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85 Cards in this Set
- Front
- Back
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what is pain
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unpleasant sensory and emotional experience associated with actual or potential tissue damage
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what is acute pain
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pain associated with tissue damage or occurs in response to tissue injury
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acute pain is _____ pain
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protective pain
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what is chronic pain
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- pain that outlasts normal tissue healing time
- underlying pathology does not explain the presence/extent of the pain |
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what is prolonged pain
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pain 3-6 months beyond onset (used to be defitinition of chronic pain- now called prolonged pain)
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what is hyperalgesia
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increased response to noxious stimuli
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what is primary hyperalgesia
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occurs at the site of injury
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what is secondary hyperalgesia
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occurs outside the site of injury
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what are the dimensions of pain
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1) sensory discriminitive
2) motivational Affective 3) cognitive evaluation |
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what is sensory discriminitive
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- tells us location, magnitude, duration, and quality of pain
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what is motivational affective dimension of pain
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responses that give us
- unpleasantness - fight/flight |
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what is the cognitive evaluatin dimension of pain
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- based on past experiences tells us the probability of outcome
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what are the receptors for pain and temperature
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pain = nociceptors
temperature = thermal receptors |
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what do nociceptors respond to
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stimuli that damage or threaten to damage tissue (actual or potential tissue damage)
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what type of fibers carry pain information
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Adelta and C fibers
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what information do Adelta fibers carry
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- unimodal.... only give mechanical information (pain)
- cooling temp (thermal) |
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what information do C fibers carry
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- polymodal..... give information on mechanical, chemical, thermal stimulation (pain)
- heating temp (thermal |
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both nociceptors and thermal receptors are ______
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free nerve endings
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what do thermal receptors respond to
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heat or cooling stimuli with the temp range that does not damage the skin
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what fibers carry thermal information
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small afferents: Adelta and C fibers
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cooling temperatures are carried on ______ fibers while heating temperatures are carried on ______ fibers
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cooling = a delta
heating = C fibers |
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besides pain and heat, what other information can C fibers carry
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itching and tickle
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which fibers carry pain and temp in the muscle/joints
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III = A delta fibers
IV = C fibers |
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which of the pain/temp fibers are myelinated
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A delta and III fibers are myelinated so go faster
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with noxious stimulus there are two waves of pain.... fast sharp pain and slow acing pain what accounds for the two responses
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fast sharp = a delta fibers getting information to the brain quickly
slow aching = c delta fibers reaching the brain more slowly |
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what chemicals activate nocieceptors
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chemicals released with inflammation (histamine, bradykinin, 5-HT, prostaglandin, ATP, H+)
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what are the two consequences following tissue injury
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1) hyperalgesia
2) peripheral sensitization |
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what is peripheral sensitization
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- lower activation threshold of nociceptor
- increased firing rate - increased release of aspartate, glutamate, substance P in dorsal horn of SC (excitatory) |
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what is the resupt of peripheral sensitization following injury
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bigger pain signal delivered to spinal cord
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what are the excitatory transmitters for pain
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- substance P
- calcitonin gene related peptide - aspartate - glutamate |
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what are the inhibitory transmitters of pain
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- GABA
- glycine - somatostatin - apha2 agonists |
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where are the inhibitory transmitters found
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descending inhibitory pathwasy
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which excitatory transmitter is increased in the spinal cord after inflammation
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glutamate
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another reason for the increase in pain with tissue injury is that inflammation activates __________
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silent nociceptors
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what are silent nociceptors
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"mechanically insensitive nociceptors/afferents"
- normally inactive and do not respond to mechanical stimuli, but after inflammation they become activated and respond to both noxious and innocuous mechanical stimuli |
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where are nociceptors found
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skin, joints, muscle, viscera (up to 50% of nociceptors in viscera are silent nocicepors!!)
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where is light touch carried vs. pain and temp in the spinothalamic tract
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pain and temp are more lateral to the light touch which is more ventral (anterolateral tract)
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what are the nerves that make up the cranial nerve V (trigeminal)
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- Opthalmic nerve
- maxillay nerve - mandibular nerve |
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what is central sensitization
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- increased excitability of pain-related central nervous system neurons
- tissue injury "sensitizes" central neurons |
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what are the 5 characteristics of central sensitization
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1) increase in receptor field size
2) increase response to noxious stimuli 3) increase response to innocuous stimuli 4) increase in spontaneous firing 5) decrease in activation threshold of spinal neurons |
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what is the receptive field
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the area in which stimulation leads to the response of a particular sensory neuron
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what are wide dynamic range spinal neurons
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increase respone to noxious and innocuous stimuli
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what is referred pain
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pain outside the area of injury
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what did the studys show to be the difference between healthy subjects and those with chronic pain as far as referred pain
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using e stim of the anterior tib,
- healty subjects pain referred distally - chronic pain sufferers pain refered both proximally and idstally |
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what are the two mechanisms to explain referred pain
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1) convergence theory
2) central sensitization |
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what is the convergence theory
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neurons can have input from several types of tissue: skin, muscle, joint, viscera
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how can drugs used for inflammation help pain
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inflammation activates silent nociceptors.... so drugs can be used to block the action potential along the first order neuron
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aspirin in particular inhibits what
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prostaglandin synthesis, which sensitizes pain receptors, so less prostaglandin = less pain
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why do we want to stimulate the descending pathways
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they release inhibitory transmitters
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what does the PAG produce
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antinociception via activation of medulla or pons
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what does the pons release to inhibit pain
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epinephrine (adrenaline)
norepinephrine (noradrenaline) |
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what does the medulla release
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serotonin
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where could opiates be released
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into the spinal cord
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what happens in the rostal ventral medulla for pain with morphine
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INHIBITS ...ON cells: increaes their firing rate immediately prior to reflex withdrawal of the tail from noxious thermal stimulation
EXCITES OFF cells: stop firing immediately before reflex withdrawal of tail |
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what factors are involved in activation of the descending pathways
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psychological, physiological, social and genetic
- noxious stim - irritants - placebo - expectations - stress mental or physical |
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where are beta endorphins released into the blood from
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pituitary gland
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where are beta endorphins released into PAG from
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hypothalamic neurons
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what are the inhibitory actions of opiods (antinociception)
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1) supresses release of glutamate or substance P from PRESYNAPTIC terminals
2) inhibits neurons by hyperpolarizing their POSTSYNAPTIC membranes |
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where are opioid receptors
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- peripheral terminals of small diameter afferents (nocicept)
- spinal cord - rostral ventral medulla - periaqueductal grey - pons - amygdala |
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how do opioid receptors get to the peripheral terminals of small diameter afferents
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- upregulated in inflammation
- made in DRG and transported to the peripheral terminal in response to injury |
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how is opiate-mediated analgesia distributed in the nervous system
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widely distributed
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where is opiate-mediated analgesia located
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in areas that modulate pain
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what controls local opioid release
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interneurons:
1) PAG 2) pons (locus ceruleus) 3) RVM 4) Dorsal horn |
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what stimulates the opiate-mediated analgesia
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1) inflammation
2) irritant 3) stress 4) exercise 5) modalities (TENS, acupunct) 6) placebo 7) drugs (morphine, codeine) |
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what is the counter irritant theory
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activation of inhibitory mechanisms via peripheral inputs
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what are examples of irritants for counter irritant theory
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- cold and heat
- electrical stimulation |
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how does the counter irritant theory activate opiod receptors in CNS
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irritant activates the supraspinal sites which cause the release of opiods into the dorsal horn, thus supressing the pain
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the gate cntrol theory is one of the first theories regarding the ________ of pain
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modulation
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how does the gate control theory work
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activation of large afferent fibers inhibits synaptic transmission of small afferent fibers
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where does the gate control theory cause an effect
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substantia gelatinosa-- lamina II of dorsal horn
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what interventious could work through the gate control theory
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NOT heat or music theory
YES to Stim and balance ex. |
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what is neuropathic pain
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pain from injury to the CNS or PNS due to direct trauma, disease process, mechanical pimpingement
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what is IASP
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a dysfunction of the nervous system
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what are the symptoms of neuropathic pain
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1) allodynia and hyperalgesia
2) dysesthesia (unpleasant/abnormal sensation) 3) paresthesia (painless abnormal sensation) |
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what are the potential mechanisms for neuropathic pain
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1) structrual reorganization of sympathetic innervations (increased sensitivity to noradrenaline)
2) central sensitization 3) disinhibition 4) neuroma formation at nerve injury 5) neuroanatomical reorganization |
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what is disinhibition
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death of inhibitory neurons in dorsal horn
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what is a neuroma
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mass growing from nerve
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how does a neuroma affect neuropathic pain
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- spontaneuous activity at a neuroma can be perceived as pain
- nerve is tryng to regenerate and is very excitable |
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what is the neuroanatomical reorganization that can happen with neuropathic pain
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following transection of peripheral nerve, dorsal horn neurons develop additional receptive fields - axonal sprouting
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what is CRPS
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comples regional pain syndrome (used to be called reflex sympathetic dystrophy)
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what is the pathology for CRPS
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- increased inflammatory neurochemicals
- impaired sympathetic regulation - central sensitization |
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what is the clinical presentation for CRPS
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- regiomnal
- severe, spontaneous pain out of proporition - skin changes (red/pale skin, sweating --> dry cold) - swelling - restricted mov't - bone changes later |
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what is the tx for CRPS
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- early intervention CRITICAL
- patient ed (USE LIMB) - drugs - ROM and AROM better than PROM - stress loading - sensory desensitization - soft tissue mob - pool therapy - possible surgery: sympathetic nerve block |
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what causes fibromyalgia
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UNKNOWN cuassified as a CNS disorder of nociception
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what is fibromyalgia
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- hx widespread pain > 3 months
- pain pain 11 out of 18 tender points on palpation |
