ANS Part 2 Flashcards

1
Q

List a few endogenous neurotransmitters of the ANS

A

epinephrine
norepinephrine
dopamine
acetylcholine

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2
Q

List the main effects of alpha1 stimulation.

A

**vasoconstriction
pupillary dilation
bladder sphincter contraction
uterine contraction
**prostate contraction

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3
Q

List the main effects of alpha2 stimulation

A

platelet aggregation
**decreased SNS outflow (CNS & nerve terminals)
vasoconstriction & vasodilation

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4
Q

List the main effects of beta1 stimulation

A

**heart: increased contractility, rate, AV node conduction velocity
renin release from kidneys

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5
Q

List the main effects of beta2 stimulation

A

**bronchodilation
**uterine relaxation
**vasodilation in skeletal muscle, heart, & lungs
**decreased GI/GU motility
**increased K+ uptake (–> hypokalemia)
tremor
**glycogenolysis (–> hyperglycemia)

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6
Q

List the main effects of dopamine1 stimulation

A

vasodilation of coronaries & renal vasculature

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7
Q

List the two synthetic catecholamines

A

dobutamine
isoproterenol

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8
Q

What can happen when giving a patient a MAO inhibitor?

A

Hypertension and tachycardia (this can lead to stroke, myocardial infarction, etc.)

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9
Q

Which receptors does epinephrine agonize?

A

a1, a2, B1, B2

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10
Q

Which receptors does norepinephrine agonize?

A

a1, a2, B1

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11
Q

Which receptor does phenylephrine agonize?

A

a1

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12
Q

Which receptor does midodrine agonize?

A

a1

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13
Q

Which receptor does clonidine agonize?

A

a2

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14
Q

Which receptor does dexmedetomidine agonize?

A

a2

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15
Q

Which receptor does dobutamine agonize?

A

B1

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16
Q

Which receptors does isoproterenol agonize?

A

B1 & B2

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17
Q

Which receptor does terbutaline & albuterol agonize?

A

B2

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18
Q

Which receptor does dopamine agonize at low doses? At medium doses? At high doses?

A

dopaminergic

medium dose = B1
high dose = a1

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19
Q

Do catecholamines or noncatecholamines have a longer duration of action?

A

noncatecholamines

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20
Q

Major adverse effect of epinephrine?

A

tachydysrhythmias
(tachycardia with rapid AV conduction that can lead to abnormal beats)

this can lead to myocardial infarction

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21
Q

Epinephrine

A
  • 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
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22
Q

Epinephrine - cardiovascular effects

A
  • increased HR, contractility, AV node conduction rate (B1)
  • vasoconstriction (a1) + vasodilation (a2, b2) –> increased SBP, decreased DBP, no change in MAP
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23
Q

Other effects of epinephrine

A

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)

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24
Q

Since norepinephrine doesn’t agonize ____, it produces the strongest _____.

A

B2; vasoconstriction

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25
Norepinephrine
- lacks B2 action: a1 vasoconstriction is unopposed - risk for metabolic acidosis - risk for tissue necrosis if extravasation - no glycogenolysis
26
Renal dose dopamine
D1, D2 agonism; increased renal, splanchnic & cerebral blood flow (vasodilation); some contractility increase (increase CO)
27
Low dose dopamine
B1 agonism, increased contractility w/o increasing HR (increased CO); same vasodilation
28
High dose dopamine
a1 agonism, vasoconstriction
29
What drug is an a1 agonist
Phenylephrine
30
Phenylephrine
a1 agonist; vasoconstriction w/ no HR or contractility agonism; baroreceptor reflex = decreased HR
31
What drug is an a2 agonist?
Clonidine & dexmedetromidine
32
three effects of alpha2 agonists
decreased blood pressure sedation analgesia
33
receptor agonized by albuterol
beta2
34
adverse effects of beta2 agonists
tremor hypokalemia hyperglycemia
35
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
36
Beta selective drugs
- isoproterenol (B1 & B2) - dobutamine (B1) - albuterol & terbutaline (B2)
37
B nonselective agonist
isoproterenol - chemical pacemaker; increased HR & contractility, bronchodilation
38
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
39
B2 agonists
- albuterol: preferred choice for asthma induced bronchospasm (inhale) - terbutaline: for asthma & premature labor (PO, subq, inhaled)
40
Ephedrine
blocks reuptake of NE; increased a1, a2 & b1
41
Nonselective or mixed selectivity adrenergic antagonists
labetalol, carvedilol
42
alpha selective antagonists
phentolamine, phenoxybenzamine, prazosin
43
Beta selective antagonists
metoprolol, atenolol, esmolol, propranolol
44
what receptors does labetalol antagonize?
B1 & B2 most strongly weakly antagonizes a1, even more weakly antagonizes a2
45
what receptor does prazosin antagonize?
a1 mostly
46
name a B1 blocker (antagonist) name a B2 blocker name a B nonselective blocker
B1 blocker = metoprolol, atenolol, esmolol B nonselective = propanolol, nadolol, timolol
47
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
48
What does a1 antagonism result in?
- vasodilation, decreased BP, orthostatic hypotension - prostate & bladder = muscle relaxation --> micturation (relieves BPH)
49
name two reasons why alpha antagonists are prescribed
hypertension BPH
50
list side effects of alpha antagonists
orthostatic hypotension (postural hypotension) reflex tachycardia (d/t baroreceptor reflex) nasal congestion (d/t vasodilation) inhibition of ejaculation
51
what is the main difference between phentolamine and phenoxybenzamine
phenoxybenzamine covalently binds the receptor = very long half life
52
What does phentolamine do?
vasodilation, decreased BP, increased HR; indicated for HTN emergencies, pheochromocytoma, or local infiltration post extravasation
53
What does phenoxybenzamine do?
noncompetitive covalent binding, very long acting
54
What does prazosin do?
a1 selective, indicated for HTN & BPH
55
list indications for administration of a beta blocker (beta antagonist)
- HTN - angina and post-myocardial infarction - tachydysrhythmias - use PRN for stage fright/anxiety prevention
56
list RELATIVE contraindications for beta antagonist administration
- AV heart block - cardiac failure - asthma - uncontrolled diabetes - hypovolemia
57
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)
58
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)
59
Nm agonism occurs where?
neuromuscular junction (the synapse between a nerve and the muscle cell)
60
Nm agonism results in _______.
skeletal muscle contraction
61
agonism of muscarinic receptors result in:
- vasodilation - **decreased heart rate - miosis - **bronchoconstriction - **increased secretions - **GI/GU motility increase (urination/defecation) - sweating - erection
62
Nonselective beta antagonists
propranolol - decreased HR, contractility & CO, decreased BP - decreased renal blood flow due to decreased BP --> Na/H2o retention
63
Cardioselective beta antagonists
- b1: metoprolol, atenolol, esmolol - atenolol = most selective B blocker, very useful in coronary artery disease
64
Mixed alpha / beta antagonists
- labetalol & carvedilol - vasodilation, decreased HR, decreased BP, CO unaffected - side effects = orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia
65
M1 receptors
- blood vessels, no nerve synapse - vasodilation if agonized
66
M2
heart, decreased HR
67
M3
- eye, lung, bladder, sweat glands, sex organs - miosis, ciliary muscle contraction, bronchoconstriction, increased secretions, urination, sweat, erection
68
M1-5
CNS, memory
69
what drug class is atropine
muscarinic antagonist aka: anticholinergic
70
what are the effects of atropine administration
- increased HR - decreased secretions - bronchodilation - mydriasis & cycloplegia
71
Muscarinic antagonists
atropine, scopolamine, glycopyrrolate, ipratropium
72
Scopolamine
crosses BBB, sedation, mydriasis, sea sickness prevention
73
Glycopyrrolate
does not cross BBB, only peripheral effects
74
Ipratropium
therapy of asthma / COPD (inhaled nasal spray to decrease systemic side effects)
75
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
76
Muscarinic agonist
bethanecholol
77
what is the indication for administration of bethanecholol?
decreased GI/GU motility
78
side effects of bethanecholol
- bradycardia - sweating - increased secretions - bronchoconstriction - miosis
79
contraindications/cautions for bethanecholol administration
bowel or bladder obstruction heart block hypotension/bradycardia asthma
80
what is an acetylcholinesterase inhibitor
medication that blocks the actions of acetylcholinesterase, which results in increased acetylcholine concentration
81
what are the contraindications to the use of acetylcholinesterase inhibitors
- bradycardia - seizures - peptic ulcer disease - GI/GU obstruction
82
AChE inhibitor effects
reverses neuromuscular blockade (MG), increases PNS tone (increased GI motility), increases CNS cholinergic activity (Alzheimers)
83
name two acetylcholinesterase inhibitors that work peripherally.
peripheral: - neostigmine - pyridostigmine
84
Neostigmine
MG, neuromuscular block reversal, improve GI motility
85
Pyridostigmine
glaucoma, MG, NMB reversal
86
what is cholinergic crisis
excessive ACh activity or muscarinic receptor stimulation
87
s/s cholinergic crisis
muscle weakness (including respiratory muscles) cramps d/t excessive GI activity salivation
88
treatment for cholinergic crisis
atropine support for respiratory system
89
what is myasthenic crisis
extreme muscle weakness (including of respiratory muscles), caused by autoimmune attack of Nm receptors)
90
what is the treatment for myasthenic crisis
acetylcholinesterase inhibitors supportive care for respiratory failure
91
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
92
What drug is a depolarizing neuromuscular blocker?
succinylcholine
93
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
94
precautions when administering a depolarizing or nondepolarizing muscle relaxant
**requires mechanical ventilation **requires sedation +/- analgesia
95
adverse effects of succinylcholine
hyperkalemia myalgias (muscle pain)
96
Duration of succinylcholine
short, breakdown by pseudocholinesterase enzyme in plasma
97
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
98
What drug is a nondepolarizing muscle relaxant?
rocuronium