diuretics 3 Flashcards

1
Q

Diuretics that block ____Na+ reabsorption receptor, which leads to _____

A

collecting tubule

decrease in K+ excretion (hyperkalemia K+-sparing)

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2
Q

Spironolactone

acts to

A

Competitive antagonist at aldosterone receptor, leads to blocks synthesis of Na+ and K+ channels - Na+-K+-ATPase

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3
Q

Triamterene / Amiloride acts as a

A
  1. Direct effect to block the Na+-channels on collecting duct lumen and decrease Na+ reabsorption
  2. No utility in HF - do not block pro-fibrotic actions of aldosterone
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4
Q

Triamterene metabolized in

A

liver

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5
Q

which drugs are K+ sparing diuretics

A
  1. spironolactone
  2. eplerenone
  3. triamterene/amiloride
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6
Q

Tx of HF by K+ sparing diuretics: Anti-remodeling action is to

A

block of aldosterone-mediated cardiac hypertrophy and fibrosis

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7
Q

K+ sparing diuretics tx HF can benefit from raising serum

A

K+ leads to counter risk of hypokalemia-induced arrhythmias from K+-wasting diuretics

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8
Q

K+ sparing diuretic adverse reactions

A
  1. hyperkalemia
  2. endocrine abnormalitiies (gynecomastia)
  3. GI upset
  4. drowsiness
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9
Q

K+ sparing diuretic: hyperkalemia can cause

A
  1. EKG changes
  2. conduction abnormalities
  3. arrhythmias
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10
Q

hyperkalemia in K+ sparing diuretic risk is increased by

A
  1. Increasing age
  2. Underlying renal dysfunction
  3. Higher doses
  4. Combined use of ACEI or ARB
  5. Use of NSAID analgesics
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11
Q

gynecomastia by spironolactone is caused by?

A

block of androgen receptor

NOT seen with eplerenone, because it is selective for aldo receptors

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12
Q

RAAS Antagonists

A
  1. ACE Inhibitors

2. AT-1 Receptor Blockers

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13
Q

ACEI action in HF

A
  1. Inhibits ACE conversion of Ang I to Ang II, which blocks Ang II-induced vasoconstriction, which decreases preload and afterload
  2. Vasodilators have less survival benefits than ACEIs
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14
Q

ACEI primary mechanism

A

decrease Ang II-induced release of aldo and moderates myocardial hypertrophy and remodeling

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15
Q

ACEI results in

A
  1. Decreases bradykinin inactivation, increasing its vasodilator action
  2. Improves endothelial function, which leads to enhancing NO action
  3. Reduces sympathetic activity
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16
Q

ACEI: prodrugs

A

are converted to the active metabolite by de-esterification in the liver

17
Q

ACEI excretion

A

Active metabolites are eliminated by the kidneys - renal dosing required