W19/L5: Anaesthetics Flashcards

1
Q

How do local anaesthetic agents work?

A

They interfere with Na+ influx to block action potentials in sensory nerves

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2
Q

What’s an example of an aminoester anaesthetic?

A

Procaine

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3
Q

What’s the duration of action of aminoesters like?

A

Relatively short ~30min

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4
Q

Why do aminoesters have a short duration of action

A

they’re hydrolysed by esterases (including AChE)

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5
Q

List 3 examples of aminoamide anaesthetics

A

Lignocaine
Bupivicaine
Ropivicaine

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6
Q

Why are the aminoamide anaesthetics longer acting?

A

They’re metabolised hepatically

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7
Q

What’s the local anaesthetic that doesn’t have a family?

A

Benzocaine

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8
Q

What features of local anaesthetics make them safe?

A

They bind reversibly
There’s no permanent nerve damage
They are administered in a way that limits systemic distribution

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9
Q

Describe the neural Na+ channel

A

Large protein with many TM domains.

Has two gates: M- and N-gate

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10
Q

Where on the Na+ channel do toxins usually bind?

A

On the extracellular side - usually causing complete & irreversible blockage.

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11
Q

Where on the Na+ channel do the local anaesthetics bind?

A

On the intracellular side

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12
Q

What are the two mechanisms of local anaesthetics interacting with the Na+ channel?

A

Hydrophobic and hydrophilic

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13
Q

How does the hydrophobic MoA of local anaesthetics work?

A

The drug in its uncharged form can enter the cell membrane and take position in the Na+ pore

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14
Q

*Skip the rest of this cause I think JZ’s explanation is wrong. Look it up!

A

..

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15
Q

What are the commonly inhaled GAs?

A

Desflurane
Sevoflurane
Isoflurane

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16
Q

What are the common IV GA’s?

A

Propofol

Thiopentone

17
Q

How can GAs affect respiration?

A

Impaired ventilation
Depression of the resp. centre
Obstruction of airways due to retention of mucosal secretions

18
Q

Why are anti-muscarinics often co-administered with GAs?

A

They decrease secretion -> reducing the likelihood of airway obstruction.

19
Q

How can GAs affect the cardiovascular system?

A
Decrease vasomotor centre function
Depress contractility
Peripheral vasodilation
Cardiac arrhythmias
Inadequate response to fall in BP or CO
20
Q

What are the two theorised MoA of GAs?

A

Lipid theory & receptor interaction theory

21
Q

What is the lipid theory of GA MoA?

A

That GAs work by getting into the lipid membrane of axons, expanding and thus affecting activity

22
Q

What evidence supports the lipid theory of GA MoA?

A
  • There;s a close correlation between lipid solubility and anaesthetic potency
  • Hyperbaric chambers can reverse anaesthesia
23
Q

What is the receptor interaction theory of GA MoA?

A

That GAs work by enhancing inhibitory systems and inhibiting excitatory systems

24
Q

What evidence supports the receptor interaction theory of GA MoA?

A

? Not actually sure - look this up!

25
Q

What (broad) treatment goals do we have for Epilepsy?

A

Modify motor nerve output: Reduce exitation