Unit 4- Diuretics Flashcards

1
Q

Acetazolamide

Drug class

A

Carbonic anhydrase inhibitors

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2
Q

Acetazolamide

Mechanism

A

Inhibits luminal carbonic anhydrase at proximal tubule –> less activity of Na/H antiporter, decreased HCO3 and Na+ (and water) reabsorption

FeNa = 5%

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3
Q

Acetazolamide

Uses

A

Decrease intraocular volume/pressure and the prevention and treatment of mountain sickness

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4
Q

Acetazolamide

Side effects

A

Increased K+ excretion and metabolic acidosis

Hepatic encephalopathy, BM depression, skin toxicity, allergic reactions

Contraindicated in cirrhotic patients;

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5
Q

Methazolamide

Drug class

A

Carbonic anhydrase inhibitors

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6
Q

Methazolamide

Mechanism

A

Inhibits luminal carbonic anhydrase at proximal tubule –> less activity of Na/H antiporter, decreased HCO3 and Na+ (and water) reabsorption

FeNa = 5%

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7
Q

Methazolamide

Uses

A

Decrease intraocular volume/pressure and the prevention and treatment of mountain sickness

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8
Q

Methazolamide

Side effects

A

Increased K+ excretion and metabolic acidosis

Hepatic encephalopathy, BM depression, skin toxicity, allergic reactions

Contraindicated in cirrhotic patients;

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9
Q

Dichlorphenamide

Drug class

A

Carbonic anhydrase inhibitors

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10
Q

Dichlorphenamide

Mechanism

A

Inhibits luminal carbonic anhydrase at proximal tubule –> less activity of Na/H antiporter, decreased HCO3 and Na+ (and water) reabsorption

FeNa = 5%

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11
Q

Dichlorphenamide

Uses

A

Decrease intraocular volume/pressure and the prevention and treatment of mountain sickness

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12
Q

Dichlorphenamide

Side effects

A

Increased K+ excretion and metabolic acidosis

Hepatic encephalopathy, BM depression, skin toxicity, allergic reactions

Contraindicated in cirrhotic patients;

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13
Q

Aminophylline

Drug class

A

Bronchodilator (Methylxanthine)

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14
Q

Aminophylline

Mechanism

A

Phosphodiesterase inhibition and enhanced signalling via increased cAMP and cGMP; works at proximal tubule; decreased HCO3 and Na+ (and water) reabsorption

FeNa = 5%; aminophylline = theophylline + ethyelenediamine (solubility agent); metabolized by liver;

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15
Q

Aminophylline

Uses

A

Reduce inflammation and bronchospasm in moderate to severe asthma, night symptoms;

NOT as diuretic

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16
Q

Aminophylline

Side effects

A

Larger doses give nausea, vomiting, CNS stimulation or seizures, tachycardia/arrythmias

cimetidine and quinoline increase blood levels

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17
Q

Mannitol

Drug class

A

Osmotic diuretic

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18
Q

Mannitol

Mechanism

A

Opposes water and sodium reabsorption at proximal tubule –> increased osmolarity of tubular fluid

FeNa = 5%; must give IV; other osmotic diuretics include glucose, urea, isorbide

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19
Q

Mannitol

Uses

A

Increased clearance of drugs, minimize renal failure (shock or surgery), decrease intraocular or intracranial pressures, diagnose oliguria

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20
Q

Mannitol

Side effects

A

Risk of pulmonary edema

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21
Q

Furosemide

Drug class

A

Loop diuretic (- charge)

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22
Q

Furosemide

Mechanism

A
  • Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption, resultant K+ loss
  • FeNa = 25%; eventually causes increase in PT reabsorption,decreases positive & negative free water clearance; decreases cortex-medulla molarity gradient;
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23
Q

Furosemide

Uses

A
  • Crisis edema (pulmonary, CHF, cirrhosis), hypercalcemia, drug toxicity/OD; severe hypertension in setting of CHF or cirrhosis
  • take before salty meals, reduce salt intake; useful in patients with renal insufficiency (GFR < 30-40)
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24
Q

Furosemide

Side effects

A
  • Hypokalemia/hypocalcemia/hypomagnesemia (–> arrhythmia), contraction alkalosis, increased BUN & creatinine, ototoxicity (esp. w/aminoglycoside)
  • Hyper -glycemia, -lipidemia, -uricemia; hypo -magnesia, -natremia; gout, photosensitivity, nephrocalcinosis, drug interactions; erectile dysfunction
  • Avoid NSAIDs
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25
Q

Bumetanide

Drug class

A

Loop diuretic (- charge)

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26
Q

Bumetanide

Mechanism

A
  • Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption, resultant K+ loss
  • FeNa = 25%; eventually causes increase in PT reabsorption,decreases positive & negative free water clearance; decreases cortex-medulla molarity gradient;
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27
Q

Bumetanide

Uses

A
  • Crisis edema (pulmonary, CHF, cirrhosis), hypercalcemia, drug toxicity/OD; severe hypertension in setting of CHF or cirrhosis
  • take before salty meals, reduce salt intake; useful in patients with renal insufficiency (GFR < 30-40)
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28
Q

Bumetanide

Side effects

A
  • Hypokalemia/hypocalcemia/hypomagnesemia (–> arrhythmia), contraction alkalosis, increased BUN & creatinine, ototoxicity (esp. w/aminoglycoside)
  • Hyper -glycemia, -lipidemia, -uricemia; hypo -magnesia, -natremia; gout, photosensitivity, nephrocalcinosis, drug interactions; erectile dysfunction
  • Avoid NSAIDs
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29
Q

Ethacrynic acid

Drug class

A

Loop diuretic (- charge)

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30
Q

Ethacrynic acid

Mechanism

A
  • Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption, resultant K+ loss
  • FeNa = 25%; eventually causes increase in PT reabsorption,decreases positive & negative free water clearance; decreases cortex-medulla molarity gradient;
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31
Q

Ethacrynic acid

Uses

A
  • Crisis edema (pulmonary, CHF, cirrhosis), hypercalcemia, drug toxicity/OD; severe hypertension in setting of CHF or cirrhosis; sulfa-free
  • useful in patients with renal insufficiency (GFR < 30-40)
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32
Q

Ethacrynic acid

Side effects

A
  • Hypokalemia/hypocalcemia/hypomagnesemia (–> arrhythmia), contraction alkalosis, increased BUN & creatinine, ototoxicity (esp. w/aminoglycoside)
  • Hyper -glycemia, -lipidemia, -uricemia; hypo -magnesia, -natremia; gout, photosensitivity, nephrocalcinosis, drug interactions; erectile dysfunction
  • Avoid NSAIDs
33
Q

Chlorthiazide

Drug class

A

Thiazide diuretic (- charge)

34
Q

Chlorthiazide

Mechanism

A

Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss

35
Q

Chlorthiazide

Uses

A

HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus

36
Q

Chlorthiazide

Side effects

A

Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine

Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions

FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance

37
Q

Hydrochlorothiazide

Drug class

A

Thiazide diuretic (- charge)

38
Q

Hydrochlorothiazide

Mechanism

A

Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss

39
Q

Hydrochlorothiazide

Uses

A

HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus

40
Q

Hydrochlorothiazide

Side effects

A

Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine

Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions

FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance

41
Q

Chlorthalidone

Drug class

A

Thiazide-like diuretic

42
Q

Chlorthalidone

Mechanism

A

Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss

43
Q

Chlorthalidone

Uses

A

Reduce stroke risk, CHF events; HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus

44
Q

Chlorthalidone

Side effects

A

Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine

Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions

FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance

45
Q

Quinethazone

Drug class

A

Thiazide-like diuretic

46
Q

Quinethazone

Mechanism

A

Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss

47
Q

Quinethazone

Uses

A

HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus

48
Q

Quinethazone

Side effects

A

Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine

Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions

FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance

49
Q

Metolazone

Drug class

A

Thiazide-like diuretic

50
Q

Metolazone

Mechanism

A

Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss

51
Q

Metolazone

Uses

A

HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus

52
Q

Metolazone

Side effects

A

Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine

Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions

FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance

53
Q

Indapamide

Drug class

A

Thiazide-like diuretic

54
Q

Indapamide

Mechanism

A

Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss

55
Q

Indapamide

Uses

A

HTN (intravascular contraction), chronic edema (cardiac insufficiency), idiopathic hypercalciuria (stones), nephrogenic diabetes insipidus

56
Q

Indapamide

Side effects

A

Hypokalemia/hypercalcemia, contraction alkalosis, increased BUN & creatinine

Hyper -glycemia, -lipidemia, -uricemia, -calcemia; hypo -magnesia, -natremia; gout, photosensitivity, impotence, drug interactions

FeNa = 8%; lethal interaction w/quinidine (v. tach –> fib, may be due to hyperkalemia); avoid NSAIDs, bile sequestrants; increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B; decreases positive free water clearance

57
Q

Amiloride

Drug class

A

K+-sparing diuretic; renal ENaC inhibitor (+ charge)

58
Q

Amiloride

Mechanism

A

Blocks Na channel and Na/H antiporter in lumenal membrane at the late distal tubule and collecting duct –> decreased K+ secretion and distal tubule acid secretion, increased Ca++ absorption

59
Q

Amiloride

Uses

A

Combination with other diuretics to prevent hypokalemia; edema, idiopathic hypercalciuria (stones); lithium-induced polyuria & toxicity, Liddle syndrome, mucocilliary clearance

60
Q

Amiloride

Side effects

A

Hyperkalemia in patients with renal failure or on ACE inhibitors

Contraindicated in patients with renal failure (hyperkalemia), ACEi/ARB use; FeNa = 2%

61
Q

Torsemide

Drug class

A

Loop diuretic (- charge)

62
Q

Torsemide

Mechanism

A

Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption, resultant K+ loss

63
Q

Torsemide

Uses

A

Crisis edema (pulmonary, CHF, cirrhosis), hypercalcemia, drug toxicity/OD; severe hypertension in setting of CHF or cirrhosis

64
Q

Torsemide

Side effects

A

Hypokalemia/hypocalcemia/hypomagnesemia (–> arrhythmia), contraction alkalosis, increased BUN & creatinine, ototoxicity (esp. w/aminoglycoside)

Hyper -glycemia, -lipidemia, -uricemia; hypo -magnesia, -natremia; gout, photosensitivity, nephrocalcinosis, drug interactions; erectile dysfunction

FeNa = 25%; eventually causes increase in PT reabsorption,decreases positive & negative free water clearance; decreases cortex-medulla molarity gradient; avoid NSAIDs, take before salty meals, reduce salt intake; useful in patients with renal insufficiency (GFR < 30-40)

65
Q

Triamterene

Drug class

A

K+-sparing diuretic; renal ENaC inhibitor (+ charge)

66
Q

Triamterene

Mechanism

A

Blocks Na channel and Na/H antiporter in lumenal membrane at the late distal tubule and collecting duct –> decreased K+ secretion and distal tubule acid secretion, increased Ca++ absorption

67
Q

Triamterene

Uses

A

Combination with other diuretics to prevent hypokalemia; edema

68
Q

Triamterene

Side effects

A

Hyperkalemia in patients with renal failure or on ACE inhibitors

Megaloblastic anemia in patients with liver cirrhosis

Contraindicated in patients with renal failure (hyperkalemia); FeNa = 2%

69
Q

Spironolactone

Drug class

A

K+-sparing diuretic; aldosterone receptor antagonist

70
Q

Spironolactone

Mechanism

A

Competes for aldosterone receptor, inhibiting mRNA transcription and translation –> decreased Na and K channels, decreased number and activity of Na-K-ATPase pumps in the late distal tubule and collecting duct –> decreased K+ secretion, distal tubule acid secretion

71
Q

Spironolactone

Uses

A

Reduction in CHF mortality (30% in NYHA class III and IV); combination with other diuretics to prevent hypokalemia; edema; primary and secondary aldosteronism; hypertension; anti-testosterone agent

72
Q

Spironolactone

Side effects

A

Hyperkalemia in patients with renal failure or on ACE inhibitors; male patients may have gynecomastia, erectile dysfunction, and loss of libido; female patients may have amenorrhea, breast soreness, and oligomenorrhea

Contraindicated in patients with renal failure (hyperkalemia); FeNa = 2%; requires a salt-restricted diet; only drug not requiring tubular lumen access

73
Q

Conivaptan

Drug class

A

Aquaretic

74
Q

Conivaptan

Mechanism

A

Vasopressin (ADH) receptor antagonist working at collecting duct –> increased free water excretion

75
Q

Conivaptan

Uses

A

Hyponatremia (SIADH, CHF)

New drug class with unproven clinical benefit

76
Q

Tolvaptan

Drug class

A

Aquaretic

77
Q

Tolvaptan

Mechanism

A

Vasopressin (ADH) receptor antagonist working at collecting duct –> increased free water excretion

78
Q

Tolvaptan

Uses

A

Hyponatremia (SIADH, CHF)

New drug class with unproven clinical benefit