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pain pathophysiology

two broad mechanisms underlying pain nociceptive neuropathic
two types of nociceptive pain somatic visceral
somatic pain pain related to ongoing activation of nociceptors that innervate bone, joint, muscle or connective tissue
visceral pain occurs when abdominal or thoracic organs are compressed, infiltrated or distended activating nociceptive receptors
neuropathic pain pain secondary to infiltration, compression, or degeneration of neurons in the central or peripheral nervous system
neuropathic pain described as a burning, tingling, or electrical (shock-like) sensation
nociceptive pain occurs as a result of the normal activation of the sensory system by noxious stimuli
nociceptors small diameter afferent neurons (with A delta fibers and C fibers) that respond to noxious stimuli; found in skin, muscle, joints and some visceral tissue
transient receptor potential (TRP) receptors receptors specific to certain types of stimuli which activate the A delta and C fibers
polymodal receptors receptors which respond to varied types of stimuli; the majority of receptors involved in pain
depolarization of primary afferent nerves a neurochemical process involving prostaglandins, bradykinins, protons, nerve growth factors produced by tissues, the inflammatory process and the neurons themselves
at the level of the spinal cord, transmission can be modulated by segmental or supraspinal neuronal pathways; processes in the glial cells of the spinal cord
neurochemistry of transmission at the spinal cord involves endorphins, neuorkinins, biogenic amines(dopamine, histamine, serotonin, norepinephrine), prostaglandins, GABA, neurotensin, cannabinoids, purines
endorphin pain modulatory pathways are made up of endogenous ligands opioid receptors
types of opioid receptors mu, delta, kappa
prolonged firing of c fibers causes release of glutamate at the level of the spinal cord
glutamate acts on these receptors in the spinal cord N-methyl-D-aspartate (NMDA)
activation of NMDA receptors in spinal cord causes central sensitization; in other words the spinal cord neuron becomes more sensitive to all inputs
NMDA receptor activation causes an increase in the response to pain stimuli and decrease in sensitivity to opioid receptor agonists
NMDA agonist will prevent central sensitization and may prevent tolerance to opioids
somatic pain described as aching, squeezing, stabbing, throbbing
visceral pain described as cramping, gnawing with a daily pattern of varying intensity; poorly localized exception: organ capsules = the pain is well localized and described as sharp, stabbing, or throbbing
type of pain that can be referred nociceptive pain of any kind
opioid drugs mimic endogenous opioid ligands at the level of the spinal cord
allodynia pain induced by non-noxious stimuli e.g., light touch
hyperalgesia increased response to a noxious stimuli; may be a result of lowered pain threshold
hyperpathia exaggerated pain responses often with after sensation and intense emotional reaction
produced by injured tissue and may lower pain threshold prostaglandins
the experience of persistent pain may induce mood disturbances (anxiety, depression); impaired coping; psychosocial concerns (loss of job, loss of identity, loss of relationships, etc)
idiopathic pain when a reasonable inference about the sustaining pathophysiology of a pain syndrome can not be made and there is no positive evidence the etiology is psychiatric
NMDA receptor a receptor that resides on the neuronal membrane of spinal thalamic tract neurons
Created by: kolsen