W19/L5: Anaesthetics Flashcards
How do local anaesthetic agents work?
They interfere with Na+ influx to block action potentials in sensory nerves
What’s an example of an aminoester anaesthetic?
Procaine
What’s the duration of action of aminoesters like?
Relatively short ~30min
Why do aminoesters have a short duration of action
they’re hydrolysed by esterases (including AChE)
List 3 examples of aminoamide anaesthetics
Lignocaine
Bupivicaine
Ropivicaine
Why are the aminoamide anaesthetics longer acting?
They’re metabolised hepatically
What’s the local anaesthetic that doesn’t have a family?
Benzocaine
What features of local anaesthetics make them safe?
They bind reversibly
There’s no permanent nerve damage
They are administered in a way that limits systemic distribution
Describe the neural Na+ channel
Large protein with many TM domains.
Has two gates: M- and N-gate
Where on the Na+ channel do toxins usually bind?
On the extracellular side - usually causing complete & irreversible blockage.
Where on the Na+ channel do the local anaesthetics bind?
On the intracellular side
What are the two mechanisms of local anaesthetics interacting with the Na+ channel?
Hydrophobic and hydrophilic
How does the hydrophobic MoA of local anaesthetics work?
The drug in its uncharged form can enter the cell membrane and take position in the Na+ pore
*Skip the rest of this cause I think JZ’s explanation is wrong. Look it up!
..
What are the commonly inhaled GAs?
Desflurane
Sevoflurane
Isoflurane
What are the common IV GA’s?
Propofol
Thiopentone
How can GAs affect respiration?
Impaired ventilation
Depression of the resp. centre
Obstruction of airways due to retention of mucosal secretions
Why are anti-muscarinics often co-administered with GAs?
They decrease secretion -> reducing the likelihood of airway obstruction.
How can GAs affect the cardiovascular system?
Decrease vasomotor centre function Depress contractility Peripheral vasodilation Cardiac arrhythmias Inadequate response to fall in BP or CO
What are the two theorised MoA of GAs?
Lipid theory & receptor interaction theory
What is the lipid theory of GA MoA?
That GAs work by getting into the lipid membrane of axons, expanding and thus affecting activity
What evidence supports the lipid theory of GA MoA?
- There;s a close correlation between lipid solubility and anaesthetic potency
- Hyperbaric chambers can reverse anaesthesia
What is the receptor interaction theory of GA MoA?
That GAs work by enhancing inhibitory systems and inhibiting excitatory systems
What evidence supports the receptor interaction theory of GA MoA?
? Not actually sure - look this up!
What (broad) treatment goals do we have for Epilepsy?
Modify motor nerve output: Reduce exitation
