22 Flashcards
define plasticity in terms of pain pathway
plasticity is the ability of the pain sensing system to change in response to input
define allodynia
stimuli that would not normally be painful is felt as painful
clinical implications of “sensitization”
- once pain is established, analgesic drugs become less effective2. with constant input over time, the pain felt by the animal increases
generalized pain pathway
conscious experience (requires integration w brain)Nociception initiates pathway through detection of tissue damage and inflammatory mediators (peripheral sensitization)TRANSDUCTION: transformation of peripheral stimulus into action potentials (depolarization of nerve)TRANSMISSION: the afferent signal is conveyed to dorsal horn of the spinal cord (via laminae)MODULATION: Processing of signs at the dorsal horn (either amplifies or suppresses signal)PROJECTION: signal taken to brain/brainstem(spinothalamic tract)PERCEPTION: cerebral cortex (thalamic or cortical level)
major classes of nociceptors
A delta: medium (1-5 microns), myelinated, mediate ACUTE fast well localized painA beta: larger, rapidly conducting myelinated fibers that respond to innocuous mechanical stimuliC-fiber: small (0.25-1.5 microns), UNMYELINATED, mediate poorly localized slow pain, HI threshold, POLYmodal
T/Fmost nociceptores are relatively nonselective ion channels
TRUENOT stimulated by voltage but rather STIMULUS (temp, chemical, mechanical forces)
define polymodal nociceptors
fibers or nociceptors that respond to MULTIPLE types of noxious stimuli (temp, chem, mechanical)
T/FMost C fibers are high threshold and poly modal
TRUEMost C fibers are high threshold and poly modal (heat and mechanical)
heat vs cold sensitive receptors in C fibers
Heat: TRPV-1Cold: TRPM-8
where are A beta nociceptors located
A beta: larger, rapidly conducting myelinated fibers that respond to innocuous mechanical stimuli (ie. light touch)innervate MERKEL CELLS, PACINIAN CORPUSCLES, HAIR FOLLICLES
receptive field of C fibers
large receptive field compared to A delta fibersThis contributes to the poorly localizing, burning, gnawing sensation that persists
conduction speeds of A delta vs C fibers
A delta: FAST 5-30 m/secC fiber: SLOW 0.5-2.0 m/sec
where does the analgesic effect of cold considered to originate from
much of the analgesic effect of cold is considered to originate due to the Inactivation of Na channels
what voltage gated ion channel is a target for local anesthetics
voltage gated SODIUM channelsinvestigation into Na1.7 voltage gated channel blockers for analgesics
Sensory information from the head enters the CNS via _____________nerve
Trigeminal nerveand then relayed to the nucleus caudalis–>thalamus and reticular formation
discrete laminae in which the spinal afferent neuron travels to the dorsal cord A delta vs C fiber
during transmission to dorsal horn A delta fibers travel and terminate in laminae 1 and 5C fibers travel and terminate in laminae 1 and 2
what are three pathways that control descending modulation of sensory input or modulate the pain response
- periaqueductal grey matter of midbrain (send descending excite or inhibit influences)2. rostroventral medulla and pons in brainstem (on, off cells)3. thalamocortical structures
main excitatory neurotransmitters released from1. brief, infrequent noxious stimuli2. frequent, severe stimuli of damaged tissue
- glutamate2. substance P
unique activity of substance P on NMDA receptor activation
neuropeptide/neurokinin/tachykininproinflammatory/excitatoryremoves the Mg block on NMDA receptors to allow for glutamate to activate NMDA receptors (with repeated stimulation and prolonged depolarization->windup pain)
clinical expression of central sensitization
- incr response to stimuli (hyperalgesia)2. expansion of receptive fields of peripheral nociceptors ( may see allodynia)3. incr in spontaneous activity (spontaneous pain)4. neuroplasticity (pain memory–phantom pain)
3 important concepts of central sensitization
- NMDA excitatory activity2. Loss of GABA-ergic and glycinergic inhibitory controls3. Glial-neuronal interactions (peripheral nerves are also damaged and release mediators)
two inhibitory NT
glycineGABA
the initial negative impact of surgical trauma and pain transmission is activation of _____________
sympathetic nervous system (sympathoadrenal and corticomedullary)release of catecholamines (changes metabolism, perfusion, CO, increases oxygen consumption, etc)
categories to assess pain in animals based on Glasgow
- posture2. restlessness3. vocalization4. attention to wound5. demeanor6. gait and ease to rise7. RESPONSE TO PALPATION
define preemptive analgesia
strategy that has the power to deter or prevent anticipated unpleasant situation or occurrencebased on preventing nociceptive input to the CNS to prevent central sensitization and post injury hypersensitivity
what is the only true way post injury hypersensitivity be prevented?
presurgical (preemptive) analgesia ALONG WITHintrasurgical AND post surgical analgesiapreemptive analgesia alone will not rid all pain post injury
Lascelles et al prospective double blinded control on timing of NSAIDs and injury in OHE model
found that preoperative carprofen was most effective in controlling pain in OHE dogs
study or pre vs post laparotomy infiltration with bupivicaine
PREincisional bupivicaine infiltration was superior
7 therapeutic modalities used to decr pain and inflammation in vet patients
- local hypo and hyperthermia2. pROM3. massage4, therapeutic exercise5. hydrotherapy6. US7. electrical stimulation
define and give advantages of multimodal (balanced) analgesia
combining drugs with different MOA1. decr dosages–>decr side effects2. synergistic effects
what areas of the pain pathway do local anesthetics work(figure 22-8 pg 246)
- modulation at the trauma site2. modulation at the peripheral nerve3. modulation of the dorsal horn
what area(s) of the pain pathway do antiinflammatories work(figure 22-8 pg 246)
- modulation at the trauma site
what areas of the pain pathway do opioids and alpha 2 agonist work(figure 22-8 pg 246)
- modulation at the dorsal horn2. modulation at higher centers (brain)
what areas of the pain pathway do 5-HT, NE, Opiodergic work(figure 22-8 pg 246)
descending modulation (via PAG, RVM)
