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55 Cards in this Set
- Front
- Back
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where are nicotinic N receptors
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all autonomic nervous system ganglia and the adrenal medulla
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what happens when nicotinic N is activated
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stimulation of parasympathetic and sympathetic POST GANGLIONIC nerves and release of EPI from the adrenal medulla
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where is nicotinic M located
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neuromuscular junction (skeletal muscle)
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what happens when Nicotinic M is activated
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contraction of skeletal muscle
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Where are muscarinic receptors
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all parasympathetic target organs and eye, heart, lung, bladder, GI tract, sex organs, blood vessels
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what happens when muscarinic receptors are activated
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meiosis, desreased heart rate, constriction of bronchi, , contraction of detrussor, salivation, defecation, increased GI motility, erection, vasodilation
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adrenergic receptor subtypes
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alpha 1, alpha 2, beta 1, beta 2
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alpha 1 location
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eye, arterioles, veins, male sex organs, bladder,
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alpha 2 location
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presynaptic nerve terminals (usually in CNS)
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response to activating Alpha 1
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mydriasis, arterioles of skin, viscera, and mucous membrane constriction, ejaculation, contraction of prostate, contraction of bladder
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activation of alpha 2
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inhibition of transmitter release
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Where are Beta 1 receptors
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heart, kidney
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what happens when Beta 1 receptors are activated
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increased heart rate, force of contraction, AV conduction, renin release
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Where are Beta 2 receptors
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arterioles of the heart, lung, skeletal muscle, bronchi, uterus, liver, skeletal muscle
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What happens when Beta 2 receptors are activated
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dilation of arterioles in heart, lung, and skeletal muscle. bronchi dilation, uterous relaxation, glycogenolysis, enhanced contraction of skeletal muscle
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Where are dopamine receptors
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kidney
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what happens when dopamine receptors are activated
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dilation of kidney casculature (to enhance circulation through kidney)
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Basic mechanisms of adrenergic receptor activation (4)
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1. direct receptor binding
2. promotion of NorEpi release 3. Inhibition of NorEpi reuptake 4. inhibition of NorEpi inactivation |
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Amphetamines are..
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adrenergic agonist (promote NorEpi release)
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Cocaine is
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adrenergic agonist inhibits norepi reuptake so there is more around the synaptic gap and it stays around longer
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types of adrenergic agonists
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catecholamines and non-catecholamines
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types of catecholamines
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NorEpi, Epi, Dopamine (all endogenous)
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types of non catecholamines
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ephedrine, phenylephrine
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oral usability of catecholamines
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not possible, will get broken down by first pass effect
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oral usability of non catecholamines
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can give orally
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duration of catecholamines
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short, 2-3 minutes
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duration of non-catecholamines
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2-3 hours
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action on the CNS by either catecholamines or non catecholamines
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both are polar and do not cross the BBB
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When a Beta 1 receptor is targeted what else may be affected
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Beta 2 receptor --spill over affect
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Specificity if receptor in reference to dosing
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The higher the dose, the less specificity
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therapeutic applications of alpha 1 receptor activation
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*hemostasis (vasoconstriction if you're bleeding to death...)
*elevation of blood pressure *mydriasis *nasal decongestion *adjunct to local anesthesia |
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how do alpha 1 receptors affect local anesthesia
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allow for a lower dose...
Epi constricts vessels, which means the anesthetic stays around longer and this decreases the amount needed |
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how to alpha 1 receptors help with nasal decongestion
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when congested vessels in the nose are dilated. alpha 1 agonist -->restricts vessels, so no more runny nose
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adverse effects of Alpha 1 receptor activation
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*hypertension (vasoconstriction of the periphery, so more blood moves to the core
*necrosis--long term (a few days) vasoconstriction of the periphery can result in the loss of toes *Reflex Bradycardia--the direct hypertension tells the baroreceptors to slow down = decrease in heart rate |
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clinical consequences of alpha 2 receptor activation
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*inhibit the release of NorEpi
*no clinical application in periphery |
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therapeutic application of Beta 1 receptors
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*cardiac arrest
*heart failure *shock *AV block |
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Negative Effects of too much Beta 1 activation
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*angina= not enough O2 to heart= chest pain
*cause arrhythmia *can increase heart size over time |
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therapeutic application of Beta 2 receptor activation
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*asthma -bronchodilation
*delay of preterm labor (tiger=no baby) |
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negative side effects of Beta 2 receptor activation
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*hyperglycemia--extra breakdown of glucose can be a big problem in diabetics
*tremor--because of skeletal muscles *possibly tachycardia as a result of bleed over to Beta 1 |
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therapeutic uses of dopamine receptor activation
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*dilates renal vasculature
*enhances cardiac performance--(usually used with Epi, not as effective as Epi) |
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signs and symptoms of anaphylactic shock
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hypotension, bronchial constriction, edema of glottis
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treatment for anaphypactic shock
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Epi
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examples of adrenergic agonists
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epinephrine, NorEpi, dopamine, isoproterenol, dobutamine, ephedrine, phenylephrine
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what to adrenergic antagonists do? (general answer)
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direct blockade of adrenergic receptors
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two major groups of adrenergic receptors
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Alpha and Beta --both adrenergic blocking agents
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therapautic applications of alpha adrenergic antagonists
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therapautic applications of alpha adrenergic antagonists
*essential hypertension *benign prostatic hyperplasia *pheochromocytoma (catecholine secreting tumor on adrenal medualla) *raynauds disease *reversal of toxicity from alpha 1 agonists |
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selectivity of alpha adrenergic blocking agents
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selectivity of alpha adrenergic blocking agents
can be selective or non selective depending on the drug *Phentolamine is non selective and blocks alpha 1 and 2 *Prazosin is selective and blocks only alpha 1 (this one is better because it is selective, but we continue to use the nonselective drug because it is cheaper, money before health..right?) |
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adverse affects of alpha adrenergic blockades
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adverse affects of alpha adrenergic blockades
*orthostatic hypotension *reflex tachycardia (due to baroreceptors) *nasal congestion *inhibition of ejaculation (because it needs vasoconstriction) |
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therapautic applications of beta adrenergic blockade drugs
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therapautic applications of beta adrenergic blockade drugs
*angina pectoris *hypertension (reduce heart rate) *cardias dysrhythmias *myocardial infarction *heart failure *migrane (vasoconstriction helps) *hyperthyroidism *stage fright (helps heart beat at normal pace, reduces sweat) *glaucoma (decrease production pf aqueous fluis |
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therapeutic consequences of beta 1 blockade
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therapeutic consequences of beta 1 blockade
*reduced heart rate *reduced force of contraction *reduced velocity of impulse conduction |
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what type of beta blocker should someone with asthma be on?
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what type of beta blocker should someone with asthma be on?
selective beta 1 blocker...if nonselective then lungs will constrict |
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Adverse effects of Beta 1 blocker
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adverse effect of Beta 1
*bradycardia *reduced cardiac output *heart failure *AV heart block |
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adverse effects of Beta 2 blocker
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adverse effects of Beta 2 blocker
*bronchial constriction *inhibition of glycogenolysis |
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what do cholinesterase inhibitors do
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what do cholinesterase inhibitors do
prevent the breakdown of Ach |
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what does atropine do to...
heart rate salivary secretions bronchi bladder tone GI tone and motility Pupil |
what does atropine do to...
heart rate: increase salivary secretions: decrease bronchi:dilate bladder tone:decrease GI tone and motility:decrease Pupil:n dilate |
