Chemical/structural: atrophy (happens w/ chronic pain) and opiod/DA dysfunction
Injury: peripheral and central sensitization
Genetics
Context: beliefs, culture, placebo, expectations
Cognition: attention, distraction, hypervigilance
Pain inhibitory center: periaqueductal gray sends messages to the thalamus that leads to profound analgesic affects
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2
Q
Generation of pain
A
Due to inflammatory events that lead to the formation of prostaglandins (COX2 pathway- inhibited by NSAIDs)
Prostaglandins sensitize skin pain receptors and makes them more prone to firing
Also regulates hypothalamic temperature control center
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3
Q
Types of pain
A
Can be chronic or acute, and nociceptive (inflammatory) or neuropathic
Nociceptive: protective response of body to trauma or inflammation, pain is relieved when inflammation is gone, responds to NSAIDs
Neuopathic: no protective purpose or biologic value, persists beyond healing, does not respond to NSAIDs
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4
Q
Factors that chronic pain influences
A
Non-opioid mediators
Endogenous opioids (placebo works on same receptors)
ANS
Respiratory center
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5
Q
Neuropathic pain
A
Caused by a lesion or disease of the nervous system
Central (stroke, MS, trauma, compression of SC, ect) or peripheral (diabetic, herpetic, etoh neuropathies, complex regional pain syndrome)
Most common neuropathic pains are lower back pain and diabetic neuropathy
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6
Q
Neuropathic pain Dx
A
Dx: spontaneous pain that’s worse at night
Exam: no sensory loss, may have allodynia (pain from cotton swab), hyperalgesia (exaggerated response to pain), or hyperpathia (summation of pain after repetitive stimulus)