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21 Cards in this Set
- Front
- Back
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depolarization
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as n+ enters we have a rise in AP which follows the all or none principle
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3 types of receptors
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mechanorecepotrs
thermal receptors nocioeptors |
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mechanoreceptors within the skin
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superficial_ meissner's corpuscle
deep- ruffinis end organ and pacinian corpuscle |
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pressure v pain cross-over
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higher up in pressure
lower in sc for pain |
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hyperasthesia
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increased sensitivity
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hyperalgesia
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increased pain response
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NSAIDS (ibuprofen)
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stops the production such as prostaglandins
-best means of modulating pain at the cellular level |
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at the reflex level
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self modulation of pain
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a-beta
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fast, acting, large myelinated fiber carrying pressure impulse
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c-fiber
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dull, slow, unmyelinated
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gate closed
gate control theory |
a-beta fibers block input to brain, there is an inhibitory interneuron acting as a gate-keeper
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higher the impulse travels
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the more disciminate the pain will be
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what is pain
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a protective sensation w/ obj/physio components and subj/emotional components
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the recognition of pain involves peripheral and central components
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transduction
transmission modulation perception |
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to call for (دعا إلى =)
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نادى بـ ، يُنادي بـ ، المُناداة بـN
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these type of receptors become increasingly sensitive following repeated or continuous stimulation
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becauseof release of k+, bradykinin, and histamine
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neuron1
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peripheral neuron contains nocioceptors ending
cell body is in the drg |
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neuron 2
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cell body is in the dorsal horn of the sc
axon crosses midline at the anterior white commissure |
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neuron 3
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cell body is in the thalamus
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what pain is more difficult to localize?
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slower, more diffuse pain because multiple synapses and interneurons can be involved at every level of the CNS
info may travel bilaterally at the sc and brainstem |
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where does modulation of sensory info occur?
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at the receptor, axons, or synapses
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