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37 Cards in this Set
- Front
- Back
vasodilator drugs
hydralazine |
Absorbed in the GI tract.
Acts on arterioles. Does not act on coronaries and veins. T1/2: 1-3 h (it can be used in the chronic therapy of hypertension) |
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hydralazine MOA
|
Don’t know
Decrease cytosolic calcium levels so have less contraction |
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hydralazine adverse effects
Vasodilation-associated adverse effects |
Excessive blood pressure drop
Flushing Dizziness, nausea & headache Tachycardia & palpitations (compensatory response) Sodium retention and edema (compensatory response |
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hydralazine adverse effects
Immunological reactions (off-target side effect |
With high dosages (>400 mg/day), there is a 10-20% incidence of a syndrome characterized by:
Arthalgia (joint pain); Myalgia (muscle pain); Skin rashes; Fever; Such syndrome resembles lupus erythematosus. |
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hydralazine
orally active? |
yesq
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hydralazine
vascular beds affected |
arterioles
|
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hydralazine
MOA |
unknown but ultimately reduces Ca++
|
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minoxidil
|
Absorbed in the GI tract.
Pro-drug sulfated after going to liver to become a vasodilator Dilates arterioles. No action on veins or coronaries. T1/2: 4 h (it can be used in the chronic therapy of hypertension) |
|
minoxidil
adverse effects: Vasodilation-associated adverse effects |
Dizziness, nausea & headache
Tachycardia & palpitations (compensatory response) Sodium retention and edema (compensatory response) |
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minoxidil
adverse effects angina (like hydralazine) |
see notes
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is tachycardia an adverse event?
|
yes
|
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minoxidil
alternate use correction of baldness |
Topical minoxidil (Rogaine) is used as a stimulant to hair growth.
topical --not systemic |
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minoxidil
orally active? |
yes
|
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minoxidil
vascular bed effected |
arterioles
|
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minoxidil
MOA |
opens K+ channel
|
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sodium nitroprusside
|
Decomposes under intestinal alkaline conditions (has to be administered IV).
T1/2: 1-2 min (needs to be continuously infused). Acts on arterioles, veins, and coronaries. Exists as a salt (sodium, is the highest conc in extracellular fluid- not enough to increase BP) |
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sodium nitroprusside
indications |
Treatment option for hypertensive emergencies.
Not indicated for chronic therapy of hypertension |
|
sodium nitroprusside can easily pass the membrane so nitric oxide gets into smooth muscle cells quickly.
|
true
|
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sodium nitroprusside adverse effects
|
Excessive vasodilation and consequent hypotension
** must be monitored closely ** |
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sodium nitroprusside adverse effects
uncommon |
cyanide intoxification
Cyanide is a byproduct of nitroprusside breakdown Cyanide might accumulate in the body |
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sodium nitroprusside
orally active |
yes
|
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sodium nitroprusside
vascular beds affected |
arterioles
veins coronaries |
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sodium nitroprusside
MOA |
release nitric oxide
|
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verapamil
|
Absorbed in the GI tract.
Acts on arterioles & coronaries. Weak effect on veins. T1/2: 4-6 h |
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verapamil
indication |
the chronic therapy of hypertension
|
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verapamil
MOA |
blocks the calcium channel
(smooth muscle cell) decreased calcium- decreased contraction |
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verapamil effects what channel?
|
L channel
|
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location of L channel
|
smooth muscle
cardiac muscle |
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properties of L channel
|
long duration
large current high threshold |
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L channel antagonists
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verapamil
dihydropyridines |
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verapamil adverse effects
Vasodilation-associated adverse effects |
Hypotension
Skin flushing Dizziness, nausea & headache Sodium retention and edema (compensatory response) Minimal compared to other vasodilators |
|
verapamil adverse effects
Bradycardia and even asystole (rare but serious |
decreased SA-AV node activity (decreased HR)
contraction force (decreased SV) |
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verapamil adverse effects
constipation |
Adverse effect likely reflects inhibition of Ca2+ channels in smooth muscle cells of the GI tract
|
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verapamil
orally active |
yes
|
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verapamil
vascular beds affected |
arterioles and coronaries
|
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verapamil
MOA |
blocks L type calcium channels
|
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other L-type calcium channel blockers
diltiazem dihydropyridines (nifedipine) orally active? |
yes
|