Pain Physiology Flashcards
physiologic pain
Normal response to a noxious stimulus, producing protective behavioural responses to potential or actual tissue damage
acute pain
sudden onset of pain, which may be severe but disappears when the stimulus is removed
chronic pain
pain that lasts several weeks to months and persists beyond the expected healing time
somatic pain
originates from damage to bone, joint, muscle, or skin;
well localized
visceral pain
originates from internal organs – stretching or twisting of viscera, mesenteries, and ligaments;
poorly localized
neuropathic pain
originates from injury to the peripheral or central nervous system (ex. nerve transection or compression)
inflammatory pain
originates from tissue damage (ex. sx, trauma, ischemia, OA, laminitis, infection)
referred pain
originates from one part of the body but perceived as occurring in another
ex: heart attach - presents as pain in left arm but damage is to the myocardium
transduction
peripheral pain receptors activated by a stimulus
transmission
signal communicated via Aδ and C-nerve fibers to spinal cord
modulation
nociceptive input modified at the spinal cord
perception
conscious recognition of pain at the cerebral cortex
mechanoreceptors respond to
stretching, compression, crushing
thermoreceptors respond to
heat and cold
chemoreceptors respond to
Neurotransmitters, prostaglandins,
autocoids (ex. Bradykinin, histamine),
acids (ex. Lactic),
cytokines (ex. TNF, IL-1, 6,8),
leukotrienes, nerve growth factor
Aδ-fibers
Myelinated, fast transmission
Acute, accurately localized, sharp, and rapid onset pain
C-fibers
Nonmyelinated, slow transmission
Chronic, diffuse, dull, burning, aching pain
spinal cord pathway
Afferent peripheral nerves (Aδ and C fibers) enter the spinal cord through the dorsal roots →
Synapse in Lamina II of the dorsal horn gray matter→
Ascend via spinothalamic and spinoreticular tracts to brain
facilitory/excitatory substances
increase pain
Substance P → NK1 receptor
Glutamate → AMPA, NMDA, kainate receptors
inhibitory substances
decrease pain
GABA, endogenous opioids
spinothalamic tract
terminates at thalamus and somatosensory cortex
Transmits easily localized, superficial pain
spinoretucular tract
Terminates in the reticular formation
Transmits deep and visceral pain
descending inhibitory pain pathways
input recieved in midbrain (periaqueductal grey matter, nucleus raphe magnus) →
axons from PAG and NRM release endorphins (endogenous opioids - serotonin and NE)→
inhibit pain transmission at level of dorsal horn
T/F head pain is different from peripheral pathways
True
mediated by trigeminal nerve (CN V)
stress response
systemic consequence of unmanaged pain
mediated by SNS
release hormones (ACTH, cortisol, vasopressin, growth hormone) and neurtotransmitters (epi, NE)
GI consequences of unmanaged pain
delayed gastric emptying, nausea, ileus
hematologic consequences of unmanaged pain
hypercoaguability
risk of thrombosis
allodynia
Pain evoked by a stimulus that does not normally cause pain
hyperalgesia
An increased or exaggerated response to a stimulus that is normally painful (heightened sense of pain)
T/F secondary hyperalgesia occurs in surrounding, undamaged tissue
True
peripheral sensitization
An increase in the activity, excitability, and responsiveness of peripheral nerve terminals, leading to primary hyperalgesia
wind up
Summation of painful stimulation IN THE SPINAL CORD, mediated by C-fibers. Contributes to central sensitization
central sensitization
An increase in nerve excitability and responsiveness in the central nervous system, particularly the spinal cord, leading to primary and secondary hyperalgesia, and allodynia
what results in “sensitizing soup”
release of H+, K+, and ATP from ruptured cells
Release of NE, histamine, bradykinin, serotonin, prostaglandins, leukotrienes, cytokines, substance P
increases intra cellular Ca and indices intracellulae signaling cascades
in peripheral sensitization high threshold Aδ and C-fiber nociceptors→
low threshold (INCREASED SENSITIVITY)
activation of silent nociceptors
peripheral sensitization clinically results in
primary hyperalgesia
what is wind up
Temporal summation and cumulative depolarization of dorsal horn neurons = Continuous stimulation of these neurons by a peripheral pain stimulus
removes normal Mg++ block on NMDA receptors (gluatmate can bind→increases pain transmission)
wind up contributes to _______sensitization
central
MoA of increased dorsal horn excitability in central sensitization
Removal of Mg++ block on NMDA receptors (wind-up)
Activation of NMDA receptors by glutamate
Increased intracellular Ca++, triggering signalling pathways and gene expression
disinhibition at the level of the spinal cord in central sensitization is due to
decreased GABA activity
central sensitization results in:
hyperalgesia
allodynia
spontaneous pain
pain memory (phantom limb pain)
preemptive analgesia
The administration of analgesic therapy before painful stimulation, used to PREVENT WINDUP
clinical goal of analgesia
reduce pain by interrupting nociception at one or multiple levels (transduction, transmission, modulation, perception)
T/F pre-emptive analgesia can prevent peripheral and/or central sensitization
true
depends on drug
decreases total analgesic requirements
interruption of nociception - transduction
Topical local anesthetics, tissue cooling
Infiltration of local anesthetic, into pleural cavity or intra-articular (+ morphine)
Systemic NSAIDS – decrease local production of inflammatory mediators
interruption of nociception - transmission
Local anesthetic nerve blockade (peripheral, plexus)
Epidural
interruption of nociception - modulation
Opioids
α-2 agonists
NSAIDS
NMDA antagonists
interruption of nociception - perception
opioids
α-2 agonists
General anesthetics
Which pain fiber would be most likely involved in transmitting sharp, fast pain?
Aδ fibers
What are the major excitatory and inhibitory neurotransmitters involved with pain transmission?
excitatory - glutamate, subtance P
inhibitory - GABA
What strategies could be used to prevent peripheral sensitization?
local blocks, topical anesthetics, NSAIDs
What strategies could be used to prevent central sensitization?
opioids
alpha 2 agonists
ketamine
Does general anesthesia prevent either peripheral or central sensitization?
No - have to add analgesia
