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N929 - Anesthesia Pharmacology > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

steps of neurotransmission

A
  • synthesis
  • storage
  • release
  • action at receptor
  • termination
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2
Q

what kind of receptor is a muscarinic cholinergic receptor

A

GPCR

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3
Q

how many types of muscarinic receptors are there?

A

5 subtypes, 2 subgroups

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4
Q

stimulatory muscarinic cholinergic receptors

A

M1, M3, M5

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5
Q

inhibitory muscarinic cholinergic receptors

A

M2, M4

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6
Q

endogenous ligand of muscarinic cholinergic receptor

A

ACh

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7
Q

autonomic effector tissues

A

heart, endothelium, smooth muscle, glands, and the CNS

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8
Q

M1

A

CNS

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9
Q

M2

A

heart

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10
Q

M3

A

smooth muscle, glands, endothelium, eye (circular and ciliary muscle)

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11
Q

M4

A

CNS

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12
Q

M5

A

CNS

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13
Q

nicotinic cholinergic receptor type

A

ligand-gated Na+ and K+ depolarizing channel

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14
Q

two subtypes of nicotinic receptor

A

NicN and NicM

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15
Q

location of nicotinic receptors

A

autonomic ganglia, skeletal muscle innervation, CNS

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16
Q

muscarinic cholinergic receptor transmission

A

ACh binds –> confirmational change –> g protein breaks off –> second messenger –> causes a cellular response

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17
Q

nicotinic cholinergic receptor transmission

A

ACh binds –> confirmational change –> channel opens and positively charged ions influx through channel

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18
Q

NicN

A

ANS ganglia (all), adrenal medulla, CNS

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19
Q

NicM

A

skeletal muscle NMJ

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20
Q

alpha adrenergic receptor type

A

GPCR

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21
Q

alpha adrenergic receptor ligand

A

NE; also EPI and Dopa in large doses

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22
Q

excitatory alpha adrenergic receptor

A

alpha1

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23
Q

alpha1 adrenergic receptor transmission

A

increase in calcium –> calmodulin activation –> increased actin/myosin interaction –> smooth muscle contraction

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24
Q

inhibitory alpha adrenergic receptor

A

alpha 2

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25
Q

alpha2 adrenergic receptor transmission

A

decrease in cAMP –> decrease in NE release

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26
Q

alpha1

A

excitatory; smooth muscle, GU sphincters (esp. bladder), most vascular smooth muscle (skin, splanchic), eye (radial muscle), heart, liver

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27
Q

alpha 2

A

inhibitory; pre-synaptic nerve terminal, platelets, pancreatic beta cells

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28
Q

beta adrenergic receptor type

A

GPCR

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29
Q

beta adrenergic receptor ligand

A

NE, Epi

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30
Q

beta adrenergic receptor transmission

A

activation of adenyl cyclase –> increase in cAMP –> increase in kinase activation and phosphorylation of protein

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31
Q

beta adrenergic receptor tissues

A

heart, kidney, liver, smooth muscle, skeletal muscle, fat cells

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32
Q

beta1

A

heart, kidney (JG cells - cause renin release)

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33
Q

beta2

A

smooth muscle (bronchiolar, uterine, etc.), vascular smooth muscle (skeletal muscle beds), liver, skeletal muscle, heart

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34
Q

beta3

A

adipose tissue

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35
Q

PSNS action

A

rest and digest

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36
Q

PSNS origin

A 
cranial nerves (III, VII, IX, X) and sacral region 
vagus nerve 90%
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37
Q

PSNS ganglia location

A

target organ

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38
Q

PSNS preganglionic length and NT

A

long, ACh

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39
Q

PSNS postganglionic length and NT

A

short, ACh

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40
Q

divergence of PSNS

A

discrete; this is because postganglionic neurons are not branched, but are directed to a specific target organ

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41
Q

PSNS receptor on postganglionic neuron

A

cholinergic

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42
Q

SNS action

A

fight or flight

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43
Q

SNS origin

A

thoracolumbar region of spinal cord; T1-T12 and L1-L5

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44
Q

SNS ganglia location

A

sympathetic chain ganglion or paravertebral chain

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45
Q

SNS preganglionic length and NT

A

short, ACh

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46
Q

SNS postganglionic length and NT

A

long, NE

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47
Q

divergence of SNS

A

diffuse; because postganglionic neurons may innervate more than one organ

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48
Q

SNS receptor on postganglionic neuron

A

adrenergic

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49
Q

exceptions to dual innervation

A
  • adrenal medulla (SNS)
  • most sweat glands (SNS)
  • kidney (SNS)
  • blood vessels (SNS)
  • piloerector muscle (SNS)
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50
Q

eye iris radial muscle

A

SNS - alpha1 - contracts (mydriasis)

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51
Q

eye iris circular muscle

A

PSNS - M3 - contracts (miosis)

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52
Q

eye ciliary muscle

A

SNS - beta2 - relaxes (far vision)

PSNS - M3 - contracts (near vision)

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53
Q

SA node

A

SNS - beta1 - accelerates (increased HR)

PSNS - M2 - decelerates (decreased HR)

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54
Q

ectopic pacemakers

A

SNS - beta1 - accelerates (increased HR)

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55
Q

contractility of myocardium

A

SNS - beta1 - increases (increased force of contraction)

PSNS - M2 - decreases (atria, decreased force of contraction)

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56
Q

skin, splanchnic blood veseels

A

SNS - alpha1 - contracts (vasoconstriction)

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57
Q

skeletal muscle blood vessels

A

SNS - beta2 - relaxes (vasodilation)

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58
Q

bronchiolar smooth muscle

A

SNS - beta2 - relaxes (bronchodilation)

PSNS - M3 - contracts (bronchoconstriction)

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59
Q

GI walls

A

SNS - alpha2, beta2 - relaxes

PSNS - M3 - contracts

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60
Q

GI sphincters

A

SNS - alpha1 - contracts

PSNS - M3 - relaxes

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61
Q

GI secretion

A

SNS - alpha2 - decreases

PSNS - M3 - increases

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62
Q

GU bladder wall

A

SNS - beta2 - relaxes

PSNS - M3 - contracts

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63
Q

GU Sphincter

A

SNS - alpha1 - contracts

PSNS - M3 - relaxes

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64
Q

Uterus (pregnant)

A

SNS - beta2 - relaxes
SNS - alpha1 - contracts
PSNS - M - contracts

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65
Q

Penis seminal vesicles

A

SNS - alpha1 - ejaculation

PSNS - M - erection

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66
Q

pilomotor smooth muscles

A

SNS - alpha1 - contracts

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67
Q

sweat glands eccrine

A

SNS - M - increases

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68
Q

sweat glands apocrine (stress)

A

SNS - alpha - increases

69
Q

liver

A

SNS - beta2, alpha - gluconeogenesis, glycogenolysis

70
Q

fat cells

A

SNS - beta3 - lipolysis

71
Q

kidney

A

SNS - beta1 - renin release from JG cells

72
Q

cholinergic muscarinic agonist drugs

A
  • acetylcholine
  • muscarine
  • pilocarpine
  • bethanechol
73
Q

cholinergic muscarinic agonist MOA

A

Receptor agonist

-acts directly on the muscarinic receptor

74
Q

cholinergic muscarinic agonist clinical uses

A
  • eye (glaucoma, contract ciliary body, increase outflow of aqueous humor)
  • GI/GU (post op ileus, post op urinary retention, xerostomia)
75
Q

cholinergic muscarinic agonist adverse affects

A 
CV: 
-decreased HR
-decreased CO and arterial pressure
-vasodilation via NO (produced by endothelial cells)
GI: increased motility
Bladder: contracts 
Lungs: bronchoconstriction 
Secretions: 
-increased sweat
-increased salivation
-increased lacrimation
-increased bronchial 
Eye: 
-miosis
-accommodation for near vision
-decreased intraocular pressure 
Toxicity antidote --> atropine
76
Q

cholinergic nicotinic agonist drugs

A
  • Succinylcholine
  • Varenicline
  • Acetylcholine
  • Nicotine
77
Q

cholinergic nicotinic agonist MOA

A

Receptor agonist

  • acts directly on the nicotinic receptor
  • NN – stimulation of post ganglionic neuronal activity (Autonomic NS); CNS stimulation
  • NM – activation of NM endplates; contraction
78
Q

cholinergic nicotinic agonist clinical uses

A
  • NN – smoking cessation (NRT, nicotine replacement therapy) (varenicline)
  • NM – depolarizing skeletal muscle paralysis (succinylcholine)
79
Q

cholinergic nicotinic agonist adverse effects

A

NN

  • CNS stimulation
  • skeletal muscle depolarization/blockade
  • HTN
  • increased HR
  • N/V/D
80
Q

AChE inhibitor (reversible) drugs

A
  • Edrophonium
  • Neostigmine
  • Pyridostigmine
  • Physostigmine
  • Donepezil
81
Q

AChE inhibitor (reversible) MOA

A
  • binds to active site and inhibits activity of AChE; undergoes hydrolysis; acidic portion slowly released and prevents ACh from binding
  • increase in ACh
  • amplifies effects at cholinergic synapses
  • indirect stimulant of nicotinic and muscarinic receptors by increased ACh
82
Q

edrophonium PK/PD

A
  • alcohol
  • short acting
  • very polar
  • onset 30-60 seconds
  • DOA – 10 min
83
Q

neostigmine PK/PD

A
  • carbamate
  • intermediate acting
  • moderately polar
  • onset 10-30 min
  • DOA – 2-4 hours
84
Q

physostigmine PK/PD

A
  • intermediate acting
  • nonpolar
  • crosses BBB
  • onset 3-8 min
  • DOA – 1 hour
85
Q

AChE inhibitors (reversible) clinical uses

A
  • reversal of NM blockade by non-depolarizing drug
  • myasthenia gravis diagnosis and treatment
  • glaucoma
  • GI-ileus
  • post op urinary retention
  • Alzheimer’s disease (donepezil)
86
Q

AChE inhibitors (reversible) adverse effects

A

Autonomic:
-increased secretions (salivary, lacrimal, bronchial, GI)
-increased GI motility
-bronchoconstriction
-bradycardia
-hypotension
-miosis; accommodation for near vision
NMJ:
-reverses NM block by non-depolarizing blocker
-improves transmission (myasthenia gravis)
-large doses – depolarizing block
CNS:
-therapeutic (dementia treatment)
-toxicity (excitation = possible convulsion; depression follows = unconscious)
Toxicity antidote –> atropine; pralidoxime

87
Q

AChE inhibitor (irreversible) drugs

A
  • Echothiophate

- Organophosphate insecticides

88
Q

AChE inhibitor (irreversible) PK/PD

A

long duration

89
Q

AChE inhibitor (irreversible) clinical uses

A
  • reversal of NM blockade by non-depolarizing drug
  • myasthenia gravis diagnosis and treatment
  • glaucoma
  • GI-ileus
  • post op urinary retention
  • non-therapeutic insecticide (organophosphate insecticide)
90
Q

AChE inhibitor (irreversible) adverse effects

A

Autonomic:
-increased secretions (salivary, lacrimal, bronchial, GI)
-increased GI motility
-bronchoconstriction
-bradycardia
-hypotension
-miosis; accommodation for near vision
NMJ:
-reverses NM block by non-depolarizing blocker
-improves transmission (myasthenia gravis)
-large doses – depolarizing block
CNS:
-therapeutic (dementia treatment)
-toxicity (excitation = possible convulsion; depression follows = unconscious)

91
Q

muscarinic antagonist drugs

A
  • atropine
  • glycopyrrolate
  • scopolamine
92
Q

muscarinic antagonist MOA

A

competitively blocks ACh from binding to the receptor and producing its effects

93
Q

muscarinic antagonist clinical uses

A 
CV: 
-tx of bradycardia 
CNS: 
-motion sickness (scopolamine) 
-Parkinson’s (boost dopamine and decrease ACh) 
Eye: 
-eye exam requiring mydriasis and cycloplegia 
Resp: 
-decreased secretions
-COPD/asthma (inhalation)
GI/GU: 
-GI hypermotility
-urinary urgency (newer M3 selective)
Other: 
-anesthetic premedication 
-cholinergic poisoning 
-AChE inhibitor toxicity
94
Q

muscarinic antagonist adverse effects

A 
CV: 
-increased HR
Resp: 
-bronchodilation
GI/GU: 
-decreased secretions/activity 
Glands/Sweat glands: 
-decreased secretions
Eye: 
-mydriasis 
-increase intraocular pressure
-cycloplegia (paralysis of accommodation) 
CNS: 
-sedation
95
Q

atropine MOA

A
  • tertiary amine
  • lipophilic
  • crosses BBB
96
Q

atropine PK/PD

A
  • half-life 4 hours (prolonged in elderly to 10 hours

- eye effects last for days

97
Q

atropine clinical uses

A
  • ophthalmic
  • tx of bradycardia
  • antidote for cholinergic agonists
  • preoperative inhibition of secretions
  • adjunct for NMBD reversal
98
Q

scopolamine MOA

A
  • tertiary amine
  • crosses BBB
  • more lipophilic than atropine
  • +++ CNS effects (amnesia)
  • +++ sedation
99
Q

scopolamine PK/PD

A
  • half-life 1-4 hours
  • onset 10 min
  • duration about 2 hours
100
Q

scopolamine clinical uses

A
  • motion sickness
  • PONV
  • preoperative for amnesia, sedation, or decrease secretions
101
Q

glycopyrrolate MOA

A
  • quaternary amine

- less CNS effects (b/c polar so unable to cross BBB)

102
Q

glycopyrrolate PK/PD

A
  • half-life 1 hour
  • onset 1 min
  • duration 7 hours
103
Q

glycopyrrolate clinical uses

A
  • pre-op cardiac dysrhythmia (vagal reflex)

- reversal of NM blockade with neostigmine

104
Q

nicotinic N antagonist (ganglionic blocker)

A

hexamethonium

105
Q

hexamethonium facts

A
  • blocks ganglionic output
  • hypertensive emergency
  • not used anymore
106
Q

nicotinic M antagonist drugs

A
  • Atracurium
  • Cisatracurium
  • Vecuronium
  • Rocuronium
  • Pancuronium
107
Q

nicotinic M antagonist MOA

A

competitively binds to nicotinic receptor at NMJ to block the action of ACh

108
Q

nicotinic M antagonist clinical use

A

skeletal muscle relaxation for surgical intubation or ventilation control

109
Q

alpha agonist drugs

A
  • Norepinephrine (alpha 1, alpha 2)
  • Phenylephrine (alpha 1)
  • Clonidine (alpha 2)
  • Dexamethasone (alpha 2)
110
Q

alpha agonist MOA

A

directly binds to activates the alpha receptor

111
Q

alpha agonist clinical uses

A 
Alpha 1: 
-Shock, systemically because of ability to vasoconstrict
-decongestant 
-ophthalmic hyperemia 
Alpha 2: 
-hypertension (central effects)
112
Q

alpha agonist adverse effects

A 
Alpha1: 
-vasoconstriction
-smooth muscle contraction (except GI)
-trophic effect BPH 
-GI/GU sphincters contract
-mydriasis 
Alpha2: 
-decrease NE release (presynaptic) 
-CNS inhibition of sympathetic outflow from VMC in the brain 
-platelet aggregation
-decrease in insulin secretion
113
Q

beta agonist drugs

A
  • Isoproterenol (beta 1 and beta 2)
  • Dobutamine (beta 1)
  • Albuterol (beta 2)
114
Q

beta agonist MOA

A

directly binds to and activates the beta receptor

115
Q

beta agonist clinical uses

A 
Beta 1: 
-acute heart failure (increases CO and BP) 
Beta 2: 
-asthma 
-COPD
-pre-term labor (to relax uterus)
116
Q

beta agonist adverse effects

A 
Beta1: 
-increased HR and contractility
-increase in renin release 
-trophic effect in heart (hypertrophy, used for chronic stable HF) 
Beta2: 
-bronchodilation
-vasodilation (esp skeletal muscle beds)
-most smooth muscle relaxes 
-skeletal muscle contracts (hypokalemia, increased K+ uptake)
-GI/GU – relaxation
-uterine smooth muscle relaxation
-glycogenolysis (liver to raise BG)
117
Q

mixed alpha/beta agonist drugs

118
Q

mixed alpha/beta agonist MOA

A
  • directly bind to and activate the alpha and beta receptors
  • which is activated depends on substance affinity for receptor
119
Q

mixed alpha/beta agonist PK/PD

A
  • rapid onset
  • brief duration
  • no oral admin because polar
  • poor CNS penetration
120
Q

NT releaser (indirect acting) drugs

A

Amphetamine

Ephedrine

121
Q

Amphetamine MOA

A
  • displaces/releases stored catecholamine NT

- secondary – inhibitis catecholamine reuptake (NET, DAT)

122
Q

amphetamine clinical uses

A

uses in ADHD, narcolepsy, appetite suppression

123
Q

ephedrine MOA

A
  • displaces/releases stored catecholamine NT

- some agonist activity at alpha and beta adrenergic receptors

124
Q

ephedrine PK/PD

A

extended duration, because not a catecholamine

125
Q

NE reuptake inhibitor (indirect acting) drugs

A
  • Cocaine

- Serotonin-Norepinephrine Reuptake Inhibitors (SNRI)

126
Q

Cocaine MOA

A
  • blocks NE reuptake by inhibiting the action of NET & DAT transporters
  • blocks sodium channels, so local anesthetic actions
127
Q

SNRI MOA

A

block NE reuptake by inhibiting NET transporter

128
Q

MAO Inhibitor (indirect acting) drugs

A
  • Tranylcypromine (non-selective A & B)

- Selegiline (selective B)

129
Q

MAOI MOA

A
  • prevent breakdown of catecholamines in presynaptic terminal so catecholamine accumulates in vesicles
  • MAO A – metabolizes NE
  • MAO B – metabolizes DA
130
Q

alpha receptor blocker drugs

A
  • Phenoxybenzamine (alpha 1, alpha 2)
  • Phentolamine (alpha 1, alpha 2)
  • Prazosin (alpha 1)
  • Yohimbine (alpha 2)
131
Q

alpha receptor blocker MOA

A

Competitively binds to the alpha receptor and blocks activity of endogenous ligand

132
Q

alpha receptor blocker clinical uses

A
  • HTN (later agent, not used a lot anymore)
  • BPH
  • pheochromocytoma (non-selective)
133
Q

alpha receptor blocker adverse effects

A
  • smooth muscle relaxation
  • decreased peripheral vascular resistance
  • decreased BP
134
Q

beta receptor blocker drugs

A
  • Propranolol (beta 1, beta 2)
  • Metoprolol (beta 1)
  • Esmolol (beta 1)
135
Q

beta receptor blocker MOA

A

Competitively binds to the beta receptor and blocks activity of endogenous ligand

136
Q

beta receptor blocker clinical uses

A
  • HTN
  • angina pectoris
  • arrythmia
  • MI
  • thyrotoxicosis
  • heart failure – chronic stable only and only select agents
  • other – infantile hemangioma, glaucoma, migraine prophylaxis, anxiety
137
Q

beta receptor blocker adverse effects

A
  • decreased HR
  • decreased force of contraction
  • decreased renin
  • anti-dysrhythmic effects (some)
  • bronchoconstriction
  • arrythmia, bradycardia
  • sedation (for those that cross BBB)
  • decreased sexual function
  • DM – blocking of glycogenolysis + blocks s/s of hypoglycemia so be careful!!
138
Q

Cholinergic Crisis Toxicity Mnemonic: (DUMBBELSS)

A
  • Diarrhea, Diaphoresis
  • Urination
  • Miosis
  • Bradycardia
  • Bronchoconstriction
  • Excitation (skeletal muscle, or CNS)
  • Lacrimation
  • Salivation
  • Sweating
139
Q

Muscarinic Agonist Mnemonic: (SLUDGE)

A
  • Salivation
  • Lacrimation
  • Urination
  • Diarrhea
  • GI Upset
  • Emesis
140
Q

Anticholinergic Memory Aid

A
  • Dry as a bone
  • Hot as a pistol
  • Red as a beet
  • Blind as a bat
  • Mad as a hatter
141
Q

Epinephrine

A

Naturally occurring catecholamine – last in the chain of synthesis

142
Q

Epinephrine receptor/MOA

A

Alpha1, alpha2, beta1, beta2, beta3
-low doses – beta effects
-high doses – alpha effects
Highest affinity for beta receptors

143
Q

Epinephrine PK/PD

A
  • metabolized in liver by CYP450
  • excreted in urine
  • half-life < 5 min
144
Q

Epinephrine dosing

A

1-20 mcg/min

145
Q

Epinephrine clinical uses

A
  • anaphylaxis
  • in combination with local anesthetics
  • cardiac arrest
  • some shock states that involve poor tissue oxygen delivery and hypotension
146
Q

Epinephrine effects

A
  • positive inotropic, chronotropic, dromotropic actions
  • increase in myocardial oxygen consumption
  • potential for arrythmia (dt dromotropic action)
  • bronchodilation
  • vasodilation
  • decrease in histamine release from mast cells
  • LOW dose – decreases SVR
  • HIGH dose – increase SVR
147
Q

Norepinephrine

A

Derived from dopamine in chain of catecholamine synthesis

148
Q

Norepinephrine receptor/MOA

A

Alpha1, beta1

-little effect on beta 2

149
Q

Norepinephrine PK/PD

A
  • metabolized in liver, kidney, plasma by CYP450
  • excreted in urine
  • half-life 1 min
150
Q

Norepinephrine dosing

A

1-20 mcg/min

151
Q

Norepinephrine clinical uses

A
  • shock

- generally used in patients with adequate CO but low SVR

152
Q

Norepinephrine effects

A
  • decrease in vital organ flow due to combo of alpha/beta stimulation
  • coronary artery perfusion increased d/t increase in DBP
  • increased renal vascular resistance, so decrease UOP
  • increase preload
  • caution in patients with peripheral tissue perfusion issues (NE may exacerbate)
  • decrease in insulin production
  • other effects usually due to potent vasoconstrictive effects
153
Q

Isoproterenol receptor/MOA

A

Beta1, beta2

No alpha activity

154
Q

Isoproterenol PK/PD

A
  • metabolized in liver by CYP450
  • excreted in urine
  • unknown half-life
155
Q

Isoproterenol dosing

A

2-20 mcg/min

156
Q

Isoproterenol clinical uses

A
  • acute asthma (not as much anymore)
  • cardiac stimulant
  • occasional use for treatment of bradycardia with heart block or torsades de pointes
  • post heart transplant for chronotropic support
157
Q

Isoproterenol effects

A
  • positive inotropic and chronotropic effects
  • decrease SVR, increase CO
  • increase myocardial oxygen consumption
  • bronchodilation
  • pulmonary vascular bed vasodilation
  • excessive tachycardia
  • myocardial ischemia (dt decreased DBP)
  • arrythmias
158
Q

Dopamine

A

derived from dopa in chain of catecholamine synthesis

159
Q

Dopamine receptor/MOA

A
  • low dose – D1 in renal, mesenteric, coronary vascular beds
  • med dose – beta1
  • high dose – alpha1
160
Q

Dopamine PK/PD

A
  • metabolized in liver, kidney, plasma by CYP450
  • 25% metabolized to NE
  • excreted urine
  • half-life 2 min
161
Q

Dopamine dosing

A

1-4 mcg/kg/min
5-10 mcg/kg/min
11-20 mcg/kg/min

162
Q

Dopamine clinical uses

A
  • shock
  • HF
  • increase blood flow to kidneys
163
Q

Dopamine effects

A
  • indirect sympathomimetic effect via release of NE from beta1 stimulation
  • increase RBF, so increase GFR and UOP
  • can cause severe limb ischemia (esp. in peds, DM, atherosclerosis, Reynaud’s)
164
Q

Dobutamine

A

synthetic sympathomimetic amine derived from isoproterenol

165
Q

Dobutamine receptor/MOA

166
Q

Dobutamine PK/PD

A
  • metabolized in liver by CYP450
  • excreted urine
  • half-life 2 min
167
Q

Dobutamine dosing

A

1-20 mcg/kg/min

168
Q

Dobutamine clinical uses

A
  • acute HF
  • cardiogenic/septic shock
  • heart stimulation for cardiac stress testing
169
Q

Dobutamine effects

A
  • strong inotropic response (but minimal chronotropy)
  • can increase or maintain BP dt increase CO and slight decrease in SVR
  • no longer used for inotropic support in surgery dt significant adverse effects

N929 - Anesthesia Pharmacology (12 decks)

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