Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHARMACOLOGY FRCA > NMBA > Flashcards

NMBA Flashcards

1
Q

Is acetylcholine an essential amino acid?

A

NO
essential NUTRIENT
it is not an amino acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what type of amine does acetylcholine have?

A

quarternary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is acetyl coA formed?

A

Acetyl-CoA is formed from oxidative decarboxylation of pyruvate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the conduction velocity of alpha motor neuron?

A

50 - 100m/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

which type of Ca channels are found pre-synaptically?

A

N type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

which receptor subunit does ACh bind?

A

alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

where is acetylcholinesterase enzyme found?

A

In clefts of the folded post synaptic membrane found in clusters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the resting membrane potenetial of muscle?

A

-90mv

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the nernst potential for Na?

A

+50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how do organophosphates work?

A

inhibit acetylcholinesterase irreversibly
cause increase ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is edrophonium?

A

Acetylcholinesterase inhibitor - used to test for myasthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does botulinum and tetanus work?

A

botulinum - hibition of SNARE proteins preventing ACh releas

tetanus - the same for GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does α-bungarotoxin venom work?

A

irreversible inhibition of nAChR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how many subunits in a 5HT3 receptor?

A

5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which family of receptors does the nACHR belong too?

A

cys loop family

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how many subunits in an AMPA receptor

A

tetramer / 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how many subunits in P2X receptor?

A

trimer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how does succinylcholine work?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how does succinylcholine act after repeated doses?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

non-depolarising

OR depolarising agent AFTER multiple doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

which patients should sux be avoided in ?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

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

A

ESES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
- piss in a pan

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
Atracurium
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 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions