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Pharmacology > Autonomic Nervous System > Flashcards

Autonomic Nervous System Flashcards

1
Q

What part of the autonomic NS responds to stress?

A

Sympathetic nervous system

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2
Q

What part of the ANS sustains homeostasis during periods of rest?

A

Parasympathetic nervous system

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3
Q

What part of the autonomic nervous system increases CO, bronchiolar dilation, and dilated pupils?

A

Sympathetic nervous system

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4
Q

The sympathetic nervous system comes from this region of the spinal cord.

A

Thoracolumbar region

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5
Q

The parasympathetic nervous system exits what part of the nervous system?

A

level of the brain, or sacral spinal cord

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6
Q

Blood vessels are directly innervated by ____ NS, but NOT directly innervated by ____ NS.

A

sympathetic; parasympathetic

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7
Q

The adrenal medulla acts just like a ____ ganglion because it is innervated by preganglionic fiber and the adrenal medulla releases compounds directly into the blood stream.

A

Sympathetic ganglion

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8
Q

Sympathetic physiology does what to heart rate, contractility, CO, blood pressure, blood flow to muscles, respiration, pupil size, blood glucose?

A

Increases it all!!!

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9
Q

What part of ANS has very short postganglionic fibers?

A

PSNS

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10
Q

Parasympathetic physiology does what to heart rate, pupil size, peristalsis and GI secretions, glucose stoarge in liver, and urinary bladder activity (micturition)?

A

PSNS decreases heart rate and pupil size; and increases peristalsis/GI secretions, glucose storage in liver, and micturition.

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11
Q

What NT do cholinergic synapses use?

A

Acetylcholine

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12
Q

Adrenergic receptors use what NT?

A

Norepinephrine

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13
Q

Sympathetic outflow uses what two kind of synapses?

A

1st = cholinergic; 2nd = adrenergic

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14
Q

Parasympathetic outflow uses what two kind of synapses?

A

Both are cholinergic

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15
Q

Describe neurohumoral transmission:

A

Presynaptic terminal depolarizes –> opens voltage gated Ca2+ channels –> calcium enters presynaptic terminal –> calcium allows vesicles to fuse with presynaptic membrane –> NT gets dumped into the cleft –> NTs bind to corresponding receptors on the postsynaptic membrane

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16
Q

List three catecholamines:

A

Norepinephrine; Dopamine; Epinephrine

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17
Q

How does epinephrine get synthesized (start from beginning)

A

Phenylalanine –> tyrosine –> DOPA –> dopamine –> norepinephrine –> epinephrine

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18
Q

What role does alpha-methylparatyrosine play in the synthesis of catecholamines?

A

It faciliatates the making of DOPA from tyrosine. Without it, concentrations of dopamine AND NE would go down.

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19
Q

List the NTs that bind to alpha receptors, ordered preferentially.

A

Epi > norepi&raquo_space; isoproterenol; (very high affinity for Epi and NE)

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20
Q

List the NTs that bind to beta receptors, ordered preferentially.

A

Isoproterenol > epi > NE (very low affinity for NE)

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21
Q

Because alpha receptors have a high affinity for NE and beta receptors have a low affinity for NE; NE is mostly a/an _____ agonist (beta or alpha)?

A

Alpha agonist (however also beta in the heart)

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22
Q

Because Epi can bind well with alpha and beta receptors; epi is considered a _____ agonist.

A

mixed agonist

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23
Q

What is the most efficient way to get NE out of the cleft?

A

Take it back up into the presynapti terminal –> usually repackaged back into granules and can be recycled in this way

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24
Q

What is MAO (monoamine oxidase)?

A

Enzyme that breaks down NTs to terminate adrenergic transmission.

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25
Q

What will cocaine do to adrenergic transmission?

A

Cocaine will inhibit neuronal uptake of NE back into presynaptic terminal –> cocaine will increase NE

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26
Q

What will reserpine do to adrenergic transmission?

A

Reserpine will inhibit the uptake of NE back into these granules (it can still be taken back up into presynaptic terminals, but stays in cytoplasm) –> decreases NE because it won’t be taken back up into granules which are needed for NE to be secreted into the cleft

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27
Q

Monoamine oxidase inhibitors increases or decreases NE in the cleft?

A

Increases NE in the cleft.

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28
Q

Adrenergic Receptors –> alpha 1s

A

These are excitatory and result in contraction of vascular smooth muscle, stimulate iris dilator muscle, stimulate GI sphincters and bladder sphincters. The end result is vasoconstriction, mydriasis, sphincter constriction.

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29
Q

Alpha 1 adrenergic receptor NTs:

A

Epi > norepi&raquo_space; isoproteronol

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30
Q

Adrenergic Receptors –> alpha 2s

A

These are presynaptic and inhibit NE release.

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31
Q

Adrenergic receptors –> beta-1s

A

Excitatory to the heart, resulting in increased cardiac function. Inhibitory to detrusor muscle, resulting in relaxation of the bladder. These receptors are positive ionotropes, chornotrops and create faster cardiac implusles.

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32
Q

Adrenergic receptors –> beta-1 NTs:

A

Iso > epi > NE

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33
Q

Adrenergic receptors –> beta-2s

A

Inhibitory –> resulting in relaxation and dilation.
Affects vascular smooth muscle, bronchiolar smooth muscle, and GI smooth muscle.
These receptors are also presynaptic - modulates NE release (stimulatory). The end result of adrenergic receptors are bronchodilation, blood vessel dilation, and GI smooth muscle relaxation.

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34
Q

Adrenergic Pharmacology = ____ Pharmacology

A

Sympathetic nervous system

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35
Q

Sympathomimetics

A

evoke responses similar to Epi and NE to increase sympathoadrenal discharge; activate (directly or indirectly) adrenergic receptors on effector cells (smooth muscle); many are chemically similar to endogenous compounds (catechoalmines and noncatecholamines)

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36
Q

Antiadrenergics

A

block effects of sympathetic NS on the body

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37
Q

_____ are direct-acting sympathomimetic amines that activate receptors whether or not presynaptic terminal is present.

A

Catecholamines

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38
Q

Dobutamine works on what adrenergic receptor, and has _____ cardioselectivity.

A

Beta-1; ionotropic

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39
Q

Isoproteronol is a ___ agonist and is a synthetic.

A

beta

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40
Q

NE is an alpha agonist that stimulates a presser response. What is a pressor response?

A

vasoconstriction/increase in blood pressure

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41
Q

Isoproterenol is mostly a ___ agonist.

A

beta

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42
Q

Effects of NE via IV

A

Remember that NE is an alpha agonist. It will cause global vasoconstriction and increase peripheral resistance. There is a large increase in blood pressure - this tells the brain to tell the heart to decrease HR; and this decrease in HR will override the increase in HR due to NE itself. You may also see increase in contractility int he heart.

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43
Q

Does NE change cardiac output?

A

NO, but it has a huge effect on vasculature

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44
Q

Effects of Epi via IV

A

Remember that epinephrine is a mixed agonist working on alpha receptors and beta receptors. Epi binds to central alpha receptors to cause vasoconstriction viscerally, increasing peripheral blood flow to muscles. Blood pressure increases. Contractility increases, HR increases and CO increases.

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45
Q

Why does CO increase with epinephrine but not norepinephrine?

A

The baroreceptors don’t override epinehprine’s increase in blood pressure because it is not as high as with norepinephrine, which is a strict alpha agonist.

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46
Q

Effect of isoproterenol

A

Remember that isoproterenol is a beta agonist. It will result in an increase in blood flow to both the muscles and viscera. Resistance and blood pressure falls (depressor effect). Increases HR and CO.

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47
Q

Effects of Catecholamines on Blood pressure: Epi vs NE

A

NE –> body wide vasoconstriction leading to increased BP;
Epi –> BP increases with vasocinstrition and myocardial stimulation; however a small constant infusion can lead to regional vasodilation (beta mediated) and decreased blood pressure; tachydardia due to acting on beta-1s; you can get a depressor response following a pressor response due to activation of beta-2s

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48
Q

Effects of catecholamines on vascular smooth muscle: cutaneous, mucosal, renal, and mesenteric arteries:

A

vasoconstriction - alpha receptors

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49
Q

Effects of catecholamines on vascular smooth muscle: in skeletal muscle? NE vs Epi

A

NE = constriction (alpha); Small amount of epi = dilation (beta2); large amount of epi = constriction (alpha); Isoproterenol = dilation

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50
Q

Effects of catecholamines on vascular smooth muscle: coronary arteries

A

dilation (beta receptors predominate

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51
Q

Effects of catecholamines on vascular smooth muscle: cerebral arteries

A

these arteries act independently of peripheral stimulation

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52
Q

Effects of Catechoalmines: Myocardium

A

Increased function; beta1s –> increased contractile force, increased rate, increased work and oxygen sometimes; often get bradycardia (decreased HR) during peak pressor response because of baroreceptor reflex which will inhibit sympathetics

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53
Q

Effects of catecholamines: respiratory and metabolic

A

Beta2s on bronchiolar smooth muscle cause relaxation; metabolism is increased –> increased blood glucose, FFAs, and lactic acid, increase oxygen consumption

54
Q

Effects of catecholamines: GI

A

decreased peristalsis (beta2); sphincters constrict (alpha); decreased secretion of digestive enzymes; increased salivary gland activity, but saliva is scant and viscous; inhibition of insulin secretion

55
Q

Effects of Catechoalmines on other smooth muscle (besides vasculature)

A

Uterine smooth muscle –> variable response; splenic smooth muscle –> contraction due to alpha - blood discharge; contraction of pilorecetor muscle (alpha); contraction of iris dilator muscle resulting in mydriasis (alpha)

56
Q

Effects of dopamine

A

vasodilation, decreased visceral vascular resistance, increased renal blood flow, myocardial stimulation

57
Q

Effects of dobutamine

A

very selective beta-1; positive ionotrope

58
Q

List drugs that are noncatecholamines that are still symapthomimetics

A

Ephedrine, Amphetamine, Phenylephrine, Methoxamine, Phenylpropanolamine

59
Q

Ephedrine effects are similar to epi, but ____ lasting.

A

longer

60
Q

Ephedrine acts on ___receptors and releases this NT.

A

adrenoreceptors; and releases NE

61
Q

Ephedrine increases…

A

blood pressure, heart rate and force, CO

62
Q

Ephedrine causes central vaso____ and peripheral vaso_____.

A

vasoconstriction, vasodilation

63
Q

What does ephedrine do to the pupil?

A

Mydriasis

64
Q

What does ephedrine due to bronchus?

A

Bronchodilation

65
Q

Does ephedrine stimulate CNS?

A

Yes

66
Q

Amphetamines release this endogenous NT

A

NE

67
Q

Amphetamine increases ___, but does not affect ___.

A

Blood pressure, CO

68
Q

Can amphetamines stimulate CNS?

A

YES

69
Q

Amphetamines are a controlled substance. True or False.

A

True.

70
Q

Phenylephrine, methoxamine, and phenylpropanolamine are non-catechoalmines, sympathomimetics, that are direct or indirect acting?

A

DIRECT via alpha1

71
Q

Phenylephrine, methoxamine, and phenylpropanolamine are pressor and depressors?

A

Pressor - peripheral vasoconstriction without cardiac effects

72
Q

Phenylephrine is mydriatic (dilation of pupil). True or False.

A

True

73
Q

Terbutaline, salbutamol, clenbuterol, and albuterol are all:

A

beta-2 selective bronchodilators

74
Q

are alpha-2 adrenergic agonists sympathomemimetics? Why?

A

No, because alpha 2 when stimulated decreases amount of NE on cleft

75
Q

What are the primary CNS effects of alpha-2 adrenergic agonists?

A

sedation - used as preanasthetic

76
Q

Xylazine and medetomidine are ___ adrenergic agonists.

A

alpha-2

77
Q

Name 2 alpha-2 antagonists that can reverse sedation

A

Atipamezole, and yohimbine

78
Q

Alpha-blockade prevents

A

pressor response

79
Q

Alpha-blockade - clinical use

A

treatment of peripheral vasospasm, visceral ischemia; shock (only with fluids on baord); urethral sphincter relaxation; pheochromocytoma; hypertension (humans

80
Q

Phenoxybenzamine, phentolamine, prazosin, and doxazosin are? are any selective?

A

alpha-blockers; prazosin and doxazosin are alpha-1 selective

81
Q

Beta-blockade

A

inhibits myocardial stimulant effects (b1)**, inhibits b2 - mediated vasodilation; bronchiolar constriction (side effect); remember, dependent on sympathetic tone

82
Q

Beta-blockade clinical use

A

Decreased cardiac workload; decreased oxygen demand (chronic heart failure); block ventricular fibrillation (anesthesia); treatment of tachycardia, tachyarrhythm

83
Q

Side effects of beta blockade

A

bronchiolar constriction, cardiac decompensation - use cautiously

84
Q

Propanolol, Atenlol, and metaprolol are ___ blockers; which ones are selective?

A

Beta blockers; atenolol and metoprolol are selective for beta-1

85
Q

What does botulinum toxin do to ACh?

A

prevents release of ACh-filled vesicles so that we don’t release ACh into the cleft

86
Q

What does acetylcholinesterase do?

A

terminates ACh located in the cleft

87
Q

Nicotnic cholinergic receptors

A

Located in most autonomic ganglia, and the adrenal medulla; excitatory effects

88
Q

Muscarinic cholinergic receptor

A

at the parasympathetic neuroeffector junctions: in heart, smooth muscle, secretory glands; at some sympathetic neuroeffector junctions; excitatory or inhibitory effects

89
Q

Parasympathomimetics act like Ach at neuroeffector organ by…

A

decreasing HR; increasing peristalsis and GI secretions, increasing glucose storage, contracting pupils and micturition

90
Q

Cardiovascular effects of parasympathomimetics

A

Decrease in peripheral resistance and blood pressure (vessel dilation) - release of NO; negative ionotropic and chronotropic effects; slowed conduction, slowed ventricular rate - can lead to atrial fibrillation, sinus arrest

91
Q

Parasympathomimetic effects on smooth muscle

A

GI motility and secretions enhanced; contraction of urinary bladder, uterus, bronchiolar smooth muscle

92
Q

Methacholine, carbachol, bethanechol are parasympathomimetics or sympathomimmetics; direct or indirect?

A

parasympathomimetics; direct acting

93
Q

methacholine, carbachol, and bethanechol are ___ esters.

A

choline

94
Q

Methacholine

A

Choline ester, parasympathomimetic; most active at muscarinic receptors, active at heart, less active at GI; depressor response - slowed HR

95
Q

Carbachol

A

choline ester, parasympathomimetic; active at both receptor types; can see adrenergic life effects

96
Q

Bethanechol

A

choline ester, parasympathomimeitc; muscarinic agonist; GI stimulation, contraction of uterine, bronchiolar, and urinary bladder smooth muscle

97
Q

Clinical use of bethanechol

A

urinary bladder atony in cats; GI hypomotility

98
Q

Clinical use of carbachol

A

used to treat glaucoma; treatment of colic, rumen atony - used as a last resort

99
Q

Pilocarpine is a _______.

A

cholinomimetic alkalide

100
Q

Actions of cholinomimetic alkalides

A

exocrine gland secretion (salivary, mucous, gastric, digestive); GI smooth muscle contraction; potent pupillary constrictor (miosis)

101
Q

Clinical use of pilocarpine

A

ocular drug: causes miosis, used in treatment of glaucoma; stimulates ciliary muscles which encourages the draining of aqueous humor to relieve glaucoma

102
Q

Toxicity of pilocarpine

A

Very toxic - colic, diarrhea, bronchoconstriction, and increased bronchial secretions, hypotension, bradycardia –> death

103
Q

Cholinesterase inhibitors depend on presence of ____ for effect.

A

ACh

104
Q

Are cholinesterase inhibitors limited to parasympathetic effects?

A

No

105
Q

Effects of cholinesterase inhibitors

A

increased peristalsis, pupillary constriction, muscular twitch, smooth muscle contraction

106
Q

Physostigmine, neostigmine, and edrophonium, and organophosphates are ____

A

cholinesterase inhibitors

107
Q

Physostigmine, neostigmine, and edrophonium: muscarinic effects

A

(remember these are cholinesterase inhibitors) parasympathomimetic activity

108
Q

Physostigmine, neostigmine, and edrophonium: nicotinic effects

A

stimulation followed by blockage of autonomic ganglia, skeletal muscle, CNS because these receptors get so excited that they stop working

109
Q

Physostigmine, neostigmine, and edrophonium: affect on adrenal medulla

A

stimulation of adrenal medulla: we have nicotinic ACh receptors at those adrenal medullary cells

110
Q

Clinical use of physostigmine

A

treatment of glaucoma - produces miosis, reduces intraocular pressure; stimulation of ruminal activity (SQ) - increases motility and peristalsis

111
Q

Toxicity of physostigmine

A

CNS depression, convulsion

112
Q

Clinical use of Neostigmine and edrophonium

A

Treatment of myasthenia gravis –> Body produces Abs to these Nicoticnic ACH receptors (prevents Ach from binding) – characterized by muscle weakness; We want to increase amount of Ach at the synapse –> increasing probability that ACH will find and bind to those receptors that are functional

113
Q

Toxicity of neostigmine

A

skeletal weakness; vomiting and diarrhea, urination, bradycardia, hypotension

114
Q

Physostigmine, neostigmine, and edrophonium are reversible or irreversible?

A

reversible

115
Q

Organophosphates are reversible or irreversible cholinesterase inhibitors?

A

reversible

116
Q

Cholinomimetic effects of organophosphates

A

profuse salivation, vomiting, diarrhea, urination, bradycardia, hypotension; muscular paralysis and CNS effects can lead to death –> too much ACh in the body for days becasue organophosphates are irreversible cholinesterase inhibitors

117
Q

How to block irreversible cholinesterase inhibitors?

A

Atropine will block muscarinic receptors and help; but it is improtant to use atropine with 2-PAM which reactivates AChE to actually fix the problem and cause dissocation from this irreversible toxin

118
Q

Parasympatholytics inhibit effects of this NT

A

ACh

119
Q

Parasympatholytics block muscarninc receptors by ___ ___

A

competitive antagonism

120
Q

Atropine is a

A

parasympatholytic

121
Q

Atropine at large doses is

A

vagolytic

122
Q

Effects of atropine

A

Dominant effect is tachycardia (dependent upon degree of vagal tone); increased CO; relaxed GI smooth muscle, decreased salivation and intestinal secretions; bronchodilation; mydriasis, urinary retension, decreased sweating in humans

123
Q

Clinical use of atropine

A

Antispasmodic –> decreases GI hypermotility, also urinary bladder and bronchioles; adjunct to general anesthesia because it decreases salivation and airway secretions and prevents bradycardia; ophthalmology - used in examination, helps prevent or treat adhesions; anitdote for anti-cholinesterase poisoning because it blocks muscarinic receptors

124
Q

Atropine toxicology

A

thirst, dysphagia, constipation, tachycardia, mydriasis because you are blocking PSNS; can be due to dog eating bunnies

125
Q

List four synthetic muscarinic antagonists

A

glycopyrrolate, tropicamide, prpantheline, isopropamide

126
Q

Glycopyrrolate

A

Synthetic muscarinic antagonist; used as a preanesthetic; less tachycardic; decreases gastric, salivary and respiratory secretions and decreases intestinal motility

127
Q

Tropicamide is mainly used for

A

ocular - mydriasis - topical administration, fewer side affects

128
Q

Propantheline and isopropamide are mainly used as

A

smooth muscle relaxants (GI, bladder)

129
Q

Nicotine is a ganglionic blocking agent. True or False.

A

True

130
Q

Nicotine effects

A

Not used clinically, first stimulates, then blocks nicotine receptors at higher concentrations - produces persistent depolarization; CNS depression; decreases HR followed by increase in HR; pressor response followed by vasodilation; excessive salivation and gastric secretion, vomiting, defecation; depolarizes muscle paralysis

131
Q

Nicotine toxicity

A

stimulation leading to depression; death from respiratory paralysis (CNS depression)

132
Q

Synthetic ganglionic blocking agents

A

skip depolarization (vs nicotine) and just go straight to blocking - effects depend on sympathetic or parasympathetic tone; GI - typically parasympathetic; heart - typically parasympathetic - tachycardia; peripheral blood vessels - typically sympathetic - vasodilation and hypotension; adrenal medulla - decreased catecholamine release - postural hypotension, syncope

Pharmacology (10 decks)

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