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NMB's Flashcards

1
Q

which subunits must be occupied to open the nicotinic receptor at the motor end plate

A

alpha and alpha (either by Ach or succ)

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2
Q

2 types of NachR’s at NMJ

A
  1. pre junctional Nn receptors present on presynaptic nerve
  2. post synaptic Nm receptors present on motor end plate of muscle
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3
Q

subunits on post synaptic nicotinic (Nm) receptor

A

2 alpha, 1 beta, 1 delta, 1 epsilon

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4
Q

subunits on extra junctional receptors and why they return

A

denervation or prolonged immobility allows for return of these receptor types (that were present in early fetal development)

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5
Q

why do extra junctional receptors increase risk for fatal hyperkalemia

A

-far more sensitive to succ and remain open for a longer period of time allowing for more Na to enter the cell
-stimulated by choline

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6
Q

extra junctional receptors and non depolarizers

A

up regulation of extra junctional receptors creates resistance to non depolarizers

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7
Q

fade during TOF is most likely caused by

A

antagonism of pre synaptic Nm receptors

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8
Q

MOA of NDNMB’s

A

competitively antagonize presynaptic Nn receptors

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9
Q

which receptor is integral to the fade mechanisn

A

presynaptic nicotinic (Nn).

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10
Q

what type of block does succ create

A

phase 1 (diminished but equal- no fade)

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11
Q

what type of block does NDNMB’s create

A

phase 2 (nerve terminal can only release avail Ach not stored Ach so fade occurs)

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12
Q

can succ cause a phase 2 block?

A

high dose, yeah
>7-10mg OR >30-60m infusion

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13
Q

post tetanic potentiation

A

none with phase 1 but yes with phase 2

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13
Q

post tetanic potentiation

A

none with phase 1 but yes with phase 2

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14
Q

most sensitive indicator for recovery of NMB

A

inspiratory force better than -40cmH2O

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15
Q

best place to measure onset of blockade

A

orbicularis oculi (closes eyelid) or corrugator supercilli (eyebrow twitch)
facial nerve (CN7)

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16
Q

best place to measure recovery blockade

A

adductor pollicis (thumb adduction) or flexor hallucis (big toe flexion)
nerve= ulnar or posterior tibial

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17
Q

TOF ratio that correlates with full recovery

A

> .9 at adductor pollicis

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18
Q

Vt and VC are normal in the setting of what amount of NMB?

A

70-80%

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19
Q

acceptable clinical end point and max % of receptors occupied when acceptable clinical endpoint is reached for tidal volume

A

> 5mL/kg and 80%

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20
Q

acceptable clinical end point and max % of receptors occupied when acceptable clinical endpoint is reached for TOF

A

no fade and 70%

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21
Q

acceptable clinical end point and max % of receptors occupied when acceptable clinical endpoint is reached for VC

A

> 20mL/kg and 70%

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22
Q

acceptable clinical end point and max % of receptors occupied when acceptable clinical endpoint is reached for sustained tetanus (50hz)

A

no fade and 60%

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23
Q

acceptable clinical end point and max % of receptors occupied when acceptable clinical endpoint is reached for DBS

A

no fade and 60%

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24
Q

acceptable clinical end point and max % of receptors occupied when acceptable clinical endpoint is reached for inspiratory force

A

> -40cmH2O and 50%

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25
Q

acceptable clinical end point and max % of receptors occupied when acceptable clinical endpoint is reached for head lift >5 seconds

A

sustained for 5 seconds and 50%

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26
Q

acceptable clinical end point and max % of receptors occupied when acceptable clinical endpoint is reached for hand grip same as pre induction

A

sustained for 5 seconds and 50%

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27
Q

acceptable clinical end point and max % of receptors occupied when acceptable clinical endpoint is reached for holding tongue blade in mouth against force

A

cant remove tongue blade against force and 50%

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28
Q

best qualitative test for neuromuscular function

A

tongue blade

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29
Q

how does succ cause bradycardia or asystole

A

stimulates M2 receptor on SA node (primary metabolite, succinomonocholine, is probably responsible)

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30
Q

how does succ cause tachycardia/HTN

A

mimics Ach at sympathetic ganglia

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31
Q

succ transiently increases IOP by

A

5-15mmHg for up to 10m

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32
Q

how does succ affect intragastric pressure and LES tone

A

increases intragastric pressure but decreases LES tone. they cancel each other out so the barrier at the GE junction is unchanged

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33
Q

different names for acetylcholinesterase at NMJ

A

genuine cholinesterase
true cholinesterase
type 1 cholinesterase
specific cholinesterase

34
Q

different names for pseudocholinesterase in plasma

A

butyrylcholinesterase
type 2 cholinesterase
false cholinesterase
plasma cholinesterase

35
Q

where is pseudocholinesterase produced and what function does it help monitor

A

produced in liver, indicator of hepatic synthetic function

36
Q

which atypical pseudocholinesterase problem can prolong succ duration

A

homozygous variant

37
Q

drugs that reduce pseudocholinesterase activity

A

metoclopramide
esmolol
neostigmine
echothiopate
oral contraceptives/estrogen
cyclophosphamide
MAOI’s
nitrogen mustard

38
Q

co existing diseases that reduce pseudocholinesterase activity

A

atypical PchE
severe liver disease
chronic renal disease
organophosphate poisoning
burns
neoplasm
advanced age
malnutrition
pregnancy (late stage)

39
Q

dibucaine test is an

A

amide LA that inhibits normal plasma cholinesterase

40
Q

outcome of normal dibucaine test

A

dibucaine inhibits normal pseudocholineseterase
normal dibucaine number is 80 which means 80% of the pseudocholinesterase is in the sample

41
Q

outcome of abnormal dibucaine test

A

does not inhibit atypical pseudocholinesterase
if the patient had a dibucaine number of 20 then the dibucaine did not inhibit the patients PchE

42
Q

PchE variant: typical homozygous
genotype:
incidence:
dibucaine #:
succ duration:

A

genotype: UU
incidence:
dibucaine #: 70-80
succ duration: 5-10min

43
Q

PchE variant: heterozygous
genotype:
incidence:
dibucaine #:
succ duration:

A

genotype: UA
incidence: 1/480
dibucaine #: 50-60
succ duration: 20-30m

44
Q

PchE variant: atypical homozygous
genotype:
incidence:
dibucaine #:
succ duration:

A

PchE variant: typical homozygous
genotype: AA
incidence: 1/3,200
dibucaine #: 20-30
succ duration: 4-8h

45
Q

define atypical plasma cholinesterase defect

A

qualitative. sufficient amounts are made theyre just not functional

46
Q

tx for patient with atypical plasma cholinesterase

A

postop mechanical ventilation and sedation is tx of choice for cost reasons but can also do whole blood, FFP, or purified human cholinesterase

47
Q

succ black box warning

A

most common is duchenne muscular dystrophy but overall the warning is for skeletal muscle dystrophy
-lack of dystrophin doesn’t allow actin and myosin to anchor which which increases sarcolemma permeability, facilitates breakdown, releases creatinine kinase and myoglobin to systemic circulation

48
Q

mild hyperkalemia presents with

A

peaked t waves and PR prolongation

49
Q

tx for hyperkalemia

A
  1. stabilize myocardium: ca chloride 20mg/kg or ca gluconate 60mg/kg
  2. shift k into cells (.3-.5mg/kg of 10% glucose solution, 1U insulin per 4-5g IV glucose, 1-2mmol/kg sodium bicarb)
  3. enhance k elimination (furosemide 1mg/kg, volume resuscitation, hemodialysis, hemofiltration)
50
Q

who is at risk for postop myalgia related to succ

A

young adults (women>men) undergoing ambulatory surgery that do not routinely engage in strenuous activity.

51
Q

what 3 drugs (and doses) can you administer before succ to help with postop myalgia

A

2mg roc
1.5mg atracurium
.3mg vec
3-5min before succ

52
Q

what to do with dose of succ if giving defasciculating dose

A

increase dose to 1.5-2mg/kg

53
Q

who should not receive a defasciculating dose

A

those with pre existing skeletal muscle disease/weakness

54
Q

who with pre existing skeletal muscle co morbidities may respond to succ with MH

A

hypokalemic periodic paralysis
malignant hyperthermia patient

55
Q

which patient population is resistant to succ but sensitive to non depolarizers

A

MG

56
Q

who with pre existing skeletal muscle co morbidities may be sensitive to non depolarizing NMB’s?

A

duchennes, Gillian barre, MS, ALS, myotonic dystrophy, huntington chorea, MG

57
Q

which patient population would respond to succ with muscle contractures that may compromise aw management?

A

myotonic dystrophy

58
Q

who with pre existing skeletal muscle co morbidities may have a hyperkalemic response to succ?

A

DMD (plus rhabdo), guillan barre, MS, ALS, charcot marie tooth, hyperkalemic periodic paralysis

59
Q

the higher the ED95, the lower the

A

potency

60
Q

short acting: mivacurium
intubation
time to max block (onset)
duration

A

intubation: .15
time to max block (onset): 3.3
duration: 16.8

61
Q

intermediate acting: cisatracurium
intubation
time to max block (onset)
duration

A

intubation: 0.1
time to max block (onset): 5.2
duration: 45m

62
Q

intermediate acting: vecuronium
intubation
time to max block (onset)
duration

A

intubation: .1
time to max block (onset): 2.4
duration: 45m

63
Q

intermediate acting: atracurium
intubation
time to max block (onset)
duration

A

intubation: 0.5
time to max block (onset) 3.2
duration 45m

64
Q

intermediate acting: rocuronium
intubation
time to max block (onset)
duration

A

intubation: .6
time to max block (onset): 1.7m
duration: 35m

65
Q

long acting: pancuronium
intubation
time to max block (onset)
duration

A

intubation: .08
time to max block (onset): 2.9m
duration: 85m

66
Q

benzylisoquinolinum compounds

A

atracurium
cisatracurium
mivacurium

67
Q

aminosteroid compounds

A

rocuronium
vecuronium
pancuronium

68
Q

how is atracurium metabolized

A

hoffman elimination and non specific plasma esterases

69
Q

how is cisatracurium metabolized

A

hoffman elimination

70
Q

how is mivacurium metabolized

A

pseudocholinesterases which explains its short DOA

71
Q

describe hoffman elimination

A

base catalyzed reaction that is dependent on normal blood pH and temperature
-faster with alkalosis and hyperthermia
-slower with acidosis and hypothermia

72
Q

toxic metabolite of benzylisoquinolinum compounds

A

laudanosine

73
Q
A
74
Q

how is rocuronium metabolized

A

biliary excretion as unchanged molecule

75
Q

metabolism of vec

A

via liver too 3OH vec

76
Q

metabolism of pancuronium

A

hepatic deacetylation to 3OH pancreatic

77
Q

drugs that potentiate NMB include

A
78
Q

electrolytes that potentiate NMB include

A
79
Q

patient factors that potentiate NMB include

A

hypothermia (decreased potassium and clearance)
gender (women>men)

80
Q

2 NMB’s that block M2 receptors in heart

A

pancuronium (moderate blockade)
roc (slight to none)

81
Q

which NMB’s release histamine

A

cisatracurium, atracurium, succ

82
Q

which NMB is most likely to cause anaphylaxis?

A

succ

83
Q

how too NMB’s cause anaphylaxis

A

they contain quarternary amines that interact with IgE, causing mast cell and basophil degranulation. this is reflected via an elevated tryptase level (peak 15-120 min after exposure)

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