Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology & Therapeutics Y2 > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

Which nervous system controls muscle innervation

A

Somatic nervous system

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

Where generally is the cell body of the alpha motor neurone

A

Spinal cord

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

How many neurons are between the cell body and muscle

A

1 single axon

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

Which horn of the spinal cord do you find the cell body of alpha motor neurone

A

Ventral horn

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

Specifically where do you find the cell body of the alpha motor neurone

A

Ventral horn of the spinal cord

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

What does CAT stand for

A

Choline acetyl transferase

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

What type of neurone do you find CAT in (X-ic receptor)

A

Cholinergic

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

What reaction does CAT catalyse

A

Acetyl CoA + choline ACh + CoA-SH

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

What is CoA-SH also known as

A

Co-enzyme A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the end plate

A

The post-synaptic membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What family of receptors does the receptor on the end plate belong to?

A

Nicotinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

With the first step being depolarisation of the presynaptic membrane, and ninth being an action potential propagating bidirectionally along the sarcolemma, describe the 9 steps and all the steps inbetween

A

1) Depolarisation of the presynaptic membrane
2) VGCC open
3) Ca2+ influx
4) ACh efflux
5) ACh binds to nicotinic ACh receptors on the end plate
6) Linked ion channel opens
7) Na+ influx
8) End plate potential reaches threshold
8) Action potential propagates bidirectionally

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

What type of receptor is the ACh receptor found on the end plate?

A

Nicotinic type-1 ion channel linked receptor

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

Which 3 molecules travel through the end plate ion channel when it opens after ACh stimulation? Which directions? What is similar of all 3 molecules that allows them to travel through together?

A

Na+ - influx
K+ - efflux
Ca2+ - influx
They are all cations

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

Is the potential that arises on the end plate of a muscle fibre graded or all or nothing?

A

Graded

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

Is the bidirectional action potential graded or all or nothing

A

All or nothing

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

What 2 factors does the size of the end plate potential depend upon

A

Amount of ACh released and how many receptors are stimulated

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

How long is a type-1 ion channel open for generally

A

Milliseconds

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

Whereabouts on a muscle fibre are the nicotinic ACh receptors usually found

A

Middle

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

Are nicotinic type-1 ion channel linked ACh receptors anion or cation channels

A

Cation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Under what circumstances is an action potential generated from an end plate potential

A

Normal

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

What enzyme breaks down ACh

A

Acetylcholinesterase

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

Where is acetylcholinesterase bound to

A

The basement membrane

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

What reaction does acetylcholinesterase catalyse

A

ACh –> acetic acid + choline

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

What is the fate of choline once it is made through the breakdown of ACh via acetylcholinesterase? What pump facilitates this

A

Can be pumped back into the presynaptic terminal through the choline pump to be reused to make more ACh

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

What are the three main neuromuscular blocking drugs

A

Tubocurarine, atracurium and suxamethonium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the two subtypes of nicotinic receptors

A

Ganglionic/(neuronal) type and muscle type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How many and what are the subunits on a nicotinic receptor

A

2 alpha, 1 beta delta and gamma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which subunit of the nicotinic acetylcholine receptor does ACh bind to

A

Alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How do drugs differentiate between ganglionic/neuronal cholinergic receptors and muscle type receptors

A

There is a slight difference in structure of the ganglionic/neuronal type and muscle type receptors that allows selectivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Local anaesthetics: what site do they target/process do they affect

A

Conduction of action potential up/down neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the mechanism of a local anaesthetic

A

They block VGSC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Can/how do anaesthetics affect muscle intervention and why? Do they have selectivity

A

Local anaesthetics can cause muscle weakness because they block VGSC which is used to propagate AP to stimulate muscle contraction. Local anaesthetics do have a degree of selectivity to the relevant sensory neurone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Baclofen is a [X] receptor [agonist/antagonist]

A

GABA receptor agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Diazepam (Valium) is a [X] receptor [agonist/antagonist]

A

GABA receptor agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Name 2 GABA receptor agonists

A

Diazepam/Valium and baclofen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How do neurotoxins facilitate death (name neurotransmitter affected and the specific system which subsequently causes death when the function is impaired). Give an example of a neurotoxin

A

Inhibit the release of ACh which causes death through impairment of respiratory muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Where do neuromuscular blocking drugs act

A

Nicotinic receptors on the end plate/post synaptic membrane

39
Q

What type of NMB drug is suxamethonium

A

Depolarising

40
Q

What type of NMB drug is tubocurarine

A

Non-depolarising

41
Q

Give an example of a depolarising NMB drug

A

Suxamethonium

42
Q

Give two examples of non-depolarising NMB drugs

A

Tubocurarine and atracurium

43
Q

Depolarising NMB drugs are [agonists/antagonists]

A

Agonists

44
Q

Non-depolarising NMB drugs are [agonists/antagonists]

A

Antagonists

45
Q

NMB [directly/indirectly] influence AP propagation

A

Indirectly

46
Q

NMB drugs [are/are not] analgesic

A

Are not

47
Q

NMB drugs [do/do not] affect consciousness, which class of drugs affect consciousness

A

Do not, general anaesthetics

48
Q

What MUST you do when administering NMB drugs to ensure patient safety

A

Assist respiration

49
Q

Describe the structure of suxamethonium, and properties of the drug (size/flexibility/rotation/efficacy/affinity/aromatics)

A

Two ACh molecules stuck together so relatively small; flexible and has rotational ability. Has both efficacy and affinity. No benzene rings.

50
Q

Describe the structure of tubocurarine/non-depolarising drugs, and properties of the drug (size/flexibility/rotation/efficacy/affinity/aromatics)

A

Big, bulky, inflexible with relatively restricted rotation. No efficacy but strong affinity (competitive antagonist). Can have benzene rings.

51
Q

Describe the MOA of suxamethonium. Mention metabolism. What is this type of depolarisation block called?

A

One suxamethonium molecule can bind to two alpha subunits and stimulate both. This overstimulates the nicotinic receptors. Suxamethonium isn’t metabolised as quick as ACh and so remains bound for so long causing so much overstimulation that the receptors switch off.
Known as a phase 1 block.

52
Q

What drug stimulates a phase 1 block

A

Suxamethonium

53
Q

What is a fasciculation and what drug causes this

A

Twitching of individual muscle fibres

54
Q

How are NMB drugs administered

A

Intravenously

55
Q

How is suxamethonium administered

A

Intravenously

56
Q

Suxamethonium is [hydrophilic/lipophilic] because of X

A

Hydrophilic because of the two quaternary ammonium groups

57
Q

Why is suxamethonium administered intravenously

A

The two quaternary ammonium groups on it make it lipid insoluble meaning it can’t cross lipid membranes and therefore wont be absorbed effectively

58
Q

How long does paralysis on suxamethonium last

A

5 minutes

59
Q

What metabolises suxamethonium and what two places is this enzyme found

A

Pdeudocholinesterase in the liver and plasma

60
Q

What are the two clinical uses of suxamethonium

A

To relax the skeletal muscle of the airways for endotracheal intubation, and as a muscle relaxant for electroconvulsive therapy

61
Q

What are the four major side effects of suxamethonium, explain them

A

Post-operative muscle pains: due to initial muscle fasciculations
Bradycardia: due to the direct muscarinic receptor stimulation of the muscarinic receptors on the heart
Hyperkalaemia: burns cause the loss of neurones in the muscle, which leads to upregulation of receptors in the skeletal muscle (deinnervation hypersensitivity). Suxamethonium then causes an exaggerated influx of sodium and also efflux of potassium.
Raised intraocular pressure: suxamethonium can cause contraction of the extraocular muscles.

62
Q

What type of NMB drugs do you give burns patients?

A

Non-depolarising

63
Q

What type of NMB drugs do you give glaucama and eye injury patients?

A

Non-depolarising

64
Q

What is deinnervation supersensitivity and give an example of what can cause this

A

Upregulation of receptors in skeletal muscle e.g. through burns

65
Q

How is bradycardia prevented when administering suxamethonium

A

Suxamethonium is administered after general anaesthetic and atropine premed -> atropine is a muscarinic receptor antagonist

66
Q

What is special of tubocurarine when it comes to non-depolarising NMB drugs

A

It is typical of all other NMB drugs, came first

67
Q

What is the MOA of tubocurarine. Mention EPP, AP and affinity, efficacy

A

Competitive antagonist, competes with endogenous ACh for the nicotinic receptor on the end plate. This prevents sufficient end plate potential being generated to stimulate an action potential. Has affinity but no efficacy.

68
Q

What % block through tubocurarine do you have to achieve to achieve full relaxation of muscles

A

70-80%

69
Q

What is the order the skeletal muscles relax in under the influence of tubocurarine

A

Extrinsic eye muscles -> small muscles of the face, limbs, pharynx -> respiratory muscles

70
Q

What is the order the skeletal muscles lose their flaccid paralysis caused by tubocurarine

A

Respiratory muscles -> small muscles of the face, limbs pharynx -> extrinsic eye muscles

71
Q

What is the little shoulder in a graph recording AP’s

A

The EPP

72
Q

What are the two major clinical uses of tubocurarine

A

Relaxation of skeletal muscles during surgical operations and to permit artificial ventilation

73
Q

Why would you use tubocurarine to relax skeletal muscles before surgical operations and what two benefits does this have to the patient

A

The NMB drug has relaxed muscles therefore means less general anaesthetic is needed which is good as it is safer and means the patient can be brought round quicker

74
Q

How does tubocurarine permit artificial ventilation

A

It relaxes skeletal muscles allowing a ventilator to take control of the patients respiration

75
Q

How do you reverse the effects of a non-depolarising blocker

A

Via anticholineesterase

76
Q

How do you reverse the effects of a depolarising blocker

A

You can’t

77
Q

The effects of [depolarising/non-depolarising] NMB drugs can be reversed

A

Non-depolarising

78
Q

Give an example of an anti-cholinesterase

A

Neostigmine

79
Q

How do anti-cholinesterase reverse the actions of a depolarising NMB

A

They prevent cholinesterase from breaking down ACh meaning they can then outcompete the tubocurarine

80
Q

What must you administer with neostigmine and why

A

Atropine as neostigmine will inhibit anticholinesterases at every cholinergic synapse and so the atropine prevents muscarinic receptor overstimulation

81
Q

How is tubocurarine administered and why

A

IV as it is highly charged/polar/lipophobic due to quaternary ammonium groups and therefore would be unable to cross the lipid bilayer to be absorbed by cells

82
Q

What does the polar nature of NMB drugs prevent them from entering

A

The BBB and placenta

83
Q

What is the duration of tubocurarine and why

A

Long, 1-2 hours bc it’s not metabolised at all n is excreted unchanged

84
Q

What are the proportions / places tubocurarine is excreted

A

70% urine 30% bile

85
Q

What would you use if someone is hepatically or renally impaired, how is this different, what is it’s duration of action

A

Atracurium, it is chemically highly unstable and is readily hydrolysed therefore lasts around 15 mins

86
Q

What effect does tubocurarine have on mast cells and why

A

Stimulates histamine release from mast cells as it is highly basic

87
Q

What effect does tubocurarine have on blood pressure and why

A

Hypotensive effect due to ganglionic nicotinic receptor blockade. Causes fall in TPR. Histamine also stimulates H1 receptors on vasculature to cause vasodilation

88
Q

What effect does tubocurarine have on heart rate and why (2 reasons why). What can this lead to

A

Tachycardia, reflex due to hypotension. May lead to arrhythmias. Also may be because of vagal ganglia blockade; Vagus puts a break on the heart

89
Q

What effect can tubocurarine have on the lungs and why

A

Bronchospasm due to histamine release

90
Q

What effect can tubocurarine have on breathing and why

A

Apnoea due to a block in skeletal muscle fibres, including respiratory muscles

91
Q

What are the 2 primary causes of the unwanted effects of tubocurarine

A

Ganglion blockade and histamine release from mast cells

92
Q

What are 5 unwanted effects of tubocurarine caused by ganglion blockade and histamine release

A 
Hypotension
Tachycardia
Bronchospasm
Excessive secretions (bronchial and salivary)
Apnoea
93
Q

What effect does tubocurarine have on secretions and why

A

Excessive secretions (bronchial and salivary) due to histamine release

Pharmacology & Therapeutics Y2 (10 decks)

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