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LCRS 1 - Pharmacology > Neuromuscular blocking drugs > Flashcards

Neuromuscular blocking drugs Flashcards

1
Q

What is the neurotransmitter at the skeletal NMJ? What receptor type does it act on?

A

Acetyl choline

Nicotinic acetyl choline receptors on the motor end-plate

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2
Q

What are the clinical uses of neuromuscular blocking agents?

A

Suxamethonium:
Endotracheal intubation - relaxes airway skeletal muscle
Muscle relaxant for electroconvulsant therapy for severe clinical depression

Tubocurarine:
Relaxation of skeletal muscles during surgery (less anaesthetic needed)
Permit artificial ventilation

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3
Q

What are unwanted effects of tubocurarine?

A
  • Ganglion block
  • Histamine release from mast cells
  • Hypotension
  • Tachycardia –> arrhythmias
  • Bronchospasm
  • Excessive secretions
  • Apnoea - tf assist breathing
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4
Q

How does tubocurarine work?

A
  • Competitive nicotinic AChR antagonist
  • Need about 70-80% block to achieve full relaxation of muscles
  • If you block enough receptors, EPP generated does not reach threshold
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5
Q

Describe the pharmacokinetics of tubocurarine

A
  • IV
  • Does not cross BBB or placenta
  • Long duration of paralysis: 40-60 mins
  • Not metabolised
  • Excreted in urine (70%) and bile (30%)
  • Any impairment in hepatic or renal fn increases duration of action
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6
Q

How does tubocurarine alter the log dose-response curve showing the response of skeletal muscle to increasing [ACh]?

A

Moves curve right without reducing the maximal response to ACh

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7
Q

How long does the paralysis caused by tubocurarine last?

A

40-60 minutes

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8
Q

Are NM blockers metabolised?

A

Depolarising - yes

Non-dp - no

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9
Q

Does tubocurarine cross the BBB?

A

No

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10
Q

Is tubocurarine metabolised?

A

Not at all

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11
Q

How does any impairment of hepatic or renal function affect the effects of tubocurarine?

A

Increases their duration of action

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12
Q

What should be coadministered with tubocurarine if there is any impairment of hepatic or renal function?

A

Atracurium (15 mins duration of action)

Then effects of tubocurarine effects are not affected by lack of liver/kidney function

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13
Q

What is the main effect of NM blockers?

A

Flaccid paralysis (no muscle tone)

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14
Q

How does suxamethonium work?

A
  • Depolarising
  • Nicotinic AChR agonist
  • Causes extended end plate DP
  • Leads to a depolarisation block of NMJ caused by overstimulation (phase 1 block)
  • Isn’t metabolised as rapidly as ACh so remains bound to AChRs - receptors quickly switch off
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15
Q

What are the effects of non-depolarising NM blockers?

A

Flaccid paralysis (no muscle tone) in particular order (reverse back to normal):

  • Extrinsic eye muscles
  • Small muscles of face, limbs, pharynx
  • Respiratory muscles
  • Fasciculations
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16
Q

Does suxamethonium cross the BBB?

A

No

17
Q

What are the unwanted effects of suxamethonium?

A

Post-operative muscle pains - due to initial fasciculations
Bradycardia - direct muscarinic action on heart
Hyperkalaemia - soft tissue injury or burns can lead to ventricular arrhytmias, cardiac arrest
Raised intraocular pressure

18
Q

How is unwanted bradycardia usually prevented when giving suxamethonium?

A

Suxamethonium has direct muscarinic action on heart
Suxamethonium is given after GA
Atropine - competitive muscarinic antagonist - given in pre med

19
Q

What is the target of NM blockers?

A

Post-synpatic nictonic AChRs on motor end plate

20
Q

What are the 2 groups of NM blockers with examples?

A
  1. Non-depolarising - competitve nicotinic receptor antagonists
    E.g. tubocurarine, atracurium
  2. Depolarising - nicotinic receptor agonists
    E.g. suxamethonium
21
Q

Why do you always assist respiration when giving NM blockers?

A

NM blockers affect respiratory muscles and cause apnoea

22
Q

Compare the structure of non-depolarising and depolarising NM blockers

A

Non-depolarising:
Big, bulky molecules
Restricted movement around bonds

DP:
2 ACh molecules linked together
Flexible, allows rotation

23
Q

What are the pharmacokinetic features of suxamethonium?

A
  • i.v. (highly charged)
  • Duration of paralysis = 5 mins
  • Metabolised by pseudocholinesterase in liver + plasma

LCRS 1 - Pharmacology (33 decks)

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