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Pharmacology Year 2 > General Anaesthetics > Flashcards

General Anaesthetics Flashcards

1
Q

What chemical did Horace Wells use as on his patients in the 1800s and what was its effects?

A

> Nitrous oxide (laughing gas)

> Didn’t lose consciousness but stopped responding to pain.

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2
Q

What did William Thomas Green Morton demonstrate as a chemical with general anaesthetic in the 1800s and what was its effect?

A

> Ether

> When inhaled caused loss of consciousness and stopped responding to pain too.

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3
Q

What chemical with general anaesthetic properties was discovered in 1846 by James Simpson and Robert Glover?

A

Chloroform

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4
Q

What are the 2 ways general anaesthetics are characterised?

A

By their chemical nature and how they are administered.

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5
Q

What 2 means can be used to induce a state of general anaesthesia?

A

1) Chemical means

2) Physical means

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6
Q

What are 2 methods for 1) Chemical 2) Physical means of inducing a stage of general anaesthesia?

A

1) Chemical means
>Inhalation (through the lungs)
>Intravenous (Directly into circulation)

2) Physical means
>Low-pressure (atmospheric) makes mammals unconscious and unresponsive to pain.
>Hypothermia (lowering temperature) especially in amphibians.

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7
Q

How is Nitrous oxide administered?

A

Inhalational (through the lungs)

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8
Q

How are Halogenated hydrocarbons, like isoflurane, administered?

A

Intravenous injection

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9
Q

How are Barbiturates, like thiopental, administered?

A

Intravenous injection

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10
Q

How are Steroids, like alfaxalone, administered?

A

Intravenous injection

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11
Q

How are Ether and Chloroform used as general anaesthetics and why are they no longer used?

A

> Liquids that vaporise at low temperatures, vapours are inhaled

> They are both highly explosive/ flammable so aren’t safe.

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12
Q

What is the Lipid Theory of Anaesthetics?

A

> Anaesthetic agents expanded the plasma membrane making them more fluid

> So The more lipid soluble the drug is, the less conc of drug is needed to render the patient unresponsive

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13
Q

What observation was the lipid theory of anaesthetics based on?

A

Based on observation of relationship between lipid solubility and the conc at which 50% of patients were unresponsive to surgical incision

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14
Q

What rule did the Lipid Theory of Anaesthetics give rise to and what does it mean?

A

It gave rise to the Meyer-Overton Rule: The potency of an anaesthetic (conc required for effect) is proportional to the conc of the anaesthetic in the plasma membrane.

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15
Q

What are 3 points that agree with the Lipid Theory of Anaesthetics?

A

Meyer-overton rule (potency was proportional to lipid solubility), pressure effect (low atmospheric pressure cuases more liquid like membrane), diverse drug structures

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16
Q

What are 4 points that disagree with the Lipid Theory of Anaesthetics and why?

A

1) Temperature effect
>Effect of temperature, induce GA state as well by lowering body temp in amphibian.
>The Lipid theory believes a more fluid bi-layer caused GA effect but lowering temp makes it more rigid.

2) Binding sites
>There was a saturation effect showing there was a limiting number of protein receptors available (showing they bind to receptors not to lipid bilayer directly)

3) Loss of activity with homologous series of lipophilic compounds
>Compounds who’s chemical structures are similar and have similar lipid solubility
>As these similar compounds get bigger they lose activity which wouldn’t be shown if the compounds just diffuse through plasma membrane

4) Increase GABAA receptor affinity for agonists
>Experiments showed general anaesthetics altered affinity for GABAA receptors for agonists.

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17
Q

What is the Protein Theory of General Anaesthetics and what does it mean?

A

The binding site of the GA on the proteins is only accessible within the plasma membrane, this explains why lipid solubility of drugs is important

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18
Q

Are there antagonists for GAs?

A

There are none

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19
Q

What method did we use to study GAs?

A

> Study on individual receptors and using sight directed mutagenesis to alter receptor binding sites to see how this impacted GA effects.

> Used to show which proteins a GA bound to

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20
Q

How do GAs work and what receptor to they effect?

A

> Increase activity of GABA at GABAA receptors.

> This increases the inhibitory neurotransmission in the CNS leading decreased APs firing.

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21
Q

How do a) Volatile (liquid that becomes gases at low temp) b)Intravenous GAs bind to GABAA receptors?

A

a) Volatile (liquid that becomes gases at low temp) GAs bind at interface of a and b subunits of GABAA

b) Intravenous GAs bind only on beta subunit of GABAA

22
Q

Why do all GAs have to be lipid soluble?

A

All receptors for GAs are found inside the plasma membrane so GAs have to be lipid soluble

23
Q

As well as GABAA receptors, what 2 other receptors do low concentrations of volatile GAs activate and what is the effect?

A

1) Activate Two Pore Domain K channels (potassium channel, role in regulating resting mV in neurons)
>Activation will hyperpolarize neuron resting mV so need more depolarisation to fire APs

2) Block NMDA receptors
>Glutamate ionotropic receptors, Glutamate is excitatory so if blocked decrease APs firing.

24
Q

What receptor does Ketamine and Nitrous Oxide (Gas) bind to?

A

Block NMDA receptors (Glutamate ionotropic receptors)

25
Q

As well as inhibiting action potential firing at the nerve terminal, what else do GAs interfere with?

A

Interfere with exocytosis of vesicles at the presynaptic membrane, so less neurotransmitter is released into the cleft.

26
Q

What is the effect of GAs inhibiting transmission of 1) Reticular formation 2) in the Hippocampus 3) in the Thalamic sensory relay nuclei (in cortex)?

A

1) Inhibition in transmission of Reticular formation –> unconscious

2) Inhibition of transmission in Hippocampus –> short term amnesia

3) Inhibition of transmission of Thalamic sensory relay nuclei parts of cortex –> analgesia

27
Q

What happens as concentrations of GA increase and what if they go too far?

A

> As concentrations increase, the amount of inhibition in CNS increases too.

> Loss of: motor control (reflexes), respiration, cardiovascular system (autonomic regulation), death due to respiratory failure.

28
Q

What are the 4 stages of Anaesthesia and what is the effect at each stage?

A

1) Analgesia
>Reduced response to pain, still partially conscious and respond.

2) Excitement
>Exaggerated reflexes, my gag or kick (dangerous)

3) Surgical Anaesthesia
>Unconscious, loss of pain response, loss of reflexes, short term amnesia.

4) Medullary Paralysis
>loss of cardiovascular reflexes and respiratory paralysis – cause death

29
Q

What stage of Anaesthesia can Nitrous Oxide achieve?

A

Stage 1 (Analgesia)

30
Q

For the ideal situation for administering a state of Anaesthesia what 4 points must occur?

A

1) Rapid induction, loss of consciousness
>Want patient to go from 1 to 3 quickly and stay there.

2) Analgesia
>No response to painful stimuli

3) Muscle relaxation (common to give neuromuscular blockers as well)
>Easier to perform incisions

4) Rapid recovery
>Rapidly reverse anaesthesia if a person is slipping from stage 3 to 4.
>Prolonged or frequent anaesthesia can cause health issues.

31
Q

What are 4 advantages about using Intravenous Anaesthetics?

A

1) As are easy to administer

2) Are highly lipid soluble, will quickly enter membranes (20-30 seconds)

3) As are so lipid soluble can enter through BBB to exert effects to inhibit CNS function.

3) Mostly they are metabolized quickly, short duration of action

32
Q

When is a good situation to use Intravenous Anaesthetics?

A

Intravenous are the ideal GA for the quick induction of anaesthesia

33
Q

What are 3 examples of intravenous anaesthetics?

A

Propofol, thiopental, etomidate

34
Q

What is advantageous to using the intravenous anaesthetic Propofol?

A

It has a short half life and is metabolised quickly, so leaves no hangover (when drug stays active inside for a while).

35
Q

What are 3 disadvantage side-effects of administering intravenous anaesthetics?

A

1) Pain at site of injection

2) Respiratory depression

3) Cardiovascular depression (etomidate doesn’t cause this)

36
Q

What are 2 disadvantages to the Intravenous Anaesthetics Thiopental?

A

> Causes hangover due to accumulation in body fat

> Has high therapeutic index, so requires a large increase in conc to get from stage 2 to stage 3.

37
Q

What class of anaesthetics is ketamine in?

A

In ‘Dissociative Anaesthetic’ class

38
Q

What are 5 effects of Ketamine and why is it not suitable for long complicated surgeries?

A

1) Sensory loss

2) Powerful Analgesia

3) Amnesia

4) No complete loss of consciousness
>Unsuitable for long/ complicated surgeries.

5) No respiratory depression (good)

39
Q

What receptor does Ketamine bind to?

A

NMDA channel inhibitor

40
Q

What are 4 side effects of Ketamine?

A

1) CV excitement, involuntary movements

2) increased intracranial pressure (hazard)

3) Hallucinations, delirium,

4) irrational behaviour on recovery

41
Q

What is 4 ways ketamine is used?

A

1) To treat depression

2) Used in pediatrics (babies)

3) Administered alongside benzodiazepine for sedation

4) Anaesthetic in veterinary

42
Q

What are 4 anaesthetics which are inhaled and which ones are halogenated drugs?

A

> Nitrous Oxide, Isoflurane, Desflurane, Sevoflurane

> Last 3 are halogenated drugs

43
Q

Why are inhaled anaesthetics useful during surgery?

A

> Can control the conc of GA quickly, drug isn’t controlled by metabolism it is controlled by breathing

44
Q

How do we control the conc of inhaled GAs and when would this be difficult?

A

> As the only route of entry and exit is via lungs,
So by controlling conc of drug in inspired air and rate of ventilation we can control conc of blood in blood and CNS

> problem if lungs are diseased/damaged

45
Q

Why can all inhaled anaesthetics easily cross the alveolar membrane?

A

As they are all small lipid molecules.

46
Q

How are inhaled anaesthetics inducted and reach target tissue in 5 steps?

A

1) Administered through inhaled air

2) Rapidly get across alveolar membranes, and due low solubility in blood and high lipid solubility will equilibrate quickly

3) They are transported around body via circulation

4) Tissues which are well perfused like lean tissues and CNS will rapidly receive the drug and will cross BBB easily due to high lipid solubility.

5) Some of the drug enters fat and accumulates, but will equilibrate slower than into CNS

47
Q

How would you a) Speed up the rate of inhaled GA delivery to CNS b) Remove the inhaled GA from CNS?

A

a) To speed up rate of delivery to CNS, increase rate of ventilation

b) To remove drug from CNS, reduce the conc of drug in inspired air and increase rate of ventilation to remove it

48
Q

Why are inhaled GAs used to maintain anaesthesia during surgery?

A

Due to the tight and easy control of the concentration reaching the CNS.

49
Q

What is the effect if administering halogenated anaesthetics to someone with malignant hyperthermia?

A

> Mutation in ryanodine receptors on SR membrane (skeletal muscles) causes activation from halogenated GAs causing increase in CA2+ in skeletal muscles causing contraction and extreme use of O2.

> Increases body temperature very high.

50
Q

How is Malignant Hyperthermia counteracted?

A

By stopping administration of inhaled gas, cooling them, and giving dantrolene intravenously, inhibitor of ryanodine receptors.

51
Q

What type of drug are general anaesthetics towards GABAA receptors?

A

Positive allosteric modulators (increase effects when GABA binds).

Pharmacology Year 2 (8 decks)

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