Vasodilators and Sympathomimetics - Kruse Flashcards Preview

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Flashcards in Vasodilators and Sympathomimetics - Kruse Deck (87)
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1
Q

ending of dihydropyridine (DHP) calcium channel blockers (CCBs)

A

-dipine

2
Q

non-DHP CCBs

A
  • diltiazem

- verapamil

3
Q

K+ channel openers

A
  • diazoxide

- minoxidil

4
Q

dopamine agonist

A

fenoldopam

5
Q

NO modulators

A
  • hydralazine
  • nitroprusside
  • isosorbide dinitrate
  • nitroglycerin
6
Q

ending of beta-andrenergic antagonist (beta-blockers)

A

-lol or -olol

7
Q

alpha1-adrenergic antagonists (alpha1-blockers)

A
  • doxazosin
  • prazosin
  • terazosin
8
Q

centrally acting sympathoplegics (alpha2-agonists)

A
  • clonidine
  • guanabenz
  • guanafacine
  • methyldopa
9
Q

MOA: DHP CCBs

A

block L-type Ca receptors (vasculature > cardiac)

10
Q

MOA: non-DHP CCBs

A

nonselective block of L-type Ca channels

11
Q

PK: CCBs

A

orally active w/ high first-pass metabolist

12
Q

CCBs given IV

A
  • nifedipine
  • clevidipine
  • verapamil
  • diltiazem
13
Q

T1/2 most CCBs

A

2-12 h

14
Q

T1/2 amlodipine

A

35-50h

15
Q

AE: DHP CCBs

A
  • xs hypotension
  • dizziness
  • HA
  • peripheral edema
  • flushing
  • tachy
  • rash
  • gingival hyperplasia
16
Q

type of DHP used to tx chronic HTN

A

slow-release and long-acting

17
Q

AE: non-DHP CCBs

A
  • dizziness
  • HA
  • periperal edema
  • constipation
  • AV block
  • brady
  • HF
  • lupus-like rash (diazetam)
  • pulmonary edema
  • coughing and wheezing
18
Q

non-DHPs causing slow HR

A

verapamil > dilitiazem

19
Q

non-DHE CCB that esp causes constipation

A

verapamil

20
Q

mechanism by which CCBs cause worsening HF

A

negative ionotropic effect

21
Q

DI: DHP CCBs

A

other vasodilators

22
Q

DI: non-DHP CCBs

A

other cardiac depressants and hypotensive drugs

23
Q

clinical uses of CCBs

A

long-term out-pt therapy for HTN, HTN emergencies, angina

24
Q

MOA: diazoxide

A

opens K channels thereby hyperpolarzing membrane and reducing contractility

25
Q

DOA: diazoxide

A

long-acting, 4-12 hours

26
Q

administration: diaoxide

A

3-4 injections at 5-15 minute intervals PRN

27
Q

AE: diazoxide

A
  • xs hypotension (> in renal failure and beta-blocker pts)
  • hyperglycemia
  • H20 + Na retantion (v rare)
28
Q

CI: diazoxide

A

-ischemic HR: causes angina, ischemia, CF

29
Q

clinical use of diazoxide

A

HTN emergencies

30
Q

MOA: minoxidil

A

opens K channels in smooth m thereby allowing hypepolarization leading to decreased contractility

31
Q

phys effect of minoxidil

A

dilation of aa, not vv; > effect than hyralazine

32
Q

AE: minoxidil

A
  • HA
  • sweating
  • hypertrichosis
  • reflex sympathetic stim
  • Na H2O retention; leads to tachy, palpitations, angina, edema
33
Q

what do you NEED to use with minoxidil and why?

A
  • beta-blocker: avoid excess sympathetic stim

- loop diuretic: avoid edema

34
Q

clinical uses of minoxidil

A
  • LT out-pt therapy of severe HTN

- topically for hair growth

35
Q

MOA: fenoldopam

A

D1 receptor agonist

36
Q

phys effects of fenyldopam

A

arteroilar dilator, naturetic

37
Q

ROA: fenyldopam

A

cont IV infusion

38
Q

T1/2: Fenyldopam

A

short - 10 min

39
Q

AE: fenoldopam

A
  • tachy
  • HA
  • flushing
40
Q

CI: fenyldopam

A

glaucoma - increased intraoccular P

41
Q

clinical uses of fenyldopam

A

HTN emergencies, peri and post-op HTN

42
Q

MOA: hydralazine

A

release of NO from endothelium causing increased cGMP

43
Q

PK: hydralazine

A

high first pass and therefore low bioavailability

44
Q

AE: hydralazine

A
  • HA, nausea, anorexia, palpitation, sweating, flushing
  • angina and arrhythmias in some pts (ischemic heart dz, reflex tachy, symp stim)
  • rare: periph neuropathy, drug F
45
Q

clinical uses of hydralazine

A
  • LT out-ppt with HTN
  • frist line in preg F w/ HTN
  • use with methyldopa for AA’s w/ HTN + HF
  • IV for HTN emergencies
46
Q

phys effects of hyralazine

A
  • aa dilation but not vv

- reflex tachy

47
Q

MOA: sodium nitroprusside

A

release of NO leading to increase cGMP

48
Q

phys effect of sodium nitroprusside

A
  • aa and vv dilation, dec BP

- pts with HF = increase CO too

49
Q

DOA: sodium nitroprussides

A

-rapid onset w short duration

50
Q

ROA: sodium nitroprusside

A

IV infusion w/ cont monitoring

51
Q

AE: sodium nitroprussides

A
  • excessive hypotension

- cyanide and thiocyanate release - potential for poisoning if used for several days

52
Q

clinical uses of sodium nitroprussides

A
  • HTN emergencies

- acute decompensated HF

53
Q

organic nitrate agents

A
  • nitroglycerin
  • isosorbide dinitrate
  • isosorbide mononitrate
54
Q

MOA: organic nitrates

A

release of NO via enzymatic metabolism

55
Q

phys effects of organic nitrates

A
  • vv dilation > aa: increased venous capacity
  • decreased vent preload
  • reduced pulmonary vasc P
  • reduces heart size
  • reduced CO
56
Q

ROA: organic nitrites

A

oral, transdermal and buccal (for longer DOA)

57
Q

DOA: organic nitrates

A
  • reach therapeudic levels w/in minutes

- effects lasts 15-30 min

58
Q

limitation of organic nitrates and how to prevent it

A

can build tolerance, need to have nitrate-free period for at least 8 hr btwn doses

59
Q

AE: organic nitrates

A
  • orthostatic hypotension
  • syncope
  • throbbing HA
60
Q

CI: organic nitrates

A

increase ICP

61
Q

DI: organic nitrates

A

hypotension w/ PDE5 inhibitors

62
Q

clinical uses of organic nitrates

A
  • HTN emergency
  • angina
  • heart failure
63
Q

when are sympathoplegic agents most effective?

A

when used with a diuretic

64
Q

Beta1-blockers do what in the kidney?

A

inhibit renin secretion

65
Q

beta-blocker not available as oral preparation

A

esmolol

66
Q

extended release beta-blockers

A
  • carvediol
  • metoprolol
  • propranolol
67
Q

beta-blockers available as parenternal preparations

A
  • atenolol
  • esmolol
  • labetalol
  • metoprolol
  • propranolol
68
Q

beta-blockers that cross the BBB

A
  • propranolol

- penbutolol

69
Q

CI: beta blockers

A
  • asthma/COPD ( benefit may outweigh risk of COPD)

- diabetes: benefits may outweigh risk in pts after MI

70
Q

AE: beta blockers

A
  • brady
  • fatigue
  • sexual dysfunction
  • depresion
  • unfavorable plasma lipid profiles (inc VLDL, dec HDL)
  • rebount HTN after sudden stopping w/ possible angina and MI
71
Q

DI: beta-bockers

A

heart block if used with verapamil or diltiazem

72
Q

clinical uses of beta-blockers

A
  • HTN
  • heart failure
  • ischemic heart disease
  • cardiac arrythmias
  • glaucoma
73
Q

clinical use for beta1-selective agonist

A
  • comorbid asthma
  • DM
  • peripheral vascular disease
74
Q

clinical use of beta2 selective agonists

A
  • bradyarrhythmias

- peripheral vascular disease

75
Q

MOA: alpha1-blocker

A

reversible antagonists at alpha 1 receptors

76
Q

phys effects of alpha1 blockers

A
  • vasoconstrcitos aa and vv
  • relax smooth mm in prostate
  • H2O and Na retention (when used w/out beta blocker)
  • no change or improvement of plasma lipid profiles
77
Q

AE: alpha 1 blockers

A
  • orthostatic hypotension
  • dizziness
  • palpations
  • HA
  • lassitude
78
Q

alpha 1 blockers have less incidence of what in comparison to non-selective alpha adrenergic blockers?

A

reflex tachy

79
Q

DI: alpha 1 blockers

A

most effective when used with other drugs (beta-blockers and diuretics)

80
Q

clinical use of alpha 1 blockers

A

concurrent HTN and BPH

81
Q

MOA: centrally acting agents (alpha 2 agonists)

A
  • reduce sympathetic outflow from vasomotor centers

- retain or increase sensitivity to baroreceptor control

82
Q

clinicl uses of central acting (alpha 2) agonists

A
  • v rare use

- methyldopa is used for HTN in pregnancy

83
Q

MOA: clonidine

A

lowers BP by reducing CO and peripheral vascular resistance

84
Q

AE: clonidine

A
  • sedation
  • dry mouth
  • depression
  • sexual dysfunction
85
Q

SAE: clonidine

A

abrupt w/drawal can lead to life-threatning HTN crisis

86
Q

MOA: methyldopa

A
  • lowers BP via reduction in peripheral vascular resistance

- variable reduction in HR and CO

87
Q

AE: methyldopa

A
  • sedation
  • dry mouth
  • lack of concentration
  • sexual dysfunction