ANS Part 2 Flashcards
List a few endogenous neurotransmitters of the ANS
epinephrine
norepinephrine
dopamine
acetylcholine
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
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
Epinephrine
- short acting, if we wanted it to last longer we’d give infusion
- indications: brochoconstriction due to asthma, acute allergic reaction, cardiac arrest, decreased myocardial activity
Epinephrine - cardiovascular effects
- increased HR, contractility, AV node conduction rate (B1)
- vasoconstriction (a1) + vasodilation (a2, b2) –> increased SBP, decreased DBP, no change in MAP
Other effects of epinephrine
mydriasis, bronchodilation, decreased GI secretions, decreased peristalsis, decreased renal blood flow, increased renin release, bladder relaxation & sphincter contraction, decreased urination, ejaculation, uterus relaxation & labor inhibition, glycogenolysis (increased plasma glucose concentration)
Since norepinephrine doesn’t agonize ____, it produces the strongest _____.
B2; vasoconstriction
Norepinephrine
- lacks B2 action: a1 vasoconstriction is unopposed
- risk for metabolic acidosis
- risk for tissue necrosis if extravasation
- no glycogenolysis
Renal dose dopamine
D1, D2 agonism; increased renal, splanchnic & cerebral blood flow (vasodilation); some contractility increase (increase CO)
Low dose dopamine
B1 agonism, increased contractility w/o increasing HR (increased CO); same vasodilation
High dose dopamine
a1 agonism, vasoconstriction
What drug is an a1 agonist
Phenylephrine
Phenylephrine
a1 agonist; vasoconstriction w/ no HR or contractility agonism; baroreceptor reflex = decreased HR
What drug is an a2 agonist?
Clonidine & dexmedetromidine
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
Beta selective drugs
- isoproterenol (B1 & B2)
- dobutamine (B1)
- albuterol & terbutaline (B2)
B nonselective agonist
isoproterenol - chemical pacemaker; increased HR & contractility, bronchodilation
B1 agonist
doputamine; B1 agonism at low doses, a1 agonism at high doses; increased contractility w/o increasing HR or BP substantially; good in chronic heart failure, dilates coronary arteries
B2 agonists
- albuterol: preferred choice for asthma induced bronchospasm (inhale)
- terbutaline: for asthma & premature labor (PO, subq, inhaled)
Ephedrine
blocks reuptake of NE; increased a1, a2 & b1
Nonselective or mixed selectivity adrenergic antagonists
labetalol, carvedilol
alpha selective antagonists
phentolamine, phenoxybenzamine, prazosin
Beta selective antagonists
metoprolol, atenolol, esmolol, propranolol
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
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
What does a1 antagonism result in?
- vasodilation, decreased BP, orthostatic hypotension
- prostate & bladder = muscle relaxation –> micturation (relieves BPH)
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
What does phentolamine do?
vasodilation, decreased BP, increased HR; indicated for HTN emergencies, pheochromocytoma, or local infiltration post extravasation
What does phenoxybenzamine do?
noncompetitive covalent binding, very long acting
What does prazosin do?
a1 selective, indicated for HTN & BPH
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
- cardiac failure
- asthma
- uncontrolled diabetes
- hypovolemia
What do beta antagonists do?
- decrease contractility / HR, better o2 supply demand balance
- bronchospasm
- vasoconstriction in skeletal muscle
- decreased renin release, decreased BP
- decreased K uptake into skeletal muscle (hyperK risk)
- decreased glycogenolysis –> hypoglycemia risk in diabetics (masks symptoms of hypoglycemia - tremor, sweating, tachycardia)
Beta antagonists clinical indications
HTN, angina management, decrease mortality in post MI patients, pre op & peri op for patients at risk of MI, suppression of tachyarrhythmias, prevention of excessive SNS activity (stage fright)
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
Nonselective beta antagonists
propranolol
- decreased HR, contractility & CO, decreased BP
- decreased renal blood flow due to decreased BP –> Na/H2o retention
Cardioselective beta antagonists
- b1: metoprolol, atenolol, esmolol
- atenolol = most selective B blocker, very useful in coronary artery disease
Mixed alpha / beta antagonists
- labetalol & carvedilol
- vasodilation, decreased HR, decreased BP, CO unaffected
- side effects = orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia
M1 receptors
- blood vessels, no nerve synapse
- vasodilation if agonized
M2
heart, decreased HR
M3
- eye, lung, bladder, sweat glands, sex organs
- miosis, ciliary muscle contraction, bronchoconstriction, increased secretions, urination, sweat, erection
M1-5
CNS, memory
what drug class is atropine
muscarinic antagonist
aka: anticholinergic
what are the effects of atropine administration
- increased HR
- decreased secretions
- bronchodilation
- mydriasis & cycloplegia
Muscarinic antagonists
atropine, scopolamine, glycopyrrolate, ipratropium
Scopolamine
crosses BBB, sedation, mydriasis, sea sickness prevention
Glycopyrrolate
does not cross BBB, only peripheral effects
Ipratropium
therapy of asthma / COPD (inhaled nasal spray to decrease systemic side effects)
Overactive bladder disorder
- can use muscarinic antagonists to treat
- OAB = urgency, frequency, nocturia, urge incontinence
- block M receptors on detrusor muscle = decreased bladder pressure & decreased urinary urgency
- large side effect profile (blocks all M receptors) –> dry mouth, blurry vision, constipation, tachycardia
Muscarinic agonist
bethanecholol
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
AChE inhibitor effects
reverses neuromuscular blockade (MG), increases PNS tone (increased GI motility), increases CNS cholinergic activity (Alzheimers)
name two acetylcholinesterase inhibitors that work peripherally.
peripheral:
- neostigmine
- pyridostigmine
Neostigmine
MG, neuromuscular block reversal, improve GI motility
Pyridostigmine
glaucoma, MG, NMB reversal
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), caused by autoimmune attack of Nm receptors)
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
What drug is a depolarizing neuromuscular blocker?
succinylcholine
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)
Duration of succinylcholine
short, breakdown by pseudocholinesterase enzyme in plasma
mechanism of action of nondepolarizing muscle relaxants
antagonize Nm at neuromuscular junction and prevent depolarization of muscle cell –> flaccid paralysis
- complete paralysis (requires mechanical vent)
- no sedation or analgesia
What drug is a nondepolarizing muscle relaxant?
rocuronium
