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Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

where are beta1 receptors located?

A

the heart and kidney

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2
Q

what do stimulated beta1 receptors lead to?

A

in heart: increased HR, increased contractility, and increased SV leading to increased CO
in kidneys: increase renin release

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3
Q

where are alpha1 receptors located?

A

blood vessels

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4
Q

what do stimulated alpha1 receptors lead to?

A

increased vasoconstriction, and increased peripheral resistance

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5
Q

equation for cardiac output

A

HR X SV

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6
Q

what does increased renin release imply?

A

increased conversion of angiotensinogen to angiotensin I

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7
Q

how is angiotensin I converted to angiotensin II?

A

ACE

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8
Q

how does angiotensin II impact the adrenal cortex?

A

increases aldosterone release

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9
Q

how does angiotensin II impact the posterior pituitary?

A

increases vasopressin or antidiuretic hormone

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10
Q

function of aldosterone

A

act on late distal tubule and collecting duct, directly impacts Na absorption and K excretion

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11
Q

what does increased Na channels and Na-K ATPase in the nephron imply?

A

increased passive diffusion of na into na channels on the luminal side (into the blood vessels), increased active transport of na into blood and K into cell via basolateral na-k atpase
NET EFFECT: sodium absorption into blood cells from lumen of nephron

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12
Q

function of vasopressin (ADH)?

A

act on V2 receptors of distal or collecting tubules, and generates aquaporin-2 (and encourages aquaporin-2 migration to luminal membrane of tubule cells), water then reabsorbed from urine to the blood stream.

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13
Q

end product of ADH?

A

water resorption, concentration of urine, reduces urine volume, increases blood volume

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14
Q

overall impact of aldosterone and ADH increase?

A

increased Na and H2O retention = increased blood pressure

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15
Q

site of action of carbonic anhydrase inhibitors?

A

proximal convoluted tubule

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16
Q

example of carbonic anhydrase inhibitor?

A

acetazolamide

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17
Q

site of action of osmotic diuretics?

A

thin descending limb, PCT, collecting duct (places where water is permeable)

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18
Q

class of mannitol?

A

osmotic diuretic

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19
Q

class of urea?

A

osmotic diuretic

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20
Q

class of glycerin?

A

osmotic diuretic

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21
Q

class of furosemide?

A

loop diuretic

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22
Q

class of bumetanide?

A

loop diuretic

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23
Q

class of torsemide?

A

loop diuretic

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24
Q

class of ethacrynic acid?

A

loop diuretic

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25
Q

site of action of loop diuretics?

A

thick ascending limb

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26
Q

class of metolazone?

A

thiazide

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27
Q

class of indapamide?

A

thiazide

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28
Q

site of action of thiazides?

A

distal convoluted tubule

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29
Q

class of triamterene

A

potassium sparing diuretic

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30
Q

class of eplerenone

A

potassium sparing diuretic

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31
Q

class of canrenone

A

potassium sparing diuretic

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32
Q

class of spironolactone

A

potassium sparing diuretic

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33
Q

class of amiloride

A

potassium sparing diuretic

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34
Q

site of action of potassium sparing diuretics

A

collecting ducts

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35
Q

class of demeclocycline

A

vasopressin antagonist

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36
Q

class of vaptans

A

vasopressin antagonist

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37
Q

site of action of vasopressin antagonists?

A

collecting ducts

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38
Q

what do most diuretics block in the renal tubules?

A

transporters on the luminal membrane of tubular cells

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39
Q

how do most diuretics reach the site of action?

A

secretion by the organic acid secretory system in the proximal convoluted tubule

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40
Q

do diuretics ever block na-k-ATPase?

A

NO

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41
Q

4 biological actions of most diuretics?

A

increased urine volume and flow, decreased na reabsorption (increased na in urine), decreased water reabsorption indirectly (increased water concentration in urine), changing urine and plasma concentration of ions

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42
Q

5 major ions affected by diuretics?

A

sodium, chloride, potassium, calcium, magnesium

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43
Q

what are diuretics majorly used to treat?

A

htn, heart failure

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44
Q

where is the organic acid secretory system located?

A

proximal convoluted tubule

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45
Q

reabsorption in the proximal convoluted tubule?

A

most reabsorption of na, k, and ions and water; nearly all glucose, AA; sodium bicarb

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46
Q

organic acid secretory system

A

secretes uric acid, antibiotics, and para-aminohippuric acid into lumen

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47
Q

reabsorption in thin descending tubule?

A

water (permeable) (urine increases in concentration), NO SALT

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48
Q

reabsorption in thick ascending tubule?

A

Na, Ca, Mg reabsorption, water impermeable (urine concentration decreased - losing ions but no water)

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49
Q

urine concentration in thin descending tubule?

A

increased concentration

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50
Q

urine concentration in thick ascending tubule?

A

decreased concentration

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51
Q

reabsorption in distal convoluted tubule?

A

Na and Ca, water impermeable

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52
Q

where in the nephron is water impermeable?

A

thick ascending tubule, distal convoluted tubule

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53
Q

where in the nephron is water permeable

A

PCT, thin descending, collecting duct

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54
Q

collecting duct reabsorption

A

Na, water if ADH and aldosterone

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55
Q

site of action of aldosterone and ADH

A

collecting ducts

56
Q

where is Na NOT resabsorbed?

A

thin limb of loop of henle

57
Q

what is the passive step of Na reabsorption?

A

passive movement of na from lumen into tubular cell mediated by transporter mechanisms

58
Q

what is the active step of na resorption?

A

movement of na from the tubular cell through the ECF to the blood, mediated by Na/K ATPase in basolateral membrane

59
Q

where is the basolateral membrane?

A

between the tubular cell and the interstitial fluid (extracellular fluid)

60
Q

% of Na reabsorption in PCT?

A

67%

61
Q

passive step of Na reabsorption in PCT?

A

Na/H exchanger

62
Q

active step of Na reabsorption in PCT, thick ascending, DCT and collecting duct?

A

Na/K ATPase

63
Q

Na reabsorption in thin descending limb?

A

NONE

64
Q

%Na reabsorption in thick ascending limb?

A

25%

65
Q

passive step of Na reabsorption in thick ascending limb?

A

Na/K/2Cl transporter

66
Q

% Na reabsorption in DCT?

A

6%

67
Q

passive step of na reabsorption in DCT?

A

NaCl transporter

68
Q

% na reabsorption collecting tubule?

A

2%

69
Q

passive step of na reabsorption in collecting tubule?

A

na ion channels

70
Q

which step do diuretics block for Na reabsorption?

A

passive steps (Na/K/2Cl, NaCl transporters and Na ion channels)

71
Q

2 routes that diuretics reach site of actions?

A

blood to site, tubular fluid to site

72
Q

which is the only diuretic that utilizes blood transport?

A

aldosterone antagonists (spironolactone)

73
Q

how do most diuretics travel from the tubular fluid to the site of action?

A

drug binds to OASS and is transported from the blood directly into the tubular lumen in the PCT

74
Q

how do aldosterone antagonists (spironolactone) reach the site of action?

A

directly from blood to site

75
Q

how do osmotic diuretics reach the site of action?

A

filtration of the substance at the glomerulus

76
Q

what large or extensively bound molecules are transferred from the blood to the renal tubules through the OASS?

A

diuretics, penicillin, uric acid, NSAIDs

77
Q

what is the effect of diuretics with frequent gout attacks?

A

diuretics compete with endogenous substances for transfer into tubular fluid and can lead to decreased uric acid secretion and increased uric acid concentrations in blood (increased uric acid in plasma, buildup of uric acid)

78
Q

most potent loop diuretic

A

bumetanide

79
Q

2 most notable characteristics of loop diuretics?

A
  1. most powerful diuretic that produce lots of urine (highest efficacy in producing na and water loss)
  2. very rapid onset of action
80
Q

benefit of very rapid onset of action of loop diuretics?

A

can be used in emergency situations (edema from heart failure)

81
Q

loop diuretic access to site of action?

A

to the tubular fluid via OASS in the PCT

82
Q

nephron site of action of loop diuretic?

A

thick ascending limb

83
Q

transporter site of action loop diuretics

A

Na/K/2Cl transporter on the luminal membrane of thick ascending limb

84
Q

which ions can move directly from lumen to blood?

A

calcium and magnesium

85
Q

5 major physiological events in thick ascending limb?

A
  1. increased Na reabsorption
  2. increased Cl reabsorption
  3. increased water reabsorption
  4. increased Ca reabsorption
  5. increased Mg reabsorption
86
Q

explain K accumulation in the thick ascending limb CELL

A

Na/K/2Cl transporter increases the [K], Na-K ATPase increases [K] in cell, which then causes the concentration gradient to move back into the lumen. this buildup of +charge drives Ca and Mg out of the lumen and into the blood.

87
Q

what is the major reason for Ca and Mg reabsorption at the thick ascending limb?

A

the buildup of + charge from K secretion into the lumen driving out the Ca and Mg

88
Q

6 pharmacological effects of loop diuretics on thick ascending limb

A
  1. decreased na reabsorption (directly)
  2. decreased cl reabsorption (directly)
  3. decreased water reabsorption
  4. decreased Ca reabsorption (indirectly)
  5. decreased Mg (indirectly)
    reabsorption
  6. decreased K reabsorption (directly)(abolishes K back diffusion into the lumen, prevents + charge buildup in luminal side, removes driving force for Ca and Mg reabsorption)
89
Q

pharmacology of loop diuretics on thick ascending limb

A

blocks Na/K/2Cl transporter

90
Q

considerations for loop diuretics?

A

hypocalcemia, hypokalemia

91
Q

drug interaction of loop diuretics?

A

NSAID decreases overall efficacy of diuretic, risk of kidney failure

92
Q

why are NSAIDs and loop diuretics contraindicated?

A

NSAID blocks renal prostaglandins (PGE2), which contribute to the diuretic effects of loop diuretics

93
Q

loop diuretic impact on prostaglandins?

A

loop diuretics increase PGE2, which decreases na and water reabsorption, decreasing blood volume and blood pressure

94
Q

what adverse side effect can the loop diuretic action of decreasing K reabsorption have?

A

decreased K plasma concentration, increasing risk of hypokalemia

95
Q

what adverse side effect can the loop diuretic action of decreasing Na and H2O reabsorption have?

A

decreases blood volume, therefore decreasing blood pressure, increasing risk of hypovalemia (orthostatic hypotension and lightheaded)and hyponatremia

96
Q

what adverse side effect can the loop diuretic action of increasing uric acid reabsorption have?

A

increased plasma uric acid concentration, increases risk for hyperuricemia and gout

97
Q

chlorthiazide classq

A

thiazide diuretic

98
Q

HCTZ class

A

thiazide diuretic

99
Q

chlorthalidone class

A

thiazide-like diuretic

100
Q

metolazone class

A

thiazide like diuretic

101
Q

indapamide class

A

thiazide like diuretic

102
Q

onset of action speed?

A

slower than loop diuretics

103
Q

which class is the most effective diuretic in lowering BP and is the first line HTN tx?

A

thiazide and thiazide-like diuretics

104
Q

thiazide/TLD nephron side of action?

A

distal convoluted tubule

105
Q

transporter targeted by thiazides?

A

NaCl transporter on luminal membrane of DCT

106
Q

how do thiazides/TLD access the DCT?

A

tubular fluid via organic acid secretory system (OSS in the PCT)

107
Q

4 major physiological events in the distal tubule?

A
  1. increased Na reabsorption
  2. increased Cl reabsorption
  3. increased water reabsorption (direct and indirect)
  4. increased Ca reabsorption
108
Q

where does Ca reabsorption occur in the distal convoluted tubule?

A

Na/Ca exchanger, driven by energy derived from the steep Na gradient (high Na outside the cell makes high Ca outside the cell, optimizing reabsorption)

109
Q

Thiazide diuretics and NaCl transporter relationship??

A

thiazide blocks NaCl channel, decreasing Na and Cl reabsorption directly, decreasing intracellular Na directly

110
Q

thiazide NaCl transporter effect on Ca?

A

increases Ca reabsorption indirectly via reduction in intracellular Na (blocked NaCl) d/t increased movement of Na from blood to cell at the Na/Ca exchanger which equals more energy input to Ca transport )increase rate of Ca movement from cell into blood) = rise in blood Ca levels

111
Q

Thiazide/TLD effect on arterioles?

A

work directly on smooth muscle cells, promote smooth muscle relaxation, most responsible for long term reduction in blood pressure

112
Q

physiologic response to smooth muscle relaxation in the arterioles?

A

vasodilation, decreased peripheral resistance, decreased blood pressure

113
Q

where is thiazide/TLD active?

A

orally

114
Q

onset of action of thiazides?

A

1-3 weeks before stable BP reduction

115
Q

duration of action of thiazides?

A

long duration (d/t vasodilation mostly and volume reduction)

116
Q

5 main effects of thiazides/TLD?

A
  1. decreased Na and H2O reabsorption
  2. relaxation of smooth muscle in arterioles
  3. decreased K reabsorption
  4. increased Ca reabsorption
  5. uric acid reabsorption
117
Q

risk of decreased K reabsorption?

A

decreased plasma K concentration, leading to increased risk of hypokalemia

118
Q

risk of increased Ca reabsorption?

A

increased plasma Ca concentration, increasing bone mineral density and decreasing risk of hip fractures

119
Q

risk of uric acid reabsorption?

A

increased plasma uric acid concentration, leading to hyperuricemia and increased gout risk

120
Q

risk of the combination decreased Na, H2O absorption and decreased peripheral resistance?

A

decreased BP that could lead to hypovolemia, orthostatic hypotension and light headedness, and hyponatremia

121
Q

what makes potassium sparing diuretics special?

A

actually increases K reabsorption, not decreased

122
Q

what are the two classes of potassium sparing diuretics?

A
  1. Na channel blockers

2. aldosterone antagonists

123
Q

amiloride class

A

K sparing, na channel blocker

124
Q

triamterene class

A

na channel blocker, Ksparing diuretic

125
Q

spironolactone class

A

aldosterone antagonist ,K sparing

126
Q

canrenone class

A

aldosterone antagonist, K sparing

127
Q

eplerenone class

A

aldosterone antagonist, K sparing

128
Q

K sparing diuretic site of action?

A

collecting ducts

129
Q

aldosterone antagonist transporter site of action

A

block aldosterone receptors in cytoplasm of collecting duct cells

130
Q

Na channel blocker transporter site of action?

A

block Na channels on luminal membrane of collecting duct

131
Q

aldosterone antagonist access to site of action?

A

transported through the blood and then directly through the lipid membrane of collecting duct cells to cytoplasmic aldosterone receptor

132
Q

na channel antagonist access to site of action?

A

tubular fluid via OASS in the PCT

133
Q

3 major aldosterone effects?

A
  1. decreased K reabsorption
  2. increased Na reabsorption
  3. increased water reabsorption (decreased water output) (passive and indirect)
134
Q

what 2 things (genetically) occur when aldosterone is released?

A
  1. binds to and activates cytoplasmic aldosterone receptor

2. aldosterone-receptor complex migrates to nucleus and binds to DNA

135
Q

what does aldosterone-receptor complex binding to DNA cause? (3)

A
  1. increased Na channel expression
  2. increased Na channel activity
  3. increased K channel expression

Pharmacology (5 decks)

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