Anaesthetics Flashcards

1
Q

Give some inhalational agents

A

Nitrous oxide IsofluraneDesfluraneSevoflurane

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2
Q

Give some intravenous agents

A

PropofolKetamine

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3
Q

What areas of the brain do anaesthetics have an effect on?

A

Reticular formation depressionThalamusHippocampus depressedBrainstem depressedSpinal cord - dorsal horn analgesia

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4
Q

Describe general anaesthesia

A

Affects the whole bodyUse inhalational and IV plus adjuvants Reversibly inhibit sensory, motor and sympathetic nerve transmission in CNSGive unconsciousness and sedation

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5
Q

Describe regional anaesthesia

A

Gives anaesthesia to large, specific regions of the bodyTransmission block between spinal cord and part of the body Occurs with spinal and epidural anaesthesiaPt remains conscious

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6
Q

Describe local anaesthesia

A

Defined peripheral nerve block e.g. tooth extraction, procedures on hands/feet.

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7
Q

Describe dissociative anaesthesia

A

Inhibition of transmission of nerve pulses between higher and lower centres of the brain. Used in kids and elderly - less susceptible to hallucinogenic effects

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8
Q

Generally, how do anaesthetics work?

A

Affect post synaptic transmission of inhibitory and excitatory ligand gated ion channels. - are weak and easily reversed reactions

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9
Q

How do anaesthetics bind to GABA mediated inhibitory channels?

A

Bind and increased sensitivity to GABA, which increased Cl- entering the cell to hyperpolarise the cell and decrease its excitability. Positive allosteric modulation

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10
Q

How do anaesthetics exert their action at glycine activated chlorides channels?

A

Bind and increase glycine sensitivity to increase Cl- entering the cell. Causes hyperpolarisation and decreases excitability. Positive allosteric modulation. V. important in inhibitory transmission in spinal cord and brainstem and reducing te response to noxious stimuli

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11
Q

How do anaesthetics exert their effect on neuronal nicotinic ACh receptors?

A

Bind and inhibit certain subtypes of receptors, by reducing excitatory Na+ currents due to ACh binding. - contributes to analgesia and amnesia rather than anaesthesia. Non-competitive antagonists

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12
Q

How do anaesthetics exert their action on NMDA receptors?

A

Bind and reduce Ca2+ currents, which are involved in synaptic responses. Nitrous oxide and ketamine exert their action here. Non-competitive antagonism

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13
Q

Describe the administration of inhalational agents

A

Fluranes are volatile liquids at room temp. Mix anaesthetic agent with oxygen, air and usually nitrous oxide. Then it is administrated via a mask with spontaneous or controlled respiration.

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14
Q

Define MAC

A

Alveolar concentration at one atmospheric pressure at which 50% of subjects fail to move to a surgical stimulus.

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15
Q

What does a lower MAC value indicate?

A

More potent anaesthetic- is more lipid soluble

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16
Q

What MAC is needed fro surgical depth?

A

1.2 - 1.5

17
Q

How can a MAC be reduced for an individual agent?

A

Use another agent in combinatione.g. N2O or fentanyl

18
Q

Define the blood:gas coefficient

A

The volume of gas in litres that can dissolve in one litre of blood

19
Q

What does a higher blood:gas coefficient indicate?

A

The gas will enter blood more readily.

20
Q

What determines the distribution of gas around the body?

A
  • relative blood supply to each organ or tissue- specific tissue uptake capacity (tissue:blood coefficient)
21
Q

Give some characteristics of different tissues regarding uptake of inhalational anaesthetics

A

Brain - slightly more than bloodSk muscle - double brainAdipose - 30 times more than brain - gives a large reservoir of anaesthetic that can redistribute during the recovery phase

22
Q

Describe elimination of inhalational anaesthetics

A

Anaesthetist withdraws anaesthesia, with adequate oxygenation. [Blood] drops, so anaesthetic moves out of tissue into venous blood where it travels to the lungs to be eliminated from the alveoli in an unchanged form.

23
Q

How does the rate of induction and the rate of recovery from inhalational anaesthetics differ?

A

Does not differ much - elimination is led by well perfused tissues, followed by muscle and then fat.

24
Q

What factors affect then length of recovery from inhalational anaesthetics?

A

Length of procedureDegree of loading in fat and muscle compartments

25
Q

How does the rate of induction differ with inhalational and intravenous anaesthetics differ?

A

IV is much quicker - seconds rather than minutes.

26
Q

What are some characteristics of intravenous anaesthetics?

A

Need further vigilance as it is harder to reverse dose related effects once administered.

27
Q

Describe propofol administration nad distribution

A

IV bolus, rapid distribution to CNS and less to muscle and fat. Redistribution occurs from CNS to other compartments.

28
Q

Give the metabolism characteristics of propofol

A

Undergoes hepaic and extrahepatic conjugation- half life of 2 hours Means there is not a post-procedural “hangover” during recovery

29
Q

Give some neuromuscular blocking agents

A

TubocurarinePancuroniumSuccinylcholine

30
Q

What do neuromuscular blocking agents do?

A

Abolish reflexes that occur with significantly invasive procedures and induce muscle relaxation.

31
Q

What are the stages of anaesthesia?

A

InductionMaintenance- adjuvant balance to maintain adequate anaesthetic depth Recovery - withdraw anaesthetics, monitor physiological function. - can administer antidotes to facilitate this

32
Q

Give the stages of anaesthetic depth

A
  1. Analgesia2. Excitement3. Surgical anaesthesia4. Respiratory paralysis and death
33
Q

Describe analgesia stage

A

Early effects on transmission in the spinothalamic tract

34
Q

Describe the excitement stage

A

Delirium and aggressive behaviour are experienced- uncommon due to rapid induction with propofol

35
Q

Describe surgical anaesthesia

A

Profound CNS depressionSkeletal muscles are fully relaxedMay need to assist breathing. MAC of 1.2-1.5Four levels of increasing depth of breathing until breathing is weak

36
Q

Describe respiratory paralysis and death

A

Above 2.2 MAC, increased risk of this stage. Severe medullary depression which can lead to respiratory and cardiac arrest and death