Anaesthetic Drugs

Question 1

Contemporary Use of Anaesthesia:

Answer 1

Question 2

Unconsciousness: Potential Drug Targets:

Answer 2

• cerebral cortex
• thalamus
• reticular activating system
• spinal cord
• GABA receptors
• glutamate receptors
• glycine receptors
• serotonin receptors

Question 3

All anaesthetic agents affect tissues by

Answer 3

depressing all excitable tissues to variable sensitivities

Question 4

All anaesthetic drugs are lipid soluble.

True or False?

Answer 4

True

Question 5

Proprofol: Method of Delivery:

Answer 5

IV

Question 6

Proprofol:

Answer 6

• lipid soluble
• rapidly perfuses the brain, relaxes the larynx
• rapidly metabolised by liver
• does not accumulate
• offset (wears off) by redistribution)

Question 7

Proprofol: Drug Class:

Answer 7

• antiemetic
• antiepileptic

Question 8

Proprofol: Side Effects:

Answer 8

• pain on injection
• abnormal movements
• hypotension

Question 9

Inhaled Anaesthetics:
- are
- side effects

Answer 9

• halogenated ethers
• post-op nausea and vomiting
• if irritant, makes gas induction difficult
• emergence phenomena

Question 10

Idea proporties of inhaled agents:

Answer 10

• stable, non-corrosive
• liquid
• vapourisable at room temp
• pleasant to inhale, bronchodilator, non-
  irritant
• low blood:gas solubility
• not metabolised

Question 11

General Anaesthesia:

Answer 11

• IV induction
• gas maintenance

Question 12

NMBAs

Answer 12

• neuromuscular blocking agents
• only given to unconscious patients

Question 13

Akinesia/Muscle reaction by

Answer 13

NMBAs

Question 14

Two classes of NMBAs:

Answer 14

• depolarising
• non-depolarising

Question 15

Label

Answer 15

insert diagram

Question 16

Depolarising NMBAs:
- eg
- receptors?
- location?
- molecular effect
- onset and offset
- half life
- metabolised by
- side effects

Answer 16

• succinylcholine
• acts on muscarinic and nicotinic receptors
• at post-synaptic membrane
• 2 Ach joined together; minimises Ach
  available to bind
• rapid onset and offset
• half life = 2mins
• metabolised by plasma cholinesterase
• multiple side effects: twitchy at first, only
  lasts for five mins (effects), muscle pains
  post-op, bradycardia because harshly
  affecting muscarinic receptors but we want
  effect of inhibition of nicotinic

stuck at receptors, can not restimulate muscle

Question 17

Non-Depolarising NMBAs:
- eg/are
- receptors?
- location?
- molecular effect
- onset and offset
- half life
- metabolised by
- side effects

Answer 17

• aminosteriod/ quaternary ammonium
  compounds
• nicotinic receptors: alpha subunit
• synaptic cleft/post-synaptic neuron
• competes with Ach by binding and blocking
  Na+ channel on nicotinic receptor
• slow onset and offset (30-40mins)

Question 18

When can prolonged paralysis during the use of succinylcholine (depolarising NMBA) as an akinesic agent?

Answer 18

cholinesterase deficiency
anything that inhibits cholinesterase

Question 19

Botulinum Toxin:

Answer 19

• intracellular toxin
• prevents vesicles of Ach binding to
  intracellular membrane preventing release
  of Ach into the synaptic cleft
• relieves muscle spasms and contractions,
  neuropathic pain and used for aesthetic
  purposes

Question 20

Are depolarising or non-depolarising more receptor-specific?

Answer 20

Non-depolarising only nicotinic
succinylcholine both muscarinic and nicotinic

Question 21

Non-depolarising NMBAs require reversal agents eg

Answer 21

• neostigmine: binds to acetylcholinesterase
  and prevents the break down of Ach in the
  synaptic cleft; will increase ach at muscarinic
  and nicotinic; activates sympathetic so given
  with atropine to block muscarinic receptors
• sugammadex: selective relaxant binding
  agent (SRBA), binds to aminosteriod non-
  depolarising NMBAs, preventing action of
  the akinesic agent (aminosteriod)