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RENAL II Exam 3 > Intro to Antihypertensive Agents IV > Flashcards

Intro to Antihypertensive Agents IV Flashcards

1
Q

amlodipine

A

calcium channel blocker

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2
Q

clevidipine

A

calcium channel blocker

-DHP

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3
Q

felodipine

A

calcium channel blocker

-DHP

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4
Q

isradipidine

A

calcium channel blocker

-DHP

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5
Q

nicardipine

A

calcium channel blocker

-DHP

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6
Q

nifedipine

A

calcium channel blocker

-DHP

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7
Q

nisoldipine

A

calcium channel blocker

-DHP

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8
Q

diltiazem

A

calcium channel blocker

-non-DHP

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9
Q

verapamil

A

calcium channel blocker

-non-DHP

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10
Q

diazoxide

A

K channel opener

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11
Q

minoxidil

A

K channel opener

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12
Q

fenoldopam

A

dopamine agonist

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13
Q

hydralaine

A

NO donor

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14
Q

nitroprusside

A

NO donor

-nitropress

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15
Q

nitroglycerin

A

NO donor

-organic nitrate

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16
Q

isosorbide dinitrate

A

NO donor

-organic nitrate

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17
Q

calcium channel blocker mechanism

A

block L-type Ca channels
-cardiac myocyte and SA and AV nodal cells

decreased vascular smooth m contraction

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18
Q

dihydropyridine mechanism

A
  • bind L-type Ca channels
  • arteriolar vasodilation predominant

**more vascular effect

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19
Q

non-dihydropyridine mechanism

A
  • bind L-type Ca channels
  • predominant cardiac effects, but also act at vascular tissues

verapamil > diltiazem

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20
Q

hemodynamics of CCBs

A
  • reduced TPR
  • reduced afterload
  • reduced O2 demand
  • non-DHPs reduce CO
  • decreased coronary vascular resistance and increased coronary blood flow
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21
Q

CCBs and cardiac muscle

A

negative inotropic effect

  • Na fast channel primary depolarization, but Ca slow channels is additional
  • Ca entry - induce Ca release from SR
  • Ca binds troponin - allows contraction

verapamil > diltiazem > DHPs (inotropic effects)

22
Q

DHPs

A

relax vascular smooth m at lower concentration than required for direct action on heart

23
Q

DHPs and cardiac muscle

A

greater vasodilatory effect

-reflex increased sympathetic tone that overcomes negative inotropic effect

24
Q

CCB effect on cardiac nodal cells

A

SA and AV node - depolarization L-type Ca channels

DHPs block channel - but don’t effect recovery of channel and ARE NOT frequency dependent

25
Q

verapamil and diltiazem

A

non-DHP CCB
-block channel, delay recovery of channel, and ARE frequency dependent

  • decreased rate of SA node depolarization and slow AV nodal conduction
  • useful for Tx of supraventricular tachyarrhythmias but dangerous for patients with slow nodal conduction
26
Q

non-DHPs

A

more cardiac effect

-decreased contractility, suppress SA automaticity, and AV conduction

27
Q

CCB pharmacokinetics

A

high 1st pass effect

28
Q

long half life CCBs

A

amlodipine, felodipine, isradipine

29
Q

DHP with long plasma half lives **

A

preferred to minimize reflex cardiac effects

  • **decreased reflex tachycardia
  • release preparations are available
30
Q

CCBs sometimes used IV

A

nifedipine, clevidipine, verapamil, diltiazem

31
Q

CCB adverse effects

A

generally very well tolerated

  • excessive vasodilation - dizzy, hypotension, HA, nausea
  • constipation** (verapamil), peripheral edema, coughing, wheezing, pulmonary edema
32
Q

non-DHP with beta blocker**

A

contraindicated

-risk for potential AV block

33
Q

non-DHP contraindications

A
  • ventricular dysfunction
  • SA or AV nodal conduction defects
  • systolic BP < 90
34
Q

CCB clinical uses

A

HTN (with other agent to counteract reflex CV response), hypertensive emergency, angina (reduced O2 demand)

35
Q

potassium channel opener mechanism

A

increased K permeability
> hyperpolarizes smooth m. membrane
> reduce probability of contraction

36
Q

diazoxide adverse effects

A
  • excessive hypotension can cause stroke/MI

- hyperglycemia

37
Q

minoxidil adverse effects

A

-HA, sweating, hypertrichosis, reflex tachycardia, edema

38
Q

with minoxidil

A

use beta-blocker and diuretic

39
Q

topical minoxidil

40
Q

potassium channel openers

A

arteriolar vasodilation

-diazoxide and minoxidil

41
Q

fenoldopam

A

D1 dopamine receptor agonist
-renal afferent arteries contain dopamine receptors
>increased blood flow to kidney

42
Q

clinical use fenoldopam

A

HTN emergency and post op HTN

43
Q

adverse effects of fenoldopam

A

tachycardia, headache, flushing

44
Q

avoid in patients with glaucoma

A

fenoldopam

-increased IOP

45
Q

hydralazine mechanism

A

released NO from endothelium

>dilates arterioles (not veins)

46
Q

clinical for hydralazine

A

first line for HTN in pregnancy (with methyldopa)

combine with nitrates -heart failure pts

47
Q

adverse effects of hydralazine

A

fluid and Na retention

  • HA, nausea, anorexia, sweating, flushing, palpitations
  • reflex tachycardia - provoke angina
  • lupus like syndrome (reversible on drug withdrawal)
48
Q

effect of organic nitrates

A 
dilate arterial and venous vessels
>decreased TPR and venous return
>decreased preload and afterload
>main relaxation of large veins (decreased venous return/preload)
>also decreased O2 demand
>smaller decreased afterload
49
Q

adverse effects of nitroprusside

A

excessive hypotension, CN poisoning

50
Q

adverse effects of nitrates

A

orthostatic hypotension, syncope, throbbing HA

51
Q

compensatory response to vasodilators

A
  • increased RAAS system

- increased sympathetic outflow

RENAL II Exam 3 (17 decks)

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