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25 Cards in this Set

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

M3 = stimulation leads to contraction and round lens (near)
radial iris muscle receptor
alpha 1 = stimulation leads to pupil dilation
circular iris muscle receptor
M3 = stimulation leads to pupil constriction