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SRNAPharmacology II > NMB- COMPLETED > Flashcards

NMB- COMPLETED Flashcards

1
Q

Depolarizing neuromuscular blocking drugs

A

Mimics acetylcholine; Competitive agonists, and generating action potentials

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2
Q

Non-depolarizing neuromuscular blocking drugs

A

Interferes with actions of acetylcholine

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3
Q

2 types on Non-depolarizing MB

A

Benzylisoquinolinium compounds

Aminosteroid compounds

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4
Q

The Main neurotransmitter is

A

Acetylcholine

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5
Q

Anticholinergic agent only work at

A

MUSCARINIC receptors

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6
Q

ACh in high concentration acts as an

A

inhibitor to vesicle release

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7
Q

Agonist will ______muscle contraction while antagonists _______muscle contraction

A

activate muscle contraction

Antagonist will prevent muscle contraction (NDNMB)

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8
Q

Patient who suffer from stroke have extra

A

EXTRAjunctional receptors

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9
Q

Nicotinic receptor at motor end plate

A

acetylchonisterase (true) metabolize ACW

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10
Q

Before succinylcholine starts working

A

you see fasciculations, Cell can’t repolarize, no new depolarization

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11
Q

Acetylcholine can’t break down

A

Succinylcholine (PSEUDOCHOLINESTERASE in plasma)

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12
Q

ACH has how many subunits

A

5

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13
Q

Ach must occupy both ______ for a conformotional change to occur

A

Alpha subunit , capable of binding Ach

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14
Q

Depolarizing Agents

A

Mimic the action of Ach but remain attached longer than ACh

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15
Q

Competitive Agents

A

Benzylisoquinoliniums

Aminosteroids

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16
Q

90% suppression of a single twitch response

A

is considered evidence of adequate drug-induced skeletal muscle relaxation

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17
Q

Laryngeal spasms associated with

A

can be treated with doses of 0.1mg/kg of succinylcholine

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18
Q

Used to measure the speed of onset and duration of NM blockade

A

• Adductor pollicis, orbicularis oculi

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19
Q

What TOF IS CONSIDERED evidence of return?

A

Traditionally TOF >0.7 has been considered evidence of return of adequate skeletal muscle strength to allow spontaneous
ventilationon

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20
Q

• Pharyngeal dysfunction and risk of aspiration exist when TOF

A

<0.9

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21
Q

Benzylisoquinoliniums NMB are

A

Cisatracurium

Atracurium

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22
Q

Aminosteroids NMB are

A

Rocuronium

Vecuronium

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23
Q

Reversal agent for aminosteroids ONLY is

A

SUGAMMADEX

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24
Q

At the neuromuscular Junction, the receptor is Nicotinic or muscarinic

A

Nicotinic

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25
Q

ACh binds to nicotinic or muscarinic

A

Nicotinic (only one at NMJ anyway)

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26
Q

Nicotinic are

A

Sodium channels and some voltage gated channels

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27
Q

ACh binds to ACh receptors —>

A

action potential of fibers and muscle movement occur

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28
Q

Presynaptic receptor are located on the

A

A-alpha motor neuron

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29
Q

Postsynaptic receptor are located on the

A

Skeletal muscle

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30
Q

After succinylcholine binds to the 2 alpha subunits, conformational change of channel allow channel to open what cations flows in and out?

A

Sodium and calcium flow in
Potassium flow OUT
Generating an end plate potential

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31
Q

Nicotinic receptors are

A

ion channels

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32
Q

When there is a voltage change Na channels

A

open and then the resultant action potential travels through muscle then open sodium channels and release CA from the SR –> The calcium allows actin and myosin to interact leading to muscle contraction

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33
Q

What is Ach broken down by ? located where ?

A

Acetylcholinesterase , at the motor end plate, adjacent to the receptor

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34
Q

ACh is broken down into

A

Acetyl and choline

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35
Q

What happens after ACh is broken down?

A

ion channels eventually close, allowing the end plate to repolarize. Calcium then return to the SR allowing the muscle to relax.

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36
Q

Succinylcholine is different in agonist of Ach receptors because

A

it remains attached longer , prolongs the depolarization state and the CELL CANNOT REPOLARIZE (cell cannot start over the cascade require to be repolarized)

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37
Q

What dose of the ED95 is required to facilitate the Endotracheal intubation ?

A

2 times ED95

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38
Q

What is considered evidence of adequate drug-induced skeletal muscle relaxation?

A

90% suppression of a single twitch response

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39
Q

Does NMB have any CNS depressant or analgesic properties?

A

NO

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40
Q

What can laryngeal spasms be treated with

A

0.1mg/kg of Succinylcholine

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41
Q

What does the nerve stimulators do?

A

Measure the speed of onset and duration of NMB

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42
Q

2 major muscles use to measure

A

Adductor pollicis

Orbicularis Oculi

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43
Q

What is evidence of return of ADEQUATE skeletal muscle strength to allow SPONTANEOUS VENTILATION

A

TOF > 0.7

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44
Q

What is the patient at risk for when TOF ratio is <0.9?

A

Pharyngeal dysfunction

Risk of aspiration

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45
Q

TOF assessment: TOF 0/4 means ______blockade, receptor occupancy is ____%.

A

Intense ; > or equal to 95%

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46
Q

TOF assessment: TOF 1/4 means ______blockade, receptor occupancy is ____%.

A

Moderate/ surgical block; 90%

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47
Q

TOF assessment: TOF 2/4 means ______blockade, receptor occupancy is ____%.

A

Moderate/surgical block; 85%

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48
Q

TOF assessment: TOF 3/4 means ______blockade, receptor occupancy is ____%.

A

Recovery; 80%

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49
Q

TOF assessment: TOF 4/4 means ______blockade, receptor occupancy is ____%.

A

Recovery; 75%

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50
Q

Faster to block : large muscle ________than fast moving muscles

A

HARDER

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51
Q

From most difficult to easier to block DAOL

A

Diaphram
Adductor Policis (open-slow)
Orbicularis Oculi
Laryngeal muscles (Thyroarythenoid muscles close gottis fast)

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52
Q

VA and NMB what effect do they have on NMB

A

Potentiate action of NMB

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53
Q

What is the charge of quarternary ammonium?

A

They are permanently charged

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54
Q

What is water soluble and HIGHLY IONIZED at physiologic pH?

A

Quaternary ammonium

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55
Q

Quaternary ammonium does not penetrate?

A

BBB, GI tract, placenta and undergo small tubular reabsorption

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56
Q

NMB will NOT affect VA but will VA affect NMB ?

A

Yes

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57
Q

Does NMB affect VA

A

No

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58
Q

What terminates the action of NMB

A

Redistribution

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59
Q

Factors affecting clearance, VD and half time

A

Age, volatile anesthetics, Hepatic or renal disease.

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60
Q

Are NMB highly bound to proteins

A

NO

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61
Q

Rate of disapperance of NMB from blood is rapid why?

A

due to distribution to tissue

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62
Q

What is potency when defining NMB?

A

The effective dose necessary to depress a single twitch depression 95%.

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63
Q

What is Duration of action when defining NMB?

A

Time from injection to onset of maximal single twitch depression

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64
Q

What is Recovery of index when defining NMB?

A

Time from 25% return of single twitch height to 75% return of single twitch height.

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65
Q

What is Clinical duration when defining NMB?

A

Time from injection to recovery of the TOF ratio to >0.7 or >0.9

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66
Q

What is the MOA mechanism of action Succinylcholine?

A

Mimics Ach and binds Ach receptor generating a muscle action potential

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67
Q

Depolarizing NMB are not metabolized by acetylcholinestrase so there is ?

A

prolonged depolarization of the motor end plate

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68
Q

Depolarizing NMB acts as AGONIST or ANTAGONIST?

A

AGONIST

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69
Q

The only DEPOLARIZING agent in clinical use is?

A

Succinylcholine

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70
Q

Low dose of succinylcholine is

A

0.5 - 1 mg/kg IV

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71
Q

Onset of low dose of Succinylcholine

A

30-60 seconds

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72
Q

What are the effects seen with PHASE I BLOCKADE? Return to function ____

A

Extensive Fasciculations (return to function in 5 mins)

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73
Q

What are the effects seen with PHASE II BLOCKADE? renal to function ____

A

NO FASCICULATIONS; 10-15 minutes

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74
Q

High dose of Succinylcholine is

A

2-4 mg/kg

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75
Q

High doses goes right to phase ____blockade

A

II

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76
Q

Less postop myalgia is associated with

A

High dose and phase II blockade

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77
Q

Metabolism of Succ is ____Compared to Ach

A

Low

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78
Q

Succinylcholine on ion channel effect

A

keep them open longer(depolarization )

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79
Q

NMB occurs because a ______post junctional junction cannot respond to subsequent release of Ach

A

Depolarized

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80
Q

Depolarizing muscular relaxant aka

A

PHASE I blockade (prolonged depolarization)

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81
Q

Explain the Phase I Block?

A

After initial excitation , sodium channel close on the cytosolic side but outer door remains open
membrane return to its RESTING STATE –> resulting in muscle relaxation and a phase I block

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82
Q

Absence of Post tetanic stimulation

A

Phase I Block

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83
Q

NO Fade with this type of Block

A

Phase I block

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84
Q

With Phase I block what happens to the Block when an Anticholinesterase Inhibitors are given?

A

Augmentation of block

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85
Q

TOF ratio > 0.7 in Phase I block

A

Can’t see fade

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86
Q

Decrease contraction with a single twitch stimulation? which Phase?

A

Phase I Block

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87
Q

Decrease in AMPLITUDE but sustained response to continuous stimulation? which Phase?

A

Phase I Block

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88
Q

The onset of Phase I block is accompanied by what?

A

Presence of Fasciculations

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89
Q

Pre and postsynaptic binding with this block?

A

Phase II Block

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90
Q

Phase II block main action is

A

Inhibits release of Ach vacuoles

Inhibits Ach receptor

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91
Q

Phase II block resemble

A

Response of nerve stimulator that is considered to be characteristic of non-depolarizing NMB

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92
Q

Succ induced phase II Block occurs with (CHR)

A

Higher doses 2-4 mg/kg
Repeated doses
Continuous infusions

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93
Q

Phase II Block occurs

A

Rapidly

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94
Q

Varying degree of phase I and II may be present how do you know PHASE I is predominant?

A

Given a reversal agent such as ANTICHOLINESTERASE will INTENSIFY THE BLOCK

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95
Q

So which agent do you given and how do you determine the block present?

A

Small dose of Anticholinesterase (Edrophonium 0.1-0.2 mg/kg ). If the small dose antagonizes the block, subsequent higher doses will further antagonize the effects/.

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96
Q

The onset of PHASE II Block is manifested initially as _______. What may be needed______

A

Tachyphylaxis ; increased dose

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97
Q

T/F majority of Succ metabolized before reaching NMJ

A

True

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98
Q

The brief duration of action of succ is due to

A

Hydrolysis by PLASMA CHOLINESTERASE (pseudocholinesterase)

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99
Q

Where is plasma cholinesterase metabolized?

A

in the liver

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100
Q

Pseudocholinesterase efficiency?

A

has enormous ability to hydrolyze Sch at a rapid rate , so only a small fraction reach the NMJ

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101
Q

Because plasma cholinesterase are not present at high concentration at the NMJ, what is the metabolism of SCH dependent on?

A

Diffusion away from the NMJ

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102
Q

What can decrease plasma cholinesterase activity?

A

Decrease hepatic production–> prolong effect

Atypical cholinesterase –> slower metabolism

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103
Q

2 ethnicities with decrease plasma cholinesterase activity?

A

Persian Jewish

Alaska natives

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104
Q

Neogstimine on plasma cholinesterase activity

A

Profound effect on plasma cholinesterase activity (30 mns after administration, activity still reduced by 50%)

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105
Q

Decrease plasma cholinesterase activity by 40% but not prolong block

A

High estrogen levels.

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106
Q

Myasthenia gravis on plasma cholinesterase

A

Decrease plasma cholinesterase and prolong block

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107
Q

What test is done to diagnose genetic disease Atypical plasma cholinesterase?

A

Dibucaine

108
Q

Atypical plasma cholinesterase usually diagnosed how>

A

when a patient experience prolonged block after admin of Succ.

109
Q

_______gene is responsible for Atypical PC

A

single gene

110
Q

A normal dibucaine test number is

A

80

111
Q

Dibucaine is a

A

LA

112
Q

Dubicaine usuallly inhibits ____% of plasma cholinesterase activity compared to _________% in the atypical enzyme

A

80%; 20%

113
Q

Dubicaine homozygous number is

A

20

114
Q

What is the significance of homozygous number 20 in dubicaine test? How many abnormal gene?

A

EXTREME: Very long blockade 6-8 hours due to presence of 2 abnormal genes

115
Q

Dubicaine heterozygous number is

A

40-60

116
Q

What is the significance of heterozygous number 40-60 in dubicaine test?How many abnormal gene?

A

Slighly prolonged block 20-30 mns

1 abnormal gene

117
Q

Resistant to Succ means

A

Increase plasma cholinesterase activity

118
Q

How does myasthenia gravis dose of succ different?

A

required 2.6 times the ED95 because of the DESTRUCTION OF ACH receptor

119
Q

Adverse effects of Succinylcholine CHIMMMS

A 
Cardiac arrhythmias
Hyperkalemia
Increased IOP, IGastricP, ICP
Malignant Hyperthermia
Myalgia
Myoglobinuria
Susttained skeletal muscle contractions
120
Q

What attenuates the or PREVENT the occurance of cardiac arrhythmias, myalgia, increase Intragastric pressure and increase ICP

A

Administration of a NON-PARALYZING dose of a NON-DEPOLARIZING NMB drug

121
Q

Doest the administration of a nondepolarizing NMB drug influence the magnitude of POTASSIUM RELEASE EVOKED?

A

NO

122
Q

Cardiac Dysrhythmias associated with Succ

A

Sinus brady, junctional, ‘sinus arrest (action of muscarinic cholinergic receptor)

123
Q

Risk of cardiac dysrhythmias increased with

A

2nd dose is given 5 minutes after initial dose.

124
Q

Atropine dose of _______ Does NOT PREVENT BRADYCARDIA to response of 2nd dose of Succ

A

<6mcg/kg

125
Q

Succinylcholine contraindicated in

A

Muscular dystrophy

126
Q

Denervation injury effect on nicotinic receptors?

A

INCREASED

127
Q

Denervation injury leading to skeletal muscle atrophy

A

MS and GBS, spinal cord and CVA (UMN lesions)

128
Q

MS , GBS, spinal cord injury and CVA and SUCC may cause

A

HYPERKALEMIC ARREST due to UPREGULATION of receptors and INCREASED POTASSIUM RELEASE

129
Q

Myalgia occurs with Phase ____ and may be perceived as ________

A

I; sore throat

130
Q

Myalgia prevented by going straight to ______block with a _____dose

A

Larger dose of succ , goes straight to PHASE II block,

131
Q

What dose myoglobinuria relfects?

A

Muscle damage damage due to fasciculations

132
Q

Intragastric pressure prevented by ________ and increase IGP increase risk of

A

Administering small dose of NDNMB ; aspiration

133
Q

Avoid Sch in patients with this eye injury although not proven______because SUCC increases ____

A

Open eye injury; IOP

134
Q

Succ and intracranial tumors safe?

A

yes , although succ increases ICP no contraindications

135
Q

Sustained skeletal muscle contraction represented by

A

MASSETER rigidity (may be hard to differentiate from MH)

136
Q

2 conditions associated with increased skeletal muscle contraction

A

Myotonia congenita and dystrophica

137
Q

Strong inductor of Malignant Hyperthermia

A

Succinylcholine

138
Q

Decision of what agent to use is determined by

A 
DDRMCC
Difference in onset
Difference in duration
Rate of recovery
Metabolism
Clearance
Cost
139
Q

Clinical classification of NDNMB

A

Short, intermediate, and long acting.

140
Q

Classification based on their molecular structures (2)

A

Benzylisoquinolinium

Aminosteroids

141
Q

Drugs similar to curare

A

Benzylisoquinolinium

142
Q

Benzylisoquinolinium identified with ______in the word

A

-acurium

143
Q

Aminosteroids has ______in the word

A

Curonium

144
Q

2 intermediate acting aminosteroids

A

Vecuronium

Rocuronium

145
Q

Non-depolarizing (ND) NMB MOA acts as

A

COMPETITIVE ANTAGONIST at the alpha subunits of the PJ nicotinic receptors

146
Q

Do NDNMB have prejunctional nicotinic receptor site? significant

A

yes; not significant

147
Q

When does NEUROMUSCULAR BLOCKADE occur?

A

When 80-90% of the RECEPTORS ARE BLOCKED

148
Q

Decreased twitch response to a single stimulus?

A

NDNMB

149
Q

FADE with continuous stimulation with NDNMB or DNMB

A

NDNMB

150
Q

Antagonism of NDNMB

A

by anticholinesterase agents

151
Q

Do NDNMB cause fasciculations?

A

NO

152
Q

Does NDNMB active MH??

A

No

153
Q

NDNMB characteristics

A

Fade (unstained response) to continous stimulation , TOF ratio <0.7

154
Q

Benzylisoquinolinium cause drug induced________

A

Release of histamine and vasoactive substances

155
Q

Narrow autonomic MARGIN of safety

A

PANCURONIUM

156
Q

Critical care myopathy occurs when drug given for _____occur more with the ______NDNMB agenst

A

> 6 days; Aminosteroids

157
Q

What INCREASE THE incidence of critical care myopathy of NDNMB?

A

Administration of GLUCOCORTICOIDS prior to the administration of NMB

158
Q

Drugs that enhance NMB Agents? VAL CDM LGC

A 
Volatile
Antibiotics -Aminoglycosides
Local anesthetics
Cardiac dysrhythmic drugs Quinidine, Lidocaine
Diuretics
Magnesium
Lithium
Ganglionic Blockers
Cyclosporins
159
Q

Dose dependent increase in NMB effects with those agents?

A

DIES (Des, Iso, En, Sevo)

160
Q

Least effect on increase in NMB with that agents

A

Nitrous

161
Q

Enhanced effect of NMB with this Antibiotics?

A

Aminoglycosides (may decrease release of Ach)

162
Q

Antibiotics with NO EFFECT on NMB

A

PCN and cephalosporins

163
Q

Small LA doses and NMB

A

Small doses enhance NMB produced by NDNMB

164
Q

Large doses of LA on NMB

A

Block NEURAL transmission

165
Q

ESTER local anesthetics compete with

A

Succ for plasma anticholinesterase

166
Q

How does Lidocaine and quinidine augment preexisting block?

A

via Na channel inhibition

167
Q

Diurectics dose that enhance NMB?

A

Furosemide 1mg/kg

168
Q

Does MANNITOL affect the degree of NMB by NMB agents

A

NO

169
Q

Chronic hypokalemia ______Dose requirements for pancuronium but __________ the dose of ________ needed to antagonize the block

A

Decrease; Increases ; NEOGSTIMINE

170
Q

How does mag affect NMB

A

Enhances NMB produced by NDNMB ( more with VEC) due to prejunctional release

171
Q

Patients clinically treated with Phenytoin are

A

resistant to the effects of NMB due to upregulations of receptors ; need HIGHER doses

172
Q

ABT; May prolong duration o f block of NDNMB

A

Cyclosporine

173
Q

Decrease the onset of action (Faster)of NMB ND

A

Hypotension Ephedrine(shunts blood to skeletal muscle)

174
Q

NDNMB Esmolol decreases CO meaning ____

A

DELAYS ONSET

175
Q

Hypothermia and NDNMB, 2 drugs

A

hypothermia prolongs the duration of NMB of pancuronium and vecuronium

176
Q

Hypothermia on atracurium?

A

Prolong effects of atracurium and decrease the continuous dose necesarry to maintain the block

177
Q

Hypokalemia and succinylcholine

A

Resistance to Succ, increase sensitivity to NDNMB

178
Q

Hypokalemia -_________ the transmembrane potential causing __________ of cell membrane

A

Increases, Hyperpolarization

179
Q

Hyperkalemia _________The transmembrane potential partially ______cell membrane

A

decreases, POLARIZING,

180
Q

Hyperkalemia and succinylcholine

A

INCREASE sensitivity to succ,

RESISTANCE TO to NDNMB

181
Q

Burns and NDNMB

A

Resistance to NDNMB

182
Q

Monitoring NM blockade with a nerve stimulator on the side effected by CVA reveals a

A

Decreased sensitivity to NMB drugs (up-regulation of nicotinic receptors)

183
Q

Monitoring NM blockade with a nerve stimulator on the CVA patient

A

may underestimate the degree NMB present at the muscles of ventilation

184
Q

Drugs class LESS LIKELY and LESS CROSS REACTIVE

A

Drugs with a SINGLE Quaternary ammonium

Roc, Pan, Vec

185
Q

Enhance effects of NDNMB______Therefore always check ____ prior to givin ND

A

Sch ; TOF

186
Q

MEN vs WOMEN which is more sensitive to NMB

A

WOMEN more sensitive (men have more skeletal mass)

187
Q

Does NDNMB agents metabolized by either acetylcholinesterase or pseudocholinesterases?

A

No

188
Q

ED 95 dose of Pancuronium

A

70mcg/kg

189
Q

Dose of ______provide adequate relaxation for intubation for 3 minutes

A

0.08 to 0.12 mg/kg

190
Q

Onset of pancuronium

A

3-5 minutes

191
Q

Long acting AMINOSTEROID

A

Pancuronium

192
Q

Duration of action of Pancuronium

A

60-90 mns

193
Q

Enhances pancuronium induce blockade

A

Respiratory acidosis

also OPPOSES ANTAGONISM with neogstimine

194
Q

Avoid in RENAL FAILURE (aminosteroid)

A

PANCURONIUM (decrease clearance)

195
Q

Need higher initial dose to have same effect of pancuronium in those patients? what about the effect?

A

Hepatic patients : effect may last longer

196
Q

Aminosteroid with modest increase in HR MAP and CO

A

Pancuronium (vagal effect

197
Q

Pancuronium and digitalis

A

Increase risk dysrhythmias

198
Q

With this drug the increase in HR may offset opiods induce bradycardia

A

Pancuronium

199
Q

Intermediate acting NDNMBS are

A

ACVR

Atracurium, Cisatracurium, Rocuronium, Vecuronium

200
Q

What makes intermediate NDNMBs different?

A

Efficience Clearance that minimize the likelihood of cumulative effects of continuous infusion

201
Q

1/3 the duration of Long acting NDNMBs

A

Intermediate acting; 20-35 mins

202
Q

Characteristics of intermediate acting NDNMBs

A

Absent cumulative effects and cardiac effets.

203
Q

Characteristics of intermediate acting NDNMBs as far as REVERSAL? time frame?

A

Reliably blocked by anticholinesterase drugs often within 20 mins

204
Q

A benzylisoquinolinium which is a mixture of 10 isomers

A

Atracurium

205
Q

Atracurium ED95 dose is

A

0.2mg/kg

206
Q

Intubation dose of Atracurium is

A

0.5 mg/kg

207
Q

Atracurium onset of action

A

3-5 minutes

208
Q

Duration of action of Atracurium

A

20-35 mins

209
Q

Maintenance dose of Atracurium

A

0.1mg/kg

210
Q

Metabolism of Atracurium

A

1/3 Undergoes HOFFMAN elimination (spontaneous degradation at physiologic temp and pH)

211
Q

Safety net drug for patient with IMPAIRED RENAL and HEPATIC (Benzoisoquinolinium)

A

ATRACURIUM

212
Q

Other metabolism mechanism of Atracurium

A

Hydrolysis 2/3

213
Q

T/ F both metabolism routes of Atracurium are independent of hepatic or renal ?

A

True

214
Q

Does Atracurium have a metabolites if yes what is it?

A

LAUDANOSINE (may lead to CNS stimulation, increase MAC and VA

215
Q

Side effects of ATRACURIUM

A

Hypotension and tachycardia (fall SVR , increase in CI)

216
Q

Atracurium: histamine release

A

NO

217
Q

Should be AVOIDED In ASTHMATICS (THINK AAA)

A

ATRACURIUM (ATRACURIUM AVOIDED ASTHMATICS)

218
Q

Should not be mixed with Barbiturates, or alkaline pH

A

ATRACURIUM

219
Q

Monoquarternary aminosteroids NDNMB

A

Vecuronium

220
Q

Intubating dose of Vecuronium

A

0.08 - 0.12 mg/kg

221
Q

ED95 dose of Vecuronium

A

50mcg/kg

222
Q

Packaged as a powder and unstable in solution

A

VECURONIUM

223
Q

Vecuronium Onset of action

A

3-5 minutes

224
Q

Duration of action

A

20-30 minutes

225
Q

More lipid soluble due to

A

monoquartery structure

226
Q

_______undergoes both Renal and hepatic excretion

A

Vecuronium

227
Q

Elimination prolonged in renal failure with this drug

A

VECURONIUM

228
Q

Slower onset of action of VECURONIUM with those patients

A

Renal failure patients

229
Q

Prolonged duration of action of VECURONIUM

A

Hepatic Cirrhosis

230
Q

Hypoventilation /Hyperventilation which one enhances Neuromuscular blockade

A

Hypoventilation

231
Q

This Aminosteroids has a large Vd

A

Vecuronium

232
Q

Cumulative effects of AMINOSTEROIDS from most to least? PVA

A

Pancuronium > Vecuronium > Atracurium

233
Q

Aminosteroid devoids of Cardiac effects even with RAPID amdinistration

A

Vecuronium

234
Q

Lack VAGOLYTICS and histamine (aminosteroids)

A

Vecuronium

235
Q

What should vecuronium be administered with and why?

A

Incidence of bradycardia (vagotonic effect)

236
Q

Decreased in clearance with elderly patients? and why?

A

VECURONIUM
Decrease hepatic and renal flow
Decrease hepatic enzyme activity

237
Q

Vecuronium in the immediate post partum period duration of action is _________

A

DOA prolonged

238
Q

Duration increase in OBESE patients

A

Vecuronium (lg Vd)

239
Q

Does Atracurium duration increase in obese patient?

A

NO

240
Q

Monoquaternary aminosteroids

A

Rocuronium

241
Q

ED95 dose of Rocuronium

A

0.3mg/kg

242
Q

Onset of action of Rocuronium

A

1-2 minutes

243
Q

Intubatind dose of Rocuronium

A

0.6 - 1 mg/kg

244
Q

The lack of potency of Rocuronium compared to Vecuronium

A

Vecuronium faster onset ( occupy more receptor faster)

245
Q

Potency and onset of action are

A

Inversely proportional?

246
Q

After the administration of ______times the ED95 the onset of Rocuronium resembles the onset of 1mg/kg of Succ

A

3-4 times

1mg/kg of Sch

247
Q

What is the ONLY non-depolarizing NMB that may be used as an alternative to Succinylcholine due to rapid onset?

A

ROCURONIUM

248
Q

Muscle more resistant to the effects of Rocuronium

A

laryngeal muscles more than Adductor POLLICIS

249
Q

large doses of Rocuronium May be delayed at the laryngeal muscles even though the

A

adductor policis appear blocked –> may cause difficult intubation .

250
Q

2 muscles for Rocuronium more resistant to blockade

A

Laryngeal adductor

Diaphram

251
Q

What does not confirm paralysis of the diaphragm and laryngeal muscles with ROC?

A

Complete suppression of single twitch response at ADDUCTOR POLICCIS

252
Q

What can cause paralysis?

A

Initiating laryngocopy at the time of peak laryngeal muscle paralysis

253
Q

ROC Renal and hepatic effects

A

modestly increase DOA

Liver disease longer DOA

254
Q

CV Rocuronium

A

no CV or release of histamine

255
Q

What is consistent with ND aminosteroid NMB agents?

A

NO HISTAMINE RELEASE

256
Q

Useful in opthtalmic procedures associated with vagal stimulation?

A

ROCURONIUM

257
Q

Bisquaternary BENZYLISOQUINOLINIUM

A

Cisatracurium

258
Q

ED95 dose of Cisatracurium

A

50mcg/kg

259
Q

Onset of duration of Cisatracurium

A

3-5 mns

260
Q

Duration of action of Cisatracurium

A

20-35 mins

261
Q

Prolonged Cisatracurium infusions are not associated

A

with prolonged effects

262
Q

Clearance of Cisatracurium

A

Hoffman Elimination

263
Q

Is nonspecific plasma esterase involved in Cisatracurium?

A

NO

264
Q

Nonplasma clearance of Cisatracurium means

A

Can be given to Renal and liver disease

265
Q

Potency Cisatracurium vs Atracurium

A

Cisatracurium because less LAUDANOSINE with cisatracurium

266
Q

Devoid of histamine and CV effects even with rapid admini Benzoisoquinoilnium

A

Cisatracurium

SRNAPharmacology II (32 decks)

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