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Year 2 Collin > Pharm 10 - NMJ blocking drugs > Flashcards

Pharm 10 - NMJ blocking drugs Flashcards

1
Q

Somatic motor nervous system uses which neurotransmitter?

A

ACh. Only a single axon

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2
Q

What enzyme is used for ACh synthesis?

A

CAT (cholinoacetyl transferase)

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3
Q

Muscle type NAChR are different to ganglionic NAChR?

A

True

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4
Q

ACh binds to the alpha subunits of the NAChR. Typically how many ACh must bind to the NAChR for it to open?

A

2

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5
Q

Baclofen is a spasmolytic. It is a —— agonist

A

GABA

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6
Q

What do local anaesthetics act on?

A

VGSC

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7
Q

Dantrolene is a spasmolytic. Where does it work and what is its mode of action?

A

Inhibits release of Ca from Sarcoplasmic reticulum stores - less powerful muscle contraction

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8
Q

What are the sites of action of drug action?

A
  1. Central processes
  2. Conduction of AP along motor neurone
  3. ACh release
  4. Depolarisation of motor end plate - AP initiation
  5. Propagation of AP along muscle fibre + muscle contraction
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9
Q

What drugs can be used to target central processes?

A

Spasmolytics - e.g. diazepam or Baclofen

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10
Q

What drugs can be used to target the conduction of AP along motor neurone?

A

Local anaesthetics

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11
Q

What drugs can be used to target ACh release?

A
  1. Ca entry blockers
  2. Neurotoxins (e.g. botulinum)
  3. Hemicholinium
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12
Q

What drugs can be used to target depolarisation of motor end plate ?

A
  1. Tubocurarine

2. Suxamethonium

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13
Q

What drugs can be used to inhibit propagation of the AP along muscle fibre?

A

Certain spasmolytics e.g. Dantrolene

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14
Q

Do neuromuscular blocking drugs work presynaptically or postsynaptically?

A

Postsynaptically

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15
Q

What are the 2 classes of neuromuscular blocking drug that work postsynaptically?

A
  1. Non-depolarising (competitive antagonists)

2. Depolarising (agonists)

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16
Q

Give an example of a non-depolarising NM blocking drug?

A

Tubocurarine

Atracurium

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17
Q

Give an example of a depolarising NM blocking drug

A

Suxamethonium

18
Q

Do NM blocking drugs affect consciousness or pain sensation?

A

No

19
Q

What must always be assisted when giving NM blocking drugs in surgery?

A

Respiration

20
Q

What is the mode of action of suxamethonium?

A

Excessively stimulates NAchR on end plate - causing extended depolarisation. Suxamethonium takes 5/6 minutes to leave the synaptic cleft

This causes “depolarisation block” (aka Phase 1 block)

21
Q

What other drug can also cause depolarising block?

A

Ecothiopate

22
Q

What can happen in the first few minutes after administering suxamethonium?

A

Fasciculations - muscle twitches

Flaccid paralysis may follow - loss of tone in SkM

23
Q

How is suxamethonium administered?

A

Intravenously

24
Q

What is the duration of paralysis with suxamethonium?

A

5 minutes (SHORT)

25
Q

What is suxamethonium metabolised by?

A

Pseudo-cholinesterase

26
Q

Name 2 uses of suxamethonium

A
  1. Endotracheal intubation

2. Muscle relaxant for ECT

27
Q

What are some unwanted effects of suxamethonium?

A
  1. Post-op muscle pains
  2. Bradycardia due to direct muscarinic action on the heart (M2 receptors) but this is usually solved by coadministration of atropine
  3. Hyperkalaemia - e.g. giving patients with soft tissue damage/burns patients is very dangerous - causes greater sodium influx and greater K efflux
  4. Increased intraocular pressure - avoid for patients with eye injuries or glaucoma
28
Q

Why is it dangerous to give burns patients/soft tissue damage patients suxamethonium?

A

De-innervation up regulation of NAChR on SkM

29
Q

What can hyperkalaemia cause (in worst case scenarios)?

A

Ventricular arrhythmias and cardiac arrest

30
Q

What is a naturally occurring 4 Ammonium compound (alkaloid) found in S.American plants?

A

Tubocurarine

31
Q

What is the mode of action of tubocurarine?

A

Competitive NAChR antagonist - competes with endogenous ACh

32
Q

What % block is needed from tubocurarine to prevent the End plate potential firing an AP?

A

70-80% BLOCK

33
Q

What are the effects of tubocurarine?

A

Flaccid paralysis

  1. Initially, extrinsic eye muscles relax (double vision)
  2. Then small muscles of face, limbs, pharynx
  3. Then, respiratory muscles
34
Q

What is tubocurarine used for?

A
  1. SkM relaxation for surgery (means less General anaesthetic is needed)
  2. Relaxes respiratory muscles, allows artificial ventilation
35
Q

What can non-depolarising blockers be reversed by?

A

Anticholinesterases (e.g. Neostigmine (+ Atropine))

36
Q

How is tubocurarine given?

A

IV

37
Q

Tubocurarine is not very lipid soluble so it doesn’t cross which 2 things?

A

BBB or placenta

38
Q

What is the duration of paralysis with tubocurarine?

A

1-2 hours

39
Q

Is tubocurarine metabolised?

A

No, it is excreted (70% urine, 30% bile)

40
Q

If there are renal/hepatic problems in the patient, you don’t give tubocurarine. What do you give instead?

A

Atracurium (15 mins DOA) - DOA not determined by liver or kidney function.

41
Q

What are the unwanted effects of giving tubocurarine?

A
  1. Ganglion block and histamine release
  2. Hypotension due to Ganglion block (TPR decrease) and histamine release (H1 receptor causing vasodilation)
  3. Tachycardia - reflex tachycardia or blockade of vagal ganglia
  4. Bronchospasm and excessive secretions (histamine release)
  5. Apnoea (always assist respiration)
42
Q

What can basic drugs do to mast cells?

A

Cause them to release histamines

Year 2 Collin (114 decks)

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