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Diuretics Flashcards

1
Q

metabolic acidosis as SE

A

Sulfanilamide

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2
Q

prototype drug

A

Acetazolamide

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3
Q
  • limited usefulness as diuretics
A

CAIs

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4
Q
  • forerunners of diuretics
A

CAIs

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5
Q

Zn metalloenzyme found in proximal tubular epithelial cells (where too??)

A

Carbonic Anhydrase

  • Luminal and basolateral membranes (type IV)
  • Cytoplasm (type III)
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6
Q

first to discover CA in mammalian kidneys

A

Davenport and Willhelmi (1941)

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7
Q

Key role in NaHCO3 reabsorption and acid secretion

A

Carbonic anhydrase

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8
Q

Inhibit the enzyme carbonic anhydrase, blocking NaHCO3 reabsorption in PCT

A

Carbonic anhydrase Inhibitors MOA

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9
Q

MOA of Carbonic Anhydrase Inhibitors

A

Inhibit the enzyme carbonic anhydrase, blocking NaHCO3 reabsorption in PCT
collecting duct as secondary site of action (blocking and secretion)

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10
Q

collecting duct as secondary site of action (blocking and secretion)

A

MOA of Carbonic Anhydrase Inhibitors

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11
Q

Extrarenal action of CAIs

A

Extrarenal actions:

  1. Decreases rate of formation of aqueous humor -> reduces IOP
  2. Frequently causes paresthesias and somnolence
  3. Anticonvulsant (acetazolamide)
  4. Increases CO2 levels in peripheral tissues; decreases CO2 levels in expired gas
  5. Reduce gastric acid secretion (large doses)
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12
Q

Decreases rate of formation of aqueous humor -> reduces IOP

A

CAIs

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13
Q

Frequently causes paresthesias and somnolence

A

CAIs

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14
Q

Anticonvulsant

A

acetazolamide

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15
Q

Increases CO2 levels in peripheral tissues; decreases CO2 levels in expired gas

A

CAIs

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16
Q

Reduce gastric acid secretion (large doses)

A

CAis

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17
Q

Dose Acetazolamide

A

125 mg half, 250 mg and quarter-scored tablets

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18
Q

1% ophthalmic suspension

A

Brinzolamide

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19
Q

2% ophthalmic suspension

A

Dorzolamide

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20
Q

primary indication is Glaucoma, no diuretic effect, no systemic effect and ↓IOP

A

Brinzolamide, Dorzolamide Topical agents

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21
Q

open-angle glaucoma

A

CAIs

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22
Q

CHF-associated and drug induced edema

A

acetazolamide

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23
Q

Epilepsy

A

(acetazolamide)

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24
Q

symptomatic relef and/or prophylaxis for acute mountain or altitude sickness

A

CAIs

*used nightly for 5 days before climbing to prevent weakness, breathlessness

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25
Q

familial periodic paralysis

A

CAIs

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26
Q

correction of metabolic alkalosis (diuretic-induced H+ excretion)

A

CAIs

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27
Q

bone marrow depression, skin toxicity, sulfonamide-like renal lesions, hypersensitivity reactions (SJS)

A

AE - CAIs

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28
Q

signs on bulla skin, deadly if on mucosa

A

SJS

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29
Q

drowsiness and paresthesias

A

AE - CAIs

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30
Q

Hepatic encephalopathy

A

AE - CAIs

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31
Q

( diversion of ammonia of renal origin from urine into the systemic circulation -> induce or worsen hepatic encephalopathy therefore drugs are contraindicated to patients with hepatic cirrhosis

A

AE - CAIs

Hepatic encephalopathy

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32
Q

calculus formation, ureteral colic

A

AE - CAIs

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33
Q

(owing to ppt of calcium phosphate salts in an alkaline urine)

A

AE - CAIs

Calculus formation, ureteral colic

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34
Q

worsening of metabolic or respiratory acidosis

A

AE - CAIs

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35
Q

Drugs are contraindicated in patients with hyperchloremic acidosis or severe COPD

A

AE - CAIs

worsening of metabolic or respiratory acidosis

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36
Q

Na+ and K+ wasting

A

AE - CAIs

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37
Q

CI for patients w/ Na+ or K+ depletion)

A

AE - CAIs

CI for patients w/ Na+ or K+ depletion)

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38
Q
  • Most effective diuretics available
A

LOOP DIURETICS

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39
Q
  • High-ceiling diuretics
A

LOOP DIURETICS

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40
Q

Highest efficacy in mobilizing Na+ and Cl- from the body

A

LOOP DIURETICS

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41
Q

*produce copious amounts of urine

A

LOOP DIURETICS

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42
Q

Act directly on the thick ascending limb of the loop of Henle to inhibit sodium and chloride reabsorption

A

LOOP DIURETICS

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43
Q

MOA of Loop diuretics

A

Act directly on the thick ascending limb of the loop of Henle to inhibit sodium and chloride reabsorption

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44
Q

Increase renal prostaglandins, resulting in the dilation of blood vessels and reduced peripheral vascular resistance (↑ renal blood flow)

A

LOOP DIURETICS

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45
Q

– impt role in mediating renin release reponse to loop diuretics

A

Prostacyclins

LOOP DIURETICS

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46
Q

Prostaglandins have a role in their diuretic action and NSAIDS like indomethacin that interfere in prostaglandin synthesis can reduce the diuretic action of these agents

A

LOOP DIURETICS

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47
Q

Decrease renal vascular resistance and increase renal blood flow

A

LOOP DIURETICS

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48
Q

Other actions of loop diuretics

A
  1. Increase renal prostaglandins, resulting in the dilation of blood vessels and reduced peripheral vascular resistance (↑ renal blood flow)
    * Prostacyclin – impt role in mediating renin release reponse to loop diuretics
    * Prostaglandins have a role in their diuretic action and NSAIDS like indomethacin that interfere in prostaglandin synthesis can reduce the diuretic action of these agents
  2. Decrease renal vascular resistance and increase renal blood flow
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49
Q

Lasix dosage form

A

Tablet and ampule

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50
Q

– greater S/E therefore limited use (a loop diuretic)

A

Ethacrynic acid

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51
Q

more potent than furosemide , ↑ use

A

Bumetanide

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52
Q

DOC: acute pulmonary edema of HF

A

LOOP diuretics

given parenterally due to rapid action

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53
Q

Ind: Hypercalcemia (+hydration)

A

LOOP DIURETICS

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54
Q

Ind: - Hyperkalemia

A

LOOP DIURETICS

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55
Q

Ind: Hyponatremia

(+ hypertonic saline

A

LOOP DIURETICS

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56
Q

Ind: Acute renal failure

oliguric to nonoliguric

A

LOOP DIURETICS

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57
Q

Ind: - Forced diuresis in drug overdose

A

LOOP DIURETICS

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58
Q

Ind: Hypertension refractory to other diuretics or antihypertensives

A

LOOP DIURETICS

59
Q

Administered orally or parenterally

A

LOOP DIURETICS

60
Q

rapid onset of action (IV)

A

LOOP DIURETICS

61
Q

duration of action is relatively brief (2 to 4 hrs)

A

LOOP DIURETICS

62
Q

secreted into urine

A

LOOP DIURETICS

63
Q

A/E Hypokalemia

TX?

A

Tx: Potassium-sparing diuretics or dietary supplementation with K+
LOOP DIURETICS

64
Q

A/E Hypomagnesemia

A

(chronic use + low dietary intake of Mg 2+) = Elderly

LOOP DIURETICS

65
Q

A/E Hyperuricemia

A

furosemide, ethacrynic acid compete with uric acid for the renal and biliary secretory systems, thus blocking its secretion and inturen causing or exacerbating gouty attacks)
LOOP DIURETICS

66
Q

A/E Ototoxicity

A

(+aminoglycosides; rapid IV > PO)
*Tinnitus- hearing impairment deafness, vertigo, sense of fullness in the ears
*vestibular function too affected
LOOP DIURETICS

67
Q

A/E - Sulfonamide-related hypersensitivity rxns

A

(Furosemide and Bumetanide)

LOOP DIURETICS

68
Q
  • synthesized to enhance potency of CAIs
69
Q
  • discovered to increase NaCl excretion
70
Q
  • Benzothiadiazine derivatives (chlorothiazide) are
71
Q
  • Most widely used diuretic drugs for tx of Hypertension
72
Q
  • Sulfonamide derivatives; related in structure to CAIs
A
  • Significantly greater diuretic activity than acetazolamide
    Thiazides
73
Q
  • Affect the distal convoluted tubule
74
Q
  • All have equal max diuretic effects, differing only in potency(expressed on a per-milligram basis) -> “ceiling diuretics”
A

*Even if increase dose of drug, it will not give ↑/enhance therapeutic action but only toxic actions
Thiazides

75
Q

Act mainly in the cortical region of the ascending loop of Henle and the distal tubule to decrease the reabsorption of Na+, apparently by inhibition of a Na+/Cl- co-transporter on the luminal membrane of the tubules

76
Q
  • first modern diuretic that was active orally and was capable of affecting the severe edema of cirrhosis and heart failure w/ a min. of S/E
A

Chlorothiazide

77
Q
  • less ability to inhibit CA than chlorothiazide
A

Hydrochlorothiazide

78
Q
  • Newer derivative used more commonly
A

Hydrochlorothiazide

79
Q
  • more potent (required dose is considerably lower)
A

Hydrochlorothiazide

80
Q
  • efficacy is exactly the same as that of the parent drug
A

Hydrochlorothiazide

81
Q

IND: - mainstay of antihypertensive medication

82
Q

IND:- HF (when additional diuresis is needed)

83
Q

IND:- Hypercalciuria

84
Q

IND:- Nephrogenic diabetes insipidus (substitute for ADH)

85
Q
  • Effective orally
86
Q
  • Most thiazides take ___ wks to produce a stable reduction in BP
A

1 to 3 wks

87
Q
  • Exhibit a prolonged biologic half-life
88
Q
  • secreted by the organic acid secretory system of the kidney
89
Q

A/E - Hypokalemia (↑common)

90
Q

A/E - Hyponatremia

91
Q

A/E - Hyperuricemia

A
  • increase serum uric acid by decreasing the amt of acid excreted by the organic acid secretory system
    Thiazides
92
Q

A/E - Hypercalcemia

93
Q

A/E - Hyperglycemia

A
  • due to impaired release of inculin and tissue uptake of glucose
    Thiazides
94
Q

A/E - Hyperlipidemia

95
Q

A/E - Volume depletion

96
Q

A/E - Hypersensitivity rxns

97
Q
  • compounds that lack the thiazide structure but like thiazides they have the unsubstituted sulfonamide groups and share same MOA
A

Thiazide -like

98
Q
  • Non-thiazide derivatives that behaves like HCTZ
A

Chlorthalidone

99
Q
  • very long duration of action ; therefore, is often used to tx Hypertension
A

Chlorthalidone

100
Q
  • given 1/d for this in
A

Chlorthalidone

101
Q
  • more potent than thiazides
A

Metolazone

102
Q
  • causes Na+ excretion in advanced renal failure
A

Metolazone

103
Q
  • lipid-soluble, nonthiazide diuretic that has a long duration of action
A

Indapamide

104
Q
  • at low doses, shows significant antihypertensive action w/ min diuretic effects
A

Indapamide

105
Q
  • metabolized and excreted by the GIT and kidneys
A

Indapamide

106
Q
  • less likely to accumulate in patients w/ renal failure
A

Indapamide

107
Q
  • act in the collecting tubule to inhibit Na reabsorption and K+ excretion
A

Potassium-sparing diuretics/ Na-channel inhibitors

108
Q
  • Major use: Tx of hypertension, most often in combination w/ a thiazide
A

Potassium-sparing diuretics/ Na-channel inhibitors

109
Q
  • discontinue exogenous K supplementation
A

Potassium-sparing diuretics/ Na-channel inhibitors

110
Q
  • close monitory of serum K levels
A

Potassium-sparing diuretics/ Na-channel inhibitors

111
Q
  • avoided in patients with renal dysfunction because of increased risk of hyperkalemia
A

Potassium-sparing diuretics/ Na-channel inhibitors

112
Q
  • synthetic steroid that antagonizes aldosterone at intracellular cytoplasmic receptor sites
A

Spironolactone

113
Q
  • Inactive spironolactone-receptor complex (does not bind to DNA -> inhibition of protein synthesis)
A

Spironolactone

114
Q
  • mediator proteins not present to stimulate Na+/K+ exchange sites
A

Spironolactone

115
Q
  • Inhibition of Na+ reabsorption and K+/H+ secretion
A

Spironolactone

116
Q

*in patients with no significant circulating levels of aldosterones, like with Addison disease (primary adrenal deficiency) , no diuretic effect of the drug occur

A

Spironolactone

117
Q

(Spironolactone + HCTZ)

118
Q
  • often given in conjunction w/ a thiazide or loop diuretic to prevent the K+ excretion
A

Aldosterone Antagonist

119
Q
  • diuretic of choice in patients with hepatic cirrhosis
A

Aldosterone Antagonist

120
Q
  • secondary hyperaldosteronism
A

Aldosterone Antagonist

121
Q
  • completely absorbed orally
A

Aldosterone Antagonist

122
Q
  • strongly bound to proteins
A

Aldosterone Antagonist

123
Q
  • rapidly converted to an active metabolite, canrenone (has mineralocorticoid-blocking activity)
A

Aldosterone Antagonist

124
Q
  • induces hepatic cytochrome P450
A

Aldosterone Antagonist

125
Q
  • Gastric upsets -> peptic ulcers
A

Aldosterone Antagonist

126
Q
  • Gynecomastia in male patients; menstrual irregularities in female patients (high doses on chronic use)
A

Aldosterone Antagonist

127
Q
  • Hyperkalemia, nausea, lethargy and mental confusion
A

Aldosterone Antagonist

128
Q
  • block Na+ transport channels, resulting in a decrease in Na+/K+ exchange
A

Triamterene and Amiloride

129
Q
  • ability to block the Na+/K+ - exchange site does not depend on the presence of aldosterone
A

Triamterene and Amiloride

130
Q
  • not very efficacious diuretics
A

Triamterene and Amiloride

131
Q
  • commonly used in combination with other diuretics usually for their potassium-sparing properties
A

Triamterene and Amiloride

132
Q
  • leg cramps
A

Triamterene and Amiloride

133
Q
  • possibility of increased blood urea nitrogen, uric acid and K+ retention
A

Triamterene and Amiloride

134
Q
  • agents that are freely filtered at the glomerulus, undergo limited reabsorption by the renal tubule, and are relatively inert pharmacologically
A

Osmotic diuretics

135
Q
  • administered in large enough doses to increase significantly osmolality of plasma and tubular fluid
A

Osmotic diuretics

136
Q
  • not useful for treating conditions in which Na retention occurs
A

Osmotic diuretics

137
Q

Increase the osmotic pressure at the PCT and LOH to prevent water reabsorption

A

Osmotic diuretics

138
Q

what about mannitol?

A
  • IV only
  • prolonged standing of mannitol (may ppt)
  • subject to heat (glass bottles); shake bottles (agitate) until clear
139
Q
  • used to maintain urine flow following acute toxic ingestion of substances capable of producing acute renal failure
A

Osmotic diuretics

140
Q
  • mainstay treatment for patients with increased intracranial pressure or acute renal failure due to shock, drug toxicities and trauma
A

Osmotic diuretics

141
Q
  • extracellular water expansion
A

Osmotic diuretics

142
Q
  • dehydration
A

Osmotic diuretics

143
Q
  • hypo- or hypernatremia
A

Osmotic diuretics

144
Q

*The expansion of extracellular water results because the presence of mannitol in the extracellular fluid extracts water from the cells and causes hyponatremia until diuresis occurs.

A

Osmotic diuretics

Pharmacology (12 decks)

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