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Renal II > Vasodilators and Sympathomimetics - Kruse > Flashcards

Vasodilators and Sympathomimetics - Kruse Flashcards

1
Q

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

A

-dipine

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2
Q

non-DHP CCBs

A
  • diltiazem

- verapamil

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3
Q

K+ channel openers

A
  • diazoxide

- minoxidil

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4
Q

dopamine agonist

A

fenoldopam

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5
Q

NO modulators

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

ending of beta-andrenergic antagonist (beta-blockers)

A

-lol or -olol

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7
Q

alpha1-adrenergic antagonists (alpha1-blockers)

A
  • doxazosin
  • prazosin
  • terazosin
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8
Q

centrally acting sympathoplegics (alpha2-agonists)

A
  • clonidine
  • guanabenz
  • guanafacine
  • methyldopa
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9
Q

MOA: DHP CCBs

A

block L-type Ca receptors (vasculature > cardiac)

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10
Q

MOA: non-DHP CCBs

A

nonselective block of L-type Ca channels

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11
Q

PK: CCBs

A

orally active w/ high first-pass metabolist

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12
Q

CCBs given IV

A
  • nifedipine
  • clevidipine
  • verapamil
  • diltiazem
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13
Q

T1/2 most CCBs

A

2-12 h

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14
Q

T1/2 amlodipine

A

35-50h

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15
Q

AE: DHP CCBs

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

type of DHP used to tx chronic HTN

A

slow-release and long-acting

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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
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18
Q

non-DHPs causing slow HR

A

verapamil > dilitiazem

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19
Q

non-DHE CCB that esp causes constipation

A

verapamil

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20
Q

mechanism by which CCBs cause worsening HF

A

negative ionotropic effect

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21
Q

DI: DHP CCBs

A

other vasodilators

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22
Q

DI: non-DHP CCBs

A

other cardiac depressants and hypotensive drugs

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23
Q

clinical uses of CCBs

A

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

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24
Q

MOA: diazoxide

A

opens K channels thereby hyperpolarzing membrane and reducing contractility

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25
DOA: diazoxide
long-acting, 4-12 hours
26
administration: diaoxide
3-4 injections at 5-15 minute intervals PRN
27
AE: diazoxide
- xs hypotension (> in renal failure and beta-blocker pts) - hyperglycemia - H20 + Na retantion (v rare)
28
CI: diazoxide
-ischemic HR: causes angina, ischemia, CF
29
clinical use of diazoxide
HTN emergencies
30
MOA: minoxidil
opens K channels in smooth m thereby allowing hypepolarization leading to decreased contractility
31
phys effect of minoxidil
dilation of aa, not vv; > effect than hyralazine
32
AE: minoxidil
- HA - sweating - hypertrichosis - reflex sympathetic stim - Na H2O retention; leads to tachy, palpitations, angina, edema
33
what do you NEED to use with minoxidil and why?
- beta-blocker: avoid excess sympathetic stim | - loop diuretic: avoid edema
34
clinical uses of minoxidil
- LT out-pt therapy of severe HTN | - topically for hair growth
35
MOA: fenoldopam
D1 receptor agonist
36
phys effects of fenyldopam
arteroilar dilator, naturetic
37
ROA: fenyldopam
cont IV infusion
38
T1/2: Fenyldopam
short - 10 min
39
AE: fenoldopam
- tachy - HA - flushing
40
CI: fenyldopam
glaucoma - increased intraoccular P
41
clinical uses of fenyldopam
HTN emergencies, peri and post-op HTN
42
MOA: hydralazine
release of NO from endothelium causing increased cGMP
43
PK: hydralazine
high first pass and therefore low bioavailability
44
AE: hydralazine
- 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
clinical uses of hydralazine
- 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
phys effects of hyralazine
- aa dilation but not vv | - reflex tachy
47
MOA: sodium nitroprusside
release of NO leading to increase cGMP
48
phys effect of sodium nitroprusside
- aa and vv dilation, dec BP | - pts with HF = increase CO too
49
DOA: sodium nitroprussides
-rapid onset w short duration
50
ROA: sodium nitroprusside
IV infusion w/ cont monitoring
51
AE: sodium nitroprussides
- excessive hypotension | - cyanide and thiocyanate release - potential for poisoning if used for several days
52
clinical uses of sodium nitroprussides
- HTN emergencies | - acute decompensated HF
53
organic nitrate agents
- nitroglycerin - isosorbide dinitrate - isosorbide mononitrate
54
MOA: organic nitrates
release of NO via enzymatic metabolism
55
phys effects of organic nitrates
- vv dilation > aa: increased venous capacity - decreased vent preload - reduced pulmonary vasc P - reduces heart size - reduced CO
56
ROA: organic nitrites
oral, transdermal and buccal (for longer DOA)
57
DOA: organic nitrates
- reach therapeudic levels w/in minutes | - effects lasts 15-30 min
58
limitation of organic nitrates and how to prevent it
can build tolerance, need to have nitrate-free period for at least 8 hr btwn doses
59
AE: organic nitrates
- orthostatic hypotension - syncope - throbbing HA
60
CI: organic nitrates
increase ICP
61
DI: organic nitrates
hypotension w/ PDE5 inhibitors
62
clinical uses of organic nitrates
- HTN emergency - angina - heart failure
63
when are sympathoplegic agents most effective?
when used with a diuretic
64
Beta1-blockers do what in the kidney?
inhibit renin secretion
65
beta-blocker not available as oral preparation
esmolol
66
extended release beta-blockers
- carvediol - metoprolol - propranolol
67
beta-blockers available as parenternal preparations
- atenolol - esmolol - labetalol - metoprolol - propranolol
68
beta-blockers that cross the BBB
- propranolol | - penbutolol
69
CI: beta blockers
- asthma/COPD ( benefit may outweigh risk of COPD) | - diabetes: benefits may outweigh risk in pts after MI
70
AE: beta blockers
- brady - fatigue - sexual dysfunction - depresion - unfavorable plasma lipid profiles (inc VLDL, dec HDL) - rebount HTN after sudden stopping w/ possible angina and MI
71
DI: beta-bockers
heart block if used with verapamil or diltiazem
72
clinical uses of beta-blockers
- HTN - heart failure - ischemic heart disease - cardiac arrythmias - glaucoma
73
clinical use for beta1-selective agonist
- comorbid asthma - DM - peripheral vascular disease
74
clinical use of beta2 selective agonists
- bradyarrhythmias | - peripheral vascular disease
75
MOA: alpha1-blocker
reversible antagonists at alpha 1 receptors
76
phys effects of alpha1 blockers
- 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
AE: alpha 1 blockers
- orthostatic hypotension - dizziness - palpations - HA - lassitude
78
alpha 1 blockers have less incidence of what in comparison to non-selective alpha adrenergic blockers?
reflex tachy
79
DI: alpha 1 blockers
most effective when used with other drugs (beta-blockers and diuretics)
80
clinical use of alpha 1 blockers
concurrent HTN and BPH
81
MOA: centrally acting agents (alpha 2 agonists)
- reduce sympathetic outflow from vasomotor centers | - retain or increase sensitivity to baroreceptor control
82
clinicl uses of central acting (alpha 2) agonists
- v rare use | - methyldopa is used for HTN in pregnancy
83
MOA: clonidine
lowers BP by reducing CO and peripheral vascular resistance
84
AE: clonidine
- sedation - dry mouth - depression - sexual dysfunction
85
SAE: clonidine
abrupt w/drawal can lead to life-threatning HTN crisis
86
MOA: methyldopa
- lowers BP via reduction in peripheral vascular resistance | - variable reduction in HR and CO
87
AE: methyldopa
- sedation - dry mouth - lack of concentration - sexual dysfunction

Renal II (7 decks)

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