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Pharmacology > Pharmacology-Renal > Flashcards

Pharmacology-Renal Flashcards

1
Q

Name the drugs that work at the PCT:

A

mannitol, acetazolamide

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2
Q

Name the drugs that work at the Thick Ascending LOH

A

loop diuretics: furosemide, ethacrynic acid

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3
Q

Name the drugs that work at the DCT

A

hydrochlorothiazide

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4
Q

Name the drugs that work at the collecting duct

A

K+ sparing diuretics

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5
Q

name the K+ sparing diuretics:

A

spironolactone, eplerenone, amiloride, triamterine

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6
Q

Mannitol – mechanism

A
  • osmotic diuretic (increases tubular fluid osmolarity), increased urine flow
  • decreased intracranial and intraoccular pressure
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7
Q

Mannitol – site of action

A

PCT

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8
Q

Mannitol – use

A

Drug overdose, hydrocephaly, glaucoma

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9
Q

Mannitol – toxicity

A

pulmonary edema, dehydration

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10
Q

Mannitol – contraindications

A

anuria, CHF

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11
Q

Acetazolamide – mechanism

A
  • carbonic anhydrase inhibitor

- self-limited NaHCO3 diuresis and reduction in total-body HCO3- stores

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12
Q

Acetazolamide – site of action

A

PCT

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13
Q

Acetazolamide – use

A
  • Glaucoma
  • Urinary alkinization, metabolic alkalosis, alt. sickness
  • pseudotumor cerebri
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14
Q

Acetazolamide – toxicity

A
  • hyperchloremic metabolic acidosis
  • paresthesias
  • NH3 toxicity
  • sulfa allergy
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15
Q

Loop diuretics – names

A

furosemide, ethacrynic acid

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16
Q

Furosemide – type of loop diuretic

A

sulfonamide loop diuretic

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17
Q

Furosemide – mechanism

A
  • inhibits cotransport system (Na+, K+, 2Cl-) of thick ascending limb
  • abolishes hypertonicity of medulla, preventing [] of urine
  • Ca2+ excretion
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18
Q

What does furosemide stimulate the release of? effects?

A

PGE, vasodilatory effect on afferent arteriole

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19
Q

What is furosemide inhibited by?

A

NSAIDS

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20
Q

Furosemide – use

A

edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia

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21
Q

Furosemide – toxicity

A 
OH DANG!
O - ototoxicity
H - hypokalemia
D - dehydration
A - allergy (sulfa)
N - nephritis (intersitial)
G - gout
22
Q

Ethacrynic acid – type of Loop diuretic

A

phenoxyacetic acid derivative ** NOT A SULFA

23
Q

Ethacryic acid – action

A

same as furosemide

24
Q

ethacrynic acid – use

A

diuresis in patients allergic to sulfa drugs

25
Q

Ethacrynic acid – toxicity

A

similar to furosemide

CAN CAUSE HYPERURICEMIA – NEVER USE TO TREAT GOUT!

26
Q

Hydrochlorothiazide – site of action

27
Q

Hydrochlorothiazide – mechanism

A
  • Thiazide diuretic
  • (-) NaCl reabsorption in early DCT
  • reduces diluting capacity of the nephron
  • decrease Ca2+ excretion
28
Q

Hydrochlorothiazide – use

A

HTN, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus

29
Q

Hydrochlorothiazide – toxicity

A
  • Hypokalemic metabolic alkalosis, Hyponatremia
  • (Hyper)GLUC: hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia
  • Sulfa allergy
30
Q

K+ sparing diuretics – names

A

SEAT – Spironolactone, Ethacrynic acid, Amiloride, Triamterene

31
Q

K+ sparing diuretics – site of action

A

cortical collecting tubule

32
Q

Spironolactone, Eplerenone – mechanism

A

competetive aldosterone receptor antagonists

33
Q

Triamterene, amiloride – mechanism

A

Block Na+ channels

34
Q

K+ sparing diuretics – use

A

hyperaldosteronism, K+ depletion, CHF

35
Q

K+ sparing diuretics – toxicity

A

hyperkalemia -> arrhythmias

36
Q

Spironolactone – toxicity

A

endocrine effects (gynecomastia, antiandrogenic effects)

37
Q

Diuretic induced electrolyte change: Urine NaCl

A
  • increase in all diuretics

- NaCl in serum may decrease as a result

38
Q

Diuretic induced electrolyte change: Urine K+

A
  • increase in all diuretics except K+sparing

- serum K+ decrease as result

39
Q

Diuretic induced electrolyte change: Decreased Blood pH

A

carbonic anhydrase inhibitors – decrease HCO3- reabsorption
K+ sparing – aldosterone blockade prevent K+ and H+ secretion
- hyperkalemia -> K+ entering all cels via H+/K+ exchanger so H+ exits and leads to more H+ in blood

40
Q

Diuretic induced electrolyte change: Increased Blood pH

A

loops and thiazides via contraction alkalosis and paradoxical aciduria

41
Q

Explain contraction alkalosis

A

volume contraction, leading to increased angiotensin II, therefore increased Na+/H+ exchange in PCT leading to increased HCO3- reabsorption

42
Q

Explain paradoxical aciduria

A
  • K+ loss leads to K+ exiting all cells (H+/K+ exchanger) in exchange for H+ entering cells
  • In low K+ state, H+ rather than K+ is exchanged for Na+ in cortical collecting tubule leading to alkalosis
43
Q

Diuretic induced electrolyte change: increased Urine Ca2+

A

with loop diuretics: decrease paracellular Ca2+ reabsorption leading to hypocalcemia

44
Q

Diuretic induced electrolyte change: decreased urine Ca2+

A

thiazides: enhanced paracellular Ca2+ reabsorption in proximal tubule and LOH

45
Q

ACE inhibitors: names

A

captopril, enalapril, lisinopril (-pril)

46
Q

Ace inhibitors: mechanism

A

(-)ACE -> decrease ATII, leading to decreased GFR by (-) constriction of efferent arterioles
- renin increase because loss of feedback inhibition

47
Q

ACE-I use

A

HTN, CHF, proteinuria, diabetic renal dz

48
Q

ACE-I prevent what two things

A

unfavorable heart remodeling and diabetic nephropathy

49
Q

ACE-I toxicity

A

“Captoprils CATCHH”

Cough (prevent inactivation of bradykinin a potent vasodilator), Angioedema, Teratogen (fetal renal malformations), Creatinine increase (decrease GFR), Hyperkalemia, Hypotension

50
Q

ACE-I contraindications

A

avoid in bilateral renal artery stenosis because ACE-I will further decrease GFR, leading to renal failure

51
Q

ARB’s: name

A

“-sartan” eg: losartan

52
Q

ARB’s – toxicity difference with ACE-I

A

do not increase bradykinin so no cough or angioedema

Pharmacology (12 decks)

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