nociception
process of encoding sensory stimuli
somatic pain
bones, skin, muscles, joint pain
referred pain
pain felt elsewhere
visceral pain
organ pain
neuropathic pain
pain from nerves
nociceptor
pain receptor
transmission
AP from site of injury to spinal cord –> spinal cord to brain stem & thalamus –> thalamus to cortex
transduction
site of injury; releases chemicals such as PROSTAGLANDINS; Substance P; etc.; then activates nociceptors which leads to an AP
perception
experience of pain
modulation
neurons from the brain stem descend down the spinal cord and release substances (e.g. endogenous opioids) to inhibit nociceptive impulses
PAIN
P - pattern
A - area
I - intensity
N - nature
Acute pain
sudden, quick onset; SNS responses; cause can be determined; brief
chronic pain
long-lasting; no SNS effect; cause/source can be difficult to determine; interferes with ADL’s
Prostaglandins
control inflammation, blood flow, formation of blood clots
COX-1
produce gastric mucus; enhance renal perfusion; assist in thrombus formation
COX-2
produces pain, edema, fever, stimulates the cycle of inflammation
Salicylism
overdose of salicylic containing compounds (e.g. aspirin)
Mu receptors
opioid receptors; analgesia; respiratory depression; sedation; euphoria; physical dependence; decreased GI motility
Kappa receptors
opioid receptor; analgesia; sedation; decreased GI motility
Delta receptors
analgesia; decreased GI motility
agonist
activates receptors
antagonist
inhibits receptors
mixed agonist-antagonist
sometimes acts as an agonist; other times acts as an antagonist
equinanalgesic dose
dose that roughly yields the same amount of analgesia to the standard dose (equivalent to 10 mg)
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Class 1 - Intro34
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Class 2 - Vital Signs and Physical Assessment41
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Class 3 & 4 - Pharmacology49
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Class 5 Pain31
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Class 6 - LOC29
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Class 7 - Perfusion28
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Class 8 - Cell Regulation48
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Class 9 - Wounds34
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Class 10 - Immunity28
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Class 12 - Anemia16
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Class 13 - Polycythemia & Leukemia27
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Class 14 - Bleeding & Clotting Disorders17
