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BMS 242 - Phys and pharm of cells > General anaesthetics > Flashcards

General anaesthetics Flashcards

1
Q

What does NO do in terms of pain?

A

Reduced RESPONSE to pain

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2
Q

What does ether do in terms of pain?

A

Reduced RESPONSE to pain

Loss of consciousness

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3
Q

What does Chloroform do in terms of pain?

A

Reduced RESPONSE to pain

Loss of consciousness

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4
Q

What is the structure of ether and chloroform?

A

Volatile liquids that turn to gas at room temperature

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5
Q

How are general anaesthetics described?

A

Into 2 categories - by the route of administration

1) Chemical
2) Physical

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6
Q

What are chemical general anaesthetics?

Examples?

A

1) Inhalational
- NO

2) Intraveous
- Steroids
- Barbiturates
- Halogenated hydrocarbons

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7
Q

What are the physical general anaesthetics?

A
  • Low-pressure

- Hypothermia

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8
Q

What do general anaesthetics do/not do?

A
  • Reduces the RESPONSIVENESS to pain

- NOT the FEELING of pain

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9
Q

How do we know that anaesthetics don’t work by working on a specific receptor?

A
  • The structure of general anaesthetics is VERY DIVERSE

- If work on a specific receptor - normally have a CONSERVED structure

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10
Q

How easily do general anaesthetics enter into membranes?

Why?

A

Easily

They are very lipophilic

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11
Q

What is the potency of general anaesthetics depends upon?

A

Closely related to the oil:gas partition coefficient (how easily they enter into the lipids)

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12
Q

What is MAC?

A

Minimum alveolar concentration

The amount of the drug needed to achieve a state of anaesthesia in 50% of proteins

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13
Q

Which anaesthetics have the highest potency?

A

Anaesthetics with the highest lipid solubility

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14
Q

How does temperature impact on anaesthesia?

A

Decrease temperature –> anaesthetic effect

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15
Q

What is the lipid theory of anesthetic action?

A

‘Molecules exert their action in the nervous system by entering into the plasma membrane

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16
Q

What are the 2 ideas of the ‘lipid theory’?

A

1) Membrane expansion

2) Increase in lipid fluidity

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17
Q

What is the ‘membrane expansion’ component of the lipid theory?

A

Lipids enter into the membrane

Causing:

  • Fat molecules in the membrane to be pushed apart
  • Altering the property of the neurons
  • Altering neuronal excitability –> entering the state of anaesthesia
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18
Q

What is the ‘increase in lipid fluidity’ component of the lipid theory?

A

Lipids enter into the membrane

Causing:

  • Lipids to become more ‘floppy’
  • Activity of the proteins within the lipids are impacted
  • Effect neuronal excitability –> entering the state of anaesthesia
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19
Q

What are the 3 arguments for the ‘lipid theory’?

A
  • Obey the Meyer-Overton rule
  • Obey the pressure effect
  • Support drug diversity
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20
Q

What is the Meyer-Overton rule?

A

Correlation between the oil:gas coefficient and the potency of the drug as a general anaesthetic

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21
Q

What is the pressure effect on general anaesthetics?

A
  • Reducing the atmospheric pressure INCREASES the potency of general anaesthetics
  • As reduce pressure - support a more fluid membrane
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22
Q

How does the lipid theory support drug diversity?

A
  • All general anaesthetics have a diverse structure

- Therefore the only thing that would affect how well they work would be how well they enter the lipid membrane

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23
Q

What are the 4 arguments against the the ‘lipid theory’?

A

1) Temperature effect
2) Binding sites
3) Loss of activity with homologous series of lipophilic compounds
4) Some drugs increase GABAa receptor affinity for agonists

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24
Q

Why does the temperature effect oppose the lipid theory?

A
  • When the temperature decrease - membranes become LESS fluid
  • But decrease temperature –> has anaesthetic effect
  • Counteracts the effect that general anaesthetics work by increasing membrane fluidity
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25
Q

How do ‘binding sites’ counteract the ‘lipid theory’?

A
  • Can see SATURATION of effect when drugs are administered

- Saturation is a classic indication of a drug that is working on a RECEPTOR, where there is a limited amount

26
Q

What did the oppositions of the ‘lipid theory’ give rise to?

Describe this theory

A

The ‘protein theory’ of general anaesthetics

There is a RECEPTOR that the drugs must bind to to exert their action

27
Q

Which receptors do some anaesthetics bind to?

What do they do here?

A

GABAa receptors

They alter the function of the GABAa receptors

28
Q

Why is the lipid solubility of the drug so important?

A

The amino acids present that the general anaesthetics interact with are part of the channel within the transmembrane domain - buried deep within the plasma membrane

29
Q

Where do gaseous anaesthetics tend to bind?

A

At the INTERFACE between 2 subunits of the GABAa receptor

30
Q

Where do intravenous anaesthetics tend to bind?

A

Bind just the beta subunit

31
Q

As well as GABAa receptors, where else can general anaesthetics bind?

A
  • Low concentrations can activate the TwoPoreDomain K channels
  • NDMA glutamate receptors
32
Q

What are the TwoPoreDomain K channels involved in?

What happens when these channels are activated by GAs?

A

Maintaining the resting, hyper polarised state of the neurons

When activated - hyper polarise the channels –> less likely to fire action potentials

33
Q

What blocks NDMA glutamate receptors?

A

NO and Ketamine

34
Q

What blocks NDMA glutamate receptors?

A

NO and Ketamine

35
Q

What type of anaesthetic is Ketamine?

A

A dissociative anaesthetic (member in its own family)

36
Q

What is the aim of all GA targets?

A

To decrease neuronal excitability

37
Q

What do electrophysiology of voltage gated Na+ channel show when GAs are applied?

A

As the concentration of the drugs increase, the current the current through the Na+ channels gets smaller

38
Q

What happens to the size of the action potential as GAs are applied?

A

Size of the action potential decreases

39
Q

How do GA affect the fusion of vesicles in the presynaptic terminal?

What does this show?

How does this impact the post synaptic site?

A

Reduced

GA may DIRECTLY interfere with synaptic transmission at the pre synaptic site

Impact at the post synaptic site:

  • Less excitation
  • Action potentials more spread out
40
Q

Where are the effects of GA at therapeutic (low) dose?

A

In the CNS and not the PNS

41
Q

Where do low concentrations of GAs act?

What does this cause?

A
  • Decrease synaptic transmission in the CNS
  • Reticular formation - unconsciousness
  • Hippocampus - reduced neuronal activity –> long term amnesia
  • Analgesia
  • Inhibition of spinal reflexes
42
Q

What do high concentrations of GAs do?

A

Loss of:
- Motor control

  • Reflexes
  • Central control of respiration
  • Regulation of the cardiovascular system
43
Q

What are the stages of anaesthesia?

What happens at each stage?

A

1) Analgesia
- Reduced responsiveness to painful stimuli

2) Excitation
- Dangerous stage (want to see through as quickly as possible)
- Exaggerated response of reflexes (even though unconscious)

3) Surgical anaesthesia
- Unconsciousness
- Loss of response to painful stimulation
- Loss of exaggerated reflexes
- Short-term amnesia (no memory of the procedure

4) Medullary paralysis
- Desperately try to avoid this stage
- Loss of cardiovascular reflexes and respiratory paralysis -cause death

44
Q

Why is it difficult to form surgery on obese patients?

A

Drugs enter the fat and NOT the CNS

45
Q

What are the advantages of intravenous anaesthetics?

A
  • Easy to administer
  • Rapid induction

-

46
Q

Why is there a rapid induction with intravenous anaesthetics?

A
  • Delivery straight into the blood
  • Brain is HIGHLY perfused –> rapidly distributed to the CNS
  • Easy to cross the BBB (lipophilic)
  • Rapid metabolism –> good induction for anaesthesia, rapid recovery (quick wear off)
47
Q

What are the disadvantages of intravenous anaesthetics?

A
  • Pain at the site of injection
  • Complex pharmacokinetics
  • Short duration of action due to redistribution
  • ‘Hangover’ effect due to accumulation in the body fat
  • Peripheral side effects
48
Q

What receptors does Ketamine block?

A

NDMA receptors

49
Q

What are the positive effects of Ketamine?

A
  • NOT a complete loss of consciousness
  • Sensory loss
  • Powerful analgesic
  • Amnesia
  • NO respiratory depression
50
Q

What are the negative effects of Ketamine?

A

No use on humans, as:
- Increased inter cranial pressure (hazard)

  • Can cause hallucinations, delirium
  • Irrational behaviour on recovery
51
Q

What are the gaseous anaesthetics?

A

NO, Isoflurane, Desflurane, Sevoflurane

52
Q

When are gaseous anaesthetics used?

IV?

A

Gaseous used to MAINTAIN surgical anaesthesia

After originally giving IV until the loss of conciousness

53
Q

How can the concentration of GA in the blood in the brain?

A

By altering:
1) The RATE of VENTILATION

2) CONCENTRATION of the drug in the inspired air

54
Q

When is there a problem with controlling the concentration of GA in the blood in the brain?

A

When the lungs are diseased or damaged

55
Q

What are the advantages of the gaseous GA?

A

1) Can easily change the concentration in the blood and brain (don’t have to wait metabolism)
2) Well tolerated, less side effects
3) Easily cross the alveolar membrane (small lipid soluble molecules)

56
Q

What do the differences between gaseous A come from?

A

The solubility of the different agents in the blood and fat

57
Q

What does the speed of induction and recovery from GA depend upon

A

Drug solubility and fat

58
Q

Describe the passage of inhaled drugs around the body?

A

1) Drug INTO the lungs
2) RAPIDLY equilibriate across the alveolar membrane
3) Blood takes the drug rapidly to the brain and any LEAN tissue (highly perfused)
4) Very quick to equilibriate between the inspired air and the tissues
5) Solubility of the drug in the blood is very low (partitions quickly into the lipids

59
Q

Do drugs bind well to proteins?

A

NO

60
Q

What can be triggered by halogenated GAs?

A

Malignant hyperthermia:

  • Body temperature increase due to rapid contraction of the muscles
  • Problems with the heart

BMS 242 - Phys and pharm of cells (13 decks)

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