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Year 2 LCRS > Pharmacology 10 - Neuromuscular Blocking Drugs > Flashcards

Pharmacology 10 - Neuromuscular Blocking Drugs Flashcards

1
Q

Describe the innervation of skeletal muscle by the somatic nervous system

A
  • Single axon

- Releases Acetylcholine

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2
Q

What type of receptors are at the neuromuscular junction?

A
  • Muscarinic acetylcholine receptors (type 1 - ion channels)
  • They are slightly different to the nicotinic acetylcholine receptors at the ganglia, so therefore can selectively be blocked by antagonists
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3
Q

List the main competitive (non-depolarising) neuromusclar drugs. What are these drugs?

A
  • Tubocurarine
  • Atracurium
    Competitive antagonists
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4
Q

Give an example of a depolarising neuromuscular blocking drug. What are these drugs?

A

Suxamethonium

Agonists

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5
Q

What are the subunits of the nicotinic receptor?

A
  • 2 alpha, where acetylcholine binds (2 molecules of acetylcholine needed)
  • beta
  • gamma
  • delta
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6
Q

What is the result of opening of nicotinic receptor channel?

A
  • Sodium influx

- Some potassium efflux

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7
Q

Where can different drugs act to block neuromuscular junctions?

A
  • Central processes (generation of action potentials in the spinal cord)
  • Conduction of nerve action potential in motor neurone
  • ACh release
  • Depolarisation of the motor end plate and action potential initiation
  • Propagation of action potential along the muscle fibre and muscle contraction
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8
Q

Which drugs act on the central processes to relax smooth muscles?

A
  • Spasmolytics

- Eg. Diazepam and Baclofen

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9
Q

Which drugs reduce conduction of the nerve action potential in the motor nerve to relax smooth muscle?

A

Local anaesthetics

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10
Q

Which drugs reduce acetylcholine release to relax smooth muscle?

A
  • Hemicholinium
  • Ca2+ entry blockers
  • Neurotoxins (eg. butolium toxin)
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11
Q

Which drugs reduce depolarisation of the motor-end plate and initiation of an action potential to relax smooth muscle?

A
  • Tubocurarine

- Suxamethonium

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12
Q

Which drugs reduce propagation of action potentials along muscle fibres and muscle contraction to relax smooth muscle?

A
  • Spasmolytics

- Eg. dantrolene

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13
Q

What do neuromuscular blockers not affect?

A
  • Consciousness
  • Pain sensation
  • When administered, respiration must be assisted until drug is inactive
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14
Q

Where do neuromuscular blocking drugs act?

A
  • Postsynaptic action
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15
Q

Why can tubocurarine bind to the nicotinic receptors?

A
  • As it has 2 quaternary amine groups

- Acetylcholine also has one of these groups

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16
Q

Why can suxamethonium bind to the receptor and activate it?

A
  • Structure is more similar to acetylcholine

- Flexible and has rotation

17
Q

Describe the mechanism of action of suxamethonium

A
  • Nicotinic receptor agonist
  • Produces an extended end plate depolarisation (also called a phase 1 depolarisation block). Therefore, the receptor is overstimulated and shuts down
  • Fasciculations are seen as the drug is administered and muscle is stimulated, followed by flaccid paralysis (muscles relax)
18
Q

Describe the pharmacokinetics of suxamethonium

A
  • IV administration
  • Paralysis lasts around 5 minutes (short acting)
  • Metabolised by pseudocholinesterase (butyrylcholinesterase) in the liver and plasma
19
Q

List the uses of suxamethonium

A
  • Endotracheal intubation (used in bronchoscopy and administer anaesthesia)
  • Muscle relaxant for ECT (electroconvulsive therapy - used to treat severe clinical depression)
20
Q

List the unwanted effects of suxamethonium

A
  • Post-oerative muscle pains (due to fasciculations)
  • Bradycardia (due to direct muscarinic action on the heart - solved by atropine administration premed)
  • Hyperkalaemia
  • Increased intraocular pressure (not used in eye injurys or glaucoma)
21
Q

Why can suxamethonium not be administered to patients with soft tissue injury or burns?

A
  • Soft tissue injury or burns decreases sensitivity to acetylcholine
  • End plate responds by increasing nicotinic receptors, attempting to amplify reduced input
  • This is denervation supersensitivity, leads to increased potassium efflux and sodium influx
  • Hyperkalaemia can lead to ventricular arrhythmias or cardiac arrest
22
Q

What is tubocurarine?

A
  • Naturally occurring tertiary ammonium compound found in plants
23
Q

Describe the mechanism of action of tubocurarine

A
  • Competitive nicotinic acetylcholine receptor antagonist

- 70-80% block necessary

24
Q

List the effects of tubocurarine

A
  • Causes flaccis paralysis
  • Double vision when the patient is conscious, small muscles of face limbs and pharynx relax, then respiratory muscles relax
  • Recovery occurs in the reverse of the order off occurrence of those effects
25
Q

Describe the effect of tubocurarine on neuromusclar transmission

A
  • ACh released at end plate, but tubocurarine is blocking the nicotinic receptors
  • Therefore, the end plate potential generated is not sufficient to stimulate muscle contraction
  • No propagation from the end plate
26
Q

List the uses of tubocurarine

A
  • Relaxation of skeletal muscles during surgical operations (therefore, less anaesthetic is needed)
  • Permit artificial ventilation, as the respiratory muscles are relaxed
27
Q

How can actions of non-depolarising blockers be reversed?

A
  • By acetylcholinesterases

- Eg. neostigmine (+atropine to prevent overstimulation of muscarinic receptors)

28
Q

Describe the pharmacokinetics of tubocurarine

A
  • IV administration
  • Does not cross the blood brain barrier/placenta
  • Duration of paralysis is 1-2 hours (long)
  • Not metabolised, excreted 70% in urine and 30% bile (therefore, be careful if there is impairment of renal/hepatic function - use atracurium instead)
29
Q

What is atracurium?

A
  • Chemically unstable non-depolarising blocker
  • Breaks down spontaneously after 15 minutes to two inactive fragments
  • Therefore, it can be used in patients with impairment of renal/hepatic function
  • Same mechanism of action as tubocurarine
30
Q

List the side effects of tubocurarine

A
  • Hypotension (due to ganglion blockade decreasing TPR and histamine release - histamine is a vasodilator)
  • Tachycardia (potentially can give rise to arrhythmias, a reflex to tachycardia, or blockade of vagal ganglia)
  • Bronchospasm and excessive secretions (histamine bronchoconstrictor)
  • Apnoea (always assist respiration)
31
Q

What causes side effects of tubocurarine?

A
  • Ganglion blockade

- Histamine release from mast cells, as tubocurarine is so basic

32
Q

How does tubocurarine affect the log dose-response curve showing response of skeletal muscle to increasing concentration of ACh?

A
  • The curve will shift right
  • Max will be reached as tubocurarine is surmountable
  • Competitive antagonist

Year 2 LCRS (128 decks)

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