NMB's

Question 1

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

Answer 1

alpha and alpha (either by Ach or succ)

Question 2

2 types of NachR’s at NMJ

Answer 2

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

Question 3

subunits on post synaptic nicotinic (Nm) receptor

Answer 3

2 alpha, 1 beta, 1 delta, 1 epsilon

Question 4

subunits on extra junctional receptors and why they return

Answer 4

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

Question 5

why do extra junctional receptors increase risk for fatal hyperkalemia

Answer 5

-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

Question 6

extra junctional receptors and non depolarizers

Answer 6

up regulation of extra junctional receptors creates resistance to non depolarizers

Question 7

fade during TOF is most likely caused by

Answer 7

antagonism of pre synaptic Nm receptors

Question 8

MOA of NDNMB’s

Answer 8

competitively antagonize presynaptic Nn receptors

Question 9

which receptor is integral to the fade mechanisn

Answer 9

presynaptic nicotinic (Nn).

Question 10

what type of block does succ create

Answer 10

phase 1 (diminished but equal- no fade)

Question 11

what type of block does NDNMB’s create

Answer 11

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

Question 12

can succ cause a phase 2 block?

Answer 12

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

Question 13

post tetanic potentiation

Answer 13

none with phase 1 but yes with phase 2

Question 13

post tetanic potentiation

Answer 13

none with phase 1 but yes with phase 2

Question 14

most sensitive indicator for recovery of NMB

Answer 14

inspiratory force better than -40cmH2O

Question 15

best place to measure onset of blockade

Answer 15

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

Question 16

best place to measure recovery blockade

Answer 16

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

Question 17

TOF ratio that correlates with full recovery

Answer 17

> .9 at adductor pollicis

Question 18

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

Answer 18

70-80%

Question 19

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

Answer 19

> 5mL/kg and 80%

Question 20

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

Answer 20

no fade and 70%

Question 21

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

Answer 21

> 20mL/kg and 70%

Question 22

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

Answer 22

no fade and 60%

Question 23

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

Answer 23

no fade and 60%

Question 24

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

Answer 24

> -40cmH2O and 50%

Question 25

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

Answer 25

sustained for 5 seconds and 50%

Question 26

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

Answer 26

sustained for 5 seconds and 50%

Question 27

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

Answer 27

cant remove tongue blade against force and 50%

Question 28

best qualitative test for neuromuscular function

Answer 28

tongue blade

Question 29

how does succ cause bradycardia or asystole

Answer 29

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

Question 30

how does succ cause tachycardia/HTN

Answer 30

mimics Ach at sympathetic ganglia

Question 31

succ transiently increases IOP by

Answer 31

5-15mmHg for up to 10m

Question 32

how does succ affect intragastric pressure and LES tone

Answer 32

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

Question 33

different names for acetylcholinesterase at NMJ

Answer 33

genuine cholinesterase true cholinesterase type 1 cholinesterase specific cholinesterase

Question 34

different names for pseudocholinesterase in plasma

Answer 34

butyrylcholinesterase type 2 cholinesterase false cholinesterase plasma cholinesterase

Question 35

where is pseudocholinesterase produced and what function does it help monitor

Answer 35

produced in liver, indicator of hepatic synthetic function

Question 36

which atypical pseudocholinesterase problem can prolong succ duration

Answer 36

homozygous variant

Question 37

drugs that reduce pseudocholinesterase activity

Answer 37

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

Question 38

co existing diseases that reduce pseudocholinesterase activity

Answer 38

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

Question 39

dibucaine test is an

Answer 39

amide LA that inhibits normal plasma cholinesterase

Question 40

outcome of normal dibucaine test

Answer 40

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

Question 41

outcome of abnormal dibucaine test

Answer 41

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

Question 42

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

Answer 42

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

Question 43

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

Answer 43

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

Question 44

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

Answer 44

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

Question 45

define atypical plasma cholinesterase defect

Answer 45

qualitative. sufficient amounts are made theyre just not functional

Question 46

tx for patient with atypical plasma cholinesterase

Answer 46

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

Question 47

succ black box warning

Answer 47

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

Question 48

mild hyperkalemia presents with

Answer 48

peaked t waves and PR prolongation

Question 49

tx for hyperkalemia

Answer 49

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)

Question 50

who is at risk for postop myalgia related to succ

Answer 50

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

Question 51

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

Answer 51

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

Question 52

what to do with dose of succ if giving defasciculating dose

Answer 52

increase dose to 1.5-2mg/kg

Question 53

who should not receive a defasciculating dose

Answer 53

those with pre existing skeletal muscle disease/weakness

Question 54

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

Answer 54

hypokalemic periodic paralysis malignant hyperthermia patient

Question 55

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

Answer 55

MG

Question 56

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

Answer 56

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

Question 57

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

Answer 57

myotonic dystrophy

Question 58

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

Answer 58

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

Question 59

the higher the ED95, the lower the

Answer 59

potency

Question 60

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

Answer 60

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

Question 61

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

Answer 61

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

Question 62

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

Answer 62

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

Question 63

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

Answer 63

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

Question 64

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

Answer 64

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

Question 65

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

Answer 65

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

Question 66

benzylisoquinolinum compounds

Answer 66

atracurium cisatracurium mivacurium

Question 67

aminosteroid compounds

Answer 67

rocuronium vecuronium pancuronium

Question 68

how is atracurium metabolized

Answer 68

hoffman elimination and non specific plasma esterases

Question 69

how is cisatracurium metabolized

Answer 69

hoffman elimination

Question 70

how is mivacurium metabolized

Answer 70

pseudocholinesterases which explains its short DOA

Question 71

describe hoffman elimination

Answer 71

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

Question 72

toxic metabolite of benzylisoquinolinum compounds

Answer 72

laudanosine

Question 74

how is rocuronium metabolized

Answer 74

biliary excretion as unchanged molecule

Question 75

metabolism of vec

Answer 75

via liver too 3OH vec

Question 76

metabolism of pancuronium

Answer 76

hepatic deacetylation to 3OH pancreatic

Question 77

drugs that potentiate NMB include

Answer 77

Question 78

electrolytes that potentiate NMB include

Answer 78

Question 79

patient factors that potentiate NMB include

Answer 79

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

Question 80

2 NMB's that block M2 receptors in heart

Answer 80

pancuronium (moderate blockade) roc (slight to none)

Question 81

which NMB's release histamine

Answer 81

cisatracurium, atracurium, succ

Question 82

which NMB is most likely to cause anaphylaxis?

Answer 82

succ

Question 83

how too NMB's cause anaphylaxis

Answer 83

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)