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Pharmacology > Pharm 10 - Neuromuscular Blocking Drugs > Flashcards

Pharm 10 - Neuromuscular Blocking Drugs Flashcards

1
Q

Describe how impulses are transmitted across synapses.

A

Action potential propagates along the presynaptic neurone –> depolarisation of presynaptic membrane –> oprening of VGCC –> calcium influx –> vesicle exocytosis

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2
Q

What type of receptor is found at the neuromuscular junction?

A

nicotinic acetycholine receptors

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3
Q

Where are these receptors found on the muscle fibre?

A

Motor end plate

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4
Q

What does depolarisation of the motor end plate cause?

A

Causes a change in end plate potential
Graded potential

Once it reaches its threshold, action potential propagates in both directions away

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5
Q

Where is acetylcholinesterase found?

A

bound to basement membrane in the synaptic cleft

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6
Q

State the three main neuromuscular blockers.

A

Tubocurarine
Atracurium
Suxamethonium

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7
Q

State the two main types of nicotinic acetylcholine receptor.

A

Ganglionic

Muscle

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8
Q

Describe the structure of nicotinic acetylcholine receptors.

A

5 subunits

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9
Q

How many molecules of acetycholine are required to activate 1 nicotinic acetylcholine receptor?

A

2

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10
Q

Name 2 drugs that are used as spasmolytics.

A

Diazepam
Baclofen

Both help GABA transmission

GABA is inhibitory so reduce epilepsy etc

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11
Q

Give some examples of conditions in which spasmolytics may be used

A

cerebral palsy and spasticity

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12
Q

What do local anaesthetics have their effect on?

A

Conduction of action potentials in motor neurones

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13
Q

Describe the action of neurotoxins.

A

inhibit the release of acetylcholine and hence block the contraction of respiratory skeletal muscle causing death

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14
Q

Describe the difference between depolarising and non-depolarising NM blockers.

A

depolarising = suxamethonium = nicotinic acetylcholine receptor agonist

non-depolarising = tubocurarine + atracurium = nicotinic acetylcholine receptor antagonist

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15
Q

How do NM blockers affect conciousness and pain?

A

They DO NOT

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16
Q

What must you always do when giving NM blockers?

A

assist respiration

17
Q

Describe the difference in structure between non-depolarising and depolarising NM blockers.

A

Non-depolarising = big, bulky molecules with limited movement around
their bonds
Suxamethonium = made up of two acetylcholine molecules that are
linked together. This is more flexible and allows rotation. As it is made
up of two acetylcholine molecules it can binds to the two alpha subunits
and activate the receptor.

18
Q

Describe the mechanism of action of suxamethonium.

A

agonist

extended end plate depolarisation leading to depolarising block of the NMJ

19
Q

What does Suxamethonium normally cause before causing the flaccid paralysis?

A

Fasciculations

20
Q

What is the duration of paralysis of suxamethonium?

A

5 mins

21
Q

How is suxamethonium metabolised?

A

by pseudocholinesterase in liver and plasma

22
Q

What are some uses of suxamethonium?

A

Endotracheal intubation

Muscle relaxant

23
Q

State 4 unwanted effects of suxamethonium.

A

1) Post surgical muscle pain because of fasciculations
2) hyperkalaemia
3) bradycardia
4) raised intraocular pressure

24
Q

Describe the mechanism of action of tubocurarine.

A

competitive nicotinic acetylcholine receptor antagonist

need to block around 70-80% of receptors

25
Q

State the order of relaxation of skeletal muscles when administering tubocurarine.

A
  • extrinsic eye muscles
  • small muscles of face limbs and pharynx
  • resp muscles
26
Q

State 2 uses of tubocurarine.

A

relaxation of muscles during surgical operations

permit artifical ventilation

27
Q

How can the actions of NM blockers be reversed?

A

Give a anti-cholinesterase

28
Q

What else would you give with an anticholinesterase?

A

atropine to stop some unwanted side effects

29
Q

How are NM blockers administered?

A

iv

30
Q

What is the duration of action of tubocurarine?

A

40 mins

31
Q

Under which conditions would you get increased duration of tubocurarine?

A

Impaired renal or hepatic functions

32
Q

What are the main unwanted effects of tubocurarine?

A
  • hypotension
  • tachycardia
  • bronchospasm
  • excessive secretions
  • apnoea

Pharmacology (10 decks)

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