics, decreases paracellular Ca++ reabsorption –>hypocalcemia
Decreases with thiazide use, enhances paracellular Ca++ reabsorption in PCT and loop of Henle

37
Q

What is the MOA of ACE inhibitors?

A

Inhibit ACE –>decrease ANGII –>decrease GFR by preventing efferent arteriole constriction
Also prevents inactivation of bradykinin –>vasodilator
Results in increased renin production

38
Q

What are the clinical uses of ACEi?

A

HTN, CHF, diabetic renal dz, prevents unfavorable heart remodeling as a result of chronic HTN

39
Q

What are the AEs of ACEi’s?

A

Cough, angioedema, teratogen (fatal renal malformations), creatinine increase as a result of dec. GFR, hyperkalemia, hypotension (esp. 1st dose)
Avoid in bilateral renal artery stenosis due to dec GFR effect

40
Q

What is the MOA of ARBs?

A

Prevent action of ANGII at AT1 receptor; no effect on bradykinin

41
Q

What are the clinical uses of ARBs?

A

Similar to ACEi

42
Q

What are the AEs of ARBs?

A

Similar to ACEi, risk of cough is reduced

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