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69 Cards in this Set

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