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46 Cards in this Set

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The catecholamines are:
epinepherine, norepinepherine, dopamine, isoproteronol (synthetic)
The precursor of all catecholamines is:
L-tyrosine
Amphetamines and epinepherine both stimulate the release of:
norepinepherine
The main effects of Guanethydine and reserpine
Catecholamine depletors-->Inhibit NE release
The classic alpha-1 agonists are:

and they:
phenylephrine, methoxamine and clonidine

stimulate alpha receptors, on both the pre and post junctional membranes
The classic alpha antagonists are:
phenoxybenzamine, phentolamine and prazosin
The classic beta agonists are:
isoproterenol, dobutamine, terbutaline and albuterol
The classic beta antagonists (blockers) are:
propranolol, metoprolol
The primary way that NE is removed from the synaptic cleft is through the __ __, which is blocked by ___.
Uptake 1 System
cocaine
Catecholamine pathway (precursors + enzymes-->product)
L-tyrosine (tyrosine hydroxylase)-->Dopa (decarboxylase)-->Dopamine (dopamine beta hydroxylase)-->NE
(Phenylethanolamine-N-methyltransferase)-->Epi
NE is taken up in the postsynaptic cell by:
Uptake 2
Pre-junctional enzyme made by mitochondria to get rid of NE (or any amine):
MAO (monoamineoxidase)
Post-junctional, extra-neuronal enzyme to get rid of NE (specifically):
COMT (catechol-o-methyltransferase)
Which adrenergic receptors typically mediate sympathetic excitation? What is the exception?
Alpha
Exception is GI tract, which is slowed down by alpha (sympathetic response redirects blood flow to where it's needed most)
Which adrenergic receptors typically mediate inhibition?
What is the exception?
Beta
Exception is the heart, which is stimulated by Beta adrenergic receptors
alpha-1 receptors are typically located where?
Post-synaptic effector cells
Alpha-2 receptors are typically located where? Why?
Pre-synaptic nerve terminal
When bound by NI, serve as a negative feedback loop to shut down NE release
Where are Beta-1 adrenergic receptors typically located? Why does that make sense?
Heart and conduction system, adipocytes
Makes sense to simultaneously increase heart contractility and the energy source for that activity (fatty acids)
Beta-2 adrenergic receptors are typically found where? Especially?
Everywhere else but heart, especially smooth muscle (vascular, GI, bladder, respiratory, etc)
Alpha-1 adrenergic receptors are similar in their signal transduction pathway as which muscarinic receptors? How so?
Odd muscarinics--M1 & M3

Use Gq-protein coupled receptors that stimulate DAG & IP3, PLC, PKC-->Ca2+ release
Why would you give an alpha-1 agonist?
Ca2+ release will cause smooth muscle contraction, especially in vasculature and bladder-->for hypotensive states and urinary incontinence
Alpha-2 adrenergic receptors are similar in their signal transduction pathway as which muscarinic receptors? How so?
Even Muscarinics--M2, M4

Stimulate Gi to inhibit adenylyl cyclase and DECREASE cAMP levels
Both Beta-1 and Beta-2 receptors use which signaling pathway? What is its function?
Stimulate Gs which activates PKA-->Ca2+ and INCREASE cardiac contractility
Which catecholamines stimulate alpha adrenergic receptors, in order of most to least?
epi>NE>ISO
Which catecholamines stimulates Beta-1 adrenergic receptors, in order of most to least?
ISO>Epi/NE
Which catecholamines stimulate Beta-2 adrenergic receptors, in order of most to least?
ISO>>Epi>>>>NE
In a patient with a normal functioning ANS, injection of NE would have what effects on blood pressure and heart rate?
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)
Epi has more of an affinity for which type of receptors? Are these receptors stimulated more at a higher or lower dose of epi?
Beta-2 receptors
Stimulated more at lower doses of epi, what would be more concurrent with natural release of epi
What effect would a LOW dose of EPI have on TPR? Why?
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
What effect would a HIGH dose of EPI have on TPR? Why?
TPR would INCREASE, because high doses of EPI will activate alpha-1 receptors, increase Ca2+ and thereby contract smooth muscle in vasculature
What effect would epi have on the heart rate?
It would increase, due to its direct effects on Beta-1 receptors and there are NO reflexes to direct effects
What effect would ISO have on TPR?
It would decrease, due to stimulation of Beta-2 receptors causing vasodilation
What effect would ISO have on blood pressure?
It would decrease, due to the decrease of TPR.
What effect would ISO have on heart rate?
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
Prazosin, a selective alpha-1 ANTAGONIST, would have what effect on TPR and BP and HR?
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
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?
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
If a pt on prazosin, a selective alpha-1 ANTAGONIST, is now given NE, what will happen to TPR, BP and HR?
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
Asthma attacks are best treated with what class of drugs?
Beta-2 agonists, which will cause bronchodilation
Why should you avoid treating patients with cardiac problems with EPI as a Beta-2 agonist for asthma?
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.
For a patient with athersclerosis and asthma, which drugs would be best to treat the asthma?
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
Sympathetic stimulation actually slows down what systems due to both alpha-1 and beta-2 stimulation?
GI, urinary, uterine-->Beta-2 relaxes smooth muscle, alpha-1 tightens sphincters
Why is EPI added to local anesthetics?
It is an alpha-1 agonist, which causes vasoconstriction in the area to prevent washout of the drug
The strongest catecholamine cardiac stimulants are
ISO and EPI
The primary use of NE is
hypotensive crises or shock, because it is a very strong vasoconstrictor
What is the best way to administer catecholamines? Why?
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
Catecholamine excretion in urine should normally be very low. If elevated, what could be the problem?
Pheocromocytoma-->tumor of the adrenal medulla, causing over production of catecholamines