Lecture 11 - General Anaesthetics Flashcards

1
Q

what is the dose response curve for general anaesthetics?

A

it is a very steep dose response curve

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2
Q

what is general anaesthetic potency proportional to?

A

liquid solubility

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3
Q

what are the three ways for chemicals to be administered?

A
  1. inhalation
  2. intravenous
  3. physical
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4
Q

lipid solubility theory for general anaesthetics

A

work at the level of the plasma membrane to either cause volume expansion or increase lipid fluidity

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5
Q

what is the Meyer-Overton rule?

A

anaesthetic effect is proportional to molar concentration of agent in liquid

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6
Q

what did binding experiments with general anaesthetics conclude?

A

there was a limited number of sites for general anaesthetics which resulted in the idea that specific receptors were involved.

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7
Q

where are binding sites accessible for general anaesthetics?

A

within the cellular membrane

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8
Q

general anaethetics interaction with ion channels

A
  • increase action of GABA at GABAa receptors.
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9
Q

where do volatile general anaesthetics bind to?

A

the interface of alpha and beta subunits of GABAa
or activate two pore domain K channels causing hypnotic effect

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10
Q

where do intravenous general anaesthetics bind?

A

only on the beta subunit of GABAa

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11
Q

what blocks NMDA receptors

A

ketamine and nitrous oxide

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12
Q

what is the action if general anaesthetics?

A

inhibits action potentials by decreasing inward currents of voltage gated sodium channels. also interferes with exocytotic process of neurotransmitters

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13
Q

what is the effect of general anaesthetics on neurotransmission at low concentrations?

A
  • synaptic transmission in CNS is decreased
  • decreased reticular information causing unconsciousness
  • inhibition of neurotransmission in hippocampus causing short term amnesia.
  • inhibition of thalamic sensory relay nuclei parts of cortex causing analgesia
  • volatile anaesthetics can inhibit spinal reflexes
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14
Q

what is the effect of general anaesthetics at high concentrations?

A
  • results in loss of motor control, reflexes, respiration and autonomic regulation.
  • in absence of artificial respiration results in death
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15
Q

first stage of anaesthetic (analgesia)

A

reduced responsiveness to a normal painful procedure

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16
Q

second stage of anaesthetic (excitement)

A
  • patient has exaggerated reflexes where they gag or kick out.
    this stage is dangerous for the person doing the procedure
17
Q

third stage of anaesthetic (surgical anaesthesia)

A
  • unconsciousness
  • patient has lost all reflexes
  • short-term amnesia
18
Q

fourth stage of anaesthetic (medullary paralysis)

A
  • loss of cardiovascular reflexes and respiratory paralysis
  • needs to be rapidly controlled
19
Q

what are the advantages of intravenous anaesthetics?

A
  • rapid induction and easy to administer
20
Q

characteristics of propofol (intravenous)

A

used for maintenance of anaesthesia and has rapid metabolism. rapid recovery so less ‘hangover’ can be useful for short surgery.

21
Q

characteristics for thiopental (barbiturate)

A

induction is 20 seconds and lasts 10 minutes because of redistribution but causes respiratory depression

22
Q

characteristics of etomidate (intravenous)

A

offers advantage of having less cardiovascular depression

23
Q

disadvantages of intravenous administration

A

pain at site of injection and complex pharmacokinetics. has a hangover due to accumulation in body fat

24
Q

characteristics of ketamine

A
  • acts as a dissociative anaesthetic and causes sensory loss
  • NMDA channel blocker
  • causes hallucinations
  • increased intracranial pressure which is a hazard.
25
Q

characteristics of inhalation anaesthetics

A
  • only route of entry and exit is via lungs
  • easy to control the concentrations
    easily cross alveolar membrane
    small amount of toxicity due to limited metabolism
26
Q

what does low blood solubility cause?

A

causes rapid induction and recovery because of concentration in alveolar space is equal to concentration in inspired air. equilibrates more rapidly with concentration in blood

27
Q

what does high lipid solubility cause?

A

increases potency but slows down recovery and equilibration in fat is much slower

28
Q

how is malignant hyperthermia triggered?

A

exposure to certain drugs used for general anaesthetics like volatile anaesthetic agents

29
Q

what does malignant hyperthermia cause?

A

drastic and uncontrolled increase in oxidative metabolism in skeletal muscle, which overwhelms bodys capacity to supply oxygen, remove CO2 and regulate temperature

30
Q

what can malignant hyperthermia lead to if not treated?

A

circulatory collapse and death

31
Q

how is malignant hyperthermia treated?

A

Dantrolene used to treat it as a ryanodine receptor antagonist and muscle relaxant given

32
Q

what type of disorder is malignant hyperthermia?

A

inherited as an autosomal dominant disorder