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GT BSN/CNL PHARM > Autonomic Nervous System > Flashcards

Autonomic Nervous System Flashcards

1
Q

What are the sympathetic and parasympathetic effects of stimulation on pupils?

A

sympathetic: dilate
parasympathetic: constrict

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2
Q

What are the sympathetic and parasympathetic effects of stimulation on salivation?

A

sympathetic: decreases saliva production
parasympathetic: increases saliva production

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3
Q

What are the sympathetic and parasympathetic effects of simulation on heart rate?

A

sympathetic: increase
parasympathetic: decrease

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4
Q

What are the sympathetic and parasympathetic effects of simulation on contractility (strength of heart contraction)?

A

sympathetic: increase
parasympathetic: decrease

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5
Q

What are the sympathetic and parasympathetic effects of simulation on the bronchi?

A

sympathetic: bronchiole dilation
parasympathetic: bronchiole constriction

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6
Q

What are the sympathetic and parasympathetic effects of simulation on the GI tract?

A

sympathetic: decreases activity
parasympathetic: increases activity

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7
Q

What are the sympathetic and parasympathetic effects of simulation on the adrenal medulla?

A

sympathetic: increases epinephrine (and some norepinephrine) release
parasympathetic: N/A

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8
Q

What are the sympathetic and parasympathetic effects of simulation on urination?

A

sympathetic: decreases urination (relaxes urinary bladder, constricts sphincter)
parasympathetic: increases urination (constricts urinary bladder, relaxes sphincter)

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9
Q

What are the sympathetic and parasympathetic effects of simulation on vasculature?

A

Sympathetic: general vascular tone. Increased sympathetic response leads to vasoconstriction.
Parasympathetic: N/A

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10
Q

Which branch of the ANS innervates sweat glands?

A

SNS

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11
Q

Which branch of ANS innervates blood vessels?

A

SNS

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12
Q

What is the somatic nervous system?

A

nerve impulses that are under voluntary control as well as reflexes

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13
Q

List a few endogenous neurotransmitters of the ANS

A

epinephrine
norepinephrine
dopamine
acetylcholine

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14
Q

What is a synapse?

A

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.

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15
Q

What neurotransmitter is released by the somatic nervous system? What receptor binds this neurotransmitter here?

A

Acetylcholine
Nicotinic (type 1) Receptor (Or Nm receptor)

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16
Q

What neurotransmitter is released into the synapse at all autonomic ganglion? What receptor binds this neurotransmitter here?

A

Acetylcholine
Nicotinic (type 2) Receptor (Or Nn receptor)

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17
Q

What neurotransmitter is released onto target organs from the parasympathetic nervous system? What receptor binds this neurotransmitter here?

A

Acetylcholine
Muscarinic (M) Receptor

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18
Q

What neurotransmitter is released onto target organs from the sympathetic nervous system? What receptors bind this neurotransmitter here?

A

Norepinephrine
Adrenergic Receptors (alpha1, alpha 2, Beta 1, Beta 2)

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19
Q

What neurotransmitter is released by the adrenal medulla? Where does this neurotransmitter go?

A

Primarily epinephrine (some norepinephrine)
It goes into the vascular circulation

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20
Q

How is acetylcholine metabolized?

A

Acetylcholinesterase (AChE)

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21
Q

How are epinephrine and norepinephrine metabolized?

A

COMT (catechol-o-methyltransferase) and
MAO (monoamine oxidase)

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22
Q

How does the baroreceptor reflex respond to low blood pressure?

A

results in vasoconstriction & increased heart rate and/or contractility (increased cardiac output)

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23
Q

How does the baroreceptor reflex respond to high blood pressure?

A

results in vasodilation & decreased heart rate and/or contractility (decreased cardiac output)

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24
Q

List the main effects of alpha1 stimulation.

A

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

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25
Q

List the main effects of alpha2 stimulation

A

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

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26
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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27
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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28
Q

List the main effects of dopamine1 stimulation

A

vasodilation of coronaries & renal vasculature

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29
Q

Agonist

A

stimulates the receptor to do what it normally does

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30
Q

Antagonist

A

blocks the normal activated receptor activity

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31
Q

Affinity

A

strength of drug binding to the receptor

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32
Q

List the two synthetic catecholamines

A

dobutamine
isoproterenol

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33
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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34
Q

Which receptors does epinephrine agonize?

A

a1, a2, B1, B2

35
Q

Which receptors does norepinephrine agonize?

A

a1, a2, B1

36
Q

Which receptor does phenylephrine agonize?

A

a1

37
Q

Which receptor does midodrine agonize?

A

a1

38
Q

Which receptor does clonidine agonize?

A

a2

39
Q

Which receptor does dexmedetomidine agonize?

A

a2

40
Q

Which receptor does dobutamine agonize?

A

B1

41
Q

Which receptors does isoproterenol agonize?

A

B1 & B2

42
Q

Which receptor does terbutaline & albuterol agonize?

A

B2

43
Q

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

A

dopaminergic

medium dose = B1
high dose = a1

44
Q

Do catecholamines or noncatecholamines have a longer duration of action?

A

noncatecholamines

45
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

46
Q

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

A

B2; vasoconstriction

47
Q

three effects of alpha2 agonists

A

decreased blood pressure
sedation
analgesia

48
Q

receptor agonized by albuterol

A

beta2

49
Q

adverse effects of beta2 agonists

A

tremor
hypokalemia
hyperglycemia

50
Q

what is an indirect agonist

A

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

51
Q

what receptors does labetalol antagonize?

A

B1 & B2 most strongly

weakly antagonizes a1, even more weakly antagonizes a2

52
Q

what receptor does prazosin antagonize?

A

a1 mostly

53
Q

name a B1 blocker (antagonist)
name a B2 blocker
name a B nonselective blocker

A

B1 blocker = metoprolol, atenolol, esmolol
B2 blocker = butoxamine
B nonselective = propanolol, nadolol, timolol

54
Q

when giving a beta antagonist for hypertension, what are side effects of using a nonselective antagonist?

A

bronchoconstriction (esp risk with asthma)
hypoglycemia (esp risk with diabetes)
hyperkalemia

55
Q

name two reasons why alpha antagonists are prescribed

A

hypertension
BPH

56
Q

list side effects of alpha antagonists

A

orthostatic hypotension (postural hypotension)
reflex tachycardia (d/t baroreceptor reflex)
nasal congestion (d/t vasodilation)
inhibition of ejaculation

57
Q

what is the main difference between phentolamine and phenoxybenzamine

A

phenoxybenzamine covalently binds the receptor = very long half life

58
Q

list indications for administration of a beta blocker (beta antagonist)

A
  • HTN
  • angina and post-myocardial infarction
  • tachydysrhythmias
  • use PRN for stage fright/anxiety prevention
59
Q

list RELATIVE contraindications for beta antagonist administration

A
  • AV heart block or symptomatic bradycardia
  • cardiac failure
  • asthma
  • uncontrolled diabetes
  • hypovolemia
60
Q

does receptor selectivity increase or decrease when the dose of medication increases

A

decrease

61
Q

what are the three types of receptors in the parasympathetic nervous system?

A

nicotinic N (N1 or Nn)
nicotinic M (N2 or Nm)
muscarinic (5 major subtypes)

62
Q

what neurotransmitter is released in the parasympathetic and somatic nervous systems

A

acetylcholine

63
Q

Nn agonism occurs where?

A

all SNS & PSNS ganglia
adrenal medulla

64
Q

Nm agonism occurs where?

A

neuromuscular junction (the synapse between a nerve and the muscle cell)

65
Q

Nm agonism results in _______.

A

skeletal muscle contraction

66
Q

agonism of muscarinic receptors result in:

A
  • vasodilation
  • **decreased heart rate
  • miosis
  • **bronchoconstriction
  • **increased secretions
  • **GI/GU motility increase (urination/defecation)
  • sweating
  • erection
67
Q

what drug class is atropine

A

muscarinic antagonist
aka: anticholinergic

68
Q

what are the effects of atropine administration

A
  • increased HR
  • decreased secretions
  • bronchodilation
  • mydriasis
69
Q

what is the indication for administration of bethanecholol?

A

decreased GI/GU motility

70
Q

side effects of bethanecholol

A
  • bradycardia
  • sweating
  • increased secretions
  • bronchoconstriction
  • miosis
71
Q

contraindications/cautions for bethanecholol administration

A

bowel or bladder obstruction
heart block
hypotension/bradycardia
asthma

72
Q

what is an acetylcholinesterase inhibitor

A

medication that blocks the actions of acetylcholinesterase, which results in increased acetylcholine concentration

73
Q

what are the contraindications to the use of acetylcholinesterase inhibitors

A
  • bradycardia
  • seizures
  • peptic ulcer disease
  • GI/GU obstruction
74
Q

name two acetylcholinesterase inhibitors that work peripherally.
name two that work in the central nervous system

A

peripheral:
- neostigmine
- pyridostigmine

CNS:
- tacrine
- donepezil
- rivastigmine
- galantamine

75
Q

what is cholinergic crisis

A

excessive ACh activity or muscarinic receptor stimulation

76
Q

s/s cholinergic crisis

A

muscle weakness (including respiratory muscles)
cramps d/t excessive GI activity
salivation

77
Q

treatment for cholinergic crisis

A

atropine
support for respiratory system

78
Q

what is myasthenic crisis

A

extreme muscle weakness (including of respiratory muscles)

79
Q

what is the treatment for myasthenic crisis

A

acetylcholinesterase inhibitors
supportive care for respiratory failure

80
Q

why do we talk about cholinergic crisis and myasthenic crisis together?

A

both exhibit extreme muscle weakness

the treatment for myasthenic crisis is a CAUSE for cholinergic crisis

81
Q

mechanism of action of succinylcholine

A

agonism of Nm at neuromuscular junction = single muscle contraction followed by flaccid paralysis

this is why it’s caused a depolarizing muscle relaxant

82
Q

precautions when administering a depolarizing or nondepolarizing muscle relaxant

A

**requires mechanical ventilation
**requires sedation +/- analgesia

83
Q

adverse effects of succinylcholine

A

hyperkalemia
myalgias (muscle pain)

84
Q

mechanism of action of nondepolarizing muscle relaxants

A

antagonize Nm at neuromuscular junction and prevent depolarization of muscle cell –> flaccid paralysis

GT BSN/CNL PHARM (26 decks)

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