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eLCRS - 팜 > PHARM 10: Neuromuscular blocking drugs > Flashcards

PHARM 10: Neuromuscular blocking drugs Flashcards

1
Q

Describe the process of neuromuscular transmission

starting from AP input.

A

AP arrives –> memb gets depolarized –> VGCC opens

–> Ca2+ influx occurs –> causes exocytosis of vesicles

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2
Q

What is the target for Ach at the neuromuscular junctions?

A

targets: nicotinic Ach receptors on the end plate

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3
Q

What does it mean by a graded potential?

A
  • depends on how much Ach is released + how many receptors are stimulated
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4
Q

Describe the process of neuromuscular transmission
starting from stimulation of nicotinic receptors

to the breakdown of Ach

A
  • nicotinic receptors are stimulated
  • -> resulting in a change in conformation + influx of Na+ ions
  • -> this causes memb depolarization aka End Plate Potential
  • -> when End plate potential reaches threshold, it generates AP that propagates in both directions from the end plate
  • -> Acetylcholinesterase is found bound to the basement memb of the synaptic cleft
  • -> and it breaks down Ach to Acetate + choline
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5
Q

What are the 3 main neuromuscular blockers?

A
  1. Tubocurarine
  2. Atracurium
  3. Suxamethonium
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6
Q

What are the 2 main subtypes of nicotinic receptors?

A
  • Ganglionic

- Muscle

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7
Q

What does Diazepam do?

A
  • it is a widely used spasmolytic

- and facilitates GABA transmission

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8
Q

What is Baclofen?

A

-Baclofen = GABA receptor agonist

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9
Q

What does both diazepam + baclofen do?

A
  • both drugs potentiates the action of GABA
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10
Q

Why are neurotoxins toxic?

A
  • they are toxic because they inhibit the release of Ach
  • and blocks the contraction of respiratory skeletal muscle –> causing death

Note: same with botulinum toxin

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11
Q

Neuromuscular blocking drug suzamethonium acts on which mechanism?

A
  • acts on depolarization of the motor end plate
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12
Q

What does Dantrolene do?

A
  • it is a spasmolytic

- which inhibits Ca2+ release in the muscle fibre

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13
Q

Which neuromuscular blockers are non depolarizing + which os depolarizing?

A

Non depolarizing:

  • tubocurarine
  • atracurium

Depolarising:
- suxamethonium

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14
Q

Where do neuromuscular blockers act on?

A
  • they act on post synaptic nicotinic receptors on the motor end plate
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15
Q

non depolarizing neuromuscular blockers are what type of ANTAGONISTS?

A

NON DEPOLARISING = competitive nicotinic receptor antagonists

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16
Q

depolarizing neuromuscular blockers are what type of AGONISTS?

A

DEPOLARISING = nicotinic receptor agonists

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17
Q

Note: when giving these drugs you need to always assist respiration because –> it has effect on respiratory muscles

A

-

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18
Q

compare the structure of non depolarizing drugs + depolarizing drugs

A

non depolarizing drugs:

  • big, bulky molecules
  • with relatively restricted movement around the bonds

depolarizing drugs (suxamethonium):

  • made up of 2 Ach molecules linked together
  • it is more flexible
  • shows rotation
  • -> one suxamethonium molecule can bind to 2 alpha subunits to stimulate receptor
19
Q

Describe the mechanism of action of suxamethonium

A
  • patient given a shot of suxamethonium (agonist)
  • which seeps into the muscle fibres
  • it then STIMULATES the nicotinic receptors
  • suxamethonium isn’t metabolized as quickly as Ach
  • so it remains bound to the nicotinic receptors
  • overstimulates receptors
  • then quickly, these receptors switch off
  • which causes a depolarization block due to overstimulation
  • -> it causes an extended end plate depolarization
  • -> which leads to depolarization block go the NMJ (phase 1 block)
  • fasciculation occurs
  • and shortly after you get flaccid paralysis
20
Q

What is the consequence of using Suxamethonium?

A
  • -> it causes an extended end plate depolarization
  • -> which leads to depolarization block go the NMJ (phase 1 block)
  • -> suxametonium then causes fasciculations, and individual fibre twitches as the drug begins to stimulate the nicotinic receptors
  • -> leads to flaccid paralysis
21
Q

Describe the pharmacokinetics of Suxamethonium

A
  • given intravenously

- duration of paralysis = 5 mins

22
Q

What are some uses of depolarizing NM blockers such as Suxamethonium ?

A
  • for endotracheal intubation

- muscle relaxant for ECT

23
Q

What are some unwanted effects of depolarizing NM blockers such as Suxamethonium ?

A
  • post operative muscle pains
  • bradycardia
    ( due to direct muscarinic action on heart)
  • hyperkalaemia
    (so if patient comes in with burns/ tissue injury avoid use –> might cause ventricular arrhythmia / cardiac arrest)
  • increase in intraocular pressure
    (avoid for eye injuries / glaucoma)
24
Q

What is Tubocurarine?

it is a non depolarizing / depolairisng ….

A
  • a non depolarizing neuromuscular blocker
25
Q

Describe the mechanism of action of non depolarizing neuromuscular blockers such as Tubocurarine.

A
  • tubocurarine = competitive nicotinic Ach receptor ANTAGONIST
  • 70-80% block –> full relaxation of muscles
  • blocking these receptors prevents end plate potential from reaching the threshold.
26
Q

What are the effect of using Tubocurarine?

A
  • effects = similar to suxamethonium

- causes flaccid paralysis

27
Q

When Tubocurarine is used whats the sequence of relaxation + recovery

A
  • skeletal muscles relax in sequence of:
    extrinsic eye muscles–> small muscles of face/limbs/pharynx –> respiratory muscles
  • skeletal muscles recover in sequence of:
    respiratory muscles –> small muscles of face/limbs/pharynx –> extrinsic eye muscles
28
Q

Describe the effect of tubocurarine on NM transmission

((LOOK AT GRAPH))

A

motor axon stimulated
but due to comp antagonists
there is reduced end plate potential
which is not sufficient to allow proppagation of ap down fibre
so no contraction of skeletal muscle –> which causes relaxation .

29
Q

What are 2 major uses of tubocurarine?

A
  1. causes relaxation of skeletal muscles during surgery
    - -> so less anesthetic need
  2. allows artificial ventilation
30
Q

The actions of non depolarizing NM blockers can be reversed with ________

A

The actions of non depolarizing NM blockers can be reversed with anticholinesterases

31
Q

How can anticholinesterases reverse the action of non depolarizing NM blockers?

A
  • if you increase Ach conc –> it can outcompete the non depolarizing blocker
32
Q

What is neostigmine?

A

reversible anti cholinesterase that can be used to reverse the action of non depolarizing NM blockers

33
Q

Why do you need to give atropine along with the neostigmine ?

A
  • when you give neostigmine, you increase the Ach conc in all other cholinergic synapse

–> so you need to give some atropine with it so that it blocks the muscarinic receptor overstimulation.

34
Q

describe the pharmacokinetics of tubocurarine

A
  • all NM blockers = IV
  • long duration of paralysis + 40-60 mins
  • not metabolized at all
  • -> excreted in urine + bile
35
Q

note: impairment of hepatic/renal system –> increases duration of action of tubocurarine.

SO you would use atracurium which isn’t affected by kidney/liver function
duration of action = 15mins

36
Q

What are some unwanted effect of Tubocurarine?

A
  • ganglion block //
  • histamine release from mast cells
  • -> hypotension
  • tachycardia
  • bronchospasm
  • excessive(bronchial/salivary) secretions
  • apnea
37
Q

How does histamine cause hypotension?

A
  • Histamine can act on H1 receptors on the vasculature –> and cause vasodilation.
38
Q

Clinical use of NM blocking drugs will most likely involve interference with which of the following physiological process?

A: Kidney function
B: Consciousness
C: Body temperature regulation
D: Pain sensation
E: Respiration
A

E : Respiration

39
Q

Which of the following effects would be observed with a non-depolarising neuromuscular block?

A: Initial muscle fasciculations
B: Irreversible nAChR blockade
C: The block would be enhanced by anti-cholinesterase drugs
D: A flaccid paralysis
E: Increased arterial pressure
A

D : A flaccid paralysis

40
Q

describe the process of neuromuscular transmission starting from synthesis of ach
and ending with the reforming of ach.

A
  1. synthesis of ach via CAT enzymes
  2. loaded onto vesicles
  3. Depolarization causes Ca2+ influx
  4. allows vesicle exocytosis –> into synapse
  5. Ach diffuses into the post synaptic neurone via cation channels
  6. nicotinic receptors on the end plate are stimulated
  7. AP is generated by influx of Na+ ions
  8. Ach in synapse cleft is broken down by acetylcholesterase –> choline + acetic acid
  9. products of metabolism (choline) –> taken up again back into neuronal cell
  10. to reform Ach
41
Q

what are the 2 groups of neuromuscular blocking drugs?

A

non depolarizing (competitive antagonists)

polarising (agonists)

42
Q

give an example of a polarizing drug

A

suxamethonium

43
Q

how is suxamethonium metabolized?

A

by pseudocholinesterase in liver + plasma

eLCRS - 팜 (36 decks)

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