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pain pathophysiology
| Question | Answer |
|---|---|
| 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
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