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69 Cards in this Set
- Front
- Back
What is a practical test for evaluation of ANS function?
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Orthostatics – decrease in SBP of more than 30 mmHg without an increase in heart rate suggests autonomic dysfunction.
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Give an alternate name for the sympathetic nervous system. Why is this name used?
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Thoracolumbar nervous system; so called because the preganglionic fibers of the nerves exit the spinal cord at the thoracic and lumbar sections.
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Give an alternate name for the parasympathetic nervous system and tell why the name is used.
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Craniosacral nervous system; because the preganglionic fibers originate in the brain and sacral spinal column.
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Which ANS fibers are myelinated?
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Preganglionic fibers.
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Which nervous system has very short preganglionic fibers?
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The sympathetic nervous system.
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Which nervous system has long preganglionic fibers?
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The parasympathetic nervous system.
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How many paired chains of sympathetic ganglia do the SNS innervate?
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22
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Which nervous system has adrenergic receptors and where are they located?
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The SNS; they are located in the effector (end) organs.
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Where are cholinergic receptors located?
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PNS – at the ganglion and the end organ.
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SNS – ganglion only.
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What type of receptors are alpha, beta and dopamine receptors?
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Adrenergic
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What is the neurotransmitter released at preganglionic neuronal site?
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Acetylcholine
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What is the neurotransmitter released at the postganglionic neuronal site?
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PNS – Acetylcholine
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SNS - Norepinephrine
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How is the action of endogenous catecholamines terminated?
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Reuptake into presynaptic terminals or enzymatic breakdown.
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What are the two principle enzymes involved in catecholamine breakdown?
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Catecholamine-O-methyltransferase (COMT) or monoamine oxidase (MAO).
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What is the end product of catecholamine breakdown?
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Vanillymandelic acid (VMA).
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Where are Alpha 1 receptors located and what is their effect on that tissue when stimulated?
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Postsynaptic membranes of vascular smooth muscle (constriction); intestinal and bladder smooth muscle (relaxation, sphincter constriction) and pancreas (inhibition of insulin secretion).
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Name some drugs that act on Alpha1 receptors.
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Alpha 1 agonist – phenylephrine
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Antagonist – Prazosin, Phentolamine, Labetolol.
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Where are Alpha 2 receptors located and what is their effect on that tissue?
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Postganglionic (presynaptic sympathetic nerve ending )(inhibits release of norepi); (postsynaptic) CNS (postsynaptic) (ups K+ conductance): Platelets (aggregation).
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Name drugs that effect Alpha 2 receptors.
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Agonist – clonidine, dexmedetomidine
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Antagonist – Yohimbe, phentolamine
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Where are Beta 1 receptors located and what effect do they have when stimulated?
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Heart (increased HR, contractility & conduction velocity); fat cells (lipolysis).
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Name some drugs that work on Beta 1 receptors
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Agonists – Dobutamine, dopamine and Isuprel; antagonists – metorpolol, esmolol, propranolol, timolol, labetalol
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Where are Beta 2 receptors located and what is their effect on that tissue?
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Blood vessels (dilation); bronchioles (dilation); uterus (relaxation); kidneys (rennin secretion); liver (glycogenolysis & gluconeogenesis); pancreas (insulin secretion).
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Name some drugs that affect Beta 2 receptors.
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Agonist – albuterol, ritodrine
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Antagonist – propranolol, timolol, labetalol
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Where are dopamine 1 receptors located and what is their effect on that tissue?
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Blood vessels (dilation).
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What drugs work on dopamine 1 receptors?
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Agonist – fenoldopam
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Antagonist - Droperidol
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Where are muscarinic receptors located and what is their effect on those tissues?
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Heart (decreased HR, contractility & conduction velocity); Bronchioles (constriction); Salivary glands (salivation); intestine (contraction, sphincter relaxation and increased secretions); bladder (contraction and sphincter relaxation).
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What does the acronym BBSLUD stand for and why is it significant?
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It describes cholinergic responses (i.e. organophosphate poisoning; mushrooms);
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B – bronchoconstriction
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B – bradycardia
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S – salivation
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L – lacrimation
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U – urination
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D - defecation
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What’s the antidote for BBSLUD? (cholinergic response)
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Atropine, scopalomine, glycopyrrolate
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Of the three anticholinergic drugs mentioned earlier, which would make your patient easiest to care for in PACU and why?
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Glycopyrrolate – it doesn’t cross the blood-brain barrier as readily and so is less likely to cause central cholinergic effect.
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Where are nicotinic receptors located and what is their effect on that tissue when stimulated?
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Neuromuscular junction (skeletal muscle contraction); Autonomic ganglia (sympathetic nervous system stimulation)
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What drugs work on nicotinic receptors?
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Agonist – succinylcholine
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Antagonist – Nondepolarizing muscle relaxants
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What are three endogenous catecholamines?
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Dopamine, norepinephrine and epinephrine
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Why might a patient with adrenal suppression be in trouble?
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No endogenous catecholamine production due to a lack of steroids.
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What is the normal ratio of epinephrine to norepinephrine production in the adrenals?
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7:01
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What is the effect of dopamine?
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At lower levels of stimulation, net result is vasodilation; however, as increasing numbers of dopamine recptors are stimulated there is stimulation of Beta 1 receptors (increased HR) and Alpha 1 receptors (vasoconstriction).
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What is the effect of norepinephrine?
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Beta 1 stimulation = increased HR; Alpha 1 stimulation = vasoconstriction. Beta 2 = some vasodilation (but offset by the vasoconstriction produced by A1) and bronchodilation.
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Why must you be careful giving norepinephrine to a pregnant patient?
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Beta 2 stimulation can cause uterine relaxation and you might wind up catching a baby.
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What is the effect of epinephrine?
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Low doses = vasodilation in muscle & cutaneous constriction with a net decrease in SVR. As the dose increases, though, Beta 1 and Alpha 1 stimulation = increased HR and vasoconstriction.
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What does epinephrine do to renal blood flow?
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Decreases it, even in low doses.
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Name two synthetic catecholamines.
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Isoproterenol & dobutamine
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Name the effects of isoproterenol.
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It is a Beta agonist, so = increased cardiac output, increased HR and increased SBP.
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What are the effects of dobutamine?
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Predominantly Beta stimulation = increased HR, cardiac output, bronchodilation; can have some Alpha stimulation
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Which endogenous catecholamine is the immediate precursor of norepinephrine and epinephrine?
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Dopamine; it is the immediate precursor to norepinephrine which in turn becomes epinephrine.
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How might you tell if your patient has high levels of catecholamines?
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You can check plasma levels or do a 24-hour urine for VMA.
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What does a pheochromocytoma do to the normal epinephrine:norepinephrine ratio and why do we care?
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Reverses it. Because norepinephrine causes predominantly vasoconstriction, this predisposes patients with pheochromocytoma to malignant HTN.
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What is the effect of clonidine?
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A2 receptor stimulation; inhibits release of norepinephrine = lower BP and sedation.
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Why might one consider epidural use of clonidine?
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In very small doses it allows CNS sedation to predominate with less effect on the blood pressure, so you might get a sleeping, normotensive patient (a good thing!)
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Name a direct sympathomimetic
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Neosynephrine.
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Which sympathomimetic is indirect?
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Ephedrine.
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Why is neosynephrine considered a direct sympathomimetic?
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Because it mimics the affect of norepinephrine and directly stimulates Alpha receptors to increase BP.
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Why is ephedrine called an indirect sympathomimetic?
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Because it does not stimulate receptors directly. Instead, it evokes release of the endogenous catecholamine, norepinephrine.
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Why might you pay particular attention to the cardiac monitor in a patient taking tricyclic antidepressants if you have to give a catecholamine or sympathomimetic?
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Because tricyclics cause arrhythmogenicity; catecholamines increase HR and automaticity and so can potentiate that affect, causing arrhythmias.
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Why do adrenal glands receive innervation from the SNS directly and not via a ganglion or synapse?
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In order to potentiate the possibly lifesaving fight or flight response; this is an area where you want an instant catecholamine surge, and the easiest way to get it is to send impulses quickly to the adrenals.
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