NMBA Flashcards

(67 cards)

1
Q

Is acetylcholine an essential amino acid?

A

NO
essential NUTRIENT
it is not an amino acid

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2
Q

what type of amine does acetylcholine have?

A

quarternary

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3
Q

how is acetyl coA formed?

A

Acetyl-CoA is formed from oxidative decarboxylation of pyruvate.

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4
Q

what is the conduction velocity of alpha motor neuron?

A

50 - 100m/s

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5
Q

which type of Ca channels are found pre-synaptically?

A

N type

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6
Q

which receptor subunit does ACh bind?

A

alpha

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7
Q

where is acetylcholinesterase enzyme found?

A

In clefts of the folded post synaptic membrane found in clusters

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8
Q

what is the resting membrane potenetial of muscle?

A

-90mv

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9
Q

what is the nernst potential for Na?

A

+50

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10
Q

are the nAChR in ANS and NMJ the same?

A

Nicotinic receptors and autonomic ganglia have different types of α and β subunits.

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11
Q

which calcium channel types are found in cardiac cells?

A

T and L types
(N type found pre-synaptically in NMJ)

T found in pacemakers
L found in pacemaker and cardiac

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12
Q

what is the difference in ryanodine cells found in cardiac vs muscle cells

A

Ryanodine RyR1 receptors are in the membrane of the sarcoplasmic reticulum; RyR2 are found in myocardial cells.

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13
Q

how do organophosphates work?

A

inhibit acetylcholinesterase irreversibly
cause increase ACh

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14
Q

what is edrophonium?

A

Acetylcholinesterase inhibitor - used to test for myasthenia gravis

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15
Q

how does botulinum and tetanus work?

A

botulinum - hibition of SNARE proteins preventing ACh releas

tetanus - the same for GABA

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16
Q

how does α-bungarotoxin venom work?

A

irreversible inhibition of nAChR

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17
Q

how many subunits in a 5HT3 receptor?

A

5

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18
Q

which family of receptors does the nACHR belong too?

A

cys loop family

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19
Q

how many subunits in an AMPA receptor

A

tetramer / 4

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20
Q

how many subunits in P2X receptor?

A

trimer

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21
Q

what is the difference between T1:T4 ratio with succinylcholine and atracurium?

A

non depolarising agents - fade i.e. T1 > T4

depolarising - no fade - phase 1 block. with repeated administration start to show fade and features of non-depolarising agents (phase 2 block)

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22
Q

how does succinylcholine work?

A

agonist of nAChR
binds causing depolarisation
then blocks receptor from further depolarisations.

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23
Q

how does succinylcholine act after repeated doses?

A

phase 2 block - fade (due to inhibition of presynaptic), post tetanic fasilitation/potentiation,

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24
Q

which NMBA show fade, post tetanic potentiation and pre-synaptic nAChR binding?

A

non-depolarising

OR depolarising agent AFTER multiple doses

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25
which patients should sux be avoided in ?
- allergy - sun apnoea - risk of high K - AKI/ burns / spinal cord injury / nerve trauma / immobility / severe sepsis - after 24 hrs. guillian barre - risk of high pressures
26
which succinylcholine genotype gives paralysis for longest - 8 to 10hours?
ESES
27
which is the most likely muscle relaxant to cause anaphylaxis?
sux
28
what are the different classes of NMBAs?
depolarising - sux non-depolarising - benzylisoquinolinums - atracurium + mevacurium - aminosteroids - roc and vec
29
where do non-depolarising NMBA bind?
a subunit of nAChR - form an ionic bond
30
what factors prolong block with non-depolarising agents?
Mg aminoglycosides - gentamicin tetracyclines TCA low Ca acidosis myasthenia gravis
31
which of the aminosteroid NMBA is monoquartnary and biquartnary - what does this mean about excretion?
monoquarternary - rocuronium and vec - more biliary excretion (30% urinary) bisquarternary - pancuronium - more urinary excretion (60% urinary) - piss in a pan
32
does rocuronium have active metabolite?
yes but very weak - 20x less active
33
does pancuronium have an active metabolite?
yes 50% the activity - hence why has such prolonged action
34
what is ED 95?
ED95 is the dose required for 95% depression of TWITCH response, where ED stands for effective dose.
35
which NMBA has most and least potency?
most - pipecuronium then vecuronium then pancuronium Atracurium then rocuronium least - rapacuronium
36
which NMBA has most potent active metabolite?
vecuronium - 80% active - however only a very small fraction made
37
how can acidity of blood change potency of non depolarsing NMBA?
The tertiary amine becomes protonated and therefore positively charged, this increases the potency. it is the quartnary amine responsible for interaction with nACh
38
what is hoffman elimination dependant on?
temp and pH
39
which of the benzylisoquinolium NMBA has 1) fastest onset 2) longest duration
fastest onset - atracurium (mivacurium is slowest) shortest duration - mivacurium (duration of cisatracurium and atracurium is the same)
40
how is atracurium metabolised? how does this compare to cis-atracurium?
Atracurium: - hoffman degradation 45% - ester hydrolysis 45% - 10% unchanged in urine cisatracurium - hoffman - 77% - ester hydolysis - <10% - 15% unchanged in urine
41
what is the half life of atracurium?
50 mins at pH 7.4 and temp 37
42
how is atracurium stored?
4 degrees pH 3.4
43
which NMBA are most likely to give histamine release?
benzylisoquinoliniums most likely atracurium and mivacurium cis-atracurium has reduced histamine release the larger the dose and faster the injection, the more likely histamine release
44
how does renal function effect benzylisoquinoliniums ?
The benzylisoquinolinium NMBAs are independent of renal excretion.
45
what type of isomers does atracurium have?
geometric and sterioisomers 4 chiral centres 10 isomers in total
46
what type of isomer is cisatracurium of atracurium?
cis-atracurium is the C1-R - Cis (15% of total atracurium isomers)
47
how many isomers of mivacurium are there? which is most abundant and least potent?
3 - Trans-trans, which comprises 58% of the mixture; cis-trans, which is 36% of the mixture; and cis-cis, which is 6% of mivacurium. cis-cis is the least potent different rates of metabolism
48
what is the water solubility of benzylisoquinoliniums like?
very water soluble Vd like ECF
49
what is oral bioavailability of NMBA agents like?
poor - no effect if taken orally
50
how is mivacurium broken down?
plasma cholinesterases (like sux) - hence affected by sux apnoea
51
is mivacurium elimination affected by liver/ kidney disease?
yes liver disease - less plasma cholinesterase production cis -cis has slow metabolism and hence is eliminated by kidneys and affected by renal failure.
52
what is the important breakdown product of atracurium? why is this important?
Hofmann elimination to laudanosine and a mono-quaternary acrylate. laudanosine - this causes epilepsy in animals - can accumulate in renal failure - otherwise inactive at NMJ
53
which has more laundanosine - atracurium or cis atracurium?
atracurium cis-atracurium - more hoffman HOWEVER more potent so less drug given so OVERALL less laudanosine
54
which type of nerve stimulator measurement device uses a piezoelectric crystal?
acceloromyograph
55
how many stimuli does the double burst stimulation have?
2x 3 stimuli
56
what is the most accurate measurement of nerve stimulation?
DBS is superior to train of four in the visual and tactile assessment of fade. However, acceleromyography is superior to both.
57
what train of four can give a sustained head lift?
0.6
58
how do edrophonium and neostigmine work?
both AChE inhibitors Edrophonium - forms weak H bonds with receptor to block it - short acting neostigmine causes carbmylation of the enzyme - needs regeneration - slightly longer acting
59
what is the half life of neostigmine?
30 mins
60
does suggamadex act at NMJ?
no
61
where is sux metabolised?
plasma cholinesterases IN THE PLASMA not NMJ
62
what are the idiosyncratic reactions to suxamethonium?
anaphylaxis, MH, apnoea
63
can the speed of onset for atracurium increase by increasing the dose?
yes - as increased conc gradient however not done in practice due to leading to histamine release and CVS instability.
64
what is the terminal half life of rocuronium?
85 mins
65
which of the muscle relaxants is associated with least anaphylaxis risk?
vecuronium
66
which muscle relaxant is most cardiostable?
vecuronium
67
how is vecuronium presented?
not stable in solution for long periods. It is presented as a white powder, which may be kept at room temperature, with an ampoule of water for reconstitution prior to use.