Autonomic Nervous System Flashcards
What are the sympathetic and parasympathetic effects of stimulation on pupils?
sympathetic: dilate
parasympathetic: constrict
What are the sympathetic and parasympathetic effects of stimulation on salivation?
sympathetic: decreases saliva production
parasympathetic: increases saliva production
What are the sympathetic and parasympathetic effects of simulation on heart rate?
sympathetic: increase
parasympathetic: decrease
What are the sympathetic and parasympathetic effects of simulation on contractility (strength of heart contraction)?
sympathetic: increase
parasympathetic: decrease
What are the sympathetic and parasympathetic effects of simulation on the bronchi?
sympathetic: bronchiole dilation
parasympathetic: bronchiole constriction
What are the sympathetic and parasympathetic effects of simulation on the GI tract?
sympathetic: decreases activity
parasympathetic: increases activity
What are the sympathetic and parasympathetic effects of simulation on the adrenal medulla?
sympathetic: increases epinephrine (and some norepinephrine) release
parasympathetic: N/A
What are the sympathetic and parasympathetic effects of simulation on urination?
sympathetic: decreases urination (relaxes urinary bladder, constricts sphincter)
parasympathetic: increases urination (constricts urinary bladder, relaxes sphincter)
What are the sympathetic and parasympathetic effects of simulation on vasculature?
Sympathetic: general vascular tone. Increased sympathetic response leads to vasoconstriction.
Parasympathetic: N/A
Which branch of the ANS innervates sweat glands?
SNS
Which branch of ANS innervates blood vessels?
SNS
What is the somatic nervous system?
nerve impulses that are under voluntary control as well as reflexes
List a few endogenous neurotransmitters of the ANS
epinephrine
norepinephrine
dopamine
acetylcholine
What is a synapse?
The endpoint of a nerve where it releases its neurotransmitter for cell to cell communication.
The recipient cell can be another nerve cell or of the target organ.
What neurotransmitter is released by the somatic nervous system? What receptor binds this neurotransmitter here?
Acetylcholine
Nicotinic (type 1) Receptor (Or Nm receptor)
What neurotransmitter is released into the synapse at all autonomic ganglion? What receptor binds this neurotransmitter here?
Acetylcholine
Nicotinic (type 2) Receptor (Or Nn receptor)
What neurotransmitter is released onto target organs from the parasympathetic nervous system? What receptor binds this neurotransmitter here?
Acetylcholine
Muscarinic (M) Receptor
What neurotransmitter is released onto target organs from the sympathetic nervous system? What receptors bind this neurotransmitter here?
Norepinephrine
Adrenergic Receptors (alpha1, alpha 2, Beta 1, Beta 2)
What neurotransmitter is released by the adrenal medulla? Where does this neurotransmitter go?
Primarily epinephrine (some norepinephrine)
It goes into the vascular circulation
How is acetylcholine metabolized?
Acetylcholinesterase (AChE)
How are epinephrine and norepinephrine metabolized?
COMT (catechol-o-methyltransferase) and
MAO (monoamine oxidase)
How does the baroreceptor reflex respond to low blood pressure?
results in vasoconstriction & increased heart rate and/or contractility (increased cardiac output)
How does the baroreceptor reflex respond to high blood pressure?
results in vasodilation & decreased heart rate and/or contractility (decreased cardiac output)
List the main effects of alpha1 stimulation.
**vasoconstriction
pupillary dilation
bladder sphincter contraction
uterine contraction
**prostate contraction
List the main effects of alpha2 stimulation
platelet aggregation
**decreased SNS outflow (CNS & nerve terminals)
vasoconstriction & vasodilation
List the main effects of beta1 stimulation
**heart: increased contractility, rate, AV node conduction velocity
renin release from kidneys
List the main effects of beta2 stimulation
**bronchodilation
**uterine relaxation
**vasodilation in skeletal muscle, heart, & lungs
**decreased GI/GU motility
**increased K+ uptake (–> hypokalemia)
tremor
**glycogenolysis (–> hyperglycemia)
List the main effects of dopamine1 stimulation
vasodilation of coronaries & renal vasculature
Agonist
stimulates the receptor to do what it normally does
Antagonist
blocks the normal activated receptor activity
Affinity
strength of drug binding to the receptor
List the two synthetic catecholamines
dobutamine
isoproterenol
What can happen when giving a patient a MAO inhibitor?
Hypertension and tachycardia (this can lead to stroke, myocardial infarction, etc.)
Which receptors does epinephrine agonize?
a1, a2, B1, B2
Which receptors does norepinephrine agonize?
a1, a2, B1
Which receptor does phenylephrine agonize?
a1
Which receptor does midodrine agonize?
a1
Which receptor does clonidine agonize?
a2
Which receptor does dexmedetomidine agonize?
a2
Which receptor does dobutamine agonize?
B1
Which receptors does isoproterenol agonize?
B1 & B2
Which receptor does terbutaline & albuterol agonize?
B2
Which receptor does dopamine agonize at low doses? At medium doses? At high doses?
dopaminergic
medium dose = B1
high dose = a1
Do catecholamines or noncatecholamines have a longer duration of action?
noncatecholamines
Major adverse effect of epinephrine?
tachydysrhythmias
(tachycardia with rapid AV conduction that can lead to abnormal beats)
this can lead to myocardial infarction
Since norepinephrine doesn’t agonize ____, it produces the strongest _____.
B2; vasoconstriction
three effects of alpha2 agonists
decreased blood pressure
sedation
analgesia
receptor agonized by albuterol
beta2
adverse effects of beta2 agonists
tremor
hypokalemia
hyperglycemia
what is an indirect agonist
drug that acts via a mechanism that is NOT directly agonizing the receptor
examples:
- blocking reuptake of neurotransmitter
- blocking metabolism of a neurotransmitter
- increasing release of neurotransmitter from presynaptic nerve terminal
what receptors does labetalol antagonize?
B1 & B2 most strongly
weakly antagonizes a1, even more weakly antagonizes a2
what receptor does prazosin antagonize?
a1 mostly
name a B1 blocker (antagonist)
name a B2 blocker
name a B nonselective blocker
B1 blocker = metoprolol, atenolol, esmolol
B2 blocker = butoxamine
B nonselective = propanolol, nadolol, timolol
when giving a beta antagonist for hypertension, what are side effects of using a nonselective antagonist?
bronchoconstriction (esp risk with asthma)
hypoglycemia (esp risk with diabetes)
hyperkalemia
name two reasons why alpha antagonists are prescribed
hypertension
BPH
list side effects of alpha antagonists
orthostatic hypotension (postural hypotension)
reflex tachycardia (d/t baroreceptor reflex)
nasal congestion (d/t vasodilation)
inhibition of ejaculation
what is the main difference between phentolamine and phenoxybenzamine
phenoxybenzamine covalently binds the receptor = very long half life
list indications for administration of a beta blocker (beta antagonist)
- HTN
- angina and post-myocardial infarction
- tachydysrhythmias
- use PRN for stage fright/anxiety prevention
list RELATIVE contraindications for beta antagonist administration
- AV heart block or symptomatic bradycardia
- cardiac failure
- asthma
- uncontrolled diabetes
- hypovolemia
does receptor selectivity increase or decrease when the dose of medication increases
decrease
what are the three types of receptors in the parasympathetic nervous system?
nicotinic N (N1 or Nn)
nicotinic M (N2 or Nm)
muscarinic (5 major subtypes)
what neurotransmitter is released in the parasympathetic and somatic nervous systems
acetylcholine
Nn agonism occurs where?
all SNS & PSNS ganglia
adrenal medulla
Nm agonism occurs where?
neuromuscular junction (the synapse between a nerve and the muscle cell)
Nm agonism results in _______.
skeletal muscle contraction
agonism of muscarinic receptors result in:
- vasodilation
- **decreased heart rate
- miosis
- **bronchoconstriction
- **increased secretions
- **GI/GU motility increase (urination/defecation)
- sweating
- erection
what drug class is atropine
muscarinic antagonist
aka: anticholinergic
what are the effects of atropine administration
- increased HR
- decreased secretions
- bronchodilation
- mydriasis
what is the indication for administration of bethanecholol?
decreased GI/GU motility
side effects of bethanecholol
- bradycardia
- sweating
- increased secretions
- bronchoconstriction
- miosis
contraindications/cautions for bethanecholol administration
bowel or bladder obstruction
heart block
hypotension/bradycardia
asthma
what is an acetylcholinesterase inhibitor
medication that blocks the actions of acetylcholinesterase, which results in increased acetylcholine concentration
what are the contraindications to the use of acetylcholinesterase inhibitors
- bradycardia
- seizures
- peptic ulcer disease
- GI/GU obstruction
name two acetylcholinesterase inhibitors that work peripherally.
name two that work in the central nervous system
peripheral:
- neostigmine
- pyridostigmine
CNS:
- tacrine
- donepezil
- rivastigmine
- galantamine
what is cholinergic crisis
excessive ACh activity or muscarinic receptor stimulation
s/s cholinergic crisis
muscle weakness (including respiratory muscles)
cramps d/t excessive GI activity
salivation
treatment for cholinergic crisis
atropine
support for respiratory system
what is myasthenic crisis
extreme muscle weakness (including of respiratory muscles)
what is the treatment for myasthenic crisis
acetylcholinesterase inhibitors
supportive care for respiratory failure
why do we talk about cholinergic crisis and myasthenic crisis together?
both exhibit extreme muscle weakness
the treatment for myasthenic crisis is a CAUSE for cholinergic crisis
mechanism of action of succinylcholine
agonism of Nm at neuromuscular junction = single muscle contraction followed by flaccid paralysis
this is why it’s caused a depolarizing muscle relaxant
precautions when administering a depolarizing or nondepolarizing muscle relaxant
**requires mechanical ventilation
**requires sedation +/- analgesia
adverse effects of succinylcholine
hyperkalemia
myalgias (muscle pain)
mechanism of action of nondepolarizing muscle relaxants
antagonize Nm at neuromuscular junction and prevent depolarization of muscle cell –> flaccid paralysis
