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Pharmacology > Anaesthetics > Flashcards

Anaesthetics Flashcards

1
Q

Name the inhalational and IV agents

A

Inhalational:

  • nitrous oxide
  • isoflurane
  • (desflurane)
  • (sevoflurane)

IV

  • propofol
  • ketamine
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2
Q

What are the effects of anaesthesia?

A 
Sedation up to unconsciousness
Amnesia
Muscular relaxation
Reflex suppression and immobilisation
Anxiolysis
Analgesia
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3
Q

How does general anaesthesia work (generally)

A

Reversible inhibit sensory. motor and sympathetic nerve transmission in the CNS to produce unconsciousness and absence of sensation

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4
Q

Which parts mediate the different effects of anaesthesia?

A

Immobilisation - spinal cord

Inhalation anaesthetics work at

  • the thalamus - unconsiousness
  • the hippocampus - amnesia
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5
Q

What is important to predict potency?

A

Lipid solubility - affects their ability to dissolve and enter cell membranes

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6
Q

What is potency?

A

The concentration of a drug needed to attain 50% of it’s maximal effect

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7
Q

What are the two main excitatory and inhibitory neurones needed in consciousness

A

Excitatory: glutamate

Inhibitory: GABA

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8
Q

Mechanism of action of propofol?

A

Agonises GABA, increases the sensitivity

This increases Cl- influx, hyperpolarising the neurone, decreasing its excitability

Stops depolarisations that would cause pain and increased consciouness etc.

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9
Q

What are the effects of propofol?

A

Potentiating GABA causes

  • anxiolysis
  • sedation
  • anaesthesia
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10
Q

What is the effect of potentiating glycine (inhibitory neurotransmitter)

A

Signalling inhibitory neurotransmission in the spinal cord and brainstem
Reduces response to noxious stimuli

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11
Q

What is the effect of inhalational anaesthetics binding to and inhibiting nicotinic ACh receptors?

A

No Na+ influx
Less depolarisation so less excitation

-analgesia and amnesia (not sedation)

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12
Q

Which neurotransmitter acts on NMDA receptors?

A

Glutamate

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13
Q

Which anaesthetics exert their effects on NMDA receptors?

A

Nitorus oxide

Ketamine

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14
Q

What do nitrous oxide and ketamine do at NMDA receptors?

A

They bind to NMDA LGIC receptors to reduce Ca2+ influx

Less excitation

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15
Q

Which are the only anaesthetics not to potentiate GABA?

A

Xenon
Nitrous oxide
Ketamine

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16
Q

What are inhaled agents combined with before being inhaled?

A

Oxygen, air and often nitrous oxide

17
Q

What is the definition of MAC?

A

Minimum alveolar concentration

-the percentage of inhaled anaesthetic that abolishes response to surgical incision in 50% of patients

18
Q

What does it mean if an inhaled agent has a low MAC?

A

It is more potent - MAC relates to its lipid solubilty

19
Q

What are standard MAC doses given to patients?

A

1.2-1.5

20
Q

What can reduce the MAC?

A

When a drug is given in combination with other agents such as nitrous oxide or fentanyl (opiate)

21
Q

What is the blood-gas co-efficient?

A

The degree of absorption across the alveoli into the blood - this has a direct effect on the concentration of drug that reaches target sites in the CNS

Describes the volume of gas in litres that can dissolve in 1L of blood

22
Q

What does it mean if a drug has a high blood gas co-efficient?

A

The more readily it will enter the blood

23
Q

What does distribution of anaesthetics depend on?

A

The relative blood supply to each organ or tissue

The specific tissue uptake capacity for the anaesthetic

24
Q

What does the tissue-blood partition co-efficient determine?

A

How readily the anaesthetic will move from the blood to a specific tissue type

25
Q

How are inhaled agents eliminated?

A

As conc in the blood drops, the anaesthetic moves out of the cell membranes, into venous blood, back to alveolus to be eliminated unchanged

Eliminated from well-perfused tissues first (brain, kidneys), then muscle, then fat

Fat and muscle can be large reservoirs, and as it diffuses out of these compartments, can enter the CNS, affecting consciousness

26
Q

What is the duration of recovery from inhaled agents proportional to?

A

Length of procedure

Degree of loading of muscle and fat compartments

27
Q

Why are IV anaesthetics combined with inhaled ones?

A

Reduces time taken to reach anaesthetic depth sufficient for surgery
Bypasses the excitement/aggression of stage II

28
Q

Protein binding of inhaled and IV agents?

A

Inhaled - low

IV - high (98%)

29
Q

Distribution of IV agents?

A

Rapidly to the CNS (well perfused)

Drug redistributes throughout the circulation into muscle and fat - large capacity for lipophilic drugs

30
Q

Metabolism and elimination of IV agents (propofol)

A

Hepatic and extra-hepatic conjugation

Half-life around 2 hours

31
Q

ADRs of general anaesthesia?

A

Post-operative nausea and vomiting (opioids)

CVS - hypotension

Post-operative cognitive dysfunction - increases with age

Chest infection

32
Q

ADRs of local anaesthetics?

A

Can block heart depolarisation

Anaphylaxis

33
Q

Uses of benzodiazepines in general anaesthesia?

A

Low dose a few hours before surgery - anxiolytic

High dose - sedation for short procedures

34
Q

Uses of propofol?

A

Rapid IV induction of anaesthesia

35
Q

Uses of nitrous oxide?

A

Contributes to analgesia via NMDA receptors

Reduces the effective MAC of flurane

Minimises recovery time

36
Q

Uses of opiates (and which ones) in anaesthetics?

A

Morphine and fentanyl
Produce analgesia

Fentanyl more potent than morphine
Induces analgesia almost immediately
Finer control of analgesic effect in surgery

Reduce MAC
Reduce risk of CVS depression by flurane

37
Q

What are the two classes of drugs that abolish reflexes and induce muscle relaxation?

A

Competitive nicotinic ACh receptor antagonists

  • tubocurarine
  • pancuronium

Nicotinic ACh receptor depolarising agonists
-succinylcholine

Flurane also potentiates neuromuscular relaxation

38
Q

What are the different depths of anaesthesia?

A

1: Analgesia - due to effects on spinothalamic tract
2: Excitement - delirium and aggressive behaviour, now uncommon due to propofol
3: Surgical anaesthesia - CNS depression, muscles relaxed
4: Death - due to medullary depression leading resp and cardiac arrest

Pharmacology (23 decks)

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