Term
| out of NE, epi, isoproterenol, & phenylephrine, which is not a catecholamine? |
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Definition
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Term
If isoproterenol is a catecholamine, why doesn't it share the same properties as the other catecholamines? |
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Definition
| It has an isopropyl group attached |
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Term
What type of receptor(s) will NE bind to? What type of receptor is NE selective for? In what ways can NE be removed from the synapse? |
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Definition
alpha and beta alpha COMT, MAO, neuronal uptake |
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Term
What type of receptor(s) will epi stimulate? What type of receptor is epi selective for? In what ways can epi be removed from the synapse? |
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Definition
alpha and beta beta COMT, MAO, and neuronal uptake |
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Term
What type of receptor(s) will isoproterenol stimulate?There's only one way Isoproterenol is removed from the synapse. Which way is it and why won't the other two methods work? |
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Definition
Isoproterenol is highly selective (not specific) for beta receptors. Isoproterenol has an isopropyl group that prevents both degradation by MAO and neuronal uptake. However, it can cross the post-junctional membrane, where COMT can degrade it. |
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Term
What receptor(s) will phenylephrine bind to? What are the way(s) Phe can be disposed of? Why will the other not work? |
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Definition
Phe is highly selective (not specific) for alpha receptors. Phe can undergo neuronal uptake and it can be degraded by MAO. Phe is not a catecholamine, so COMT will not work. |
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Term
| What are the orders of potency for the alpha receptor? the beta receptor? |
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Definition
E, NE > P > I I > E, NE > P So very little E and NE would be required and a lot of I would be required to stimulate alpha receptors. |
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Term
T or F Isoproterenol cannot have 100% effect by stimulating alpha receptors. |
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Definition
| False. Even though it would require a very large amount of isoproterenol, it could still have a maximum effect. The DRC would just move to the right. |
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Term
| What is heart block? Out of NE, Epi, Phe, and Iso, which agonist(s) would work best? |
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Definition
| Heart block is where the atria beat more often than the ventricles. Epi and Iso can stimulate the beta receptors in the heart to increase the dromotropic effect. |
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Term
| We know beta agonists work for intrinsic asthma, but how do they work for allergic asthma? |
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Definition
| They cause bronchodilation and they bind to beta receptors on mast cells to inhibit mediator (ie, histamine & leukotriene) release. |
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Term
For people w/ peripheral vascular disease, we want vasodilation. Out of NE, epi, Phe, and Iso, which would we want to use? |
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Definition
| Just isoproterenol. Epi is also selective for beta receptors, but epi will also bind to the alpha receptors and it's actually used for vasoconstriction. |
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Term
What class does methoxamine belong to? What receptor is it selective for? What is it used for? How is it disposed of? |
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Definition
direct acting adrenergic agonist alpha 1 Hypotension & PAT (in PAT, it causes vasoconstriction which leads to parasympathetic activity) Through the urine. |
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Term
What class does clonidine belong to? What receptor is it selective for? What's it used for? What's its mechanism? |
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Definition
Clonidine is a direct acting alpha 2 agonist that is used for HTN. It stimulates alpha 2 receptors in the CNS to decrease sympathetic activity. |
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Term
What class does dobutamine belong to? Explain the condition that dobutamine used for? How does dobutamine work? How is dobutamine disposed of? |
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Definition
Direct acting beta 1 agonist Usually given as a racemic mixture, dobutamine is for heart failure. Heart failure is where the heart isn't pumping enough blood. The heart then becomes engorged w/ blood. If the heart is hogging all the oxygenated-blood, all of the other tissues are starving for oxygen. Dobutamine stimulates beta 1 receptors in the SA node, which increases the inotropic effect and makes the heart a more effective pump. Heart failure is when the heart isn't pumping enough blood, blood becomes engorged in the heart, and the heart becomes enlarged, so the tissues never get fed. COMT metabolizes dobutamine. |
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Term
What class does terbutaline belong to? What is terbutaline used for? |
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Definition
direct acting beta 2 adrenomimetic bronchial asthma and mast cell inhibition |
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Term
| What are the adverse effects of alpha adrenomimetics? What are the contraindications? |
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Definition
Adverse effects (think eyes, nose, periphery) rebound congestion ischemia (reduction of peripheral blood flow) photphobia (mydriasis) Contraindications T2DM (b/c it inhibits beta cells from releasing insulin) HTN Narrow-angle glaucoma |
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Term
What class does tyramine belong to? How is tyramine disposed of? How does tyramine work? When is tyramine dangerous? |
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Definition
indirect acting adrenomimetic MAO It is taken up into the nerve ending through an active process (just like NE is taken up). It causes NE to pool up. Then, it causes NE to be released extravesicularly. NE is not exocytosed. Tyramine can be dangerous when taken with an MAO inhibitor. |
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Term
What class does ephedrine belong to? How does it work? What is it used for? Compared to tyramine, how is it disposed of? |
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Definition
mixed acting adrenomimetic Indirectly, it has the same mechanism as tyramine. It can also act directly on alpha 1, beta 1, and beta 2 receptors. nasal decongestant and bronchodilator B/c it is not degraded by MAO or COMT, it lasts longer than tyramine. |
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Term
What class does amphetamine belong to? What is its mechanism(s) of action? |
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Definition
mixed acting adrenomimetic It has the same indirect mechanism as tyramine and ephedrine. However, it is lipid soluble, so it doesn't rely on the active transport pump for reuptake (even though it can use it). It can also act in the periphery, where it causes NE release. The NE then stimulates alpha 1 receptors in the blood vessels to cause vasoconstriction. |
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Term
What class do imipramine and amitriptyline belong to? How do they work? |
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Definition
tricyclic antidepressants The block the neuronal uptake mechanism, thereby potentiating the effects of NE, epi, & any direct acting drug. They also block the reuptake of indirect acting drugs like tyramine and ephedrine. |
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Term
Why will a tricyclic antidepressant not potentiate the effects of isoproterenol? |
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Definition
| Isoproterenol can't be taken up into the nerve ending anyway, b/c of its isopropyl grp. |
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Term
Why are COMT inhibitors used for parkinsons? |
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Definition
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Term
| Why would MAO inhibitors and COMT inhibitors have little effect on the amount of NE and Epi? |
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Definition
| B/c they are not the primary means of disposal. |
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Term
| Explain the 2 ways an MAO inhibitor function as an antihypertension agent. |
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Definition
Think MAO: SIF and tyramine 1) ganglionic blockade: When MAO is inhibited, dopamine builds up inside of SIF cells. ACh then stimulates SIF cells to release dopamine. The dopamine causes a hyperpolarization, which decreases transmission through the autonomic ganglia. Consequently, NE doesn't stimulate alpha receptors in the blood vessels, and vasodilation occurs. 2) formation of false transmitter: Low amounts of tyramine will not cause problems w/ MAO inhibitors. The tyramine will get into vesicles, & it will get transformed into octopamine. The octopamine will eventually take over the NT inside the vesicle, & it will be exocytosed. It is a false NT, b/c it has no effect on alpha or beta receptors. Consequently, alpha receptors won't be stimulated, & vasodilation will occur. |
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Term
| What are COMT inhibitors and MAO inhibitors mainly used for? |
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Definition
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Term
What class does phentolamine belong to? What will it do to the dose response curve? |
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Definition
It's an adrenolytic and an alpha adrenergic antagonist (it's not selective for either of the alpha receptors) It will shift the DRC to the right, since it is a competitive reversible antagonist. |
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Term
What class does phenoxybenzamine belong to? What does phenoxybenamine do the dose response curve? |
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Definition
It's an adrenolytic and an alpha adrenergic antagonist. It is an irreversible antagonist, so it will shift the DRC to the right and reduce the max effect. |
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Term
What class does prazosin belong to? How is prazosin different from phenoxybenzamine and phentolamine? What does prazosin do to the dose response curve? |
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Definition
alpha adrenergic antagonist It is highly selective for alpha 1 receptors. It is a competitive antagonist, so it shifts the DRC to the right and the max effect can still be achieved. |
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Term
| Why are alpha adrenergic antagonists used for hemorrhagic shock? |
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Definition
| Hemorrhagic shock occurs when the bp goes way down after blood loss. When you lose alot of blood, sympathetic activity causes vasoconstriction. The best tx is whole blood, but it's difficult to give whole blood, when the blood vessels are constricted. Alpha adrenergic antagonists are used then to block the alpha 1 receptors on blood vessels to stimulate vasodilation. |
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Term
| Which alpha adrenergic antagonist is preferred for HTN? Why? |
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Definition
| Prazosin is preferred for its high alpha 1 selectivity. Phenoxybenzamine and phentolamine would also bind to alpha 2. If they are bound to alpha 2, they are preventing NE from binding to alpha 2. If NE can't bind to alpha 2, it cannot regulate its release. Consequently, there would be lots of NE stimulating alpha receptors, causing increased HTN. |
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Term
What is pheochromocytoma? What is the best tx for it? What drug is used? |
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Definition
| Pheochromocytoma cells are tumor cells that secrete too much NE and epi. The best tx is to surgically remove the tumor cells. However, during surgery, more NE and epi is released. Alpha adrenergic antagonists can then be used to relieve HTN. |
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Term
| What class of adrenergic drugs are used for benign prostatic hyperplasia? How do they work? |
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Definition
Alpha adrenergic antagonists can block alpha receptors on the urethra and prostate gland, causing them too relax. |
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Term
| Explain 4 adverse effects of alpha antagonists |
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Definition
1) hypotension 2) tachycardia - when the bp goes too far down, a sympathetic reflex can occur & increase the HR. 3) nasal congestion 4) impotence - if alpha receptors are blocked, there will be no ejaculation. |
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Term
| What is tamsulosin used for? What receptor is it specific for? |
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Definition
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Term
What is the difference b/w metoprolol and propranolol? Who would you not give propranolol to? What would these beta blockers do the dose response curve? |
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Definition
Metoprolol is specific for beta 1 receptors. Propranolol is non-specific for beta receptors, meaning it could block the beta 2 receptors in the bronchial tubes of an asthmatic, which would work against albuterol. So, you wouldn't give propranolol to an asthmatic. They would shift the DRC to the right, but they would not effect the max effect. |
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Term
How are beta-blockers used for cardiac arrhythmias and myocardial ischemia? |
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Definition
Cardiac arrhythmias - A beta blocker would prevent NE and epi activity on the beta receptors in the heart, thereby relaxing the heart. Myocardial ischemia - the heart is working too hard, & it can't get enough blood & oxygen. This is due to overstimulation of the beta receptors. |
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Term
| What are the 3 theories used to explain the effects of beta-blockers on HTN? |
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Definition
1) they block beta receptors in the CNS, thereby inhibiting sympathetic activity. 2)they block renin release from JAG cells. 3) they block beta receptors in the heart to reduce systolic bp. |
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Term
How are beta-blockers used for open-angle glaucoma? |
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Definition
| They can decrease formation of aqueous humor. |
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Term
| Why wouldn't you want to give a beta-blocker to a diabetic? |
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Definition
Normally, if a diabetic becomes hypoglycemic (maybe b/c they took too much insulin), glycogenolysis would occur to increase blood glucose levels. A beta-blocker would inhibit glycogenolysis. Another reason a beta-blocker shouldn't be given to a diabetic is b/c it could mask tachycardia. Tachycardia is a warning signal to a diabetic that they are hypoglycemic. |
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Term
| What does guanethidine do? |
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Definition
| It prevents vesicles from binding to the membrane. This inhibits exocytosis of NE. Prolonged use can lead to NE depletion. Guanethidine can also prevent the neuronal uptake mechanism. |
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Term
| What does a-methyl tyrosine do? Concerning NE depletion, how is it different from Guanethidine? What is it used for? |
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Definition
| It inhibits tyrosine hydroxylase, thereby inhibiting NE synthesis and causing NE depletion. Guanethidine may lead to NE depletion as a secondary effect, whereas it's a primary effect w/ a-methyl tyrosine. It is used for pheochromocytoma |
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Term
What does reserpine do? What is it used for? How is it unique from guanethidine and a-methyl tyrosine? What is its most severe side effect? |
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Definition
| It prevents storage of NE in the vesicles, leading to NE depletion. It's used for HTN. It is unique, b/c it is lipid soluble, it can enter the CNS and cause depletion of amines (eg, NE, serotonin, and dopamine). The lack of these amines would lead to severe mental depression. Many suicides have been reported. |
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Term
| What does a-methyldopa do? What's its therapeutic use? What drug is it very similar to? |
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Definition
Most of a-methyldopa's activity takes place in the CNS. It is considered a "new NT". It takes the place of dopa. It enters the vesicle and gets converted to a-methylnorepinephrine. Then, it gets exocytosed into the synapse, binds to alpha 2 receptors, and inhibits sympathetic activity. It's used for HTN, & it's similar to clonidine. |
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Term
What does d-Tubocurarine do? What is the order of blockade? What is the antidote? |
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Definition
It is a competitive antagonist that causes paralysis by blocking the NM receptors. 1) Small, fast-moving muscles like fingers & toes. 2) limbs, neck, trunk 3) intercostal muscles 4) diaphragm Neostigmine is the antidote. |
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Term
| What are the therapeutic uses for d-Tubocurarine? |
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Definition
| It's used as a muscle relaxant during anesthesia and during electroshock therapy (ECT). |
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Term
| What are the 2 depolarizing antagonists. How do they work? |
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Definition
| Decamethonium and Succinylcholine are selective for NM receptors (but they will bind to NN receptors). They bind to them (I think they bind partially, so that ACh can bind too), & partially depolarize the muscles (the resting membrane potential is kept below threshold). Then, when ACh tries to depolarize the muscle, it doesn't work, b/c they're already depolarized (partially). |
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Term
| How is succinylcholine degraded? |
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Definition
| bCHe in the blood. Consequently, succinylcholine probably has the shortest 1/2 life of all of the NM blocking agents. |
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Term
What are the therapeutic uses for the depolarizing antagonists? What is the antidote for the depolarizing antagonists. What is the adverse effect from the depolarizing antagonists that you could avoid if one of your ancestors had it? |
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Definition
The therapeutic uses are the same as they are for d-Tubocurarine: surgical anesthesia & ECT The only antidote is artificial air; not even neostigmine could depolarize a partially depolarized membrane. Malignant hyperthermia |
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