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Maddy - CPR II - some pharm > Diuretics > Flashcards

Diuretics Flashcards

1
Q

MOA furosemide

A

blocks Na-K-2Cl cotransporter in thick ascending limb, directly inhibiting reabsorption of Na+ and Cl-

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2
Q

spironolactone effects

A

K+ sparing diuretic

  • blunts ability of aldosterone to promote Na+/k+ exchange
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3
Q

spironolactone MOA

A

competitive antagonist of aldosterone receptors

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4
Q

spironolactone clinical app

A
  • counteracts K+ loss induced by other diuretics
  • tx of primary aldosteronism
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5
Q

toxicities of spironolactone

A
  • hyperkalemia
  • amenorrhea, hirsutism, gynecomastia, impotence
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6
Q

furosemide effects

A

increased excretion of water, sodium, potassium, chloride, magnesium, Ca2+

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7
Q

furosemide clinical app

A
  • manages edema
  • decreases preload
  • rapid dyspnea relief
  • HTN
  • ACUTE DECOMPENSATED HEART FAILURE
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8
Q

toxicities of furosemide

A
  • hypokalemia
  • hyponatremia
  • hypocalcemia
  • hypomagnesemia
  • hyperglycemia
  • hyperuricemia
  • ***it’s a sulfa drug so watch for allergies
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9
Q

hydrochlorothiazide MOA

A

blocks Na/Cl cotransporter in distal convoluted tubule

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10
Q

hydrochlorothiazide effects

A

increases urinary excretion of sodium and water, potassium, and magnesium

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11
Q

hydrochlorothiazide clinical app

A
  • HTN
  • edema
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12
Q

toxicities of hydrochlorothiazide

A
  • orthostatic hypotension
  • hypokalemia
  • hypomagnesemia
  • hyponatremia
  • hypochloric metabolic alkalosis
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13
Q

compare torsemide with furosemide

A

longer half life, better oral absorption, works better in heart failure

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14
Q

compare bumetanide with furosemide

A

more predictable oral absorption

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15
Q

when would you use ethacrynic acid instead of furosemide

A

non-sulfonamide loop diuretic reserved for those with sulfa allergies

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16
Q

MOA amiloride

A

blocks epithelial sodium channels (ENaC) in collecting ducts

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17
Q

effects amiloride

A
  • causes small increase in Na+ excretion
  • blocks major pathway for K+ elimination so K+ is retained (K+ sparing)
  • H+, Mg2+, and Ca2+ excretion decreased
18
Q

clinical app amiloride

A

counteracts K+ loss induced by other diuretics in tx of HTN or HF

19
Q

half life and administration amiloride

A

given orally

half life 6-9 hours

20
Q

toxicities amiloride

A

hyperkalemia

  • hyponatremia
  • hypovolemia
  • hyperchloremic metabolic acidosis
  • dizziness, fatigue, HA
  • n/v/d
21
Q

MOA triamterene

A

similar to amiloride (K+ sparing diuretic)

22
Q

MOA eplerenone

A

aldosterone receptor antagonist

(more selective aldosterone antagonist than spironolactone)

23
Q

clinical app eplerenone

A

approved for use in post-MI HF and alone or in combo for tx of HTN

24
Q

MOA conivaptan

A

non-peptide arginine casopressin receptor antagonist

affinity for V1A and V2 receptors

25
Q

effects conivaptan

A

promotes excretion of free water (without loss of serum electrolytes)

  • increases urine output
  • decreases urinary osmolality
  • increases plasma osmolality
26
Q

clinicap app conivaptan

A

tx of euvolemic and hypervolemic hyponatremia in pts who are hospitalized, symptomatic, and not responsive to fluid restriction

27
Q

problems with too rapid serum Na+ correction when using conivaptan

A

can lead to seizures, osmotic demyelination, coma, or death

28
Q

administration of conivaptan

A

IV

29
Q

toxicities conivaptan

A
  • orthostatic hypotension
  • fatigue
  • thirst
  • polyuria, bedwetting
30
Q

MOA tolvaptan

A

V2 receptor antagonist

31
Q

what patients do you give tolvaptan to

A

only patients in a hostpial where plasma sodium can be closely monitored

32
Q

how long do you treat with tolvaptan

A

less than 30 days for hyponatremia because longer use can cause potentially fatal hepatotoxicity

33
Q

clinical app tolvaptan

A

tx for hyponatremia

used to slow progression of adult PKD

34
Q

mannitol MOA

A

osmotic diuretic

  • it is unabled to be reabsorbed –> keeps water in the PCT lumen –> water is delivered to the distal portions of the nephron –> much of it is ultimately excreted
  • acts throughout body to pull water out of cells
35
Q

adverse effects mannitol

A

ECF volume acutely increased –> exacerbates HF

HA, nausea, vomiting, electrolyte imbalances

36
Q

therapeutic uses of mannitol

A

prophylaxis of renal failure

reduction of intracranial and intraocular pressure

37
Q

MOA acetazolamide

A

carbonic anhydrase inhibitor

bicarbonate ion remains in PCT –> H+ cycling is lost –> inhibits Na+/H+ exchange –> Na+ bicarbonate diuresis

38
Q

therapeutic uses carbonic anhydrase inhibitors

A

urinary alkalinization

metabolic alkalosis

glaucoma

acute mountain sickness

39
Q

adverse effects acetazolamide

A

hyperchloremic metabolic acidosis

nephrolithiasis

potassium wasting

40
Q

MOA and therapeutic use metolazone

A

thiazide diuretic

used as adjunct diuretic in tx of CHF

41
Q

MOA and therapeutic uses chlorthalidone

A

thiazide diuretic

often preferred by hypertension specialists

Maddy - CPR II - some pharm (18 decks)

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