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33 Cards in this Set
- Front
- Back
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What effect do AChe Inhibitors have:
- at NM junction? - at post-gang M sites? - at ganglia? |
NM: flaccid paralysis
post-gang M: either ↑stimulation (contraction & secretion) OR hyperpolarization (inhibitory response) ganglia: depolarization & enhanced transmission |
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Imipramine
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interferes with NET at CNS adrenergic synapses
TCA, bedwetting |
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entacapone
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peripheral COMT inhibitor
Parkinsons (given w/ levodopa) |
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tolcapone
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peripheral & brain COMT inhibitor
Parkinsons (given w/ levodopa) |
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tranylcypromine
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nonselective MAOI
- potentiates tyramine effects |
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selegiline
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selective & reversible MAOB inhibitor
adjunct Parkinsons treatment |
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propranolol
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ß blocker
HTN, angina, tachycardia, migrain, palsy, ↓MI |
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phenoxybenzamine
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α blocker
HTN due to pheochromocytoma (adrenal tumor) |
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phenelzine
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MAOI
depression |
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isocarboxazid
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MAOI
depression |
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trimethapan
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ganglionic blocker (selective & noncompetetive) 4°
vasodilator |
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hexamethonium
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nACh antagonist, ganglionic blocker
paralysis |
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tubocurarine
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1°: motor end plate blocker
2°: autonomic ganglia blocker |
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succinylcholine
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selective NM blockade
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atopine
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M antagonist
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pirenzepine
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M1 antagonist
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tripitramine
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M2 antagonist
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darifenacin
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M3 antagonist
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phenylephrine
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α1 agonist
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clonidine
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α2 agonist
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isoproterenol
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ß1 & ß2 agonist
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dobutamine
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ß1 agonist
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terbutaline
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ß2 agonist
bronchodilation w/ minimal effects on heart |
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metoprolol
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ß1 antagonist
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atenolol
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ß1 antagonist
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prazosin
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α1 antagonist
α2b & α2c >>> α2a |
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yohimbe
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α2 antagonist
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hemicholinium (HC-3)
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blocks choline transport → limits ACh synthesis
- synthetic |
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vesimicol
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blocks ACh transport into vesicles
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botulinum toxin
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blocks ACh release
inj. used for cosmetic, opthalmologic, palsy |
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α-methyltyrosine
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inhibits tyrosine hydroxylase → no NE synthesis
pheochromocytoma (adrenal tumor) |
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methyldopa
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inhibits L-amino decarboxylase → false transmitter α-methylnorepinephrine
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reserpine
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blocks VAMT-2 uptake of amines → depletion of transmitters
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