Pain

  1. nocioception
    process of transduction, transmission, perception, and modulation of pain
  2. T or F, nocioception varies widely among individuals?
    F, similar
  3. T or F, pain experience and response is similar among individuals?
    F, varies widely
  4. pain threshold
    point where a stimulus is perceived as painful
  5. pain tolerance
    max intensity of pain that an individual can endure before they want action taken
  6. how do pain threshold and pain tolerance vary among individuals?
    • threshold is fairly uniform
    • tolerance varies widely
  7. 2 major classifications of pain
    nocioceptive and neuropathic
  8. 2 types of nocioceptive pain
    somatic or visceral
  9. nocioceptive pain
    results from ongoing stim of nerves from a noxious stim
  10. somatic pain
    • type of nocioceptive pain
    • identifiable focal point
    • follows nerve distribution
    • well localized, sharp, pain at point of stimulus
  11. visceral pain
    • type of nocioceptive pain
    • diffuse and can be referred to another area
    • dull and vague
  12. What type of pain med does nocioceptive pain respond best to?
    NSAIDs and opioids
  13. neuropathic pain
    • caused by abnormal processing of painful stimuli
    • CNS dysfunction allows for spontaneous excitation leading to severe pain
    • peripheral or central generation
    • difficult to treat
    • described as burning, tingling, or shock like
  14. T or F, neuropathic pain may be associated with subjective numbness, loss of sensation, or weakness
    T
  15. What type of pain med is effective in treating neuropathic pain?
    • Adjunctive meds 
    • NSAIDs and opioids are not very effective
  16. Adjunctive analgesic
    • med used primarily for other reasons than analgesia
    • ex: TCA, anti-convulsant meds
  17. acute pain
    • mostly nocioceptive
    • peripheral nocioceptive response is activated by noxious stimuli
    • associated with neuro endocrine stress response proportional to level of stimulus
    • resolves within a few days to weeks
  18. chronic pain
    • lasts longer than course of disease or injury (1-6 months post healing)
    • nocioceptive or neuropathic
    • psych or enviro factors play a major role
  19. What nerve fibers carry pain sensation?
    • A delta and C fibers
    • sensory (afferent)
  20. Describe the pain that A-delta fibers carry
    • fast pain, AKA 1st pain
    • fibers are myelinated
    • sharp prickling pain that is acutely localized
    • duration coincides with duration of the stimulus
  21. Describe the pain that C fibers carry
    • slow pain, AKA 2nd pain
    • unmyelinated
    • burning and diffuse pain
    • pain may exceed the duration of the stimulus
  22. Acute pain is ___ (fast or slow?) pain and is carried by ___ fibers
    • fast
    • A-delta
  23. Chronic pain is ___ (fast or slow?) pain and is carried by ___ fibers
    • slow
    • C
  24. Deafferentiation pain
    • chronic pain associated with a loss of sensory input
    • ex: amputation
  25. T or F, chronic pain is complex and involves changes in the nervous system both centrally and peripherally?
    T
  26. Neospinothalamic tract
    • fast A-delta fibers travel via this pathway
    • synapse at lamina 1 and 5
    • pain travels to midbrain (thalamus)
  27. Main afferent (sensory) pathway of the spinal cord
    spinothalamic
  28. paleospinothalamic
    carries slow (C fiber) pain transmission to reticular formation in the brain stem
  29. What are the 2 divisions of the spinothalamic tract?
    neospinothalamic and paleospinothalamic
  30. Where do afferent C fibers synapse in the spinal cord?
    lamina 2 and 3
  31. substantia gelatinosa
    • AKA lamina 2
    • afferent C fibers synapse here in the spinal cord
    • plays a major role in processing and modulating nocioceptive input
    • major site of action of opioids
  32. What part of the spinal cord receives all the afferent neuron activity?
    dorsal horn
  33. dorsal horn
    principle site of modulation of pain by both ascending and descending neuro pathways
  34. pain pathway is the _____ tract
    spinothalamic
  35. T or F, pain sensations cross the spinal cord?
    T
  36. Describe the path of pain sensations traveling in either A-delta or C nerve fibers
    • synapse in the dorsal horn of the SC
    • ascend 1-3 segments in the tract of lissauer
    • synapse with a 2nd order neuron
    • crosses midline 
    • ascends via contralateral spinothalamic tract to the brainstem
  37. What are the 2 types of 2nd order neurons?
    • nocioceptive- serve only noxious stimuli
    • wide dynamic range neurons- carry noxious and non-noxious stimuli
  38. What type of neurons are capable of wind up
    wide dynamic range neurons
  39. What is "wind up"
    • with repeat stimulation, wide dynamic range neurons increase their firing rate in a graded fashion
    • preemptive analgesia is thought to prevent this
  40. periaqueductal grey
    • grey matter in the mid brain
    • when there is afferent stimulation of the periaqueductal grey the efferent (downward) pathway is activated
  41. How is the periaqueductal grey area stimulated?
    when there is afferent stimulation of the periaqueductal grey the efferent (downward) pathway is activated
  42. Major NT released from C fibers
    substance P
  43. T or F, release of substance P activates the arachidonic pathway?
    T
  44. How does the substantia gelatinosa modulate pain?
    • c fibers synapse with inter neurons in the SG
    • this causes substance P to be released
    • SG releases enkephalins which decreases the release of substance P
    • this decreases the number of action potentials in the interneuron pain pathway and ultimately the pain perception is decreased
  45. Major NT released from A delta fibers
    glutamate, an excitatory NT
  46. substance P works via what receptor
    NK-1
  47. glutamate works via what receptor
    NMDA
  48. What are examples of alpha 2 adrenergic agonists?
    clonidine and precedex
  49. activation of the alpha 2 receptor leads to...
    where are the receptors located?
    • pain inhibition
    • dorsal horn of the spinal cord
  50. ketamine MOA
    NMDA antagonist
  51. What are the old names for opioid receptor 1?
    2?
    3?
    • 1= mu
    • 2= delta
    • 3= kappa
  52. supra spinal analgesia is mediated primarily by ____
    mu 1, although mediated by all opioid receptors
  53. spinal analgesia is mediated primarily by ____
    mu 2, although mediated by all opioid receptors
  54. what opioid is unique in that it is a potent mu receptor agonist but has minimal kappa and delta activity?
    remi
  55. properties of mu 1 receptor activation
    decreased HR, euphoria, low abuse potential, urine retention
  56. properties of mu 2 receptor activation
    resp depression and physical dependence
  57. properties of delta receptor activation
    resp depression and physical dependence
  58. properties of kappa receptor activation
    dysphoria, sedation, low abuse potential
  59. T or F, opioids stimulate different receptors than the body's endorphins and enkephalins?
    F, opioids stimulate the same receptors
  60. how does spinal analgesia work?
    • opioid is injected into the spinal or epidural space
    • it diffuses into the substantia gelatinosa (lamina 2)
    • unites with opioid receptors in the nerve terminal 
    • release of substance P is reduced and 
    • transmission of nerve impulses thru the substantial gelatinosa is inhibited
  61. IV opioids affect what area of the brain
    periaqueductal grey in the midbrain
  62. what is primary hyperalgesia
    • increased pain sensitivity
    • mediated by release of substances from damaged tissues
    • type of peripheral pain modulation
    • prostaglandins are released after tissue damage, phospholipids form, arachidonic cascade is set off
  63. what is secondary hyperalgesia
    • increased pain sensitivity
    • type of peripheral pain modulation
    • neurogenic inflammation
    • mediated by substance P
    • allogens? are released from the damaged tissue (bradykinin, 5HT3) and can irritate nerve endings leading to pain
  64. is wind up an example of central or peripheral pain modulation?
    central
  65. 3 types of central modulation
    • wind up
    • receptor field expansion
    • hyper excitability of flexion reflexes
  66. what is receptor field expansion?
    • a type of central pain modulation
    • dorsal horn neurons increase their receptor fields such that adjacent neurons become responsive to stimuli to which they were previously unresponsive
  67. what are the 2 pathways of arachidonic acid breakdown?
    • cyclooxygenase to prostaglandins to bradykinin and O2 free radicals leading to inflammation and pain
    • lipoxygenase to leukotrienes to inflammation
  68. allogen
    • pain producing substance
    • all end products of arachidonic acid breakdown are allogens
  69. what are examples of meds that interrupt the arachidonic acid breakdown pathway?
    corticosteroids, NSAIDs, tylenol, ASA
  70. what systemic effects can tissue injury have?
    • anxiety and demoralization
    • DVT (decr flow and Plt aggregation)
    • muscle splinting
    • PNA (immobile)
    • coronary ischemia (increased O2 consumption)
    • poor wound healing (increased cortisol and hyperglycemia)
  71. T or F, activation of the RAAS and immunosuppression may result from tissue damage and pain
    T
  72. what are risk factors for reap depression with PCA use?
    • OSA
    • older age
    • basal infusion
    • hypovolemia
  73. most common SE of opioid PCA
    • itching
    • nausea
    • ileus
  74. risk of using demerol in an elderly or renal failure pt
    accumulation of normeperidine leading to seizures, anxiety, tremors, myoclonus
  75. why might clonidine be added to an epidural
    • alpha 2 agonist
    • reduces sympathetic outflow from the brain stem; inhibit 2nd order neurons in the dorsal horn of the spinal cord
    • sedation is dose related
  76. dose of nalaxone recommended for respiratory depression but to avoid reversal of analgesia
    0.04 mg increments
  77. epidural onset time is directly proportional to
    lipid solubility
  78. fent is highly ____ ____ and thus has a ___ onset
    • lipid soluble
    • fast
  79. fent can cause (early or late) resp depression
    early (fast onset and short DOA)
  80. morphine is ___ and thus has a ___ onset
    • hydrophilic
    • slow
  81. which has more rostral spread- morphine or fentanyl?  why
    morphine, it's water soluble and thus diffuses out of the CSF slowly and thus can travel up toward the brain
  82. morphine can cause (early or late) resp depression
    late
  83. Patho r/t complex regional pain syndromes
    SNS dysfunction
  84. T or F, neuropathic pain is easily treated with opioids
    F
  85. T or F, a different opioid at an equianalgesic dose may be effective in treating chronic pain
    T
  86. how do TCA work to decrease neuropathic pain?
    block NMDA mediated activity
  87. how do SSRIs work to decrease neuropathic pain?
    • block reuptake of serotonin and NE
    • serotonin is an important INHIBITORY NT in the pain pathway
  88. how do anti-convulsants help with chronic pain?
    • alter ion channels along the nerve fiber and block the action potential and thus the painful stimuli
    • helpful for neuropathic pain
  89. reasonable treatment goals for LT pain management
    • reduction of pain intensity
    • increased physical functioning
    • proper medication use
    • improvement of sleep, mood, and interactions with others
    • return to work for normal daily activities
Author
ariadne9
ID
272273
Card Set
Pain
Description
P.I.A.
Updated