Anaesthesia and analgesia Flashcards

1
Q

4 phases of nociceptive pain:

A

Tenderness Tells Possible Misery
Transduction
Transmission
Perception
Modulation

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2
Q

What is transmission?

A

The action potential travels through a first order neuron to the spinal cord:
A-beta (fast, myelinated, large) - touch
A-delta (fast, myelinated, small) - mechanical, thermal
C (slow, unmyelinated) - mechanical, chemical, thermal
They go to the dorsal horn and the rexed laminae (greymatter) of spinal cord -> decussation (contralateral ventral horn) -> up 5 ascending tracts (spinothalamic tract to the thalamus and spinomesencephalic tract to periacqueductal grey to medulla)

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3
Q

What is transduction?

A

Turns signal of noxious stimuli (chemical/thermal/mechanical) into an electrical stimulus (action potential).

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4
Q

what is perception?

A

3rd order neuron sends information to the appropriate somatosensory cortex. The limbic system is contacted.

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5
Q

what is modulation?

A

Descending neurons from the brain release substances that inhibit transmission of painful impulses and produce motor resoibse ti aviud oaub

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6
Q

what are the 3 main endogenous mechanisms for pain modulation?

A
  1. descending inhibitory nerve system (serotonin, norepinephrine), synapse dorsal horn of spinal cord
  2. endogenous opioid system (inhibitory neuron): enkephalins, endorphins, dynorphins. Gate control: interneuron release these substances in response to stimulus of A-beta fibre that block pain signaling
  3. peripheral modulation on terminal nociceptors: decrease Ca2+ entry and inhibit neurotransmitter release
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7
Q

Opioid receptors are located in:

A

Brain: thalamus, limbic system
Spinal cord: substantia gelatinosa

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8
Q

Explain ion trapping in COX-2 selective NSAIDs

A
  • NSAIDs are weak acids that become lipid soluble in the highly acidic environment of the stomach
  • Penetrate easily into gastric cells -> readily trapped in the more alkaline environment
  • High local concentration of NSAID in the GI mucosa
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9
Q

what is serotonin syndrome?

A

Overactivation of peripheral and central postsynaptic 5-HT1A and 5-HT2A receptors

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10
Q
A
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