Autonomic Nervous System Flashcards
1
Q
What part of the autonomic NS responds to stress?
A
Sympathetic nervous system
2
Q
What part of the ANS sustains homeostasis during periods of rest?
A
Parasympathetic nervous system
3
Q
What part of the autonomic nervous system increases CO, bronchiolar dilation, and dilated pupils?
A
Sympathetic nervous system
4
Q
The sympathetic nervous system comes from this region of the spinal cord.
A
Thoracolumbar region
5
Q
The parasympathetic nervous system exits what part of the nervous system?
A
level of the brain, or sacral spinal cord
6
Q
Blood vessels are directly innervated by ____ NS, but NOT directly innervated by ____ NS.
A
sympathetic; parasympathetic
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
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!!!
9
Q
What part of ANS has very short postganglionic fibers?
A
PSNS
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.
11
Q
What NT do cholinergic synapses use?
A
Acetylcholine
12
Q
Adrenergic receptors use what NT?
A
Norepinephrine
13
Q
Sympathetic outflow uses what two kind of synapses?
A
1st = cholinergic; 2nd = adrenergic
14
Q
Parasympathetic outflow uses what two kind of synapses?
A
Both are cholinergic
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
16
Q
List three catecholamines:
A
Norepinephrine; Dopamine; Epinephrine
17
Q
How does epinephrine get synthesized (start from beginning)
A
Phenylalanine –> tyrosine –> DOPA –> dopamine –> norepinephrine –> epinephrine
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.
19
Q
List the NTs that bind to alpha receptors, ordered preferentially.
A
Epi > norepi»_space; isoproterenol; (very high affinity for Epi and NE)
20
Q
List the NTs that bind to beta receptors, ordered preferentially.
A
Isoproterenol > epi > NE (very low affinity for NE)
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)
22
Q
Because Epi can bind well with alpha and beta receptors; epi is considered a _____ agonist.
A
mixed agonist
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
24
Q
What is MAO (monoamine oxidase)?
A
Enzyme that breaks down NTs to terminate adrenergic transmission.
25
What will cocaine do to adrenergic transmission?
Cocaine will inhibit neuronal uptake of NE back into presynaptic terminal --> cocaine will increase NE
26
What will reserpine do to adrenergic transmission?
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
27
Monoamine oxidase inhibitors increases or decreases NE in the cleft?
Increases NE in the cleft.
28
Adrenergic Receptors --> alpha 1s
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.
29
Alpha 1 adrenergic receptor NTs:
Epi > norepi >> isoproteronol
30
Adrenergic Receptors --> alpha 2s
These are presynaptic and inhibit NE release.
31
Adrenergic receptors --> beta-1s
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.
32
Adrenergic receptors --> beta-1 NTs:
Iso > epi > NE
33
Adrenergic receptors --> beta-2s
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.
34
Adrenergic Pharmacology = ____ Pharmacology
Sympathetic nervous system
35
Sympathomimetics
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)
36
Antiadrenergics
block effects of sympathetic NS on the body
37
_____ are direct-acting sympathomimetic amines that activate receptors whether or not presynaptic terminal is present.
Catecholamines
38
Dobutamine works on what adrenergic receptor, and has _____ cardioselectivity.
Beta-1; ionotropic
39
Isoproteronol is a ___ agonist and is a synthetic.
beta
40
NE is an alpha agonist that stimulates a presser response. What is a pressor response?
vasoconstriction/increase in blood pressure
41
Isoproterenol is mostly a ___ agonist.
beta
42
Effects of NE via IV
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.
43
Does NE change cardiac output?
NO, but it has a huge effect on vasculature
44
Effects of Epi via IV
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.
45
Why does CO increase with epinephrine but not norepinephrine?
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.
46
Effect of isoproterenol
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.
47
Effects of Catecholamines on Blood pressure: Epi vs NE
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
48
Effects of catecholamines on vascular smooth muscle: cutaneous, mucosal, renal, and mesenteric arteries:
vasoconstriction - alpha receptors
49
Effects of catecholamines on vascular smooth muscle: in skeletal muscle? NE vs Epi
NE = constriction (alpha); Small amount of epi = dilation (beta2); large amount of epi = constriction (alpha); Isoproterenol = dilation
50
Effects of catecholamines on vascular smooth muscle: coronary arteries
dilation (beta receptors predominate
51
Effects of catecholamines on vascular smooth muscle: cerebral arteries
these arteries act independently of peripheral stimulation
52
Effects of Catechoalmines: Myocardium
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
53
Effects of catecholamines: respiratory and metabolic
Beta2s on bronchiolar smooth muscle cause relaxation; metabolism is increased --> increased blood glucose, FFAs, and lactic acid, increase oxygen consumption
54
Effects of catecholamines: GI
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
Effects of Catechoalmines on other smooth muscle (besides vasculature)
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
Effects of dopamine
vasodilation, decreased visceral vascular resistance, increased renal blood flow, myocardial stimulation
57
Effects of dobutamine
very selective beta-1; positive ionotrope
58
List drugs that are noncatecholamines that are still symapthomimetics
Ephedrine, Amphetamine, Phenylephrine, Methoxamine, Phenylpropanolamine
59
Ephedrine effects are similar to epi, but ____ lasting.
longer
60
Ephedrine acts on ___receptors and releases this NT.
adrenoreceptors; and releases NE
61
Ephedrine increases...
blood pressure, heart rate and force, CO
62
Ephedrine causes central vaso____ and peripheral vaso_____.
vasoconstriction, vasodilation
63
What does ephedrine do to the pupil?
Mydriasis
64
What does ephedrine due to bronchus?
Bronchodilation
65
Does ephedrine stimulate CNS?
Yes
66
Amphetamines release this endogenous NT
NE
67
Amphetamine increases ___, but does not affect ___.
Blood pressure, CO
68
Can amphetamines stimulate CNS?
YES
69
Amphetamines are a controlled substance. True or False.
True.
70
Phenylephrine, methoxamine, and phenylpropanolamine are non-catechoalmines, sympathomimetics, that are direct or indirect acting?
DIRECT via alpha1
71
Phenylephrine, methoxamine, and phenylpropanolamine are pressor and depressors?
Pressor - peripheral vasoconstriction without cardiac effects
72
Phenylephrine is mydriatic (dilation of pupil). True or False.
True
73
Terbutaline, salbutamol, clenbuterol, and albuterol are all:
beta-2 selective bronchodilators
74
are alpha-2 adrenergic agonists sympathomemimetics? Why?
No, because alpha 2 when stimulated decreases amount of NE on cleft
75
What are the primary CNS effects of alpha-2 adrenergic agonists?
sedation - used as preanasthetic
76
Xylazine and medetomidine are ___ adrenergic agonists.
alpha-2
77
Name 2 alpha-2 antagonists that can reverse sedation
Atipamezole, and yohimbine
78
Alpha-blockade prevents
pressor response
79
Alpha-blockade - clinical use
treatment of peripheral vasospasm, visceral ischemia; shock (only with fluids on baord); urethral sphincter relaxation; pheochromocytoma; hypertension (humans
80
Phenoxybenzamine, phentolamine, prazosin, and doxazosin are? are any selective?
alpha-blockers; prazosin and doxazosin are alpha-1 selective
81
Beta-blockade
inhibits myocardial stimulant effects (b1)**, inhibits b2 - mediated vasodilation; bronchiolar constriction (side effect); remember, dependent on sympathetic tone
82
Beta-blockade clinical use
Decreased cardiac workload; decreased oxygen demand (chronic heart failure); block ventricular fibrillation (anesthesia); treatment of tachycardia, tachyarrhythm
83
Side effects of beta blockade
bronchiolar constriction, cardiac decompensation - use cautiously
84
Propanolol, Atenlol, and metaprolol are ___ blockers; which ones are selective?
Beta blockers; atenolol and metoprolol are selective for beta-1
85
What does botulinum toxin do to ACh?
prevents release of ACh-filled vesicles so that we don't release ACh into the cleft
86
What does acetylcholinesterase do?
terminates ACh located in the cleft
87
Nicotnic cholinergic receptors
Located in most autonomic ganglia, and the adrenal medulla; excitatory effects
88
Muscarinic cholinergic receptor
at the parasympathetic neuroeffector junctions: in heart, smooth muscle, secretory glands; at some sympathetic neuroeffector junctions; excitatory or inhibitory effects
89
Parasympathomimetics act like Ach at neuroeffector organ by...
decreasing HR; increasing peristalsis and GI secretions, increasing glucose storage, contracting pupils and micturition
90
Cardiovascular effects of parasympathomimetics
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
Parasympathomimetic effects on smooth muscle
GI motility and secretions enhanced; contraction of urinary bladder, uterus, bronchiolar smooth muscle
92
Methacholine, carbachol, bethanechol are parasympathomimetics or sympathomimmetics; direct or indirect?
parasympathomimetics; direct acting
93
methacholine, carbachol, and bethanechol are ___ esters.
choline
94
Methacholine
Choline ester, parasympathomimetic; most active at muscarinic receptors, active at heart, less active at GI; depressor response - slowed HR
95
Carbachol
choline ester, parasympathomimetic; active at both receptor types; can see adrenergic life effects
96
Bethanechol
choline ester, parasympathomimeitc; muscarinic agonist; GI stimulation, contraction of uterine, bronchiolar, and urinary bladder smooth muscle
97
Clinical use of bethanechol
urinary bladder atony in cats; GI hypomotility
98
Clinical use of carbachol
used to treat glaucoma; treatment of colic, rumen atony - used as a last resort
99
Pilocarpine is a _______.
cholinomimetic alkalide
100
Actions of cholinomimetic alkalides
exocrine gland secretion (salivary, mucous, gastric, digestive); GI smooth muscle contraction; potent pupillary constrictor (miosis)
101
Clinical use of pilocarpine
ocular drug: causes miosis, used in treatment of glaucoma; stimulates ciliary muscles which encourages the draining of aqueous humor to relieve glaucoma
102
Toxicity of pilocarpine
Very toxic - colic, diarrhea, bronchoconstriction, and increased bronchial secretions, hypotension, bradycardia --> death
103
Cholinesterase inhibitors depend on presence of ____ for effect.
ACh
104
Are cholinesterase inhibitors limited to parasympathetic effects?
No
105
Effects of cholinesterase inhibitors
increased peristalsis, pupillary constriction, muscular twitch, smooth muscle contraction
106
Physostigmine, neostigmine, and edrophonium, and organophosphates are ____
cholinesterase inhibitors
107
Physostigmine, neostigmine, and edrophonium: muscarinic effects
(remember these are cholinesterase inhibitors) parasympathomimetic activity
108
Physostigmine, neostigmine, and edrophonium: nicotinic effects
stimulation followed by blockage of autonomic ganglia, skeletal muscle, CNS because these receptors get so excited that they stop working
109
Physostigmine, neostigmine, and edrophonium: affect on adrenal medulla
stimulation of adrenal medulla: we have nicotinic ACh receptors at those adrenal medullary cells
110
Clinical use of physostigmine
treatment of glaucoma - produces miosis, reduces intraocular pressure; stimulation of ruminal activity (SQ) - increases motility and peristalsis
111
Toxicity of physostigmine
CNS depression, convulsion
112
Clinical use of Neostigmine and edrophonium
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
Toxicity of neostigmine
skeletal weakness; vomiting and diarrhea, urination, bradycardia, hypotension
114
Physostigmine, neostigmine, and edrophonium are reversible or irreversible?
reversible
115
Organophosphates are reversible or irreversible cholinesterase inhibitors?
reversible
116
Cholinomimetic effects of organophosphates
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
How to block irreversible cholinesterase inhibitors?
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
Parasympatholytics inhibit effects of this NT
ACh
119
Parasympatholytics block muscarninc receptors by ___ ___
competitive antagonism
120
Atropine is a
parasympatholytic
121
Atropine at large doses is
vagolytic
122
Effects of atropine
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
Clinical use of atropine
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
Atropine toxicology
thirst, dysphagia, constipation, tachycardia, mydriasis because you are blocking PSNS; can be due to dog eating bunnies
125
List four synthetic muscarinic antagonists
glycopyrrolate, tropicamide, prpantheline, isopropamide
126
Glycopyrrolate
Synthetic muscarinic antagonist; used as a preanesthetic; less tachycardic; decreases gastric, salivary and respiratory secretions and decreases intestinal motility
127
Tropicamide is mainly used for
ocular - mydriasis - topical administration, fewer side affects
128
Propantheline and isopropamide are mainly used as
smooth muscle relaxants (GI, bladder)
129
Nicotine is a ganglionic blocking agent. True or False.
True
130
Nicotine effects
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
Nicotine toxicity
stimulation leading to depression; death from respiratory paralysis (CNS depression)
132
Synthetic ganglionic blocking agents
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
