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46 Cards in this Set
- Front
- Back
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The catecholamines are:
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epinepherine, norepinepherine, dopamine, isoproteronol (synthetic)
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The precursor of all catecholamines is:
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L-tyrosine
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Amphetamines and epinepherine both stimulate the release of:
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norepinepherine
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The main effects of Guanethydine and reserpine
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Catecholamine depletors-->Inhibit NE release
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The classic alpha-1 agonists are:
and they: |
phenylephrine, methoxamine and clonidine
stimulate alpha receptors, on both the pre and post junctional membranes |
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The classic alpha antagonists are:
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phenoxybenzamine, phentolamine and prazosin
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The classic beta agonists are:
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isoproterenol, dobutamine, terbutaline and albuterol
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The classic beta antagonists (blockers) are:
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propranolol, metoprolol
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The primary way that NE is removed from the synaptic cleft is through the __ __, which is blocked by ___.
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Uptake 1 System
cocaine |
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Catecholamine pathway (precursors + enzymes-->product)
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L-tyrosine (tyrosine hydroxylase)-->Dopa (decarboxylase)-->Dopamine (dopamine beta hydroxylase)-->NE
(Phenylethanolamine-N-methyltransferase)-->Epi |
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NE is taken up in the postsynaptic cell by:
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Uptake 2
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Pre-junctional enzyme made by mitochondria to get rid of NE (or any amine):
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MAO (monoamineoxidase)
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Post-junctional, extra-neuronal enzyme to get rid of NE (specifically):
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COMT (catechol-o-methyltransferase)
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Which adrenergic receptors typically mediate sympathetic excitation? What is the exception?
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Alpha
Exception is GI tract, which is slowed down by alpha (sympathetic response redirects blood flow to where it's needed most) |
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Which adrenergic receptors typically mediate inhibition?
What is the exception? |
Beta
Exception is the heart, which is stimulated by Beta adrenergic receptors |
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alpha-1 receptors are typically located where?
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Post-synaptic effector cells
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Alpha-2 receptors are typically located where? Why?
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Pre-synaptic nerve terminal
When bound by NI, serve as a negative feedback loop to shut down NE release |
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Where are Beta-1 adrenergic receptors typically located? Why does that make sense?
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Heart and conduction system, adipocytes
Makes sense to simultaneously increase heart contractility and the energy source for that activity (fatty acids) |
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Beta-2 adrenergic receptors are typically found where? Especially?
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Everywhere else but heart, especially smooth muscle (vascular, GI, bladder, respiratory, etc)
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Alpha-1 adrenergic receptors are similar in their signal transduction pathway as which muscarinic receptors? How so?
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Odd muscarinics--M1 & M3
Use Gq-protein coupled receptors that stimulate DAG & IP3, PLC, PKC-->Ca2+ release |
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Why would you give an alpha-1 agonist?
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Ca2+ release will cause smooth muscle contraction, especially in vasculature and bladder-->for hypotensive states and urinary incontinence
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Alpha-2 adrenergic receptors are similar in their signal transduction pathway as which muscarinic receptors? How so?
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Even Muscarinics--M2, M4
Stimulate Gi to inhibit adenylyl cyclase and DECREASE cAMP levels |
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Both Beta-1 and Beta-2 receptors use which signaling pathway? What is its function?
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Stimulate Gs which activates PKA-->Ca2+ and INCREASE cardiac contractility
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Which catecholamines stimulate alpha adrenergic receptors, in order of most to least?
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epi>NE>ISO
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Which catecholamines stimulates Beta-1 adrenergic receptors, in order of most to least?
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ISO>Epi/NE
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Which catecholamines stimulate Beta-2 adrenergic receptors, in order of most to least?
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ISO>>Epi>>>>NE
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In a patient with a normal functioning ANS, injection of NE would have what effects on blood pressure and heart rate?
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BP increases, and baroreceptors cause a reflex bradycardia in response (don't see tachy like you might think unless pt has abnormal vagal nerve, as in diabetic neuropathy)
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Epi has more of an affinity for which type of receptors? Are these receptors stimulated more at a higher or lower dose of epi?
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Beta-2 receptors
Stimulated more at lower doses of epi, what would be more concurrent with natural release of epi |
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What effect would a LOW dose of EPI have on TPR? Why?
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It would decrease it, because it is binding mainly to Beta-2 receptors, which will dilate peripheral vasculature to allow for more blood flow to skeletal muscle in a fight or flight reaction
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What effect would a HIGH dose of EPI have on TPR? Why?
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TPR would INCREASE, because high doses of EPI will activate alpha-1 receptors, increase Ca2+ and thereby contract smooth muscle in vasculature
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What effect would epi have on the heart rate?
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It would increase, due to its direct effects on Beta-1 receptors and there are NO reflexes to direct effects
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What effect would ISO have on TPR?
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It would decrease, due to stimulation of Beta-2 receptors causing vasodilation
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What effect would ISO have on blood pressure?
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It would decrease, due to the decrease of TPR.
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What effect would ISO have on heart rate?
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It would increase a lot (tachycardia) for two reasons:
1. Direct agonist effect of ISO on Beta-1 receptors 2. Reflex tachy due to sudden drop in TPR & BP |
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Prazosin, a selective alpha-1 ANTAGONIST, would have what effect on TPR and BP and HR?
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TPR DECREASES slightly because decreasing sympathetic tone on vasculature
BP DECREASES because of decreased TPR HR INCREASES SLIGHTLY due to reflex tachy, NO direct effects b/c ~no alpha-1 receptors on heart |
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If a pt on prazosin, a selective alpha-1 ANTAGONIST is now given EPI, what will happen to TPR, BP and HR? What is the name of this effect?
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EPI works on both alpha and beta receptors. With the alpha's blocked, EPI can only stimulate betas, which cause a DECREASE in TPR, a DECREASE in BP and an INCREASE in HR due to B-1 direct effect AND reflex tachy
EPI REVERSAL |
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If a pt on prazosin, a selective alpha-1 ANTAGONIST, is now given NE, what will happen to TPR, BP and HR?
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Alpha-1's are blocked, so since NE is an alpha-1 AGONIST, nothing much will happen to TPR or BP.
NE will INCREASE HR because of pure effect on Beta-1 receptors, alpha's are blocked so can't create a reflex bradycardia |
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Asthma attacks are best treated with what class of drugs?
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Beta-2 agonists, which will cause bronchodilation
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Why should you avoid treating patients with cardiac problems with EPI as a Beta-2 agonist for asthma?
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Because EPI can leak into pulmonary circulation and subsequently coronary circulation, causing increased contractility due to EPI stimulating Beta-1 receptors and therefore increased Oxygen demand. If there is athersclerosis, pt will suffer ischemia because demand for O2 is greater than the supply can be, due to blockage.
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For a patient with athersclerosis and asthma, which drugs would be best to treat the asthma?
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SELECTIVE Beta-2 agonists, such as albuterol or terbutylene, because do not interfere with Beta-1 receptors, which would increase heart contractility and increase O2 demand and cause ischemia in the heart
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Sympathetic stimulation actually slows down what systems due to both alpha-1 and beta-2 stimulation?
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GI, urinary, uterine-->Beta-2 relaxes smooth muscle, alpha-1 tightens sphincters
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Why is EPI added to local anesthetics?
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It is an alpha-1 agonist, which causes vasoconstriction in the area to prevent washout of the drug
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The strongest catecholamine cardiac stimulants are
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ISO and EPI
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The primary use of NE is
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hypotensive crises or shock, because it is a very strong vasoconstrictor
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What is the best way to administer catecholamines? Why?
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IV. IM ok in the case of epi pen, and CANNOT take orally due to first pass metabolism-->will be degraded by MAO and COMT immediately
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Catecholamine excretion in urine should normally be very low. If elevated, what could be the problem?
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Pheocromocytoma-->tumor of the adrenal medulla, causing over production of catecholamines
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