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PHARMACOLOGY FRCA > NMBA > Flashcards

NMBA Flashcards

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)

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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

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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
Q

which patients should sux be avoided in ?

A

burns / spinal cord injury / nerve trauma / immobility / severe sepsis - after 24 hrs

guillian barre

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26
Q

which succinylcholine genotype gives paralysis for longest - 8 to 10hours?

A

ESES

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27
Q

which is the most likely muscle relaxant to cause anaphylaxis?

A

sux

28
Q

what are the different classes of NMBAs?

A

depolarising - sux
non-depolarising
- benzylisoquinolinums - atracurium + mevacurium
- aminosteroids - roc and vec

29
Q

where do non-depolarising NMBA bind?

A

a subunit of nAChR - form an ionic bond

30
Q

what factors prolong block with non-depolarising agents?

A

Mg
aminoglycosides - gentamicin
tetracyclines
TCA
low Ca
acidosis
myasthenia gravis

31
Q

which of the aminosteroid NMBA is monoquartnary and biquartnary - what does this mean about excretion?

A

monoquarternary - rocuronium and vec - more biliary excretion (30% urinary)

bisquarternary - pancuronium - more urinary excretion (60% urinary)

32
Q

does rocuronium have active metabolite?

A

yes but very weak - 20x less active

33
Q

does pancuronium have an active metabolite?

A

yes 50% the activity - hence why has such prolonged action

34
Q

what is ED 95?

A

ED95 is the dose required for 95% depression of TWITCH response, where ED stands for effective dose.

35
Q

which NMBA has most and least potency?

A

most - pipecuronium
then vecuronium
then pancuronium
then rocuronium
least - rapacuronium

36
Q

which NMBA has most potent active metabolite?

A

vecuronium - 80% active - however only a very small fraction made

37
Q

how can acidity of blood change potency of non depolarsing NMBA?

A

The tertiary amine becomes protonated and therefore positively charged, this increases the potency.

it is the quartnary amine responsible for interaction with nACh

38
Q

what is hoffman elimination dependant on?

A

temp and pH

39
Q

which of the benzylisoquinolium NMBA has
1) fastest onset
2) longest duration

A

fastest onset - atracurium (mivacurium is slowest)

shortest duration - mivacurium (duration of cisatracurium and atracurium is the same)

40
Q

how is atracurium metabolised? how does this compare to cis-atracurium?

A

Atracurium:
- hoffman degradation 45%
- ester hydrolysis 45%
- 10% unchanged in urine

cisatracurium
- hoffman - 77%
- ester hydolysis - <10%
- 15% unchanged in urine

41
Q

what is the half life of atracurium?

A

50 mins
at pH 7.4 and temp 37

42
Q

how is atracurium stored?

A

4 degrees
pH 3.4

43
Q

which NMBA are most likely to give histamine release?

A

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
Q

how does renal function effect benzylisoquinoliniums ?

A

The benzylisoquinolinium NMBAs are independent of renal excretion.

45
Q

what type of isomers does atracurium have?

A

geometric and sterioisomers
4 chiral centres
10 isomers in total

46
Q

what type of isomer is cisatracurium of atracurium?

A

cis-atracurium is the C1-R - Cis
(15% of total atracurium isomers)

47
Q

how many isomers of mivacurium are there? which is most abundant and least potent?

A

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
Q

what is the water solubility of benzylisoquinoliniums like?

A

very water soluble
Vd like ECF

49
Q

what is oral bioavailability of NMBA agents like?

A

poor - no effect if taken orally

50
Q

how is mivacurium broken down?

A

plasma cholinesterases (like sux) - hence affected by sux apnoea

51
Q

is mivacurium elimination affected by liver/ kidney disease?

A

yes liver disease - less plasma cholinesterase production

cis -cis has slow metabolism and hence is eliminated by kidneys and affected by renal failure.

52
Q

what is the important breakdown product of atracurium? why is this important?

A

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
Q

which has more laundanosine - atracurium or cis atracurium?

A

atracurium

cis-atracurium - more hoffman HOWEVER more potent so less drug given so OVERALL less laudanosine

54
Q

which type of nerve stimulator measurement device uses a piezoelectric crystal?

A

acceloromyograph

55
Q

how many stimuli does the double burst stimulation have?

A

2x 3 stimuli

56
Q

what is the most accurate measurement of nerve stimulation?

A

DBS is superior to train of four in the visual and tactile assessment of fade. However, acceleromyography is superior to both.

57
Q

what train of four can give a sustained head lift?

A

0.6

58
Q

how do edrophonium and neostigmine work?

A

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
Q

what is the half life of neostigmine?

A

30 mins

60
Q

does suggamadex act at NMJ?

A

no

61
Q

where is sux metabolised?

A

plasma cholinesterases
IN THE PLASMA

not NMJ

62
Q

what are the idiosyncratic reactions to suxamethonium?

A

anaphylaxis, MH, apnoea

63
Q

can the speed of onset for atracurium increase by increasing the dose?

A

yes - as increased conc gradient
however not done in practice due to leading to histamine release and CVS instability.

64
Q

what is the terminal half life of rocuronium?

A

85 mins

65
Q

which of the muscle relaxants is associated with least anaphylaxis risk?

A

vecuronium

66
Q

which muscle relaxant is most cardiostable?

A

vecuronium

67
Q

how is vecuronium presented?

A

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.

PHARMACOLOGY FRCA (12 decks)

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