Term
| Where do we see the following neurotransmitters;NE, DA, Epi? What do they bind? What system are we talking about? |
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Definition
Norepinephrine (NE); Neurotransmitter for most organs and cardiac & smooth muscle (binds all but β2)
Dopamine (DA); Activates D1 causing renal and mesenteric vasodilation
Epinephrine (Epi); Is from the adrenal medulla and acts on all adrenoceptors (α & β)
-We are talking about the postganglionic neurotransmitters for the sympathetic autonomic nervous system (SANS)
-We also see ACh to M receptors for SANS to sweat glands and piloerector muscles, but that's the only cholinergic |
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Term
| Where do we see ACh used? |
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Definition
-All direct transmission from the CNS uses ACh and nicotinic receptors (Nn for preganglionic, and Nm for motor)
-Also see it with M receptors for all postganglionic PANS, and for sweat glands in SANS |
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Term
| What is particular about β2 receptors? |
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Definition
-They are typically not innervated
-They bind Epi (from adrenal medulla), but not NE |
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Term
| What would be the PANS equivalent of a β agonist (produces similar effect)? |
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Definition
-An M antagonist
-They have opposing effects |
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Term
| What is a difference in secretions indicative of? |
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Definition
-Muscarinic receptor involvement
-The PANS controls all secretions (except sweat) |
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Term
| From physiology, how is BP calculated? How is CO calculated? |
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Definition
-It is the product of the total peripheral resistance (TPR) and cardiac output (CO)
BP = TPR x CO
CO = HR x SV (stroke vol.) |
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Term
| If we use a drug to raise BP, how would the body respond? Go through the process? |
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Definition
-Eventually, it will cause reflex bradycardia
-Would be for something like shock
-(+)BP-->baroreceptor stimulation-->(+)PANS & (-)SANS-->(-)HR [bradycardia]
-It would be the same, but the reverse for a drug lowering BP (for hypertension), giving *tachycardia (bad if our patient already has *angina!) |
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Term
| What are the stimulated receptors for increasing and decreasing TPR, and how? GIve drugs that could do it? What are the receptors responsible for reflex action, and what is the reflex action? How could we block the reflex action then? |
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Definition
-We would alter TPR to effect the BP (e.g. NE can preferentially target α-->vasoconstriction, and isoproterenol can target β2-->vasodilation)
-Raise TPR(+α1)-->reflex bradycardia (+M2; PANS)
-Lower TPR(+β2)-->reflex tachycardia (+β1; SANS)
-To block reflex bradycardia, we would block M2
-To block reflex tachycardia, we would block β1
-Ganglionic blockade will block all reflex action (but blocks both PANS and SANS because they all use Nn) |
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Term
| So if we have a hypertensive patient, how do we want to treat? How about for a patient in shock? |
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Definition
-Hypertensive; β2 agonist, B1 antagonist
-Shock; α agonist, M2 antagonist |
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Term
| What is the hormonal feedback loop, and when do we have to worry about it? |
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Definition
-It is only a concern when we are trying to decreasing blood pressure (treat hypertension)
-Lower BP means lower renal perfusion, resulting in the release of *renin
-Renin-->Angiotensin II-->aldosterone
-Angiotensin II causes vasoconstriction
-Aldosterone causes salt and water retention
-Overall; (+)TPR x (+)CO = (++)BP
-In other words, the BP goes right back up to where it was |
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Term
| So, overall what do we have to worry about when treating hypertension? So how could we treat it and avoid the negative effects? |
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Definition
-Tachycardia (from ANS feedback) and salt and water retention (from endocrine feedback)
-Could use a β2 agonist with β1 blocker (tachy) and an ACE inhibitor (retention) |
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Term
| What is mydriasis? What is it's opposite? |
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Definition
-Dilation of the pupil
-Miosis is the opposite |
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Term
| What is the SANS receptor for pupil action? What will stimulation of it cause? |
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Definition
| -α1 stimulation will cause mydriasis |
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Term
| What controls the pupil size? What controls accommodation? |
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Definition
-The pupil size has dual control by the PANS (M) and SANS (α1)
-Accommodation is controlled only by the PANS via M receptors
-Similar to how vasodilation and vasoconstriction is controlled mostly by the SANS |
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Term
| So if we have a patient that comes in with miosis, what two kinds of drugs could they have used? How would we differentiate? |
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Definition
-Because of the dual control, it could be an *M agonist or an α1 antagonist
-We can tell the difference based on accommodation; anytime M receptors are involved, there will be blurred vision
-In this case, we would need an M agonist, which would produce (+)accommodation, and things far away would be blurry |
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Term
| What is cyclopegia? When would we see it? What else wold we see? |
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Definition
-It is the relaxation of the ciliary muscles so that only things far away can be seen (M receptors only)
-With it, because we know a M blocker must have been used, we would also expect to see *mydriasis |
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