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73 Cards in this Set
- Front
- Back
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how is an adrenergic signal terminated?
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reuptake of catecholamines by presynaptic terminal (primary)
diffusion of catecholamines away from synaptic cleft biotransformation of catecholamines by MAO and COMT (occurs in cells , not in the cleft) |
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what is MAO?
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monoamine oxidase
enzyme that catalyzes the carboxylation of NE |
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what is COMT?
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catechol-O-methyltransferase
enzyme that catalyzes two methoxylations on the aromatic ring of NE |
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where in the cell is the enzyme, MAO?
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monamine oxidase is a mitochondrial enzyme
(widely distributed in the tissues of the body) |
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where in the cell is the enzyme, COMT?
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catechol-O-methyltransferase is a cytosolic enzyme
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what were MAO inhibitors originally used to treat?
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hypertension
many compounds that would act as false transmitters are chewed up by MAO before they enter presynaptic vesicles when MAO is inhibited, these compounds can now act as false transmitters |
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what happens to tyramine in the presence of an MAO inhibitor?
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tyramine is allowed to enter the adrenergic nerve terminal and is converted to octopamine
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what are the effects of octopamine?
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octopamine is a false transmitter
it replaces NE in the presynaptic vesicles, displacing NE into the cytoplasm where it is degraded it decreases heart rate it decreases total peripheral resistance therefore decreases blood pressure |
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how does the activity of octopamine at the adrenergic receptors compare to that of NE?
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octopamine is inactive at adrenergic receptors
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what is the current, though rare, use for MAO inhibitors?
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treat depression
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what is the Wine and Cheese syndrome?
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an acute, life-threatening toxicity associated with the use of MAO inhibitors
it is caused by eating foods high in tyramine that would usually be rapidly degraded by MAO, but under the influence of MAO inhibitors it cannot |
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what foods are high in tyramine?
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wine
cheese highly processed dairy products beer caviar |
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what mechanism prevents tyramine absorption?
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flora of the gut destroys tyramine so that it cannot be absorbed
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what happens to most of the tyramine that is absorbed?
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first pass effect of portal circulation results in degradation by the liver
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what happens to any tyramine that reaches a nerve terminal under normal conditions?
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degraded by MAO in the nerve terminal
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what happens to tyramine from the diet when a patient is on an MAO inhibitor?
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tyramine is absorbed quickly and reaches the nerve terminal where it displaces norepi
this results in a large sympathetic response |
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what are ergot alkaloids?
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complex of naturally occurring compounds from wheat rust
(wheat mold) |
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what is the effect of Ergot alkaloids on the action of epinephrine?
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epinephrine administration increases blood pressure, however when ergot alkaloids are administered and followed by a dose of epinephrine the blood pressure drops instead
"epi reversal" |
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what is the effect of Ergot alkaloids on the action of norepinephrine?
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when norepi is administered, blood pressure increases, however when ergot alkaloids are administered and followed by a dose of norepi there is no change in blood pressure
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what are the conclusions reached by the Dale study in 1906?
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both epi and norepi interact with a populaiton of adrenergic receptors that cause constriction of vascular smooth muscle resulting in increased B.P.
epi interacts with an additional population of receptors that cause relaxation of vascular smooth muscle resulting in decreased arterial pressure, but norepi doesn't there must be two populations of adrenergic receptors |
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what was studied in the 1947 Alquist study?
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ability of a series of representative sympathomimetic amines to interact with adrenergic receptors in different tissues
used epi, norepi, and isoproterenol |
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what is the relative potency of epinephrine, norepi, and isoproterenol in vasoconstriction?
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EPI > NE >> ISO
alpha type receptors |
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what is the relative potency of epinephrine, norepi, and isoproterenol in uterine contraction?
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EPI > NE >> ISO
alpha type receptors |
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what is the relative potency of epinephrine, norepi, and isoproterenol in pupillary dilation?
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EPI > NE >> ISO
alpha type receptors |
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what is the relative potency of epinephrine, norepi, and isoproterenol in GI inhibition?
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EPI > NE >> ISO
alpha type receptors |
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what is the relative potency of epinephrine, norepi, and isoproterenol in vasodilation?
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ISO > EPI > NE
beta type receptors |
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what is the relative potency of epinephrine, norepi, and isoproterenol in uterine inhibition?
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ISO > EPI > NE
beta type receptors |
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what is the relative potency of epinephrine, norepi, and isoproterenol in myocardial stimulation
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ISO > EPI > NE
beta type receptors |
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what were the results of the Land study of 1967?
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found two types of beta receptors, and norepi only acts at one of them
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what are the functions of beta-1 receptors?
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cardiac stimulation
renin secretion |
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what are the functions of beta-2 receptors?
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vascular dilation
bronchiolar relaxation |
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what hormones bind to beta-1 receptors?
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NE
epi isoproterenol |
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what hormones bind to beta-2 receptors?
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epi
isoproterenol |
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when you think of beta-2 receptors, think ___________________________________________
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smooth muscle relaxation
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what type of adrenergic receptors are found on juxtaglomerular cells?
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beta-1 receptors
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what did the Land study demonstrate about Dale's observation of epi reversal?
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norepi leads to vascular constriction
epi has the ability to cause vascular constriction or dilation ergot alkaloids were serving to block the alpha response so that the beta response could be seen |
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according to the Land study of 1967, what adrenergic receptors dominate?
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alpha-receptors
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what type of agonist is isoproterenol?
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pure beta agonist (only beta-1 and beta-2)
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what are the effects of NE administration on the TPR, BP, and heart rate?
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TPR increases
B.P. increases HR decreases |
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why does the HR decrease on administration of NE, even though the beta-1 receptors of the heart are stimulated?
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the baroreceptor reflex was triggered by the high BP
vagus dominates to cause a reduced HR |
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describe the sensitivity of alpha and beta receptors on administration of epinephrine
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at low doses, beta-2 receptors are more sensitive to epi than alpha receptors and cause vasodilation
at high doses, alpha receptors are more sensitive and cause vasoconstriction |
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what is the effect of epi administration?
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B.P. increases mildly despite vasodilation because of the increasein HR due to beta-1 stimulation
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what is the effect of epi administration on TPR, HR, and BP?
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TPR decreases because of beta-2 receptor stimulation (causing vasodilation)
HR increases because of beta-1 receptor stimulation BP increases mildly |
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what is the effect of isoproterenol administration on TPR, HR, and BP?
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TPR decreases because of beta-2 receptor stimulation
HR increases because of beta-1 receptor stimulation BP decreases initially but then there is a huge SNS response which leads to arrhythmias |
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to what adrenergic receptors does norepi bind?
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alpha-1 receptors
beta-1 receptors |
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to what adrenergic receptors does isoproterenol bind?
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beta-1 receptors
beta-2 receptors |
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to what adrenergic receptors does epinephrine bind?
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alpha-1 receptors
beta-1 receptors beta-2 receptors |
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what are the effects of alpha-1 receptor stimulation?
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vasoconstriction -> inc. TPR -> inc. BP
mydriasis (pupillary dilation) increased closure of internal sphincter of bladder |
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what are the effects of alpha-2 stimulation?
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inhibition of NE release from presynaptic terminals (alpha-2 receptors are on the presynaptic terminals and inhibit further release of NE)
Inhibition of Insulin release from beta-cells (alpha-2 receptors are also on beta cells of the pancreas) |
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what are the effects of beta-1 stimulation?
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tachycardia
increased myocardial contractility |
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what are the two locations where alpha-2 receptors can be found?
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presynaptic nerve terminals (inhibitory to prevent further NE release)
pancreatic beta-cells (inhibitory to inhibit insulin release) |
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what is the effect of beta-2 stimulation?
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vasodilation -> slightly decreased peripheral resistance
bronchodilation increased release of glucagon -> increased muscle and liver glycogenolysis relaxed uterine smooth muscle |
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what should be the first thing to come to mind when you think of beta-2 receptors?
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smooth muscle
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what type of adrenergic receptors are found on beta cells to inhibit insulin release?
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alpha-2 receptors
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what type of adrenergic receptors are found on alpha cells to increase glucagon release?
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beta-2 receptors
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what adrenergic receptors mediate the relief of bronchospasm?
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beta-2 receptors
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what adrenergic receptors mediate the relief of acute hypotension?
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alpha receptors
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what adrenergic receptors mediate the stimulation of myocardium?
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beta-1 receptors
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what adrenergic receptors mediate vasoconstriction of periphery for better perfusion of the heart?
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alpha receptors
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what is the effect of cardiac arrest on peripheral vessels?
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causes vasodilation
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why should isoproterenol not be given to patients suffering from cardiac arrest?
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isoproterenol shows only beta effects, but the alpha effect is very important
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what are the uses of epinephrine?
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Tx of acute hypersensitivity reactions
Tx of cardiac arrest adjunct to local anesthetics |
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why is epinephrine used as an adjunct to local anesthetics?
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local vasoconstriction mediated by alpha receptors increases the duration of action of the anesthetic by keeping it in the area for a longer period of time
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what are the problems with the administration of epinephrine?
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causes myocardial arrhythmias and infarction
dramatic hypertension which can lead to acute pulmonary edema and death no oral administration |
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why does epinephrine cause myocardial arrhythmias and infarction?
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too much beta-1 stimulation can lead to changes in conduction of the electrical impulse across the heart
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why does epinephrine cause dramatic hypertension?
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alpha effect of epi on vascular smooth muscle
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why are catecholamines ineffective if administered orally?
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poor absorption
first pass effect degradation by MAO |
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why is dopamine better to treat shock than NE?
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dopamine won't reduce renal blood flow, whereas NE will
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what is the effect of NE in patients with shock?
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increased blood pressure
increased heart rate |
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what are the uses for isoproterenol?
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HTN and CHF
can be used for asthma but will cause myocardial stimulation |
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what is the effect of dopamine on the renal vasculature?
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causes vasodilation -> increases renal blood flow in patients with shock
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what is the main use of dopamine? how is this done?
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one of the main uses of dopamine is the treatment of shock
a continuous IV infusion is titrated to the dose needed to stimulate some or all of the adrenergic receptors |
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describe the titration of dopamine and the effect it has on adrenergic receptors
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at slight doses, beta-one receptors are stimulated
at higher doses, alpha receptors are stimulated |
