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Gen Exam 2 > NMB agents > Flashcards

NMB agents Flashcards

1
Q

Endrophonium (does/doesn’t) cross the blood-brain barrier bc…

A

does NOT
it is a quaternary amine.

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1
Q

Do muscle relaxants provide amnesia?

A

NO

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2
Q

Neuromuscular junction consists of:

A

-Prejunctional: motor nerve ending
-cleft: AChAse
-Postjunctional: Highly folded muscle fiber

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3
Q

what causes a muscle contraction?

A

-ACh binds to nicotinic cholinergic receptor (postsynaptic)

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4
Q

Nerve stimulation

A

-Depolarization reaches nerve terminal
-voltage-gated Ca channels open
-calcium enters the nerve terminal
-Storage quanta Vesicles (presynaptic) release acetylcholine (ACh) into the cleft
-ACh diffuses cleft
-ACh binds to nicotinic cholinergic receptor at postsyn. end plate
-muscle contraction

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5
Q

each quanta contains ____ ACh molecules

A

5,000 to 10,000

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6
Q

⭐️
Which subunits do NMBs work on?

A

the 2 alpha subunits

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7
Q

Only ___ subunits are capable of binding ACh

A

the 2 alpha

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8
Q

If both the alpha subunits are occupied, what happens?

A

conformational change
central channel opens

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9
Q

What ions enter and exit when the 2 alpha subunits are occupied?

A

Na & Ca in
K out

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10
Q

____ occurs, and a muscle contraction happens

A

action potential

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11
Q

Postjunctional receptors have ___ subunits

A

5

2 alpha, 1 beta, 1 delta, and 1 epsilon (ADULT)

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12
Q

How many ACh molecules are needed to open the post jxnl receptor channel?

A

TWO

one or none = closed

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13
Q

causes vesicles of acetylcholine to fuse with the nerve membrane

A

influx of calcium within the terminal

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14
Q

ACh combines with and activates which receptor?

A

nicotinic receptors on motor end plate

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15
Q

release of ___ from intracellular stores stimulates an interaction between __ and ___. This results in a muscle contraction.

A

Ca
myosin
actin

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16
Q

Why do we use muscle relaxants?

A

-Optimize surgical conditions
-Prevent unwanted movement
-Facilitate tracheal intubation **
-Improve mechanical ventilation

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17
Q

The primary purpose of using NMB is to

A

achieve adequate relaxation of the upper airway, vocal cords, and diaphragm to facilitate intubation and surgery

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18
Q

Prolonged opening and increased ion flow (Hyperkalemia) can occur with (up/down) regulation.

A

up

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19
Q

Increased Extrajunctional Receptors
(up regulation or down?)

A

upregulation

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20
Q

Upregulation

A

stimulation of NMJ decreases over days (severe burns, immobilization, infxn, sepsis, prolonged use of NMBAs in ICU, CVAs)

increased immature nAChrs

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21
Q

immature nAChRs will have increased sensitivity to ____ but decreased sensitivity to ___.

A

-increased sensitivity to ACh and SCh (more nACHr’s being depolarized)

-decreased sensitivity to Nondepolarizers (more nACHr’s to block

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22
Q

Chronic neostigmine use will affect jxnl receptors by…

A

downregulating them

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23
Q

Pts w/ myasthenia gravis may experience (up/down) regulation due to chronic neostigmine use.

A

down-regulation

(Neostigmine: cholinesterase inhibitor; increases ACh levels at nerve terminals)

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24
Q

T/F
NMBAs are anesthetics

A

NO

not anesthetics
do not cause amnesia

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25
Q

Which causes awareness?
NMBA
not enough anesthesia

A

not enough anesthesia

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26
Q

T/F
Complete paralysis is required for all surgical cases

A

false

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27
Q

⭐️
Main site of action of NMBA

A

nicotinic cholinergic receptor (nAChRs)
at the endplate, which connects to the muscle

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28
Q

T/F
Neuromuscular Blocking Agents is synonymous with paralytic.

A

True

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29
Q

Most poisonous creature on planet

A

Golden PoisonFrog

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30
Q

T/F
Paralytics exist in nature.

A

True
pufferfish
Golden PoisonFrog

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31
Q

all 4 twitches will be full-strength if…

A

No muscle relaxation

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32
Q

With muscle relaxation….

A

there will be decreased strength

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33
Q

depolarizer or non?

A

depolarizer block

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34
Q

depolarizer or non?

A

non-depolarizer block

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35
Q

Which NMBAs show fade?

A

non-depolarizers

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36
Q

Potency

A

the relationship between twitch depression and dose

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37
Q

median dose that corresponds to 50% twitch reduction (among average population)

A

ED50

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38
Q

ED95

A

corresponds to 95% block (useful relaxation when twitch abolished)

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39
Q

Do we use ED50 or ED95 more when deciding doses for NMBAs?

A

ED95
we want what will get pt adequately paralyzed, full relaxed

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40
Q

Duration of Action
Time of injection to return of ___% twitch height

A

25 or 1 twitch (1 twitch out of 4 twitches)

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41
Q

T/F
Duration of action is dose-dependent

A

True

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42
Q

T/F
Inhalational agents & NMBAs have a synergistic effect.

A

True
IA can prolong NMB duration

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43
Q

Recovery Index

A

Time interval between 25% and 75% twitch height

Speed of recovery

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44
Q

Only depolarizing agent

A

Succinylcholine

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45
Q

Depolarizing a muscle actually ____ it and keeps it in a relaxed state.

A

fatigues

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46
Q

Succinylcholine

A

“Depolarizes” at postsynaptic nAChRs

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47
Q

Nondepolarizing

A

“Competes” for active binding sites on nAChRs

Aminosteroid (Rocuronium, Vecuronium, Pancuronium)

Benzylisoquinolinium (Mivacurium, Atracurium, Cisatracurium)

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48
Q

How does depolarizing NMB work?

A

Depolarizes:

occupies 2 alpha subunits
opens channel
ions in
depolarizes muscles
muscle is fatigued
stays in relaxed state

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49
Q

How does non-depolarizing NMB work?

A

competes for nicotinic sites

binds to 1 alpha subunit
prevents opening
muscle cannot contract

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50
Q

Mimics ACh

A

depolarizing/succinylcholine

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51
Q

Prolonged depolarization of the motor end-plate will….

A

inactivate Na channels

increases influx of K

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52
Q

Can a muscle contract while ACh is bound to the receptor?

A

No
can only contract once it diffuses off receptor

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53
Q

What is the resemblance between ACh and Suxx?

A

Suxx = two ACh molecules

allows Suxx to sit on top of receptor and bind two alpha subunits

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54
Q

When given may cause fasciculations before total paralysis

A

Succinylcholine

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55
Q

⭐️
Succinylcholine dosing (adult)

A

1 -1.5 mg/kg IV

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56
Q

Succinylcholine onset

A

1 min

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57
Q

Succinylcholine duration

A

5-15 mins

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58
Q

T/F
We can achieve paralysis even if one of the alpha subunits is occupied by succinylcholine and the other by ACh.

A

True
Both alpha subunits must be occupied, can be 1 ACh and 1 suxx; or both occupied by suxx

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59
Q

fastest onset, the shortest duration, and greatest reliability (i.e., narrowest onset variability around the mean) of any NMBA

A

Succinylcholine

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60
Q

All NMBAs interact with ____ and block muscle membrane ____, leading to ___ paralysis.

A

α subunits of the nicotinic cholinergic receptors

depolarization

flaccid

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61
Q

reversal of ____ block is limited

A

nondepolarizing

(cholinesterase inhibitors have a ceiling effect)

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62
Q

___% of the IV dose of Suxx is hydrolyzed in the plasma before reaching the myoneural junction.

A

90

plasma cholinesterase eats it up before it gets to the receptor

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63
Q

pseudocholinesterase breaks suxx into…

A

succinylmonocholine and choline

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64
Q

Recovery from suxx occurs when…

A

SCh diffuses away from the NMJ

5-6 mins

SCh = succinylcholine

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65
Q

____% of administered suxx reaches the NMJ

A

10%

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66
Q

Plasmacholinesterase is also called:

A

Butyrylcholinesterase
Pseudocholinesterase

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67
Q

Factors that lower pseudocholinesterase

A

severe liver disease
old
pregnancy
malnutrition
burns
anticholinesterase drugs
Reglan
oral contraceptives

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68
Q

Plasmacholinesterase
Synthesized in the ___ and found in the ___.

A

liver
plasma

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69
Q

Which drug decreases plasma cholinesterase (PChE) activity more?
Edrophonium
neostigmine

A

neostigmine

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70
Q

Abnormal Plasma Cholinesterase testing

A

Dibucaine number

reflects quality of cholinesterase enzyme (ability to hydrolyze SCh) not the quantity that is circulating in plasma

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71
Q

T/F
Dibucaine number reflects quantity of cholinesterase enzyme

A

False
quality (ability to hydrolyze SCh)

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72
Q

Lower dibucaine numbers mean (shorter/longer) duration of drug action.

A

longer

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73
Q

How do anesthesia providers usually determine that their pt has abnormal PChE (plasma cholinesterase)?

A

On the spot. The patient will not recover from paralytic. Twitches not returning when expected.

Will have to recover in ICU

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74
Q

Which type of PChE are we most concerned with?
-homozy. typical
-heterozy. atypical
-homozy. atypical

A

homozygous atypical
both genes are mutated

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75
Q

T/F
Succinylcholine can be given as an infusion.

A

False
Will cause Phase II block

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76
Q

What causes Phase II block?

A

(Suxx)

continued dosing, a phase I block can develop into a phase II block

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77
Q

⭐️
T/F
Succinylcholine is an antagonist, making it a paralytic.

A

False
NMJ nicotinic AGONIST

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78
Q

Succinylcholine prevents (depolarization/repolarization).

A

repolarization

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79
Q

Phase II block

A

(Repeated SCh doses or an IV continuous infusion)

muscles are no longer receptive to acetylcholine released by the motor neurons

“I’m phase 2 faded”

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80
Q

Suxx
CV effects

A

Sinus bradycardia
junctional
arrest (esp peds)

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81
Q

When giving suxx to kids, mix it with ____.

A

atropine

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82
Q

Suxx
if a second dose is given within 5 minutes of first dose, we increase the risk of…

A

cardiac arrest

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83
Q

CV effects of suxx are due to…

A

its action @ cardiac muscarinic cholinergic (M2) receptors
mimics ACh

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84
Q

Preventing myalgias from SChE (suxx)

A

pretreat with non-depolarizer or NSAIDs

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85
Q

SChE myalgias are usually due to _____, and affect ____ muscles.

A

fasciculations
big skeletal muscles

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86
Q

SCh can elevate plasma potassium by ___ mEq/dL in healthy patients.

A

0.5

caution in renal pts (K already high)

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87
Q

Conditions to avoid SChE

A

renal Dz
burns
severe abdominal Infections
severe metabolic acidosis

upregulation of AChR
hemiplegia, paraplegia, muscular dystrophies, Guillian-Barre syndrome

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88
Q

Which paralytic should we avoid in a pt with a recent diagnosis of Guillian-Barre syndrome?

A

SChE (suxx)

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89
Q

Conditions associated with upregulation of extrajunctional AChR

A

hemiplegia
paraplegia
muscular dystrophies
Guillian-Barre syndrome
burns

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90
Q

Succinylcholine risk specific to children

A

massive rhabdomyolysis –> renal failure

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91
Q

Which paralytic is better for children?
succinylcholine
rocuronium

A

rocuronium

suxx risks:
-asystole
-hyperK
-massive rhabdomyolysis –> renal failure

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92
Q

Which paralytic is associated w/ MH?

A

SchE

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93
Q

Primary sign of MH

A

Masseter/jaw spasm

Jaw will lock up
cannot scissor jaw open

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94
Q

Best NMB for full stomach

A

Suxx
Increases intragastric pressure

increases lower esophageal tone (LES) helps prevent vomitus entering airway

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95
Q

NMB to avoid in open eye injury

A

Suxx
increases IOP

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96
Q

SChE (increases/decreases) ICP.

A

increases

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97
Q

Malignant Hyperthermia triggers

A

halogenated agents & succinylcholine

Activates Ryanodine receptor from the sarcoplasmic reticulum

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98
Q

Malignant Hyperthermia

A

-Massive uncontrolled release of Ca++ from the sarcoplasmic reticulum
-activates uncontrolled – constant (hypermetabolic) muscle contraction state

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99
Q

T/F
ACh is more competitive and more easily bound to alpha subunits than non-depolarizing NMB.

A

False
NDNMB are more competitive than ACh
can push ACh off receptors

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100
Q

T/F
Non-depNMB only need to occupy one of the alpa subunits to elicit their paralytic effect.

A

True

2 NDNMB = closed
1 NDNMB + ACh = closed

2 ACh = open

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101
Q

Classes of Non-depolarizing muscle relaxant (NDMR)

A

Aminosteroid
(Rocuronium, Vecuronium, Pancuronium)

Benzylisoquinolinium
(Mivacurium, Atracurium, Cisatracurium)

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102
Q

Know dis
-dose
-onset
-duration

A
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103
Q

Nondepolarizing Muscle Relaxants
MoA

A

Competitively antagonize the presynaptic receptors (one or both alpha subunits) to decrease release of Ach (fade on TO4)

104
Q

Depolarizing NMB are ____.
Non-depolarizaing are ____.
(agonist/antagonist)

A

Depo = agonIst

non-depo = competitive antagonist

(Every home DEPO has a mansplainer, who thinks he’s some AGONIST to women)

105
Q

Almost always given IV

A

NonDepoMB

106
Q

Rocuronium (Zemuron) is ____ acting.

A

intermediate

107
Q

T/F
Rocuronium (Zemuron) is know to cause histamine release.

A

True
rare tho

108
Q

Rocuronium (Zemuron)
CV effects

A

no effect of BP or HR

109
Q

Using Rocuronium with suxx

A

use rocuronium to defasciculate

110
Q

Rocuronium is (high/low) potency.

A

low
takes more molecules for effect

111
Q

Rocuronium
intubating dose

A

0.6 mg/kg

112
Q

Rocuronium
RSI dose

A

1.2 mg/kg

113
Q

Rocuronium
defiscic dose

A

5 mg

114
Q

Rocuronium
maintenance/repeat dosing

A

0.1 mg/kg PRN

115
Q

Rocuronium
onset

A

1-2 mins (dose-dependent)

116
Q

Rocuronium
duration

A

30 min or up to 70 minutes after RSI dose

117
Q

Rocuronium elimination
___% hepatic
___% renal

A

70% liver
30% renal

118
Q

Best NMB for short laparoscopic procedures

A

Rocuronium

119
Q

Has greatest assoc. w/ anaphylaxis than any other drug given in anesthesia

A

Rocuronium

(stats could be inflated b/c we give rocuronium A LOT)

120
Q

T/F
We must be aware of active metabolites with Rocuronium.

A

False
no real metabolites

121
Q

Vecuronium (Norcuron) benefits

A

No histamine release
Cardiac stable

122
Q

Vecuronium (Norcuron) is ___ potency

A

medium

123
Q

Vecuronium (Norcuron) is ____ acting.

A

intermediate

124
Q

Vecuronium (Norcuron) precipitates with ____.

A

thiopental

125
Q

Vecuronium (Norcuron)
induction/intubation dose

A

0.1 mg/kg

126
Q

Vecuronium
Pretreatment/priming with ___% of intubation dose given ___ min before intubation dose.

A

10%

3-5 min

127
Q

Which NMB agent do we see pre-dosing before intubation?

A

Vecuronium
onset of action is longer than rocuronium

128
Q

Vecuronium
recovery

A

25-40 min (25% recovery)

45-60 min(95% recovery)

129
Q

Vecuronium metabolite has ___% potency of parent drug.

A

(3-desacetyl): 60% potency of vecuronium

130
Q

What’s unique about a patient’s response to Vecuronium?

A

same dose will give same, predictable duration of action (on that given day, may change next day)

131
Q

Pancuronium (Pavulon)
initial dose

A

0.1 mg/kg

132
Q

longest acting aminosteroid NMB

A

Pancuronium (Pavulon)

133
Q

Pancuronium (Pavulon)
CV effects

A

Vagolytic effects: modest tachycardia due to M2 antimuscarinic stimulation

Direct sympathomimetic effects: norepine release and reduced uptake of norepinephrine by adrenergic nerves

134
Q

T/F
Histamine release occurs with Pancuronium.

A

False

135
Q

T/F
Pancuronium increases HR and CO.

A

True

136
Q

Used in Cardiac surgery to counteract the bradycardia associated with high-dose opioid dosing

A

Pancuronium

137
Q

Potential for significant postoperative residual blockade

A

Pancuronium

very long acting

138
Q

Pancuronium
Maintenance dose

A

0.02 mg/kg

139
Q

Pancuronium
onset

A

2-5 min

140
Q

Pancuronium
duration

A

60-100 min

141
Q

T/F
Pancuronium is mostly metabolized by the liver

A

False
Hepatic metabolism 20%
Urinary excretion (40-70%)

142
Q

Pancuronium metabolite

A

(3-OH pancuronium): 50% potency

143
Q

NMB best for renal and liver Dz

A

Benzylisoquinolines

144
Q

Potency: relationship between ____ ___ and dose.

A

twitch depression

145
Q

ED50

A

median dose that corresponds to 50% twitch reduction

146
Q

ED95

A

corresponds to 95% block (useful relaxation when twitch abolished)

147
Q

Undergoes Hoffman elimination

A

Benzylisoquinolines

148
Q

Hofmann Elimination

A

Spontaneous, non-enzymatic, non-organ dependent chemical breakdown at physiologic temperature and pH

149
Q

____ increases Hofmann Elimination.

A

Increased Temp = increased Hoff Elim

150
Q

Beware of histamine release, esp if giving quickly

A

Mivacurium (Mivacron)

151
Q

Mivacurium (Mivacron)
recovery

A

rapid

152
Q

Mivacurium (Mivacron)
metabolism

A

Hydrolysis by plasma cholinesterase

153
Q

Atracurium metabolism is by the same enzymes that degrade ___ and ___.

A

esmolol and remifentanil

154
Q

Mivacurium (Mivacron)
onset

A

1 min

“MIV only takes a MIN!”

155
Q

Mivacurium (Mivacron)
duration

A

10-20 min

156
Q

Mivacurium (Mivacron)
intubation dose

A

0.2 mg/kg

157
Q

Mivacurium (Mivacron)
infusion dose

A

5-8 mcg/kg/min infusion

158
Q

Atracurium (Tracrium) is ____ acting.

A

intermed

159
Q

Atracurium (Tracrium)
metab

A

Hofmann Elimination 30% and ester hydrolysis 60%

160
Q

Laudanosine

A

Primary metabolite of Atracurium

-seizure activity
-tertiary amine
-CNS stimulant

161
Q

Atracurium (Tracrium)
dose

A

0.5 mg/kg

162
Q

Atracurium (Tracrium)
histamine release?

A

some
potential for skin flushing, tachycardia and hypotension

163
Q

Atracurium (Tracrium)
onset

A

2-3 min

164
Q

Atracurium (Tracrium)
duration

A

20-35 min

165
Q

Atracurium (Tracrium)
recovery

A

60-70 min = 95% recovery

166
Q

Cisatracurium (Nimbex) is __ acting

A

intermed

167
Q

Potent cis-cis isomer of Atracurium

A

Cisatracurium (Nimbex)

168
Q

Cisatracurium (Nimbex)
metabolism

A

30% Hofmann elimination

metabolite breakdown by nonspecific esterase metabolism

169
Q

Cisatracurium (Nimbex)
dose

A

0.15-0.2 mg/kg IV

170
Q

Cisatracurium (Nimbex)
onset

A

2-3 min

peak: 4-7 min

171
Q

Cisatracurium (Nimbex)
peak effect

A

4-7 min

172
Q

Cisatracurium (Nimbex)
duration

A

40-70 min

173
Q

Cisatracurium (Nimbex)
recovery

A

20-35 min
93 min = 90%

174
Q

Why use cistracurium or atracurium instead of rocuronium or vecuronium?

A

ESRD
dialysis

175
Q

drugs that enhance NMBA effects(8)

A

Inhalational agents (direct effect on postjunctional receptors)

Local anesthetics: potentiate both NDMA and depolarizers

Antibiotics (streptomycin/neomycin/aminoglycosides): depress the NMJ

Hypercarbia

Acidosis

Hypothermia

Anticonvulsants (Acute administration)

Magnesium

176
Q

How do volatiles enhance NMBs?

A

direct effect on postjunctional receptors

177
Q

How do L.A.’s enhance NMBs?

A

potentiate both NMDA and depolarizers

**NMDA: N-methyl D-aspartate (like ketamine)

178
Q

How do antibiotics enhance NMBs?

A

depress the NMJ

streptomycin/neomycin/aminoglycosides

179
Q

We would expect (longer/shorter) NMB action in an acidotic patient.

A

longer

hypercarbia & acidosis enhances NMBA effects

180
Q

We would expect (longer/shorter) NMB action in a patient being treated for acute seizures.

A

longer

Anticonvulsants (Acute administration) enhance NMBA

181
Q

We would expect (longer/shorter) NMB action in a parturient patient being treated with magnesium.

A

longer

Mag enhances NMBA effects

182
Q

How would hypothermia affect NMB activity?

A

prolongs
decreasing receptor sensitivity and ACh mobilization

183
Q

T/F
ED95 values are safe for older ppl.

A

False
Decreased total body water and serum albumin… reduced volume of distribution

184
Q

old ppl require (higher/lower) NMB doses

A

lower

185
Q

How would hypoK affect NMB activity?

A

prolongs

potentiates NMBA

can decrease the effectiveness of anticholinesterases on reversal

186
Q

How would hypermag affect NMB activity?

A

prolongs duration
by inhibiting calcium channels

187
Q

Acidosis prolongs NMB effects by…

A

interfering with effects of anticholinesterases

188
Q

Hypercarbia prolongs NMB effects by…

A

leads to acidosis

interferes with antagonism

189
Q

used to diagnose myasthenia gravis

A

edrophonium

if weakness resolves after giving it = + diagnosis

190
Q

the enzyme responsible for rapid hydrolysis of released ACh

A

AChASe
acetylcholinesterase

191
Q

AChASe can catalyze ACh at ___ molecules per active site per second

A

4,000

note: a quanta is ~5,000-10,000 ACh molecules

192
Q

__% of released ACh is hydrolyzed during its diffusion across the synaptic cleft before reaching the nicotinic receptor

A

50%

193
Q

Anticholinesterase/Acetylcholinesterase Inhibitors

A

Neostigmine
Edrophonium
Pyridostigmine

194
Q

Selective Relaxant Binding Agent

A

Sugammadex

195
Q

Mechanisms to reverse NMBA (5)

A

-Diffuse away
-Metabolized
-Excreted
-Encapsulated (sugammadex)
-Reversed with an Anticholinesterase

196
Q

Acetylcholinesterase Inhibiting Agents/Anticholinesterase
MoA

A

-Block ACh breakdown by AChAse

-increase ACh [ ] in cleft

-more ACh to compete with remaining NMBA

-Causes normal muscle contraction

197
Q

Anticholinesterases have (PNS/SNS) effects due to….

A

PNS

stimulate muscarinic Ach receptors in the heart, lungs, and GI tract

198
Q

Anticholinesterase
PNS side effects

A

Bronchoconstriction
increased salivation
increased bowel motility

199
Q

Acetylcholinesterase Inhibiting Agents are usually given with ___.

A

an Anticholinergic (Antimuscarinic)

glycopyrrolate
atropine

200
Q

T/F
Acetylcholinesterase Inhibiting Agents have no ceiling effect.

A

False
they do

Maximal inhibition: when 100% of acetylcholinesterase has been inhibited

201
Q

Acetylcholinesterase Inhibiting Agents
maximal inhibition:

A

-more doses will not improve recovery
-risk paradoxical muscle weakness

-weakness: desensitization of Ach receptors –> transmission failure –> depolarization block

202
Q

Why do we see paradoxical muscle weakness at max Anticholinesterase effect?

A

desensitization of Ach receptors –> transmission failure –> depolarization block

203
Q

Neostigmine (Prostigmin)

A

Inhibits hydrolysis of ACh by AChAsE

Blocks AChAse at all cholinergic synapses –> PNS (bradycardia, GI effects)

204
Q

Neostig is a ____ amine.

A

QUAT amine (does not cross BBB)

205
Q

glycopyrrolate decreases _____ side effects of Neostigmine

A

muscarinic

206
Q

T/F
Neostig reduces risk of PONV

A

False
may increase

207
Q

When to Reverse with Neostigmine

A

moderate & deep block

only if spontaneous NMB recovery (4 tactile TOF counts are visible at the adductor pollicis)

208
Q

T/F
Neostig is fast acting.

A

False
slow

209
Q

Neostigmine
dose

A

0.04-0.08 mg/kg (max 5mg)

210
Q

Glyco + Neostig

A

For every 1 mg of Neostigmine mix with 0.2 mg Glyco (sometimes less)

mix or give separately

211
Q

Neostigmine
onset

A

15 mins
depends on twitches

212
Q

Neostigmine
duration

A

1-2 Hours

213
Q

Neostigmine
metab & excretion

A

Hepatic metabolism

urinary excretion

214
Q

What happens if we don’t give atropine with edrophonium?

A

bradycardia!

215
Q

T/F
atropine crosses the BBB

A

True

216
Q

Sugammadex (Bridion)
mechanism

A

Eight sugars arranged in a ring specifically designed to ENCAPSULATE

217
Q

Sugammadex is a modified γ-
______.

A

cyclodextrin

218
Q

Sugammadex
solubility

A

-highly water soluble

-hydrophobic cavity: encapsulate steroidal NMBAs, especially rocuronium > vecuronium

219
Q

T/F
Sugammadex has no effect on Acetylcholinesterase or cholinergic receptors.

A

True

220
Q

T/F
Sugammadex efficacy depends on depth of the NM blockade.

A

False
Independent of depth of neuromuscular blockade

221
Q

Sugammadex vs. other reversal agents

A

No real undesirable effects like anticholinesterases

222
Q

T/F
Sugammadex is an anticholinesterase.

A

False
modifiedγ-cyclodextrin

223
Q

Sugammadex dosing

A

Immediate reversal: 16 mg/kg
routine (deep block): 4 mg/kg
routine (moderate): 2 mg/kg

224
Q

Sugammadex has no interaction with which medications?

A

succinylcholine & benzylisoquinolines

225
Q

Sugammadex immediate reversal dosing (16 mg/kg) may cause:

A

-bradycardia (cardiac arrest)
-headache
-hypoTN
-N/V
-anaphylaxis
-hypersensitivity (pruritus and urticaria)

226
Q

Using ____ may inactive birth control.

A

Sugammadex
must tell pt to use alt. contraception for 1 week

227
Q

___ mg of Sugammedex is needed to encapsulate 1 mg of rocuronium.

A

4

228
Q

T/F
Sugammadex works well for renal Dz pts.

A

False
not recommended

229
Q

Sugammadex is incompatible with….

A

verapamil
ondansetron
ranitidine

230
Q

We must wait ____ before giving Roc/Vec if Sugammadex was used for NMB reversal.

A

24 H
Suga is still removing aminosteroids

231
Q

What NMBA should we use if we need to reparalyze after using Sugammadex?
Ie: emergent return to OR <24 H postop

A

nonsteroidal
Suxx

232
Q

T/F
High dose Sugammadex decreases aPTT, PT, and INR.

A

False
increases

233
Q

Sugammadex anaphylaxis

A

Airway edema
bronchospasm
CV collapse

esp higher doses

Within 5 minutes of administration

234
Q

Sugammadex anaphylaxis treatment

A

-titrated to response: small boluses of epinephrine (10-20 mcg)

-Benadryl
-dexamethasone
-famotidine

235
Q

T/F
Physostigmine crosses the BBB.

A

True
tertiary amine

236
Q

T/F
Quaternary amines cross the BBB.

A

False
tertiary amines cross the BBB

“Trespassing tertiaries”

they are “quarentined” out!

237
Q

only anticholinesterase that crosses the blood brain barrier

A

Physostigmine
tertiary amine

238
Q

Organophosphate poisoning
What do we give?

A

Atropine first
Then Physostigmine (must be given w/in timeframe or else toxic changes in brain will kill pt)

239
Q

T/F
Physostigmine is used for reversal of muscle relaxants

A

False
Not used for reversal of muscle relaxants

240
Q

Physostigmine use

A

treat anticholinergic toxicity

241
Q

anticholinergic toxicity
S/S

A

-flushing
-dry skin
-mucous membranes
-mydriasis + loss of accomdtn
-AMS
-fever
-urinary retention

“cant see, cant pee, cant spit, cant shit”

242
Q

anticholinergic toxicity
CNS effects

A

restless, shivers, agitation, disoriented

243
Q

(anticholinergic toxicity)
Types of anticholinergics

A

-atropine
-scopolamine
-antihistamines
-antipsychotics
-cyclic antidepressants

244
Q

Cholinergic Crisis/Syndrome

A

-Excessive use/overdose of cholinesterase inhibitors or organic pesticides

245
Q

Cholinergic Crisis/Syndrome
mechanism

A

Excessive ACh peripherally and centrally

246
Q

Cholinergic Crisis/Syndrome
S/S

A

miosis, salivation, bronchoconstriction, bradycardia, abdominal cramping, weakness, lacrimation,

dysphoria, confusion, seizures, coma

247
Q

Cholinergic Crisis/Syndrome
Treatment

A

Atropine 35-70 mcg/kg

Pralidoxime 15 mcg/kg Q20 min

Benzos

248
Q

Cholinergic Crisis
Muscarinic & Nicotinic Sx

A
249
Q

Cholinergic vs Myasthenic Crisis
(definition)

A

Cholinergic crisis: excess activity of Ach

Myasthenia Gravis: decrease in Ach activity d/t auto-reactive antibodies attacking nicotinic Ach receptors on postsynaptic membranes

249
Q

How do your differentiate Cholinergic vs Myasthenic Crisis?

A

Give edrophonium

muscle strength improves = MG

no improvement/worse = Cholinergic crisis

250
Q

Cholinergic vs Myasthenic Crisis
S/S

A

**Tensilon = edrophonium

251
Q

T/F
Every pt that gets a NMBA should get a reversal agent.

A

True

252
Q

Clinical Signs of Muscle Weakness

A

-Blurry/double vision
-Face weak/numb
-general weakness

PACU:
-Gen. weakness
-reported difficulty completing 5-second eye opening
-Difficult visually tracking/ speaking

253
Q

Residual neuromuscular blockade

A

-reintubation
-Impaired oxygenation and ventilation (may be blamed on Opioids)
-Impaired pulmonary fxn
-risk of aspiration & pneumonia
-Pharyngeal dysfunction
-Delayed PACU discharge

254
Q

Signs of Neuromuscular Recovery

A

-Tidal volume
-Negative inspiratory force
-Grip strength
-5-second head lift (not a sensitive test for residual block)
-Ability to protrude the tongue

255
Q

T/F
5-second head lift is a sensitive test for residual block.

A

False
it is not

256
Q

Are these reliable signs of return of muscle strength

A

NO

Gen Exam 2 (7 decks)

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