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
characteristics of inhalation anaesthetics
- 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
what does low blood solubility cause?
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
what does high lipid solubility cause?
increases potency but slows down recovery and equilibration in fat is much slower
28
how is malignant hyperthermia triggered?
exposure to certain drugs used for general anaesthetics like volatile anaesthetic agents
29
what does malignant hyperthermia cause?
drastic and uncontrolled increase in oxidative metabolism in skeletal muscle, which overwhelms bodys capacity to supply oxygen, remove CO2 and regulate temperature
30
what can malignant hyperthermia lead to if not treated?
circulatory collapse and death
31
how is malignant hyperthermia treated?
Dantrolene used to treat it as a ryanodine receptor antagonist and muscle relaxant given
32
what type of disorder is malignant hyperthermia?
inherited as an autosomal dominant disorder