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Anesthesia Pharm > NMBA > Flashcards

NMBA Flashcards

Exam 3

1
Q

ACh is synthesized in nerve terminal by ____ ; _____ in presence of ________ ____________.
Each vesicle is referred to as a ______.

A

Choline
Acetyl coenzyme A

Choline acetyltransferase
Quantum

80% in vesicles
20% nonvesicle reserve

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2
Q

What do you call the sm electrical potentials from Ach being released from vesicles?
What is the amt of mv?
What is the sum of this potential called?

A

Mepps (miniature end plate potentials
0.5-1
end plate potential

Action potential= all or nothing.

Threshold needs to be reached

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3
Q

What is required for transmitter release of ACh to occur?

A

Ca and cAMP

5x more ach is released than needed to create action potentia

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4
Q

What is ACh hydrolyzed to ?

What hydrolyzes it?

A

Choline; Acetate-diffuses away

Choline reuptake into nerve terminal
Acetylcholinesterase—ach destroyed less than 1ms after release.

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5
Q

Where on the nAChR does ACh bind?

What type of change occurs to receptor and what does it lead to?

A

2 agonist on alpha subunit must bind
Ligand gated–entry of Neurotransmitters.

Conformational change –>Na channel open–>Na in–>depolarize membrane + action potential–>Action potential–>Ca released from sarcoplastic reticulum

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6
Q

How many subunits on the post junctional nAChR?

Name them

A

5 (pentameric)

2-Alpha
1-Beta
1-delta
1-Epsilon

complex transmembrane glycoprotein core (250,000 daltons)

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7
Q

What is a nAChR competitive agonist? Antagonist?

A

Sux

NDMB

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8
Q

(True/False) Sux is hydrolyzed by Acetylcholinesterase?

Where does hydrolysis occur?

A

False

Plasma

Plasma cholinesterase/pseudo/butyrocholinesterese–Synthesized in liver

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9
Q

How is sux action terminated?

A

Diffusion away from NMJ and to plasma.

Hydrolyzed by plasma cholinesterase there.

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10
Q

when agonist bind to ___ subunits but do NOT cause a ________ change to open Na channel. This is called what?

A

Alpha

Conformational

Desensitization .

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11
Q

Medications like Cocaine, abx, and Quinidine cause this..

A

Closed channel blockade

Drug reacts around mouth of channel, prevents passage of ions

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12
Q

Closed channel blockade

A

Drug reacts around mouth of channel and prevents passage of ion.

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13
Q

NDMB at large doses can lead to this.

A

Open channel blockade.

Drug enters channel but doesnt pass all the way (gets stuck)
Prevents flow of ions.

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14
Q

What proliferates w/ decreased neural activity?

What is different about its structure?

A

Extrajunctional Receptors

Gamma instead of epsilon//stays open longer-allow for lg amt of K efflux.

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15
Q

What pt population may have an increase in extrajunctional receptors?

A 
Bedrest
Burn
Spinal cord
Sepsis
Trauma

Gamma instead of epsilon–open longer–more K efflux

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16
Q

What are the extrajunctional receptors more sensitive to?

A

agonist-DMB–Sux

less (resistant) to NDMB(antagonist)–give More

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17
Q

(True/False) Extrajunctional receptors are less sensitive to antagonist (NDMB) have to admin More of it

A

True

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18
Q

Which VA potentiate the effects of NDMR the most?

A

Des > Sevo > Iso

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19
Q

What are 2 functions of prejunctional receptors?

A

Inhibit release of Ach from presynapse

Stimulate production of Ach in nerve terminal

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20
Q

Can you get post tetanic facilitation w/ sux?

A

no

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21
Q

NMBA (5)

Structure

A 
Ionized
Water Soluble
Limited Lipid solublility
Placenta--No
BBB--No

Quarternary ammonium groups

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22
Q

For NMBA the Vd is influenced by what?

What is the Vd?

A

Age
Liver/renal disease

similar to ECF (14L)–water soluble

not highly protein bound.

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23
Q

What are the long acting NMBA?

A

Pancuronium

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24
Q

What are the intermediate acting NMBA?

A

Atracurium
Cisatracurium
Rocuronium
Vecuronium

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25
Q

IAs excluding _________ potentiate the effects of _______ via ______.
dosing should be ________.

A

Nitrous

NDMR
Ca channels.
Decreased

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26
Q

NMBA could be used to treat what conditions.

A 
Intubation-facilitate
Laryngospasm-sux
O2 utilization-dec
Surgical conditions-enhance
Truncal rigidity w/opioids
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27
Q

For NDMR what is the recommended dose to facilitate intubation?

A

2xED95

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28
Q

What is the dose needed to produce ______ suppression of single twitch?
What is adequate depression for surgical relaxation?

A

95%
ED95

90% (3 responses abolished w/TOF)

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29
Q

The duration of action of Roc is longer in the adductor muscle of larynx than the adductor pollicis.
(True/False)

A

False

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30
Q

Do NMBAs cause the majority of anaphylactic reactions during anesthesia?

A

Yes

Sux & Roc

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31
Q

What group of NMBA are more likely to cause histamine release and what is this r/t?

A

Benzyquinoliniums
Atracurium
Cis–says in ppt but usually doesnt
Mivacurium

Tertiary amine

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32
Q

electrostatic attraction occurs at all cholinergic sites btw _________ and ________.

A

AChR ; NH4 groups

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33
Q

What influences the degree of CV effects?

Maximal autonomic blockade occurs when?

A

Length of Carbon chain separating NH4+ groups.

NH4+ separated by 6Cs. (hexamethonium)

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34
Q

______ chains are more specific to nACHrs where?

Maximal NM blockade is achieved when?

A

Longer
NMJ

10Cs present (decamethonium)

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35
Q

Sux ED95 dose?
Intubation dose?
onset?
Duration?

A

0.25-0.5mg/kg
1mg/kg

30-60sec
5-10min

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36
Q

Depolarization is ________ and the depolarized membrane cant respond to additional agonist.
This is referred to as ________.
This can lead to this s/e

A

Sustained

Phase 1 blockade
Fasciculations
Sux–attaches 1 or 2 alpha subunits

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37
Q

Repeated doses of sux can cause ________

A

phase 2 blockade–? r/t desensitization, ion channel block or sux in cytoplasm.

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38
Q

Decreased contractile force in response to single twitch//sustained tetany w/ decreased amplitude//TOF ratio >0.7 and no PTF is seen w/ which NMBA..
Augmentation after anticholinesterase.
What type of blockade is this an example of?

A

Sux

Phase 1 blockade

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39
Q 
TOF ratio <0.7//
Decreased amplitude and tetanic face//
Antagonized by anticholinesterase //
Abrupt onset, manifest as tachyphylaxis 
is seen w/ \_\_\_\_\_\_\_.
A

Phase 2 blockade
Sux

Resembles NDMR

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40
Q

Sux is metabolized by what enzyme to _______________.

If the enzyme level is below this percentage DOA will be prolonged.

A

plasma cholinesterase–made in liver

Succinylmonocholine/ choline—>Succinic Acid and choline

75%

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41
Q

What can lead to decreased levels of plasma cholinesterase?

A 
Birth Control
Old
Burns
Pregnant
MAOI
Malnutrition
Esmolol
Neostig
Reglan
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42
Q

What is the test used for detection of atypical plasma cholinesterase?
Normal #?
Heterozygous?
Homozygous?

A

Dibucaine–Inhibits activity of normal plasma cholinesterase by:
80%
40-60-Modest (1:480)
20-NMB may last hrs(1:3200)

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43
Q

Myasthenia Gravis pt are ________ to Sux, r/t_________ in functional nAChRs, dose of sux would have to be ________.

A

resistant

Decrease

Increased

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44
Q

Which NMBA produces the greatest histamine release?

What symptoms could manifest?

A

Sux–lg or rapid admin

Reduced BP–anaphylaxis rx-(sympathetic ganglia),
Bronchospasm
Face/Truncal flushing

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45
Q

Sinus Brady could be seen after admin of this medication in which population?
What causes this and how could it be pretreated?

A

Sux
Peds or admin of 2nd dose soon after 1st.
NDMR or atropine decreases incidence
Stimulation of cardiac postganglionic mAChRs

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46
Q

True/False

Admin of smaller dose of Sux attenuates hyperkalemic response.

A

False

Pre treatment w/ NDMR doesnt protect against hyperK+

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47
Q

Myalgia is observed in what parts of the body most?
Which pt population is more at risk?
What can yo use as pretreatment/treatment?

A

Neck
Abdomen
Pharynx
Back

Young/healthy/athletes–more muscles

NDMR (defasiculating dose)
tx w/ NSAIDs

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48
Q

Sux can increase (3)?

A

ICP
IOP
Intra gastric pressure–risk aspiration–
increase HR, BP–sympathetic ganglia

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49
Q

Which NDMR is a mixture of 2 stereoisomers? Which configuration is 1/10 as potent as others.

A

Mivacurium-short acting

Cis-Cis

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50
Q

ED95-0.08mcg/kg

Intubation 0.25 mg/kg

A

Mivacurium-short acting

51
Q

Mivacurium
Onset:
DOA:
Hydrolyzed:

A

2-3min

10-20min

Plasma cholinesterase

52
Q

ED95: 0.04 mg/kg
intubation: 0.2mg/kg

A

Cisatracurium

53
Q

Intermediate acting NMBA onset; DOA

Roc?

A

3-5min
20-35min (30)

Roc onset 1-2min

Atra/Cis/Vec

54
Q

How is Cisatracurium metabolized?

What are the metabolites?

A

Hoffman- at body ph and temp

Laudanosine-cleared renally

55
Q

Which NMBA may be epileptogenic?

A

Atracurium— a bisquaternary benzylisoquinolinium

laudonasine-CNS stimulant.

56
Q

ED 95: 0.2 mg/kg

Intubation 0.5mg/kg

A

Atracurium

57
Q

Atracurium metabolism

A

Hoffman & hydrolysis non-specific plasma esterases

Produce laudanosine–renal clearance

58
Q

Which NMBA causes an increased HR and decrease BP? at what concentration? What do you see at greater dose?

A

Atracurium
>2x ED95
Facial/truncal flush 3xED95

Histamine release

59
Q

True/False
Decrease the dose in elderly pt receiving atracurium.
How about in Peds?

A

False–no change

Peds 1-6mo decrease 50%–more rapid recovery infants

60
Q

Which NMBA is considered a CNS stimulant?

A

Atracurium

Increases MAC in animals
Epileptogenic

61
Q

Which NMBA has the highest incidence among all periop drugs of anaphylaxis?

A

Roc

62
Q

Sustained contraction of this muscle is common in children. What must you differentiate this from?

A

Masseter muscle (trismus)

Malignant Hyperthermia

Sux not recommended in children

63
Q

rare, autosomal dominant disorder involving defective ________ receptors, which control release of _____ in _______ and leads to hypermetabolism.

A

ryanodine
Ca//Sarcoplasmic reticulum

Malignant hyperthermia–tx dantrolene

64
Q

S/S Malignant Hyperthermia

A 
Acidosis-metabolic
Tachy
Rhabdo
O2 consumption
Hyperpyrexia
Hypermetabolism
Hypercarbia
65
Q

What percent blockade by NDMR doesnt produce evidence of blockade by single twitch?

A

70%

66
Q

What percentage blockade is required to interrupt transmission of chemical signal?

A

80-90%

67
Q

TOF w/ no fade & VC could be seen w/ what % of receptor blockade?

A

70%

somewhat uncomfortable

68
Q

Head lift 180 degrees for 5 sec, & sustained hand grip represents what percentage blockade?

A

50%

69
Q

Tidal volume of 5ml/kg represents what percent blockade?

A

80%

70
Q

What is indicative of 60% receptor blockade?

A

DBS//no fade

Sustained tetany//no fade

71
Q

A right shift of the dose response curve could be seen when?

A

Competitive antagonist
Desensitization

Agonist w/ lower receptor affinity

72
Q

Tetanic stimulation before & after administration of a _______ dose of Sux is similar to the normal response to a _______

A

Large//NDMR

Post tetanic stimulation
Phase 2 blockade w/ sux

73
Q

Which agent has a narrow autonomic margin of safety?

Which agent has a wider autonomic margin of safety?

A

Pancuronium

Vecuronium//Cis//Roc

74
Q

The difference btw the required dose for NM blockade and the dose for circulatory effects is known as?

A

autonomic margin of safety

75
Q

CV effects are r/t what 2 things?

A

Histamine (prostacyclin release)

Antagonism of muscarinic and nicotinic receptors in ANS

76
Q

Which medications enhance NDMR & DMR?

A

Abx-aminoglycosides (decrease prejunctional ACh by competing w/ Ca)
Antiarrhythmic
LocalAnesthetic
Lithium

77
Q

Which medications only enhance NDMR?

A

Magnesium–esp Vec–inhibits Ca

Diuretics–lasix Inhibit cAMP–>dec ACh output

78
Q

Which medication inhibits cAMP leading to (inc or dec) in ACh output?

A

Lasix

Dec

enhances NDMR

79
Q

Upper motor neurons located in ________. synapse w/ lower motor neurons on the ______ horn of the spinal cord. Which is the ____ matter on the _____/efferent.

A

Cerebral cortex
Anterior
Gray
Ventral

80
Q

Single twitch is seen w/ blockade of the _________ nicotinic receptors

A

Post synaptic

81
Q

Resting membrane potential is _____ mv. depolarization occurs w/ stimulation of ___ channels to open. Threshold is reached at ____mv and action potential created.

A

-90

Na
-45

82
Q

Sudden influx of ___ is sufficient to _____ the membrane and create an ________.

A

Na
depolarize
action potential
Skeletal muscle contraction.

83
Q

Opening of the channel pore w/ post junctional receptors converts and amplifies signal to _______.

A

electrical currents.

84
Q

At large doses _____ may _____ the open receptor pore.

A

NDMR

Block

85
Q

______ activate opening of the receptor pore when ____ are activated.
Activity is terminated by ______ away from the ____,

A

DMR–Sux

Both alpha subunits

Diffusion//NMJ

86
Q

NM blockade w/ ______ occurs because the ______ post junctional membrane cannot respond to additional agonist.

A

DMR-SUX

depolarized

87
Q

Extrajunctional receptors are highly sensitive to ______ but less sensitive to _____.

A

agonist–sux

antagonist–NDMR–Give more

88
Q

W/ extrajunctional receptors you have to administer more/less of the NDMR?

A

More—less sensitive.

89
Q

______ receptors located:
synapse-preganglionic and postganglionic PSNS & SNS
and _____.

A

Nicotinic

NMJ

90
Q

Muscarinic receptors located where.

A

Synapse postganglionic PSNS and end organ/tissue.

91
Q

What is the primary pharmacologic effect of NMBA?

A

Block transmission of nerve impulses at NMJ

92
Q

Vd influenced by 3 things?

A

Age
Renal/hepatic disease
14L-vd NMBA

93
Q

VAs potentiate effects of NDMR via _____.

Dosing should be ____.

A

ca channels
decreased
Des>Sevo>Iso

?decrease sensitivity of post junctional membrane to depolarization.

94
Q

ED95 is dose necessary to produce _________ in response to ______ in 50% of population

A

95% suppression

single twitch

95
Q

What is the recommended dose for tracheal intubation?

Surgical relaxation?.

A

2xED95

90% depression

96
Q

The alpha subunits have at least one N that makes them

A

Quarternary ammonium group

97
Q

Abnormal response to sux may be due to what?

A

Desensitization
ion channel block
or entry of sux into skeletal muscle cytoplasm

Phase 2 block

98
Q

Dibucaine test is used to diagnose ____

A

atypical plasma cholinesterase

99
Q

Increase in HR and BP occur w/ ____

A

Sux

Sympathetic ganglia activity

100
Q

masseter muscle (trismus) is common in ____ w/ this med

A

PEDS
Sux—Not reccommended

differentiate from MH

101
Q

w/ NDMR _____ receptor blockade doesnt produce evidence of block w/ single twitch.
What amt of receptor occupation will?

A

70%

80-90%

102
Q

Which medication is typically agonized by anticholinesterase meds?

A

DMR–Sux.

NDMR-antagonized

103
Q

which med has a narrow autonomic margin of safety?

Wider?

A

Pancuronium

vec/roc/cis

104
Q

CV effects r/t ____ & ______. is from antagonism of ____ receptors

A

histamine & prostacyclin

muscarinic and nicotinic at ANS

105
Q

males are _____ sensitive to NDMR than women

A

less

22% less required by woman.

106
Q

Which NDMR increases HR, MAP, CO, increases in AV conduction and increased myocardial O2 consumed.

A

Pancuronium

antagonism cardiac muscarinic

ischemia in pt w/ CAD

107
Q

Priming dose?

A

20% of ED95- NDMR

then after induction give the rest of INDUCTION dose (2xED95)–NDMR

108
Q

Defasciculating

A

20% ED95 of NDMR before induction. then give larger dose of SUX

109
Q

Cumulative effect w/ renal disease

A

Panc >Vec > Atra

110
Q

Which med is unstable in solution

A

Vec–in powder needs reconstitute.

Does not antagonize mAChRs
´ Does not cause mast cell degranulation

111
Q

Which med has similar potency in peds as adults but more rapid onset in infants. longer doa in infants.

Prolonged DOA elderly r/t lower clearance

A

Vec

112
Q

Liver &; Renal disease can prolong w/

A

Vec–monoquartenary aminosteroid

Roc–monoquartenary aminosteroid

113
Q

Laudonasine is metabolite of _____.
Cleared _____
Has ____ effects.

A

Atracurium
Cisatracurium

Renally

CNS stimulant–increased MAC in animals
Epileptogenic–only Atra
Atra> cis

114
Q

Infants 1-6 months need 1/2 of the adult dose w/ this med.

Recovery is more ____ in infants.

A

Atracurium

Rapid

Old–no change in dose.

115
Q

Rapid admin of this med = histamine –3xED95—

2xED95 w/ this med you gent increased HR and decreased BP.

A 
mivacurium-3x
decreases map (transient)

Atracurium-2x//3x-facial/truncal flush

116
Q

Which NMBA is excreted unchanged in Bile?

& renal is >30%

A

Roc–monoquartenary aminosteroid

liver/renal can prolong function

117
Q

Deacytylation occurs w/ which 2 meds. compound 50% as potent as parent.

A

Vecuronium–

Pancuronium–(20% hepatic & 80% unchanged in urine)—prolonged liver, renal, biliary, cirrhosis, old

118
Q

resistance to NDMR is seen w/ _______

A

thermal injury

119
Q

paresis/hemiplegia causes _______ w/ ______.

A

Resistance on affected side w/ NDMR

120
Q

Ganglionic blockers

A

Delay onset and prolong DOA of NDMR

121
Q

Dilantin

A

Decreases NDMR effect

122
Q

Cyclosporin

A

Prolongs NDMR

123
Q

Hyperkalemia

A

enhances DMR

Resistance to NDMR

124
Q

Hypokalemia

A

Resistance DMR

enhance NDMR

Anesthesia Pharm (2 decks)

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