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pharmacology > 3. Neuromuscular Blockers, Reversal Agents, Muscarinic Antagonists > Flashcards

3. Neuromuscular Blockers, Reversal Agents, Muscarinic Antagonists Flashcards

1
Q

nicotine receptor location

A

autonomic ganglia

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2
Q

nicotine action

A

agonist
or
antagonist

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3
Q

nicotine use

A

smoking cessation

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4
Q

succinylcholine receptor location

A

NMJ

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5
Q

succinylcholine action

A

agonist
or
antagonist

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6
Q

rocuronium receptor location

A

NMJ

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7
Q

rocuronium action

A

antagonist

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8
Q

pancuronium receptor location

A

NMJ

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9
Q

pancuronium action

A

antagonist

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10
Q

vecuronium action

A

antagonist

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11
Q

botulinum toxin receptor location

A

NMJ

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12
Q

botulinum action

A

indirect acting antagonist

*inhibiting SNARE proteins so no NT can be released

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13
Q

botulinum use

A

cosmetic
blepharospasm
cervical dystonia
focused msucle relaxant

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14
Q

nicotinic receptor antagonists

A

nicotine
succinylcholine
rocuronium
pancuronium
vecuronium
botulinum toxin

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15
Q

nicotinic receptor type

A

ion channel

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16
Q

how many Ach molecules binding to NAchR provide max effect?

A

2 Ach bind to alpha subunits

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17
Q

how is Ach broken down?

A

acetycholineesterase

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18
Q

direct agonist

A

acting on the nAchR

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19
Q

agonist/antagonist

A

stimulate initially
stay bound longer which would be an antagonist to target NT

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20
Q

fetal receptors

A

enhanced response to D agent
relative resistance to ND agent

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21
Q

margin of safety

A
  • 10% need to be activated to initial muscle Action Potential
  • more NT than needed for each AP
  • significant reserve capacity
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22
Q

Clinical evidence of block

A

75% of nicotinic receptors occupied by antagonist before clinical evidence of block

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23
Q

Complete suppression

A

95% nicotinic receptors occupied by antagonist

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24
Q

NMBs structure

A

NCH4+ functional group
functional duplicates of ACh
cations

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25
Q

Cations absorption

A

poor PO
avoid CNS penetration
- poor BBB passage

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26
Q

Depolarizing MR MOA

A

acts as agonist
then antagonist to Ach

binds Ach receptor
persistent depolarization of endplate
blocks Ach until it diffuses away

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27
Q

Depolarizing MR metabolism

A

slower than Ach

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28
Q

Non-Depolarizing MR MOA

A

competitive antagonist

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29
Q

Depolarizing MR Phase 1 block

A

depolarizing phase
persistant –> paralysis

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30
Q

Depolarizing MR phase 2 block

A

only happens w/lgr than recc doses or infusions

desensitizing phase
blocks conversion from depolarization to non-depolarizing block

MR blocks Ach

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31
Q

Depolarizing MR metabolism

A

slower than Ach
- not degraded by AchE

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32
Q

Non-depolarizing MR

A

competitive with Ach to bind w/nicotinic recepotr of end plate
bloc inhibits Ach from binding

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33
Q

how to reverse NDMR

A

AChE inhibitor
- neostigmine

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34
Q

surmountable

A

block can eventually be overcome

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35
Q

succinuylcholine onset/duration

A

rapid onset
- low lipid solubilty
- cation effect
- water soluble

short duration of action
- diffuses away quickly

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36
Q

Prolong Succinycholine duration

A

increase dose
continuous ijnfusion
decrease rate of metabolism

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37
Q

Succinylcholine metabolism

A

quick metabolism by pseudocholinesterase (plasma)

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38
Q

Succinylcholine DOA factors

A

hypothermia
- decrease hydrolysis
low enzyme (psuedocholinesterase)
- pregnancy, liver disease, renal fail
- drug interactions
- prolong 2-20 min
genetic
- heterozygotes (20-30min duration)
- homozygotes (4-8 hrs)

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39
Q

drugs that decrease psuedocholinesterase activity

A

neostimine
metoclopramide
esmolol
oral contraceptives
dibucaine
echothiophate
phenelzine
pancuronium

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40
Q

dibucaine number

A

measures enzyme function

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41
Q

dibucaine normal enzyme

A

80%

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42
Q

dibucaine homozygote number

A

20%

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43
Q

Succinylcholine drug interactions

A

cholinesterase inhibitors
- prolong phase 1 block
- reduce metabolism of sux
- pts w/myasthenia gravis/glaucoma

Nondepolarizing agents
- small dose may be antagonistic
- in phase 2 block, NDMR enhances
block

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44
Q

Succinylcholine dose

A

2 x ED95
ED95 = 0.35-0.5 mg/kg

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45
Q

Succinylcholine dose neonate

A

larger weight-based dose
(lgr mg/kg)

  • higher Vd
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46
Q

Succ continuous infusion

A

2 mg/mL or 1 mg/mL
need nerve stimulation

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47
Q

Succ CV effects

A
  • may act at ganglia and muscarinic receptors
  • depends on underlying state
    • leads to bradycardia w/elevated vagal tone
    • peds more susceptible
  • fasciculation
  • hyperkalemia (incr serum0.5 mEq/L)
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48
Q

Manage Succ bradycardia

A

Atropine/Glycopyrrolate

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49
Q

denervation injury due to receptor upregulation

A

immature isoform
more spread out receptors
widespread depolarization
extensive K release
risk peaks 7-10 days post trauma

burn, trauma, neurological conds

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50
Q

Succinylcholine contraindication

A

underlying neuromuscular disease
risk of malignant hyperthermia
allergy to succ
homozygous atypical cholinesterase
[K] > 5.5 mEq/L

51
Q

hyperkalemia management

A

insulin (prevents hypoglycemia)
calcium gluconate (for cardiac arrest)
dialysis (reduce K level)

52
Q

succinycholine pharmacologic effects

A

muscle pain
pressure increases
- intragastric
- intraocular
- ICP
masseter muscle rigidity (MMR)
malignant hyperthermia
generalized contraction
prolonged paralysis
histamine release

53
Q

NDMR onset/duration

A

slower onset
longer duration

compared to succinycholine

54
Q

NMDR potency vs onset

A

more potent
= smaller dose
= slower onset

55
Q

NMDR goals

A

facilitate atraumatic intubation
rapid intubation
require complete relaxation of:
- oral cavity
- larynx
- diaphragm
- abdomen

56
Q

NDMR increased intubation dose

A

larger dose increase conc at NMJ
risk prolonged duration of action

57
Q

NMDR priming

A

2 injection
10-15% of full dose 5 min before induction

58
Q

NMDR Volume of Distribution (Vd)

A

central compartment
NMJ

single dose - redist to preipheral compartment

repeat dose - saturates central compartment

59
Q

NMDR plasma cholinesterase clearance

A

mivacurium

60
Q

NMDR hoffman elimination

A

atracurium
cisastracurium

61
Q

NMDR hepatic clearance

A

vecuronium
rocuronium

62
Q

NMDR renal clearance

A

pancuronium
doxacurium

63
Q

NMDR duration of action - intermediate acting

A

atracurium
cisatracurium
rocuronium
vecuronium

64
Q

NMDR duration of action - long acting

A

pancuronium

65
Q

lower ED95

A

more potent

66
Q

higher ED95

A

less potent

67
Q

NDMR pharmacology effets

A

minimal CV effects
- pancuronium - vagolytic
prevents succ fasciculation
no hyperkalemia
histamine release
hypothermia prolong block
respiratory acidosis potentiate block

68
Q

NDMR drug interactions - additive

A

des>sevo>iso>nitrous
pan>vec/atracurium

ca++ channel blockers
aminoglycoside abx

69
Q

NMDR drug interactions -inhibitive

A

reversal agents
- suggamadex
- neostigmine

70
Q

atracurium

A

onset: intermediate
DOA: intermediate
CV: stable
- some hypotension/tachycardia
- decrease SVR
bronchospasms in asthmatics
toxic metabolite: laudanosine
rare anaphylaxis

71
Q

cisatracurium

A

onset: intermediate
DOA: intermediate
no HR/BP change
no histamine release
toxic metabolite: laudanosine

72
Q

pancuronium

A

onset: intermediate
DOA: long
vagolytic
- hypertension
- tachycardia
renal elimination
liver metabolizes

73
Q

vecuronium

A

onset: intermediate
DOA: intermediate
no BP/HR changes

74
Q

rocuronium

A

onset: fast
DOA: intermedaite
no metabolism
renal/hepatic elimination
less potent = lgr dose needed

75
Q

recovery index

A

offset speed to recover from 25% to 75% twitch height

76
Q

intubation MR

A

succinylcholine
- rapid onset / short duration
- rapid sequence induction

77
Q

continued paralysis

A

NDMR
permit reduced depth of anesthesia

78
Q

peripheral nerve stimulator

A

tetany
twitch
TOF

79
Q

fade

A

reduction of evoked response indicative of ND block

80
Q

clinical recovery

A

correlates w/absence of fade

81
Q

single twitch stimulation

A

twitch height remains normal until 75% ACh receptors blocked

82
Q

single twitch disappears when

A

90-95% receptors occupied

83
Q

TOF

A

train of four monitopring
progressive fade as relaxation increases

84
Q

TOF disappearance of 4th

A

75% block

85
Q

TOF disappearance of 3rd

A

80-85% block

86
Q

TOF disappearance of 2nd

A

85-90% block

87
Q

TOF disappearance of 1st

A

90-98% block

88
Q

clinical relaxation requires ____% block

A

75-95% block

89
Q

TOF ratio

A

ratio of response to 1 and 4 twitches

90
Q

Recovery TOF ratio

A

> = 0.9

amp4/amp1

91
Q

cholinesterase inhibitors act…

A

indirectly

enhance activity of Ach receptor, not directly acting on it

92
Q

Cholinesterase inhibitors act on which esterases?

A

acetylcholinesterase
butyrylcholinesterase
pseudocholinesterase

93
Q

cholinesterase inhibitors impact ______receptors

A

nicotinic
muscarinic

increase ACh ability to act at nAChR and mAChR

increased duration of ACh presence at cholinergic receptors

94
Q

cholinesterase inhibitors MOA

A

bind to AChE
blocks ACh from binding to enzyme
ACh increases
ACh has increased duration of time present at receptors

95
Q

acetylcholinesterase inhibitor types

A

1) alcohol structure - edrophonium
2) carbamic acid esters - neostigmine

96
Q

edrophonium

A

reversibly binds
short-lived (2-10 min)

97
Q

neostigmine

A

carbamylated enzyme more resistant to hydration
prolongs release (30min-6hrs)

98
Q

acetylcholinesterase inhibitor clinical uses

A

myasthenia gravis
alzheimers
glaucoma
reversal of neuromuscular blockers

99
Q

nicotinic effects of AChE inhibitors

A

ACh able to bind
increase muscle contractility

100
Q

muscarinic effects of AChE inhibitors

A

ACh binds (throughout entire body)
parasympathetic response

**need antimuscarinic to block the parasympathetic effects

101
Q

neuromuscular blocker reversal

A

dose based on degree of block
determined by nerve stim response
pt needs spont recovery prior to dosing

102
Q

when to give neuromuscular blocker reversal?

A

sustained head lift
vital capacity
tidal volume

103
Q

neostigmine onset/duration

A

onset: 5-10 min
duration: 1 hr

104
Q

pyridostigmine onset/duration

A

onest: 10-15 min
duration: >2 hr

105
Q

edrophonium onset/duration

A

onest: 1-2 min
duration <1 hr

106
Q

sugammadex

A

selective neuromuscular reversal agent
- only for aminosteroid NDMR
- Roc/Vec

107
Q

Sugammadex FDA indication

A

reversal of neuromuscular blockade in surgery or ICU

108
Q

Sugammadex MOA

A

encapsulates free molecule form of roc

109
Q

sugammadex metabolism

A

no metabolites

110
Q

sugammadex elimination

A

renal

111
Q

sugammadex drug interaction

A

can bind w/endogenous steroids
may need more when magnesium and aminoglycosides are present

112
Q

sugammadex minimum effective dose

A

2 mg/kg

113
Q

sugammadex re-dosing

A

must wait 24 hrs before able to redose w/roc or vec

114
Q

sugammadex adverse effects

A

overall well tolerated
bitter tast
recurrence of block
irregular movement during recovery
Cost $$$

115
Q

antimuscarinic drugs

A

atropine
glycopyrrolate

116
Q

antimuscarinic absorption

A

Cation limits absorption/distribution

117
Q

antimuscarinic metabolism

A

susceptibility to cholinesterase

118
Q

antimuscarinic CV effects

A

normal hemodynamics
reverse bradycardia
block direct acting agonists

119
Q

antimuscarinic reverses

A

parasympathetic effects
stimulates:
bonchodilation
increase HR
decrease GI motility
dry secretions
urinary incontinense

120
Q

antimuscarinic side effects

A

tachycardia
mydriasis
urinary retention
decreased GI motility
eldery (CNS impacts)

121
Q

antimuscarinics are combined w/cholinesterase inhibitors

A

to minimize muscarinis adverse effects associated w/reversal agents

122
Q

antimuscarinic distribution

A

robinul does not cross BBB/placenta
more selective for heart/salivary glands

123
Q

atropine onset/duration

A

onset: faster
duration: shorter

124
Q

glycopyrrolate onset/duration

A

onset: slower
duration: longer

pharmacology (9 decks)

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