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L36 Diuretics Flashcards

1
Q

How do the kidneys control the ECF volume?

A

By adjusting NaCl and H2O excretion

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2
Q

The glomeruli produce ___ ml/min ultrafiltrate; ___ ml/min of urine is formed.

A

120; 1

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3
Q

To maintain NaCl balance, approximately ___ lbs of NaCl must be reabsorbed by the renal tubules on a daily basis.

A

3

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4
Q

What happens when NaCl intake exceeds output?

A

Edema develops

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5
Q

What do diuretics do, generally?

A

Increase urine volume, Na+ excretion, and Cl- excretion; they reduce ECF volume by decreasing NaCl content

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6
Q

What is reabsorption?

A

Movement of a substance from the tubule to the blood

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7
Q

What is secretion?

A

Movement of a substance from the blood to the tubule

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8
Q

What is excretion?

A

Movement of a substance from the collecting tubule into the urine

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9
Q

What is reabsorbed in the proximal convoluted tubule?

A 
85% of filtered HCO3
60% of filtered NaCl
60% of water
80-90% of filtered K+
70% of filtered Ca2+
100% of organic solutes
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10
Q

What is reabsorbed in the thin descending limb of the Loop of Henle?

A

Water

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11
Q

What is reabsorbed in the thick ascending limb of the Loop of Henle?

A

25% NaCl
NO water
25% Ca2+
100% Mg2+

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12
Q

What is reabsorbed in the distal convoluted tubule?

A

10% NaCl
NO water
5% Ca2+ (regulated by PTH)

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13
Q

What is reabsorbed in the collecting tubule?

A

2-5% NaCl

Water (regulated by ADH)

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14
Q

What is secreted in the collecting tubule?

A

K+ and H+ (regulated by aldosterone)

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15
Q

Where does acetazolamide act and what does it do, broadly?

A

Inhibits CA in the proximal convoluted tubule, leading to inhibition of 85% of NaHCO3 reabsorption

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16
Q

Where do osmotic agents (mannitol) act and what do they do, broadly?

A

Limits water reabsorption in the water-permeable segments of the nephron - PCT, TDL, CT (when ADH is present)

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17
Q

Where do loop diuretics (Lasix) act and what do they do, broadly?

A

Inhibits Na/K/2Cl cotransport in the thick ascending limb of Henle’s loop

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18
Q

Where do thiazides act and what do they do, broadly?

A

Inhibit NaCl co-transport in the distal convoluted tubule

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19
Q

Where do potassium sparing diuretics act and what do they do, broadly?

A

Inhibit aldosterone actions or Na+ channels in the collecting tubule

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20
Q

Where do ADH antagonists act and what do they do, broadly?

A

Prevent ADH-stimulated reabsorption of water in the collecting tubule

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21
Q

What is the primary therapeutic goal of diuretic use?

A

Reduction of edema

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22
Q

Except for spironolactone and some ADH antagonists, diuretics generally exert their effects…

A

…from the luminal side of the nephron

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23
Q

How do most diuretics (besides mannitol) get into the tubule fluid?

A

Secretion across the PT (organic acid/base secretory pathway)

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24
Q

How does mannitol get into the tubule fluid?

A

Filtration at the glomerulus

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25
Q

What two major issues can reduce diuretic effectiveness?

A
  1. Decreased renal blood flow/renal failure

2. Drugs that compete for the secretory pump

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26
Q

Which drug competes for acidic drugs? Which drug competes for basic drugs?

A

Acidic: probenecid
Basic: cimetidine

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27
Q

The apical side of the epithelial cells face the ___; the basolateral side faces the ___.

A

Lumen; blood

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28
Q

What drives sodium reabsorption in tubule epithelial cells?

A

Na/K ATPase at the basolateral side of the epithelial cells (3 Na out, 2K in)

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29
Q

Describe the Na and K concentrations in the tubule epithelial cells.

A

Low Na, High K

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30
Q

Describe the ion transport in the proximal convoluted tubule.

A

Apical side:

  1. Na/H exchanger (Na in, H out)
  2. Cl/base exchanger (Cl in, base out)

Inside the cell: CA converts CO2 and H2O to H2CO3, which becomes H+ and HCO3. The H+ is used in the Na/H exchanger. the HCO3 is used on the basolateral side.

Basolateral side:

  1. Na/K ATPase (K in, Na out)
  2. HCO3 transporter (out)
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31
Q

What is the net effect of transport in the PCT?

A

Reabsorption of Na+ and bicarbonate

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32
Q

What is the MOA of acetazolamide?

A

Reversible inhibition of CA

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33
Q

What are the pharmacodynamics of acetazolamide?

A

Inhibition of reabsorption of bicarbonate in the PCT

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34
Q

Describe the absorption and timing of effects of acetazolamide.

A

Well-absorbed orally
Effect begins in 30 minutes, maximum at 2 hours
Duration of effect: 12 hours

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35
Q

How does acetazolamide get into the tubule?

A

Organic acid transporter

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36
Q

What are the adverse effects of acetazolamide?

A
  1. Metabolic acidosis
  2. Hypokalemia
  3. Calcium phosphate stones
  4. Drowsiness, parasthesias
  5. Hypersensitivity
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37
Q

What are the contraindications of acetazolamide?

A
  1. Cirrhosis (increased urine pH reduces NH3 secretion, increasing serum NH3)
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38
Q

What are the 3 other CA inhibitors?

A
  1. Dichlorphenamide
  2. Methazolamide
  3. Dorzolamide
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39
Q

Discuss the relative potencies of dichlorphenamide and methazolamide to acetazolmide.

A

Dichlorphenamide: 30x more potent
Methazolamide: 5x more potent

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40
Q

How is dorzolamide used?

A

Topically for ocular use

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41
Q

What are the clinical indications of acetazolamide?

A
  1. Diuretic agent (weak, okay backup)
  2. Glaucoma
  3. Urinary alkalinization (OD, stones)
  4. Acute mountain sickness
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42
Q

What is the MOA of mannitol?

A

Osmotic diuresis in PCT, DTL, CT (w/ADH)

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43
Q

Discuss the pharmacodynamics of mannitol.

A

Expansion of intravascular volume that leads to a powerful diuretic effect once it reaches the kidney

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44
Q

Describe the absorption and half-life of mannitol.

A

IV injection only; half-life = 1.2 hours

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45
Q

Generally, when are adverse effects seen with mannitol?

A

When filtration is impaired

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46
Q

What are the adverse effects of mannitol?

A
  1. Reduced GFR retains mannitol in the ECF, which moves water out of the cells into the ECF, worsening edema/heart failure. Na+ follows, leading to hyponatremia.
  2. Acute pulmonary edema
  3. Dehydration
  4. Headache/nausea/vomiting
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47
Q

What are the contraindications of mannitol?

A

CHF, renal failure, pulmonary edema

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48
Q

What are the clinical indications of mannitol?

A
  1. Maintain/increase urine volume (treat/prevent acute renal failure, promote excretion of toxic substances)
  2. Reduce intracranial pressure
  3. Glaucoma
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49
Q

What is the difference in epithelium in the thin and thick segments of the Loop of Henle?

A

Thin: simple squamous
Thick: simple cuboidal

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50
Q

Describe the ion transport in the thick ascending limb.

A

Apical:

  1. Na/K/2Cl cotransporter (all 3 in)
  2. K transporter (out) - creates + charge in lumen, which drives paracellular diffusion of Ca2+/Mg2+ into the blood

Basolateral:

  1. Na/K ATPase (K in, Na out)
  2. K/Cl transporter (both out)
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51
Q

What is the most efficacious diuretic class?

A

Loop diuretics

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52
Q

What is the MOA of furosemide (Lasix)?

A

Inhibition of Na/K/Cl cotransport & vasodilation

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53
Q

What are the pharmacodynamics of furosemide?

A

Inhibition of the cotransporter reduces Na/K/Cl reabsorption, as well as Ca2+/Mg2+ due to loss of + luminal charge

Renal vasodilation improves renal blood flow

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54
Q

Describe the absorption, half-life, and duration of furosemide.

A

Rapid oral absorption; 1-1.5 hours half-life; duration = 2-3 hours

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55
Q

How does furosemide get into the tubules?

A

Organic acid transporter

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56
Q

What are the adverse effects of furosemide?

A
  1. Hyponatremia/hypokalemia/hypomagnesemia
  2. Dehydration
  3. Metabolic alkalosis
  4. Mild hyperglycemia
  5. Ototoxicity
  6. Hypersensitivity
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57
Q

What are the indications of furosemide?

A
  1. Acute pulmonary edema
  2. Edema w/CHF
  3. Acute hypercalcemia
  4. Acute hyperkalemia
  5. Hypertension
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58
Q

What are the 3 other loop diuretics?

A
  1. Bumetanide
  2. Torsemide
  3. Ethacrynic acid
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59
Q

Discuss the relative potency of bumetanide compared to furosemide.

A

40x more potent

60
Q

Discuss the relative half-lives of bumetanide and torsemide compared to furosemide.

A

Bumetanide: 1 hour
Torsemide: 3 hours (5-6 hour duration of action)

61
Q

Which loop diuretic has better oral absorption that furosemide?

62
Q

Why is ethacrynic acid a last resort?

A

Used only when others exhibit hypersensitivity, as it is nephrotoxic and ototoxic

63
Q

Describe the ion transport in the distal convoluted tubule.

A

Apical:

  1. Na/Cl transporter (both in)
  2. Ca2+ channel (in)

Basolateral:

  1. Na/K ATPase (K in, Na out)
  2. Na/Ca antiporter (Na in, Ca out)
  3. Receptor for PTH
64
Q

What does PTH control in the DCT?

A

Ca2+ reabsorption

65
Q

What is the most commonly used class of diuretics?

66
Q

What is the MOA of hydrochlorothiazide?

A

Inhibition of Na/Cl contransporter in the distal tubule

67
Q

What are the pharmacodynamics of hydrochlorothiazide?

A

Produces relatively mild diuresis and increased Ca2+ reabsorption

68
Q

Describe the absorption and half-life of hydrochlorothiazide.

A

Good oral; half-life = 2.5 hours

69
Q

What are the adverse effects of hydrochlorothiazide?

A
  1. Hyponatremia/hypokalemia
  2. Dehydration
  3. Metabolic alkalosis
  4. Hyperuricemia
  5. Hyperglycemia
  6. Hyperlipidemia (increased LDL)
  7. Weakness, fatigue, paresthesias
  8. Hypersensitivity
70
Q

What are the indications of hydrochlorothiazide?

A
  1. Hypertension
  2. CHF
  3. Reduced Ca2+ excretion to prevent kidney stones
71
Q

What are 4 other thiazide diuretics?

A
  1. Chlorothiazide
  2. Metolazone
  3. Indapamide
  4. Chlorthalidone
72
Q

Discuss the relative potencies and half-lives of the 4 thiazide diuretics to hydrochlorothiazide.

A

Chlorothiazide: 1/10 potency, 1.5 hours half life

Metolazone: 10x more potent, 4-5 hours half life

Indapamide: 20x more potent, 10-22 hours half life

Chlorthalidone: same potency, 44 hour half-life

73
Q

What is the most efficacious thiazide diuretic?

A

Metolazone

74
Q

What are the two types of cells in the collecting tubules?

A

Principal and intercalated

75
Q

Describe the ion transport in the principal cells of the collecting tubule.

A

Apical:

  1. Na, K, H2O channels (Na/H2O in, K out)
  2. Cl- (paracellular transport in - net negative charge of Na absorption > K secretion repels Cl- and attracts K into the lumen)

Basolateral:
1. Na/K ATPase (K in, Na out)

76
Q

___ regulates expression of Na/K ATPase and channels in the principal cells.

A

Aldosterone

77
Q

___ regulates water channels and water reabsorption in the principal cells.

78
Q

Describe the ion transport in the intercalated cells of the collecting tubule.

A

Apical:
1. H+ ATPase (H+ out)

Basolateral:
1. HCO3/Cl antiporter (HCO3 out, Cl in)

79
Q

The H+ ATPase of the intercalated cells is regulated by ___.

A

Aldosterone

80
Q

Discuss how hypokalemia arises in the setting of acetazolamide and other CA inhibitors.

A

These drugs increase HCO3 in the tubule, leading to increased lumen negative potential. In the collecting tubule, this enhances K+ efflux from the principal cells, leading to hypokalemia.

81
Q

Discuss how hypokalemia arises in the setting of loop and thiazide diuretics.

A

These drugs increase Na/Cl, leading to increased lumen negative potential. In the collecting tubule, this enhances K+ efflux from the principal cells, leading to hypokalemia.

82
Q

Discuss how metabolic alkalosis arises in the setting of loop and thiazide diuretics.

A

These drugs increase Na/Cl, leading to increased lumen negative potential. In the collecting tubule, this enhances H+ efflux from the intercalated cells, leading to metabolic alkalosis.

83
Q

What are potassium sparing diuretics?

A

Agents often given to avoid hypokalemia that accompanies CA inhibitors, loop diuretics, and thiazide diuretics

84
Q

When are potassium sparing diuretics contraindicated?

A

Setting of hyperkalemia or in patients on drugs or with diseases states likely to cause hyperkalemia (diabetes mellitus, multiple myeloma, tubulointerstitial renal disease, renal insufficiency)

85
Q

What are 2 common drugs that can cause hyperkalemia?

A

Potassium supplements and ACE inhibitors

86
Q

What is the MOA of spironolactone?

A

Competitive inhibition of the aldosterone receptor + anti-androgenic effects (decreases testosterone synthesis, competitively inhibits DHT receptor)

87
Q

Discuss the pharmacodynamics of spironolocatone.

A

Causes mild diuresis due to decreased Na+ reabsorption secondary to aldosterone inhibition; spares K+/H+

88
Q

Describe the onset of action of spironolocatone.

A

Slow, takes days to have an effect

89
Q

What are the adverse effects of spironolactone?

A
  1. Hyperkalemia (most important)
  2. Metabolic acidosis
  3. Gynecomastia/amenorrhea/impotence/decreased libido
  4. GI upset (peptic ulcers)
  5. CNS effects (headache, fatigue, confusion)
90
Q

What is eplerenone?

A

Competitive antagonist of aldosterone binding (more expensive, but not anti-androgen efects)

91
Q

How does spironolactone cause metabolic acidosis?

A

By blocking aldosterone binding, Na+ and H+ channels are expressed less. This decreases the lumen negative potential and reduces the driving force for H+, which remains in the blood, leading to decreased pH.

92
Q

What are the indications of spironolactone?

A
  1. Primary hyperaldosteronism
  2. Secondary hyperaldosteronism
  3. Liver cirrhosis
  4. Hypertension
93
Q

What is the MOA of amiloride?

A

Blocks Na+ channels in the principal cells

94
Q

Discuss the pharmacodynamics of amiloride.

A

Blocking Na+ influx decreases the driving force for K+ efflux, so K+ is spared

95
Q

What is the half-life of amiloride?

96
Q

How does amiloride get into the tubules?

A

Secreted via the organic base transporter

97
Q

What are the adverse effects of amiloride?

A
  1. Hyperkalemia (exacerbated by NSAIDs)
  2. GI upset (nausea, vomiting, diarrhea)
  3. Muscle cramps
  4. CNS effects (headache, dizziness, etc.)
98
Q

How does amiloride cause hyperkalemia?

A

Blocking Na+ influx decreases the lumen negative potential and reduces K+ efflux

99
Q

What are the clinical indications of amiloride?

A
  1. Edema
  2. Hypertension
  3. Combined with other diuretics to reduce K+ loss
100
Q

What is the MOA of triamterene?

A

Blocks Na+ channels in the principal cells

101
Q

Discuss the pharmacodynamic of triamterene?

A

Blocking Na+ influx decreases the driving force for K+ efflux so K+ is spared; active form can precipitate and obstruct tubular flow

102
Q

What is the half-life and relative potency of trimaterene to amiloride?

A

4 hours; 10x less potent

103
Q

How does triamterene get into the tubules?

A

Secreted via the organic base transporter

104
Q

What are 2 old ADH antagonists and what are kind of drugs are they?

A
  1. Demeclocycline (tetracycline antibiotic)
  2. Lithium (treatment of mania)

Both are nephrotoxic

105
Q

What is the MOA of Tolvaptan?

A

ADH antagonism; elective antagonist of vasopressin V2 receptor; induces increased, dose-dependent production of dilute urine without altering electrolyte balance

106
Q

How is Tolvaptan absorbed and what is its half-life?

A

Oral; 6-8 hours

107
Q

What are the 3 V2 receptor antagonists?

A

Tolvaptan
Mozavaptan
Lixivaptan

108
Q

What is the V1a and V2 receptor agonist?

A

Conivaptan

109
Q

What are the adverse effects of ADH antagonists?

A
  1. Hypernatremia
  2. Thirst
  3. Dry mouth
  4. Hypotension
  5. Dizziness
110
Q

What are the indications of ADH antagonists?

A
  1. SIADH
  2. Euvolemic/hypervolemic hyponatremia
  3. CHF
111
Q

What is conivaptan used for?

A

IV formulation for the treatment of euvolemic hyponatremia

112
Q

What are the potassium wasting diuretics?

A

CA inhibitors, loop agents, and thiazides

113
Q

What are the 3 determinants of capillary filtration?

A
  1. Hydrostatic pressure
  2. Oncotic pressure
  3. Capillary permeability
114
Q

How does edema occur?

A

Increased capillary hydrostatic pressure with decreased plasma oncotic pressure; this setting favors filtration over absorption

115
Q

What do diuretics do in the setting of edema?

A

Decrease capillary hydrostatic pressure and increase plasma oncotic pressure to favor absorption over filtration.

116
Q

In renal disease, you can get a urinary loss of albumin - how does this lead to systemic edema?

A

Hypoalbuminemia alters starling forces

117
Q

In renal disease, you can get a reduced GFR - how does this lead to systemic edema?

A

Reduced GFR leads to renal Na+ retention

118
Q

In liver cirrhosis, you can get increased pressure in hepatic sinusoids - how does this lead to systemic edem?

A

This increased pressure causes exudation of fluid into the peritoneal cavity. In addition to causing ascites, this leads to plasma volume depletion. The RAA system is activated, leading to renal Na+ retention and edema. Note that hypoalbuminemia also leads to plasma volume depletion and its downstream effects.

119
Q

Hepatic cirrhosis is resistant to ___, but this diuretic is effective.

A

Resistant to loop diuretics; aldosterone receptor antagonists are effective

120
Q

How can heart disease lead to systemic edema?

A

In right ventricular dysfunction, hypotension leads to renal Na+ retention. Left ventricular dysfunction also leads to hypotension and its downstream effects. It also leads to increased pulmonary venous pressure and pulmonary edema.

121
Q

Thiazide/loop diuretics can be effective in treating CHF, but they may cause what problem if aldosterone is high?

A

Excessive K+ loss, leading to hypokalemia. This can increase risk of coronary events, stroke, and sudden death

122
Q

What is a good alternative diuretic to prevent hypokalemia-induced cardiac dysfunction in CHF?

A

Spironolactone, or combining ACE inhibitors with thiazide or loop diuretics (NEVER with spironolactone)

123
Q

What drug is indicated in right heart failure?

A

Oral loop diuretics

124
Q

What drugs i indicated in left heart failure (acute)/

A

IV loop diuretics

125
Q

What is hyponatremia?

A

Serum Na+ concentration <136 mEg/L

126
Q

What are the symptoms of hyponatremia?

A

Headache/disorientation, fatigue, hallucinations, respiratory arrest, seizures, coma, and death (CNS symptoms)

127
Q

What are some causes of hypovolemic hyponatremia?

A

Diarrhea, vomiting, excessive sweating

128
Q

What is an effective treatment for hypovolemic hyponatremia?

A

Infusion of 0.9% saline

129
Q

What are some causes of euvolemic hyponatremia?

A

SIADH, hypothyroidism, adrenal insufficiency

130
Q

Can a saline infusion be used to treat euvolemic hyponatremia?

A

No - it may be ineffective or worsen the hyponatremia

131
Q

What are some causes of hypervolemic hyponatremia?

A

CHF, cirrhotic liver disease, nephrotic syndrome

132
Q

Can a saline infusion be used to treat hypervolemic hyponatremia?

133
Q

What drug has been shown to increase serum [Na+] and urine output while decreasing urine osmolality?

A

AVP receptor antagonists

134
Q

For uncomplicated HT, what drug should be used?

A

Thiazide diuretic

135
Q

What happens in nephrogenic diabetes insipidus?

A

Disruption of ADH effects leading to the inability to concentrate urine (leas to polyuria)

136
Q

What can be used to treat nephrogenic diabetes insipidus?

137
Q

Most kidney stones contain ___.

138
Q

Why are thiazides useful in some patients with calcium oxalate stones?

A

They decrease Ca2+ concentration by promoting reabsorption in the DCT

139
Q

What is hypercalcemia?

A

Marked elevation of serum calcium >14 mg/dL

140
Q

What causes hypercalcemia?

A

Malignancy or primary hyperparathyroidism

141
Q

What are the symptoms of hypercalcemia?

A

Nausea, vomiting, alterations of mental status, abdominal/flank pain, constipation, lethargy, depression, weakness and vague aches, polyuria, headache, coma

142
Q

What is used to treat hypercalcemia?

A

Loop diuretic with hydration; AVOID thiazide diuretics (would exacerbate)

143
Q

What are some causes of diuretic resistance?

A
  1. NSAID co-administration
  2. CHF/chronic renal failure
  3. Nephrotic syndrome
  4. Hepatic cirrhosis
144
Q

What do NSAIDs cause diuretic resistance

A

They block PG-induced increase in RBF (vasodilation). They increase expression of Na/K/2Cl cotransporter in TAL. Finally, they compete for organic acid transporter in PCT.

145
Q

What is loop + thiazide combination therapy used for?

A

In patients refractory to one or the other (may be too robust and lead to K+ wasting)

146
Q

What is K+ sparing + loop or thiazide combination therapy used for?

A

Prevention of hypokalemia (avoid in renal insufficiency)

PT 1 (34 decks)

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