CH. 49

• nocioreceptors


  pain receptors; activated by tissue damage
• conduction via A fibers

  acute pain from mechanical or thermal stimuli.
• conduction via C fibers

  more long-lasting chemical/thermal stimulation sensitize to brain to chronic pain
• what stimulates noceioreceptors

  tissue chemical mediators (prostaglandins)
• what blocks prostaglandin synthesis

  NSAIDS
• specificity theory

  pain has its own receptors and pathways
• pattern theory


  pain shares receptor and pathways response to stimulation pattern
• gate control theory


  tactile input to cord from adjacent areas can modulate pain
• neuromatrix theory

  brain contains dispersed neural network that perceives pain
• what receptors are activated due to tissue damage

  nocioreceptors
• A fibres

  acute pain from mechanical or thermal stimulation
• C fibres


  more long-lasting chemical/thermal stimulation sensitize brain to chronic pain
• What tissue chemical mediators stimulate nocioreceptors?

  prostaglandins
• What blocks prostaglandin synthesis?

  NSAIDS
• what is the mediator released during a tissue injury

  substance p, prostaglandins, serotonin, acetylcholine
• what mediator is released for A fibres in the spinal cord

  Glutamate
• what mediator is released for C fibers in spinal cord

  substance P
• what does substance P do

  diffuse to nearby synapses, prolongs and enhances pain
• A delta fibres


  myelinated, fast pain, mechanical, thermal stimuli, localized
• C Fibres

  unmyelinated, slow, more diffuse, chemical , mechanical or thermal.
• Where are free nerve endings found

  skin, periosteum, vessel walls, joint surfaces, fall cerebra and tentorium
• what stimuli excite pain receptors

  mechanical thermal chemical
• what stimuli are responsible for fast pain

  mechanical and thermal
• what stimuli are responsible for slow pain

  mechanical, thermal, chemical
• hyeralgesia


  pain receptors adapt poorly over time. causes increased firing as stimulus continues common in slow pain
• what is the pathway responsible for pain

  spinothamalic pathway
• free nerve endings

  pain, heat, cold
• merkel disks


  touch
• Krause end bulbs

  touch
• root hair plexus


  touch
• messier corpuscles

  touch
• pacinian corpuscles

  pressure
• ruffini endings

  pressure
• Fast pain is stimulated by

  mechanical or thermal damage: transmitted to cord on type alpha fibres
• slow pain is stimulated by

  chemical or persistent mechanical/thermal damage transmitted to cord on type c fibers
• rate of tissue damage is determined by

  pain perception, temp >45*c
• chemical pain stimuli during tissue damage is causes by

  an increase in bradykinin release
• ischemia pain is caused by

  lactic acid and bradykinin release
• muscle spasm


  ischemia and stimulation of machanoreceptors
• what is the pathway for slow chronic pain

  paleospinothalamic tract