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ANPH 510 pharm 2 mccarver > NMB > Flashcards

NMB Flashcards

0
Q

depolarizers mimic __

the only depolarizer left __

A

acetylcholine

succinycholine

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1
Q

Can NMB’s cross the bbb?

A

no, thus cannot produce anesthesia, only work at the neuromuscular junctions

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2
Q

do non depolarizers mimic or block acetylcholine at the neuromuscular junction?

A

non depolarizers block

depolarizers (succs) mimics

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3
Q

name some aminosteroid non-depolarizers

A

anything the ends in -onium like:
vecurONIUM
rocurONIUM
pancurONIUM

onium kind of looks like onion, so onions must be aminosteroids

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4
Q

name some benzylisoquinoliniums

A

anything that ends in -curium:
atraCURIUM
cisatraCURIUM

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5
Q

what are the characteristics of a phase 1 block?

A

reduction in amplitude of single twitch, NO FADE WITH TETANY OR TOF

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6
Q

what are the characteristics of a phase 2 block?

A

reduction in amplitude of single twitch, FADE with tetany and TOF

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7
Q

how is potency of NMBs measured?

A

the dose required to reduce the amplitude of single twitch 95%, measured under nitrous-barb-opioid anesthesia

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8
Q

the ED95 is not enough to intubate on, so typically we give __x the ED95 to intubate

A

2x

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9
Q

since the cords are fast twitch, which is a more accurate indicator of optimal NMB, adductor pollicis or obicularis oculi?

A

obicularis oculi, blinking is a fast-twitch muscle movement

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10
Q

do NMB affect fast or slow twitch muscles first?

why?

A

fast, fortunately for us there are more receptors at fast muscles, so the NMB equilibrates more quickly there

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11
Q

fortunately for us, to paralyze the diaphragm requires __x the dose required to paralyze the adductor pollicis or obicularis oculi

A

2x

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12
Q

single twitch gives __-junctional data

A

post

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13
Q

tetanus and TOF gives __-junctional data

A

pre

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14
Q

trick question, do depolarizers exhibit Wedensky inhibition?

A

no, depolarizers (succs) do not exhibit fade with TOF (wedensky)

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15
Q

if your clueless attending injects an unlabeled syringe of clear medication into a patient who subsequently develops paralysis, how can you determine if it was a depolarizer or a non-depolarizer?

A

do TOF, non-depolarizer will exhibit fade, whereas depolarizing succs does not exhibit fade.

single twitch won’t tell you because you can’t see fade with a single twitch.

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16
Q

why can’t NMBs cross the BBB and cause CNS effects, cross the placenta, etc?

A

because they are quaternary ammonium groups, highly ionized, water soluble, and poorly lipid soluble, thus they have a small volume of distribution

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17
Q

what is the INITIAL reason for decreased concentrations on NMBs

A

redistribution

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18
Q

are NMBs highly protein bound?

A

nope, but with reduced vD such as in hypovolemia, greater effects will be seen due to increased plasma concentrations

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19
Q

for laryngospasm, doses of succs as low as ___mg/kg may be sufficient

A

0.1

20
Q

patients should have a TOF >0.7 for spontaneous ventilation. what the heck does that mean?

A

it means that your fourth twitch is at least 70% of the amplitude of the first twitch.

21
Q

concentration and dosage of succs

A

20 mg/ml

1-1.5 mg/kg

22
Q

concentration and dose of vec

A

concentration 1 mg/ml

dose 0.1 mg/kg

23
Q

concentration and dosing roc

A

concentration 10 mg/ml

dose 0.6-1 mg/kg (1mg/kg to intubate in 1 minute)

24
Q

concentration and dose of nimbex/cisatracurium

A

concentration 2 mg/kg
dose 0.1 mg/kg

don’t let the concentration of nimbex trip you up, it has twice the concentration of vec because it’s got such a long drug class name - benzylisoquinolinium

25
Q

what does a molecule of succs consist of?

A

two molecules of ACH linked by acetate methyl groups

26
Q

what is the difference between succs and the other NMBs?

A

succs actually binds to and ACTIVATES the receptor (thus fasciculations), whereas benzylisoquinoliniums and aminosteroids BLOCK BUT DON’T ACTIVATE the receptor (thus no fasciculations)

27
Q

why don’t NMBs work on cardiac, GI, and other smooth muscle junctions?

A

NMBs only work on cholinergic receptors, not muscarinic or nicotinic receptors

28
Q

what is common to all NMBs?

A

quaternary ammonium group with at least 1 charged nitrogen atom

29
Q

the five post-junctional subunits are:

A

2 alphas
1 beta
1 gamma
1 delta

the sorority that Paul Meadows was in during his college days

30
Q

how wide is the synaptic cleft?

A

20-30 nm

31
Q

are pre-junctional nerve endings myelinated or non-myelinated?

A

NON-myelinated

32
Q

what class is acetylcholine?
how is it synthesized?
how many molecules of ACH in a quanta?

A
  • quaternary ammonium ESTER
  • acetylation of choline, controlled by enzyme choline acetylase
  • 1000 molecules in a quanta
33
Q

do non-depolarizers cause a conformational change in the alpha subunits?

A

no, only succs (depolarizer) causes the conformational change and opens ion channels, fasciculations, etc. Non-depolarizers block one or the other alpha subunit

34
Q

why should you pretty much always reverse your patients?

A

because occupation (or blockade) of up to 70% of receptors will not show any evidence of block by single twitch test, thus your patient will be weak but you wouldn’t know it by testing with nerve stimulator

35
Q

how many alpha subunits do you gotta block before neurotransmission fails?

A

80-90%

36
Q

paralysis is complete at __ to __ % occupancy, but adequate muscle relaxation is __ to __%

A

90-95% occupancy is complete

85-90% is adequate

37
Q

If you do a TOF and the fourth twitch is absent, that equals approximately __-__% suppression of a single twitch

A

70-75%

38
Q

Let’s say your patient recently had a stroke and is hemiplegic, which side should you place your nerve stimulator?
what about a patient with parkinsons, MS, or muscular dystrophy?
-what about para/quadriplegic?

A
  • the UNaffected side for stroke
  • no change for Michael J Fox (parkinsons) or MS, or muscular dystrophy
  • para/quad will have increased sensitivity to NDNMBs
39
Q

burn patients and NDNMBs?

A

resistance to NDNMBs, begins at 10 days, peaks at 40 days, declines after 60 days, >30% BSA

40
Q

what is the autonomic margin of safety?

A

the difference between the NMB dose and the dose producing circulatory effects

the greater the margin, the safer the drug

41
Q

what is critical illness myopathy?

A

patients who received prolonged NMB for mechanical ventilation >6 days may have significant weakness persisting for several months

42
Q

what factors enhance NDNMB activity?

sevo at 2, just got some gentamycin abx, had a regional block with LA, is on digoxin and lasix, got some mag in the unit, takes lithium and just got a ganglionic blocker for autonomic dysreflexia. Also is hypothermic

A 
volatiles
aminoglycosides
LA
anti-dysrhythmics
diuretics
Mg++
lithium
ganglionic blockers
hypothermia
43
Q

what does hypotension do to NDNMB?

A

slow onset, prolong duration

44
Q

let’s say you decide not to reverse your patient, take them to the PACU where they get too much morphine and develop respiratory acidosis, what happens to their NDNMB?

A

increases it, re-curarization

45
Q

how do volatiles enhance NDNMB?

A

volatile induced depression of CNS

46
Q

Ester LA’s compete for plasma cholinesterases and therefore prolong the effects of __

A

succs

47
Q

gorillacillin

A

a medical slang term for any of the big bad antibiotics with very broad coverage

ANPH 510 pharm 2 mccarver (7 decks)

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