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Year 2 Pharmacology > Cardiovascular pharmacology VI > Flashcards

Cardiovascular pharmacology VI Flashcards

1
Q

thiazide diuretics block what transporter? where?

A
  1. NaCl cotransporter

2. distal convoluted tubule

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2
Q

what is the main thiazide diuretic agent?

A

chlorthalidone

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3
Q

what are the effects of thiazide diuretics?

A
  1. more sodium in the lumen
  2. pull water into lumen
  3. promote calcium reabosorption (decrease calcium excretion)
  4. vasorelaxation
  5. risk of hypokalemia
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4
Q

what are the clinical applications of thiazide diuretics?

A
  1. hypertension
  2. edema control - CHF
  3. hypercalciuria
  4. nephrolithiasis
  5. nephrogenic diabetes insipidus
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5
Q

what is the mechanism of action for inhibitors of renal epithelial sodium channels?

A
  1. block epithelial sodium channels on principal cells in late DCT and initial connecting tubule and the cortical collecting ducts
  2. modest natriuresis and prevention of potassium loss
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6
Q

what are the clinical indications of inhibitors of renal epithelial sodium channels?

A
  1. potassium sparing in hypokalemic alkalosis

2. combined with loop diuretics to prevent hypokalemia

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7
Q

what is the main inhibitor of renal epithelial sodium channels agent?

A

amiloride

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8
Q

what is the mechanism of action for aldosterone receptor antagonists?

A
  1. blocks aldosterone receptors in renal collecting tubules
  2. decrease sodium reabsorption - natriuresis
  3. decrease loss of potassium in exchange for sodium
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9
Q

what is the main aldosterone receptor antagonists

A

spironolactone

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10
Q

what are the other therapeutic effects of spironolactone?

A
  1. prevents LV remodeling and cardiac fibrosis
  2. prevents sudden cardiac death
  3. lowers BP
  4. improves vascular health
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11
Q

what are the clinical applications of spironolactone?

A
  1. edema and hypertension
  2. adjunctive for heart failure
  3. primary hyperaldosteronism (body thinks there is not enough intravascular water)
  4. refractory edema associated with hyperaldosteronism
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12
Q

what are the adverse effects of spironolactone?

A
  1. HYPERKALEMIA
  2. metabolic acidosis
  3. effects due to binding other steroid receptors
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13
Q

what are the hemodynamic and hormonal effects of diuretic therapy?

A
  1. BP - decrease
  2. BV and CO - drops
  3. total body sodium and weight - decrease
  4. TPR - drop over time
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14
Q

definition: hypertensive urgency

A
  1. no associated acute end organ damage
  2. BP can be reduced over hours to days
  3. SBP over 180 or DBP over 120
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15
Q

definition: hypertensive emergency

A
  1. acute end organ damage

2. BP must be reduced within minutes to hours

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16
Q

definition: hypertensive crisis

A
  1. end organ damage

2. BP must be reduced within minutes to hours

17
Q

definition: resistant hypertension

A

BP that is uncontrolled despite use of 3 or more antihypertensive drugs (one must be a diuretic)

18
Q

how do antihypertensive agents work in calculation form?

A

MAP = CO x TPR

CO = HR x SV

19
Q

juxtaglomerular cells are stimulated by what factors?

A
  1. increased catecholamines

2. decreased serum potassium

20
Q

juxtaglomerular cells are inhibited by what factors?

A
  1. increased serum potassium

2. increased tubular sodium effect at the macula densa

21
Q

what is the role of the juxtaglomerular cells?

A

stimulates renin release, which converts angiotensinogen to angiotensin I

22
Q

what converts angiotenin I to angiotensin II?

A

angiotensin converting enzyme?

23
Q

what is the effect of angiotensin on aldosterone?

A

stimulates

24
Q

what is the effect of aldosterone on renal potassium excretion?

A

increase

25
Q

aldosterone is stimulated by what factors?

A
  1. increased serum potassium

2. ACTH

26
Q

aldosterone is inhibited by what factors?

A
  1. decreased serum potassium
  2. dopamine
  3. ANP
  4. heparin

Year 2 Pharmacology (70 decks)

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