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25 Cards in this Set
- Front
- Back
Indomethacin
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- a prostaglandin inhibitor used to rapidly close a patent ductus arteriosus (connects aorta to pulmonary artery)
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Prostaglandin E1
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used to prevent closure of ductus arteriosus in patient with transposition of the great arteries (Tetralogy of Fallot)
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Creatinine Clearance Change
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decreases 1% per year after age 20
**therefore drug dose should be decreased in patients over 70 in proportion to fall in creatinine clearance |
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reduced baro-receptor sensitivity in elderly
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(baro-receptor normally compensates for marked changes in BP)
- leads to greater reduction in BP by angiotension converting enzyme (ACE) inhibitors - leads to decreased sensitivity to hypotensive effects of beta antagonists |
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hemicholinium
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inhibits the high affinity Na+-choline cotransporter in cholinergic neurons
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vesamicol
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inhibits the H+-ACh antiporter that transports ACh into storage vesicles in cholinergic neurons
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Botulinum toxin
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prevents the calcium induced fusion of vesicles with the plasma membrane of cholinergic neurons
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AChE inhibitors
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inhibit membrane bound AChE from degrading ACh into choline and acetate in the synaptic cleft of cholinergic neurons
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SNARE proteins
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proteins that interact to tether synaptic vesicles close to the plasma membrane
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tyrosine
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precursor of all catecholamines
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alpha - methyltyrosine
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inhibits tyrosine hydroxylase (rate limiting step in catecholamine syn) in adrenergic neurons
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reserpine
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inhibits vesicular monoamine transport (VMAT) involved in filling or refilling of synaptic vesicles with dopamine or NE respectively in adrenergic neurons
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cocaine
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inhibits the selective NE transporter that takes released NE back into the presynaptic terminal of an adrenergic neuron
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clonidine
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alpha 2-agonist that stimulates presynaptic autoreceptor that results in decreased release of NE in adrenergic neurons
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positive chronotropy
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increases the rate of contraction
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positive inotropy
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increases the force of contraction
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tyramine & guanethidine
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indirect acting sympathomimetics that are trasnported into the nerve terminal and into synaptic vesicles displacing the NE stored in vesicles --> causes a release of NE
**after chronic use, MAO will deplete the NE remaining in the cytoplasm causings a rapid tyramine & guanethidine tachyphylaxis |
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amphetamine & ephedrine
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displaces NE from its synaptic vesicles similarly to tyramine & directly stimulate alpha & beta adrenoreceptors & inhibit MAO
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MAOIs
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prevent deamination of catecholamines following reuptake into presynaptic terminals --> allows more CAs to accumulate and be released with each action potential
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phenelzine, iproniazid, tranylcypromine
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nonselective MAOIs
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clorgyline
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Selective MAO-A inhibitor (preferentially metabolizes serontonin)
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selegiline
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Selective MAO-B inhibitor
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ciliary muscle receptors
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beta1 = stimulation causes relaxation and lens flattens (far)
M3 = stimulation leads to contraction and round lens (near) |
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radial iris muscle receptor
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alpha 1 = stimulation leads to pupil dilation
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circular iris muscle receptor
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M3 = stimulation leads to pupil constriction
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