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Neuropharmacology > Lecture 11 > Flashcards

Lecture 11 Flashcards

1
Q

What are the main neurophysiological changes of anaesthesia?

A
  • unconsciousness - loss of response to painful stimuli (analgesia) - loss of reflexes
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2
Q

General anaesthetics definition

A

Act in the brain to cause a loss of consciousness

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3
Q

What are general anaesthetics used for?

A
  • operations (induction and maintenance) - experimentally
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4
Q

What are the types of general anaesthetics?

A
  • inhalation - IV infusion
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5
Q

What were the first anaesthetics?

A
  • ether - nitric oxide - chloroform - barbiturates - halothane - isoflurane
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6
Q

What is the structure=-activity relationship amongst general anaesthetics?

A

There is no strict structure-activity relationship

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7
Q

According to Guedel (1937) how many stages of anaesthesia are there?

A

Four

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8
Q

Describe Stage 1 of anaesthesia

A
  • awake but drowsy- distorted perception - analgesia at the end - used for obstetrics (gas and air)
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9
Q

Describe Stage 2 of anaesthesia

A
  • most dangerous phase - loss of consciousness - exaggerated reflexes - CSN stimulation= uncontrolled actions - irregular breathing and cardiac dysrhythmia
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10
Q

Describe Stage 3 of anaesthesia

A
  • surgical anaesthesia (desirable state) - regular breathing - cough and vomit reflex depressed - initial pupil constriction before dilation - large skeletal muscles relax - BP drop
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11
Q

Describe Stage 4 of anaesthesia

A
  • depression of medulla oblongata (respiratory centres) - further reduction in breathing, BP, pulse etc
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12
Q

Why are Guedel’s stages difficult to measure?

A
  • depends on muscular movements= cannot detect clinical signs in paralysed patients - use of multiple agents obscures signs
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13
Q

How does the EEG monitor the depth of anaesthesia?

A

The amplitude of the high frequency components falls with an increase at lower frequencies

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14
Q

What are some factors worth considering when using EEG?

A
  • frequency changes are agent dependent - various pathophysiological events affect EEG e.g. hypotension, hypoxia
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15
Q

What is the Patient State Index?

A

One method of assessing hypnosis and compares large numbers of EEGs during induction, maintenance and emergence

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16
Q

What is the Cerebral Function Monitor?

A

Semi-logarithmically signal that represents the overall electrocortical background activity of the brain

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17
Q

What is the Bispectral Index monitor?

A

Measures muscular and cortical activity using single, small flexible sensor applied to forehead and temporal region

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18
Q

What are the major theories of GA mechanisms of action?

A
  • lipid theory - protein theory - combination of both (lipid/protein interface)
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19
Q

According to the lipid theory, how do GA work?

A

GA agents dissolve in membrane leading to - changes in bilayer thickness - changes in order parameters e.g. EC50 - changes in curvature elasticity, Changes affect proteins present in membrane

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20
Q

What are the pieces of evidence supporting the lipid theory?

A
  • pressure reversal - no defined chemical structure of GAs - Meyer-Overton correlation
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21
Q

What is the Meyer-Overton correlation for anaesthetics?

A

As the olive oil:gas partition coefficient increases, the lower the potency of an anaesthetic drug is needed to induce anaesthesia e.g. nitrogen is a poor anaesthetic compared to chloroform

22
Q

What are the issues of the lipid theory?

A
  • stereoisomers= only one is active - new compounds do not fit MO correlation - increase carbon chain length= cut off effect (increasing solubility does not increase effectiveness) - non-immobilisers (similar structure no effect) - small temperature changes produce similar changes in membrane density and fluidity but do not produce anaesthesia
23
Q

According to the protein theory, how do GAs work?

A

GAs bind to specific membrane proteins - GABA-A receptor (inhibitory) - 2 pore K+ channels (control resting potential) - NMDA receptor (excitatory)

24
Q

What evidence supports the protein theory?

A
  • mutate channels in animal models and either reduce/increase anaesthetic potency - manipulate binding pocket of receptors which GA acts upon
25
Q

What is the criteria for identifying relevant anaesthetic protein targets?

A
  • reversibly alters target function at clinically relevant concentrations (MAC) - protein target expressed in appropriate anatomical location in brain/spinal cord - stereo selective effects in-vivo parallel actions on the target in vitro - target exhibits appropriate sensitivity and insensitivity to model and non-anaesthetic compounds
26
Q

What are the brain areas associated with the sleep-wakefulness cycle?

A
  • ventrolateral pre-optic nuclei - tuberomamalary nuclei - locus coeruleus - laterodorsal tegmental nuclei - pedunculopontine tegmental nuclei - basal forebrain
27
Q

What are the properties of an ideal anaesthetic?

A
  • rapid action and recovery - minimal irritant properties - miscible with air/oxygen (no risk of explosion) - analgesic - muscle relaxant
28
Q

What is the minimum alveolar concentration?

A

Alveolar partial pressure of an inhaled anaesthetic which prevents movement in response to a standard noxious stimulus in 50% of patients

29
Q

Do we want a high or a low MAC?

A

Low MAC- require less anaesthetic in order to induce anaesthesia

30
Q

What does a greater solubility in blood mean for anaesthetics?

A
  • blood acts as a reservoir - reduced rate of rise of alveolar partial pressure - reduced rate of rise of brain partial pressure - slower rate of anaesthesia onset
31
Q

What does the blood/gas solubility co-efficient determine?

A

How a general anaesthetic distributes itself in the blood - low coefficient= rapid onset and offset e.g. nitrous oxide - high coefficient= slower onset and offset e.g. ether

32
Q

What is the rate of equilibration of inhalation anaesthetics in lean tissues e.g. brain?

A
  • rapid equilibration - fast perfusion - small partition coefficient
33
Q

What is the rate of equilibration of inhalation anaesthetics in fat?

A
  • slow equilibration - slow perfusion - large partition coefficient
34
Q

Why is there slower recovery from longer operations?

A

Longer operations give more time for anaesthetic to equilibrate in fat compared to muscle= long time to remove from body

35
Q

Does halothane equilibrate more quickly in vessel-rich or vessel-poor tissue?

A

Vessel-rich

36
Q

Would a drug with fast induction have a long or short recovery?

A

Short

37
Q

What determines the rate of recovery from an anaesthetic?

A

Rate of reduction of alveolar partial pressure

38
Q

What are factors that decrease the length of recovery?

A
  • reduction of the inspired concentration - high alveolar ventilation - low blood gas solubility - short duration of anaesthesia (little anaesthetic dissolved in low perfusion tissue_
39
Q

What are examples of intravenous anaesthetics?

A
  • propofol - thiopental - etomidate - ketamine
40
Q

Propofol as an intravenous anaesthetic

A
  • potentiates GABA-A receptors - induction agent - mood altering and antiemetic properties - maintenance agent- total intravenous anaesthesia with an opioid - apnoea (respiratory depression) and fall in blood pressure
41
Q

Thiopental as an intravenous anaesthetic

A
  • potentiates GABA-A receptors- barbiturate that induces anaesthesia - lipid soluble and crosses BBB - slowly metabolised by liver- sedative effects can persist - poor analgesic and muscle relaxant - cardiorespiratory depression
42
Q

Etomidate as an intravenous anaesthetic

A
  • anaesthesia induction - rapid recovery with no hangover
43
Q

Ketamine as an intravenous anaesthetic

A
  • hallucinations - abuse potential and dependence - peadiatric anaesthesia - useful for repeated administration - novel treatment for depression
44
Q

What are examples of inhalation anaesthetics?

A
  • halothane - isoflurane - sevoflurane - desflurane
45
Q

Effects of inhalation anaesthetics

A
  • fast loss of consciousness, smooth induction and recovery (but IV is preferred) - dose dependent lowering of mean arterial pressure - depress respiration leading to the increase in arterial CO2 level and impairment of O2 exchange - brain metabolic rate decreases even though cerebral blood flow increases - relaxation of skeletal muscles by a central action
46
Q

Halothane as an inhalation anaesthetic

A
  • potent, smooth induction, non-irritant - moderate muscle relaxation for abdominal surgery - severe hepatotoxicity
47
Q

Isoflurane as an inhalation anaesthetic

A
  • less potent than halothane - BP fall - depresses respiration - muscle relaxation and potentiate muscle relaxants - less of a risk of hepatotoxicity than halothane
48
Q

Nitrous oxide as a general anaesthetic

A
  • maintains anaesthesia and analgesia - low potency for anaesthesia alone so used with other agents - obstetrics (gas and air) for labour
49
Q

Neuromuscular blocking drugs as general anaesthetics

A
  • light levels of anaesthesia - relax tracheal tube for intubation- need assisted respiration
50
Q

Examples of neuromuscular blocking drugs

A
  • atracurium - cisatracurium - mivacurium - suxamethonium
51
Q

What are other types of medication used clinically?

A
  • proton pump inhibitors (prevent acid aspiration) - muscarinic antagonists (dry secretions) - sedatives (benzodiazepines) - non-opioid analgesic (NSAIDs) - opioid analgesics

Neuropharmacology (15 decks)

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