Anaesthesia in Research Flashcards

1
Q

What are the subgroups of neuromuscular blocking agents?

A

Non-Depolarising blockers (nicotinic antagonists)

Depolarising blockers (nicotinic agonists)

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2
Q

What is curare?

A

An example of a non-depolarising neuromuscular blocker used by indigenous South Americans to paralyse prey

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3
Q

What are neuromuscular blocking agents?

A

Drugs that act on the neuromuscular junction (at the muscle itself) rather than through the CNS

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4
Q

How can using neuromuscular blockers reduce damage to muscle in surgery?

A

It makes muscles lose all tone, there is less damage because the muscle was not rigid when it was manipulated

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5
Q

What type of receptor are nAChRs and what is their purpose?

A

ION channel receptors - purpose is to bring in Sodium ions

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6
Q

How do non-depolarising neuromuscular blockers work?

A

They block nAChRs, therefore no influx of sodium ions, therefore no depolarising to threshold for voltage gated calcium channels, insufficient calcium liberated from SR, no contraction.

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7
Q

What kind of antagonists are non-depolarising neuromuscular blockers?

A

Competitive antagonists

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8
Q

What are the antidotes for non-depolarising neuromuscular blockers and how do they work?

A

Acetylcholinesterase inhibitor - less AChE, more ACh in the synapse which outcompetes the blocker.

New antidote is 4-aminopyridine - makes lots of ACh get released from presynaptic neutron, so there is enough to outcompete

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9
Q

What are the side effects of administering AChE inhibitors as an non-depolarising NMB antidote, and how can this be managed?

A

Increase in parasympathetic signalling (mucous, tears, stomach acid, bladder contraction etc). Managed by administering directly to muscle to avoid it going systemic

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10
Q

Why is atracurium unique as a non-depolarising neuromuscular blocker?

A

It is broken down chemically, not enzymatically, so it doesn’t need to get to a source of enzymes to get broken down.

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11
Q

Why do we have many different non-depolarising NM blocker drugs?

A

Because they also have a range of “other effects” that need to be considered like some induce histamine release, some drop BP etc

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12
Q

How does depolarising NM blocker work?

A

nAChR agonist.
PHASE I -
1. Small muscle jerks/contractions
2. Desensitisation of receptor due to ongoing “noise”(~30sec)

PHASE II -

  1. Drug is metabolised, and the metabolite succinylmonocholine is itself an ANTAGONIST therefore acts like non-depolarising NM blocker
  2. Blocks Na influx
  3. No threshold for Ca channels
  4. No Ca to open SR
  5. No contration
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13
Q

What is the antidote for Succinylcholine, and what is important to remember about it?

A

Pseudcholinesterase. However 1 in 2000 people have an enzyme variant. That means the paralysis lasts hours instead of minutes

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14
Q

What are risks associated with depolarising neuromuscular blockers?

A
  • muscle pain during induction
  • can cause hyperkalaemia
  • can cause malignant hyperthermia
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15
Q

Why is it necessary to intubate any patients with neuromuscular blockers?

A

Neuromuscular blockers paralyse skeletal muscles, respiratory muscles are skeletal muscles, patient must be intubated or will asphyxiate

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16
Q

What are the 2 main targets for muscle relaxants?

A

GABA signalling or Ryanodine receptors

17
Q

How are GABAa and GABAb receptors different?

A

GABAb receptors exist as dimers