Intro to Antihypertensive Agents IV Flashcards Preview

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Flashcards in Intro to Antihypertensive Agents IV Deck (51):
1

amlodipine

calcium channel blocker

2

clevidipine

calcium channel blocker
-DHP

3

felodipine

calcium channel blocker
-DHP

4

isradipidine

calcium channel blocker
-DHP

5

nicardipine

calcium channel blocker
-DHP

6

nifedipine

calcium channel blocker
-DHP

7

nisoldipine

calcium channel blocker
-DHP

8

diltiazem

calcium channel blocker
-non-DHP

9

verapamil

calcium channel blocker
-non-DHP

10

diazoxide

K channel opener

11

minoxidil

K channel opener

12

fenoldopam

dopamine agonist

13

hydralaine

NO donor

14

nitroprusside

NO donor
-nitropress

15

nitroglycerin

NO donor
-organic nitrate

16

isosorbide dinitrate

NO donor
-organic nitrate

17

calcium channel blocker mechanism

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

decreased vascular smooth m contraction

18

dihydropyridine mechanism

-bind L-type Ca channels
-arteriolar vasodilation predominant

**more vascular effect

19

non-dihydropyridine mechanism

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

verapamil > diltiazem

20

hemodynamics of CCBs

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

21

CCBs and cardiac muscle

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

DHPs

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

23

DHPs and cardiac muscle

greater vasodilatory effect
-reflex increased sympathetic tone that overcomes negative inotropic effect

24

CCB effect on cardiac nodal cells

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

verapamil and diltiazem

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

non-DHPs

more cardiac effect
-decreased contractility, suppress SA automaticity, and AV conduction

27

CCB pharmacokinetics

high 1st pass effect

28

long half life CCBs

amlodipine, felodipine, isradipine

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DHP with long plasma half lives **

preferred to minimize reflex cardiac effects

-**decreased reflex tachycardia

-release preparations are available

30

CCBs sometimes used IV

nifedipine, clevidipine, verapamil, diltiazem

31

CCB adverse effects

generally very well tolerated

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

32

non-DHP with beta blocker**

contraindicated
-risk for potential AV block

33

non-DHP contraindications

-ventricular dysfunction
-SA or AV nodal conduction defects
-systolic BP < 90

34

CCB clinical uses

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

35

potassium channel opener mechanism

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

36

diazoxide adverse effects

-excessive hypotension can cause stroke/MI
-hyperglycemia

37

minoxidil adverse effects

-HA, sweating, hypertrichosis, reflex tachycardia, edema

38

with minoxidil

use beta-blocker and diuretic

39

topical minoxidil

baldness

40

potassium channel openers

arteriolar vasodilation
-diazoxide and minoxidil

41

fenoldopam

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

42

clinical use fenoldopam

HTN emergency and post op HTN

43

adverse effects of fenoldopam

tachycardia, headache, flushing

44

avoid in patients with glaucoma

fenoldopam
-increased IOP

45

hydralazine mechanism

released NO from endothelium
>dilates arterioles (not veins)

46

clinical for hydralazine

first line for HTN in pregnancy (with methyldopa)

combine with nitrates -heart failure pts

47

adverse effects of hydralazine

fluid and Na retention
-HA, nausea, anorexia, sweating, flushing, palpitations
-reflex tachycardia - provoke angina
-lupus like syndrome (reversible on drug withdrawal)

48

effect of organic nitrates

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

adverse effects of nitroprusside

excessive hypotension, CN poisoning

50

adverse effects of nitrates

orthostatic hypotension, syncope, throbbing HA

51

compensatory response to vasodilators

-increased RAAS system
-increased sympathetic outflow