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Anaesthesia > Pain and Anagesia > Flashcards

Pain and Anagesia Flashcards

1
Q

Define Pain.

A

Integration and processing of nociceptive input by the brain allowing it to be recognised as pain (cortical recoginition)

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2
Q

Define nociception.

A

Information regarding a noxious insult relayed from periphery to the CNS

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3
Q

Outline the three aspects of pain (S, M, C)

A
  1. Sensory - Recognition 2. Motivational - Affective 3. Cognitive - Evaluative (recognise consequences)
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4
Q

Name the different types of pain.

A

Phys/Path Somatic/ Visceral Acute/ Chronic

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5
Q

Describe the difference between somatic and visceral nociceptors.

A

S - numerous and widespread, small receptive fields, assoc with skin, muscle, bone & joints, respond to chemical, thermal and mechanical stimuli. V - sparsely distributed, large receptive fields, respond to ischemia, distenstion and inflammation, stimuli threshold depends on area affected rather than intensity.

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6
Q

Describe the difference between somatic and visceral pain.

A

S - localised to site of injury, sharp/ stabbing pain. V - Poorly localised and diffuse pain, autonomic associated, may be referred.

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7
Q

Functional/ anatomical adaptation of NS in response to environment/ physiological processes. What can be the consequences of this process?

A

Neuroplasticity - hyperalgesia, allodynia, chronic pain

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8
Q

Allodynia

A

Normally innocuous stimuli being percieved as painful

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9
Q

Hyperalgesia

A

Exaggerated response to normally painful stimuli

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10
Q

Define multimodal analgesia.

A

Formulation of an analgesic plan which affects multiple steps in the nociceptive pathway: transduction, transmission, modulation and perception

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11
Q

Describe the different stages of the nociceptive pathway.. (x4)

A
  1. Transduction - Applied stimuli converted into an electrical signal (AP) by activation of nerve end receptors
  2. Transmission - Conduction of impulses to and from the CNS (& of ascending and descending impulses within the CNS)
  3. Modulation - Alteration at the spinal cord level due to alteration of neuronal sensitivity and NT release
  4. Perception - CNS centres - RAS, thal/hypothal, cingulation gyrus, amygdala, hippocampus, cortex
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12
Q

Name and describe nociceptor receptors..

A
  • Free nerve endings
  • Higher activation thresholds than specialised receptors
  • A delta and C fibres
  • Prolonged stimution results in sensitisation
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13
Q

Which nociceptive have the highest activation thresholds?

A

A delta fibres < C fibres

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14
Q

Name substances which can cause activation of nociceptors.

A
  1. Cell damage products - prostaglandin E2, H+, K+, ATP, Leucotrienes
  2. Sensory nerve endins - substance P, CGRP
  3. Plasma, platelets and mast cells - hisamine, bradykinin and serotonin
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15
Q

What is peripheral sensitisation?

A

When inflammatory mediators and products of cell damage lower nociceptor threshold and recruit silent nociceptors.

Results in primary hyperalgesia, primary allodynia

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16
Q

How do NSAIDs act to produce analgesia?

A

COX inhibitors - they reduce the production of inflammatory mediators which cause receptor sensitisation (transduction and modulation effects)

17
Q

Describe the difference between COX 1 and 2 receptors.

A

COX 1 - constitutive - maintain GI mucosa, platelet aggregation and renal blood flow

COX 2 - inducible - BUT also expressed consititutively in CNS, kidney, eye and repro organs

18
Q

What factors can lead to differences in NSAID action?

A
  1. COX selectivity of the drug
  2. Selectivity differs between species
  3. Individual variation
  4. Affects LOX pathway
19
Q

What is the function of a first order neurone?

Name the three main types we are concerned with and where they synapse.

A

Transmits information from the periphery to CNS

Cell body in DRG, axon extends into grey matter of dorsal horn of spinal cord:

  • Aδ fibres – synapse in laminae I and V. First pain; mechanical and thermal stimuli
  • C fibres – synapse in laminae I and II. Interneurones connect with lamina V. Dull persistent pain; chemical, mechanical and thermal stimuli
  • Aβ fibres – synapse in laminae II, III, IV, V.
20
Q

What are the two main types of 2nd order neurone?

Describe their function.

A
  1. Inter-neurones - within the grey matter
    1. Excitatory/ inhibitory - modulation of pain signals
  2. Projection neurone - ascend spinal cord to higher centres
    1. Nociceptive specific, high threshold
    2. Adelta and c fibres only
    3. Wide dynamic range
21
Q

Name the five different anatomical tracts of projection neurones.

A
  • spinothalamic
  • spinoreticular
  • spinomesencephalic
  • spinohypothalamic
  • spinocervical
22
Q

Sodium channel blockers which prevent generation and propagation of APs

A

Local Anaesthetics

23
Q

What is the function of a third order neurone?

A
  • processing, integration and recognition of a harmful or painful experience
24
Q

Do animals need to be conscious to percieve pain?

A

Yes

25
Q

Which centres of the brain are involved in pain perception?

A
  • reticular activating system
    • affective and motivational aspects
  • thalamus and hypothalamus
    • sensory, discriminatory and affective aspects
  • cingulate gyrus
    • behavioural responses
  • amygdala
    • learned responses (anxiety and fear)
  • hippocampus
    • memory
  • locus coeruleus
    • behavioural (arousal) responses
  • cortex
    • conscious perception
26
Q

Which substances are involved in neuronal modulation?

A
  • Excitatory transmitters increase cation (Na+/Ca2+) conductance of axonal membrane
    • presynaptically increasing transmitter release
    • postsynaptically destabilising membrane potential or increasing expression and sensitivity of receptors
  • Glutamate + aspartate act on N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate receptors (ligand gated non-specific cation channels)
  • Substance P and neurokinin A act on neurokinin (G-protein coupled) receptors
27
Q

How do inhibitory transmitters work to modulate neuronal substances?

A
  1. Increased Cl- conductance of axonal membranes - causes hyperpolarisation of glycine and GABAa receptors
  2. Increased K+ conductance of axonal membrane - GABAa - prevents NT release
28
Q

Outline the pain gate theory.

A
  • Input from Aδ or C fibres inhibits activity of inhibitory interneurones facilitating nociceptive signalling
  • Innocuous sensory input from Aβ fibres activates inhibitory interneurones suppressing nociceptive signalling
29
Q

Outline descending inhibition.

A

Periaquaductal grey tracts which project to the spinal cord. They contain endogenous opioids and opioid receptors and are inhibitory to ascending pain neurones.

30
Q

Outline the MOA of paracetamol.

A
  • weak PG synthesis inhibitor (better centrally than peripherally)
  • stimulates descending serotonergic inhibitory pathways
  • inhibits reuptake of endogenous cannabinoids
  • acts centrally at modulation stage of nociceptive pathway
31
Q
  1. A mu partial agonist
  2. A mu antagonist, kappa agonist
  3. 2 mu agonists

Sort these - Butorphanol, pethidine, morphine, methadone, fentanyl, buprenorphine

A
  1. Buprenorphine
  2. Butorphanol
  3. Others
32
Q

Order these opioids in terms of their duration of effect.

Butorphanol, buprenorphine, pethidine, morphine, methadone, fentanyl

A

Fentanyl, Butrophanol, Pethidine, Morphine, methadone, Buprenorphine

33
Q

Describe the mechanism of action of alpha-2-agonists.

A

Agonise Alpha2 adrenoceptors

Activate descending serotonergic and noradrenergic inhibitory pathways

Analgesia synergists with opioids

34
Q

Describe central sensitisation

What can it result in?

A

Increased second order neurone activity due to recruitment and upregulation of post synaptic receptors in response to sustained or massive release of excitatory neurotransmitters.

Interneurone mediated sensitisation of adjacent primary afferents decreasing their threshold for recruitment.

Can lead to secondary hyperalgesia and secondary allodynia

Anaesthesia (10 decks)

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