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Renal > 05.12 - Diuretics, Aquaretics (Bahouth) > Flashcards

05.12 - Diuretics, Aquaretics (Bahouth) Flashcards

1
Q

CA Inhibitor

A

Acetazolamide

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2
Q

___ may be effective in patients w/ impaired renal function when class 1 thiazides are not

A

Metolazone, Indapamide (class 2 thiazides)

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3
Q

2 main conditions that cause ADH release

A

Elevation in plasma osmolarity >280; Depletion of ECV

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4
Q

2 Organic Base K-Sparing Diuretics

A

Triametrene, Amiloride

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5
Q

2 Types of Na Channels in IMCD

A

(1) CNG: Amiloride-sensitive, cyclic nucleotide gated cation channel; (2) Low-conductance highly-selective Na ENaC channel

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6
Q

3 Clinical uses of Osmotic Diuretics

A

Intra-cranial pressure, Intra-ocular pressure, Dialysis disequilibrium syndrome

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7
Q

3 Drugs classes associated with SIADH

A

Psychotropics, Sulfonylureas, Vinca Alkyloids

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8
Q

3 Net Effects of Loop Diuretics

A

(1) Significant NaCl loss; (2) Increase excretion of K, H; (3) Increase excretion of Ca, Mg

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9
Q

4 Clinical uses of CA inhibitors

A

Cysteinurea, Intra-ocular pressure, Seizures, Mountain sickness

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10
Q

4 Therapeutic Uses of Loop Diuretics

A

(1) Edema of cardiac, hepatic, or renal origin; (2) Pulmonary edema; (3) Hypercalcemia; (4) Protect against renal failure

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11
Q

A poor response to Thiazides may reflect

A

Either an overwhelming load of dietary Na, or impairted renal capacity to excrete Na

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12
Q

Action of ANP

A

Binds NP receptor-A, activates GC and increases cGMP

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13
Q

Action of BNP

A

Binds NP receptor-A, activates GC and increases cGMP

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14
Q

Action of CNP

A

Binds NPR-B in vascular SM cells –> Relaxation

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15
Q

Action of Demeclocycline

A

Antagonizes ADH at V2R’s

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16
Q

Activation of V1 receptor activates

A

Gq-PLC-IP3 pathway –> Mobilizes Ca –> Vasoconstriction

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17
Q

Advantages of Torsemide

A

Also lowers BP; Longer Half Life

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18
Q

Best tolerated drug classes for monotherapy in HTN

A

Diuretics, ACEi’s

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19
Q

Bindin of ADH to V2 receptor activates

A

Gs-cAMP, PKA –> Insertion of AP-2, p-lation of urea transporter

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20
Q

Bumetanide vs Furosemide

A

Bum is 40x more potent

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21
Q

Class 2 Thiazides

A

Metolazone, Indapamide

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22
Q

Clinical effects of Nesiritide

A

(1) Increase Na excretion; (2) Useful in CHF

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23
Q

Clinical Uses of Spironolactone

A

Diuretic in combo with HCTZ; CHF, Cirrhosis

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24
Q

Clinical Uses of Triametrene, Amiloride

A

Combined with HCTZ to decrease K excretion

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25
Q

Common preventable cause of diuretic resistance

A

Co-administration of NSAID with Loop

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26
Q

Concentration of urine in Mannitol use

A

Hypoosmotic (losing free water)

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27
Q

DDAVP is also used in

A

Bleeding disorders, Nocturnal Enurisis

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28
Q

Desmopressin

A

Highly selective V2R agonist

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29
Q

Difference between Loop and Osmotic

A

Loop have high [Na] in urine

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30
Q

Diuretic of choice in Cirrhosis

A

Spironolactone

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31
Q

Diuretic to use in Chronic Renal Failure

A

Loop

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32
Q

Diuretic to use in Mild CHF

A

Thiazide, Loop

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33
Q

Diuretic to use in Moderate or Severe CHF

A

Loop

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34
Q

Diuretic to use in Nephrotic Syndrome

A

Loop

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35
Q

Do PG’s increase or decrease with Loop Diuretics?

A

Increase

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36
Q

Drug interactions of Furosemide

A

Li, Indomethacin, Probenecid, Warfarin

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37
Q

Effect of ADH on urea transport

A

V2 –> PKA p-lates urea transporter –> inc. permeability of CD to urea

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38
Q

Effect of Furosemide on K, H, Ca, Mg

A

Increases secretion of all

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39
Q

Effect of Furosemide on Renal PG’s and Venous capacitance

A

Increases both

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40
Q

Effect of Osmotic Diuretics on PCT

A

Osmotically inhibit Na/H2O reabsorption

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41
Q

Effect of Thiazides on Ca, Mg

A

Decrease excretion of Ca, Increase secretion of Mg

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42
Q

Effect of Thiazides on Na, K, Cl

A

Loss of all three –> Hypokalemia

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43
Q

Effect of Triametrene, Amiloride on Na, K, H

A

Weak excretion of Na; Inhibit secretion of K, H

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44
Q

Eplerenone vs Spironolactone

A

Lower affinity for AR’s so less side effects

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45
Q

Found in urine, paracrine regulator of Na transport

A

Urodilantin

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46
Q

Furosemide vs Indomethacin

A

NSAIDs inhibit PG effect of Furosemide

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47
Q

Furosemide vs Probenecid

A

Compete for secretion by Organic Acid Transporter

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48
Q

Furosemide vs Warfarin

A

Compete for protein binding

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49
Q

General MOA Acetazolamide

A

CA Inhibitor

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50
Q

General MOA Mannitol

A

Osmotic Diuretic

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51
Q

General MOA of AVP, DDVAP

A

V2R Agonism, Collecting Duct

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52
Q

General MOA of Conivaptan, Tolvaptan

A

V2R Antagonism, Collecting Duct

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53
Q

Given in large doses, Osmotic Diuretics

A

increase osmolarity of plasma

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54
Q

Highly selective V2R agonist

A

Desmopressin

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55
Q

How are Loop diuretics administered

A

IV in hypertensive crisis or in Acute Pulmonary Edema

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56
Q

How are Thiazides unlike Loops

A

Thiazides decrease secretion of Ca

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57
Q

How do Load-Dependent Principal cells work

A

The more Na is delivered, the more is absorbed in exchange for K secretion

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58
Q

How do Loop Diuretics affect Macula Densa

A

MD thinks very little Na, so it secretes PG’s –> Increase RBF and FF

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59
Q

How do PG’s affect actions of Loops

A

Reduce Na re-absorption in distal nephron, antagonize ADH, distribute renal blood from cortex to JG

60
Q

How does Furosemide reach the luminal symporter

A

Secreted by Organic Acid Transporter

61
Q

How does Furosemide travel in blood

A

Extensively protein bound

62
Q

How does Hypovolemia lead to Hyponatremia

A

Hypovolemia stimulates ADH-mediate retention of H20

63
Q

How does Nesiritide increase Na excretion

A

Inhibits CNG_nonspecific cation channel in IMCD; Inhibits RAAS

64
Q

How will V2R agonist affect Central vs Nephrogenic DI

A

Increase urine osmolarity in central by not nephrogenic

65
Q

In CHF, Cirrhosis, or Nephrotic Syndrome, hypovolemia is exacerbated by

A

Diuretics

66
Q

In what condition is Mannitol contraindicated

A

CHF

67
Q

Indications for Vaptans

A

Significant Hypervolemic and Euvolemic Hyponatremia (including patients with HF, Cirrhosis, SIADH)

68
Q

Inhibiting CA results in loss of what in urine

A

Bicarbonate

69
Q

K-Sparing Diuretics are useful in what patients

A

At risk of K depletion; Hyperuricemia

70
Q

Late DCT, CD Principal cells are involved in __ re-absorption and __ secretion

A

Na reabsorption, K secretion

71
Q

Like Loops, Thiazides require

A

secretion into tubular fluid to exert effect

72
Q

Loop Diuretics

A

Furosemide, Bumetanide, Torsemide

73
Q

Loop that also lowers BP

A

Torsemide

74
Q

MOA of Loop Diuretics

A

Inhibit Na-K-2Cl symporter in TALH

75
Q

MOA of Thiazide Diuretics

A

Inhibit NaCl reabsorption in the Na-K Aldosterone-independent sement of distal tubule

76
Q

MOA of Triametrene, Amiloride

A

Inhibit Na re-absorption in late distal tubule (sodium load segment)

77
Q

MOA of Vaptans

A

Selective V2R antagonists

78
Q

Most popular drug for HTN

A

HCTZ

79
Q

Most potent class of diuretics in mobilizing NaCl

A

Loop

80
Q

Most Thiazides are ineffective when

A

GFR < 30-40 mL/minute

81
Q

Net Effect of Aldosterone Antagonists

A

Increase excretion of Na; Inhibit secretion of K, H

82
Q

Net effect of Osmotic Diuretics

A

Significantly increase urine

83
Q

On which part of nephron do Triametrene, Amiloride act

A

Late Distal Tubule, Sodium Load segment

84
Q

On which part of nephron does Furosemide act

A

TALH

85
Q

Osmolarity of urine with ADH present

A

1200

86
Q

Osmolarity of urine without ADH

A

50

87
Q

Osmotic Diuretic

A

Mannitol

88
Q

Patients with what type of HTN show better responses to Thiazides

A

Volume-dependent HTN (low renin)

89
Q

Pharmacokinetics of Furosemide

A

Short half-life; Extensively protein-bound

90
Q

Pharmacokinetics of Vaptans

A

CYP3

91
Q

Physiological effects of Aldosterone

A

NaCl transport enhanced; Increased secretion of K, H+

92
Q

Retention phenomena of Thiazides

A

Hyperuricemia, Hypercalcemia

93
Q

Role of Renin in Loop Diuretic use

A

Potently increased

94
Q

Route of Acetazolamide

A

Oral

95
Q

Route of HCTZ

A

Oral

96
Q

Route of Mannitol

A

Injection

97
Q

Selective V2R antagonists

A

MOA of Vaptans

98
Q

SIADH Tx:

A

Water restriction, Loops, Demeclocycline, Vaptans

99
Q

Side effects of Acetazolamide

A

Metabolic Acidosis, K loss (hypokalemia)

100
Q

Side effects of Furosemide

A

Hypokalemia, Ototoxicity; Elevated BUN, Hyperglycemia, Hyperuricemia

101
Q

Side effects of Mannitol

A

Volume overload (don’t use in CHF)

102
Q

Side effects of Nesiritide are related to

A

its narrow therapeutic index

103
Q

Side effects of Spironolactone

A

Hyperkalemia; AR: Gynecomastia, Hirsutism, Uterine Bleeding

104
Q

Side effects of Triametrene, Amiloride

A

Hyperkalemia, Megaloblastic Anemia in cirrhosis

105
Q

Side effects of Vaptans

A

Hyperglycemia, GI disturbances, Clotting probs

106
Q

Sodium loss in Thiazides results in chronic

A

Reduced GFR

107
Q

Spironolactone vs Canrenone

A

Sp is a pro-drug that is extensively metabolized; Can is active metabolite with longer half-life

108
Q

T/F: Diuretics only reduce mortality from HTN when used with BB’s

A

False, effective alone or in combo

109
Q

T/F: Nesiritide reduces mortality in CHF

A

FALSE

110
Q

Therapeutic Uses of Thiazides

A

Edema, Hypercalciurea, Essential HTN, Osteoporosis, Nephrogenic Diabetes Insipidus

111
Q

Thiazides are widely used to treat

A

Mild or Moderate HTN

112
Q

Tx of Central DI

A

Selective V2R agonists

113
Q

Tx of Nephrogenic DI

A

Thiazide Diuretics

114
Q

Type A Principal cells are regulated by

A

Hormone: Aldosterone

115
Q

Type B Principal cells are regulated by

A

Load dependent

116
Q

Type of channel in Aldosterone Sensitive Channel

A

Aldosterone-Sensitive ENaC Channel: Na-K/H

117
Q

Type of channel in Na-K Aldosterone-independent segment

A

Na-Cl symporter

118
Q

Type of Channel in Sodium Load Segment

A

ENaC Channel: Na-K/H

119
Q

Type of channels affected by Aldosterone in DCT

A

Epithelial Sodium Channels (ENaC) are increased

120
Q

Urine with Acetazolamide use

A

Alkaline, bicarbonate loss into it

121
Q

Urodilatin arises from same precursor as

A

ANP

122
Q

Use of Loop Diuretics for Non-Pulmonary edema

A

Oral use in Cardiac, Hepatic, or renal origin edema (GFR<30)

123
Q

Uses of V1R agonists

A

Post-op Ileus; Esophageal varices; Acute Hem Gastritis

124
Q

V2R agonism

A

Arginine Vasopressin, Desmopressin (DDAVP)

125
Q

V2R Ant-agonism

A

Conivaptan, Tolvaptan

126
Q

What causes acidosis with CA inhibitors

A

Enhanced chloride reabsorption

127
Q

What is substituted for Furosemide in patients receiving Warfarin

A

Bumetanide

128
Q

When are class 1 Thiazides perferably used

A

When GFR >50

129
Q

When are class 2 Thiazides used

A

More potent, so when GFR<50 but greater than 30

130
Q

When are K-Sparing Diuretics contraindicated

A

Significant Renal Insufficiency (GFR<75); Other K-retaining conditions

131
Q

When are Loop used over Thiazides

A

Severe Htn unresponsive to Thiazides, especially w/ renal insufficiency, cardiac failure, cirrhosis

132
Q

Where do CA inhibitors mostly act

A

Proximal Tubule (90%), Distal (10%)

133
Q

Where do CNP’s originate

A

Endothelium and Kidneys

134
Q

Where do Loop Diuretics act

A

Inhibit Na-K-2Cl symporter in TALH

135
Q

Where do Vasopressin and Desmopressin act

A

Collecting duct, V2R agoism

136
Q

Where is V1 receptor found

A

Vascular SM

137
Q

Where is V2 receptor found

A

Principal Cells in Renal CD

138
Q

Which are more potent anti-hypertensives: Thiazides or K-Sparing

A

Equipotent

139
Q

Which class of drugs creates largest volume of urine

A

Osmotic Diuretics

140
Q

Which is preferred: Terlipressin or 8-arg vasopressin

A

Terlipressin has less side effects

141
Q

Which parts of nephron have Aquaporin-1

A

Proximal Convoluted Tubule, Descending Limb

142
Q

Which parts of nephron have Aquaporin-2

A

Collecting Duct

143
Q

Why are Thiazides only mild diuretics

A

Act on distal tubule, which only absorbs 5% of Na

144
Q

Why is Nesiritide useful in CHF

A

Decreases SVR, Decreases LVP, Increases CO

145
Q

Wide margin of safety; Dose-response curve influence by renal disease

A

Furosemide

Renal (31 decks)

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