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pharmacology > HTN moa + > Flashcards

HTN moa + Flashcards

1
Q

Thiazides moa

A

inhibit reabsorption of Na+ and Cl- by the DCT causing them to be excreted in urine

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2
Q

thiazide like moa

A

inhibit reabsorption of Na+ and Cl- by the DCT causing them to be excreted in urine

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3
Q

Loops moa

A

MOA: inhibit NKCC2 and inhibit Na Cl and K reabsorption in the thick ascending loop of henle. They increase the loss of K, Ca, and Mg

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4
Q

loops se

A

hypokalemia, may need supplement

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5
Q

loops bbw

A

potent diuretics

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6
Q

Usually used for heart failure not HTN

A

loops

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7
Q

Extremely powerful diuretics

A

loops

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8
Q

K+ sparing moa

A

MOA: blocks ENaC (epithelial Na channel) so that Na absorption is decreased and inhibit loss of K+ in the collecting tubule independent of mineralocorticoids

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9
Q

K+ sparing se

A

hyperkalemia

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10
Q

K+ sparing bbw

A

can cause hyperkalemia and if not corrected can be fatal

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11
Q

K+ sparing contraindications

A

hyperkalemia, don’t use with K+ supplements

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12
Q

Eplerenone- ________ aldosterone antagonist

A

selective

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13
Q

Less potent than spironolactone

A

Eplerenone

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14
Q

Spironolactone- _______ aldosterone antagonist

A

nonselective

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15
Q

Aldosterone receptor blockers/antagonists moa

A

bind to mineralocorticoid receptor in collecting duct of the kidney to inhibit aldosterone

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16
Q

what does aldosterone do

A

increases Na reabsorption and K excretion

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17
Q

SE Aldosterone receptor blockers/antagonists

A

SE= gynecomastia, sexual dysfunction (bc it works on mineralocorticoid receptors)

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18
Q

Carbonic anhydrase inhibitor moa

A

MOA: inhibits carbonic anhydrase in the PCT of the kidney. Therefore BP, intracranial pressure, and intraocular pressure are lowered

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19
Q

Carbonic anhydrase

A

allows reabsorption of bicarbonate, Na, and Cl

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20
Q

Carbonic anhydrase inhibitor SE

A

SE= metabolic acidosis (bc eliminates the bicarbonate), and hyponatremia

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21
Q

osmotic moa

A

MOA: facilitates the release of H2O by inhibiting the renal tubular reabsorption of Na and Cl. This causes cerebral edema, intracranial pressure, and CSF volumes are reduced

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22
Q

osmotic is used in

A

eye surgery

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23
Q

ACE inhibitors MOA

A

MOA: blocks ACE so angiotensin 1 cannot be converted to angiotensin 2. They reduce the afterload by dilating efferent arterioles. Blocking ACE also inhibits the breakdown of bradykinin

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24
Q

ACE Inhibitors se

A

SE= cough (bc bradykinin is not broken down, which is an inflammatory mediator), angioedema of the face, lips, and throat, hyperkalemia

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25
Q

ACE Inhibitors contra

A

Contraindications: hx of angioedema, do not use if also taking Aliskiren

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26
Q

ACE Inhibitors caution

A

Cautions: ACEI + ARBs = no benefit; less effective in african americans

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27
Q

ACE Inhibitors bbw

A

BBW: stop if pregnant; category D

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28
Q

Angiotensin II receptor blockers (ARBs) moa

A

MOA: inhibits angiotensin 2 from binding to its receptors so vasoconstriction cannot occur and aldosterone cannot be secreted

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29
Q

Angiotensin II receptor blockers (ARBs) se

A

SE= hyperkalemia and angioedema (no cough like with ACEI)

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30
Q

Angiotensin II receptor blockers (ARBs) contra

A

Contraindications: do not use with Aliskiren

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31
Q

Angiotensin II receptor blockers (ARBs) bbw

A

BBW: stop if pregnant category d

32
Q

Direct renin inhibitors moa

A

MOA: competitively inhibits renin so angiotensinogen cannot be converted to angiotensin 1

33
Q

Direct renin inhibitors se

A

SE=hyperkalemia, angioedema

34
Q

Direct renin inhibitors contra

A

Contraindications: do not use with ACEI or ARBs

35
Q

Direct renin inhibitors bbw

A

BBW: D/C if pregnant category d

36
Q

Dihydropyridines moa

A

MOA: selectively inhibits L type calcium channels in vascular smooth muscle (mainly) and cardiac muscle cells causing decreased bp

37
Q

Dihydropyridines se

A

SE= peripheral edema

38
Q

non Dihydropyridines moa

A

MOA: non selectively inhibits L type calcium channels in vascular smooth muscle and SA and AV nodes which decreases hr… therefore it can have antiarrhythmic properties

39
Q

Verapamil- can lead to _____

A

constipation

40
Q

non Dihydropyridines se

A

SE= bradycardia and constipation (in verapamil)

41
Q

non Dihydropyridines caution

A

Cautions: grapefruit juice can enhance oral absorption

42
Q

Centrally active alpha 2 agonists moa

A

MOA: stimulates alpha 2 adrenoceptors in the brainstem causing reduced sympathetic outflow (less NE) causing dec bp

43
Q

Centrally active alpha 2 agonists se

A

SE= drowsiness, feeling tired

44
Q

Centrally active alpha 2 agonists caution

A

Caution: do not D/C suddenly bc it can cause rebound HTN

45
Q

Peripherally acting alpha 1 adrenergic blockers moa

A

MOA: blocks postsynaptic alpha 1 receptors causing decreased bp

46
Q

Peripherally acting alpha 1 adrenergic blockers se

A

SE= postural HTN, syncopal episode in the 1st dose

47
Q

Intrinsic sympathomimetic activity (ISA)

A

beta blocker that shows agonist and antagonist activity at the beta 1 receptors

48
Q

Beta blockers are _____ inotropes- slow the HR by blocking EPI at beta receptors

A

negative

49
Q

which beta blocker has isa activity

A

acebutolol

50
Q
  • used for eye drops in glaucoma
A

Betaxolol

51
Q

Cardioselective beta blocker moa

A

MOA: competitively block beta adrenergic stimulation at beta 1 receptor causing a dec HR

52
Q

Cardioselective beta blocker se

A

SE= bradycardia, impaired peripheral circulations/cold extremities

53
Q

Cardioselective beta blocker bbw

A

BBW: D/C gradually over 1-2 wks when used for a long time

54
Q
  • also used for glaucoma
A

Timolol

55
Q

ISA activity; crosses BBB so can be used for migraines and stage fright

A

pindolol

56
Q

non Cardioselective beta blocker moa

A

MOA: nonselective competitive beta 1 and 2 blockers cause dec BP

57
Q

non Cardioselective beta blocker se

A

SE= bradycardia, bronchospasms, impaired peripheral circulations/cold extremities

58
Q

non Cardioselective beta blocker contra

A

Contraindications: asthma and COPD

59
Q

non Cardioselective beta blocker bbw

A

BBW: D/C gradually over 1-2 wks when used for a long time

60
Q

Combination Alpha and Beta blockers moa

A

MOA: block alpha 1 to cause vasodilation and block beta 1 to cause dec HR/BP

61
Q

Combination Alpha and Beta blockers se

A

SE= postural HTN, bronchoconstriction, impaired peripheral circulations/cold extremities

62
Q

Combination Alpha and Beta blockers contra

A

Contraindications: asthma, bronchospasm, COPD

63
Q

Combination Alpha and Beta blockers caution

A

Caution: sudden D/C can exacerbate angina and lead to MI

64
Q

Hydralazine cauion

A

Caution: can cause drug induced SLE, D/C to avoid rapid side in BP

65
Q

Minoxidil se

A

SE= hypertrichosis (excessive hair growth), hirsutism

66
Q

Minoxidil caution

A

Caution: only used for severe HTN

67
Q

Minoxidil bbw

A

BBW: can cause cardiac issues that’s why it’s not 1st line trmt

68
Q

used for immediate reduction of BP in hypertensive crisis

A

Nitroprusside

69
Q

Direct vasodilators

moa

A

MOA: vasodilated arterioles and relaxes smooth muscle, but causes reflex sympathetic stimulation of the heart (so they are usually prescribed with a beta blocker too)

70
Q

direct vasodilators se

A

SE= hypotension

71
Q

Used in severe/malignant HTN and emergency HTN

A

Dopamine receptor agonist: vasodilator

72
Q

Dopamine receptor agonist: vasodilator moa

A

MOA: selective postsynaptic dopamine (D1) receptor agonist; stimulates D1 receptors to raise intracellular cAMP causing vasodilation

73
Q

Rapid onset and short duration… that’s why it’s only used in emergencies

A

Dopamine receptor agonist: vasodilator

74
Q

Postganglionic adrenergic neuron blockers

moa

A

MOA: irreversibly blocks H+ coupled vesicular monoamine transporter VMAT1 and VMAT2 which reduces monoamines in the synaptic cleft

75
Q

Postganglionic adrenergic neuron blockers

se

A

SE= depression bc serotonin and dopamine can’t get to the receptors

pharmacology (16 decks)

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