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17 Cards in this Set

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define Nociception
it refers to the detection , transduction, and transmission of noxious stimuli. Nociceptors are free nerve endings
Peripheral afferent nerve fibers:
describe A neurons
Large myelinated; low threshold for activation; impulse speed 5-100m/sec (fast); A delta mediate pain sensation; A alpha transmit motor and proprioceptive impulses; A beta and gamma cutaneous touch and pressure.
Peripheral afferent nerve fibers:
describe B neurons
medium size; myelinated; speeds 3-14 m/sec; higher threshold- lower excitability than A, & lower than B; postganglionic sympathetic and visceral afferents belong to this class
Peripheral afferent nerve fibers:
describe C neurons
unmyelinated; speeds 0.5 to 2 m/sec (slow); composed of preganglionic autonomic fibers and pain fibers. Most of them modulate nociceptive stimuli
Spinal cord and Brain pathways;
what is a First order neuron (FON)
A peripheral afferent neuron that has cell body located in dorsal root ganglion and sends its projections into the dorsal horn; synapses with 2nd order afferent neuron (SON); FON also communicate with cells bodies of SNS, and ventral motor nuclei
Spinal cord and brain pathways:
What is a second order neuron (SON)
its cell body lies in the dorsal horn, axons cross over contra lateral hemisphere of spinal cord. they ascend in the lateral spinothalamic tract to the thalamus. It sends branches to reticular formation, nucleus raphe magnus, periaqueductal gray, & other brainstem areas.
Spinal cord and brain pathways:
What is a second order neuron (SON)
In the thalamus- SON synapses with third order aff neurons, which sends projections into sensory cortex. SON can be nociceptive specific or wide dynamic range neurons;
Modulation of Nociception-Peripheral:
how does it occur?
peripheral modulation occurs by liberation or elimination of allogenic substances
Modulation of Nociception- Peripheral:
what are allogenic mediators that activate nociceptors?
Neurotransmitters such as substance P, glutamate, K, H+, lactic acid, serotonin, bradykinin, histamine, prstaglandins. These all sensitize and excite nociceptors and mediate inflammation. They come from damaged cells, mast cells, plasma & platelets
Modulation of Nociception- Peripheral:
How can you inhibit the activation?
NSAIDS , ASA, COX 2 inhibitors, inhibit PG mediated sensitization of peripheral nociceptors. Na channel blockers (LA) modulate pain as well.
Modulation of Nociception- Spinal:
What are the excitatory substances that activate pain pathways?
Modulation in spinal cord results from NTs in the dorsal horn or spinal reflexes that send efferent impulses back to periph nociceptor field. Modulation results from activation of excitatory amino acid transmitters: L glutamate, aspartate, VIP, calcitonin, neuropeptide Y. Substance P is found in synaptic vessels of unmyelinated C fibers it can enhance/aggravate pain
Modulation of Nociception- Spinal:
What are the inhibitory substances that regulate pain pathways?
Inhibitory substances regulate afferent impulses in the dorsal horn. they include GABA, glycine, enkephalins, beta endorphins, norepi, dopamine, adenosine, Ach, M receptors
Modulation of Nociception- Spinal:
explain the positive feed back loop
afferent modulating mechanisms at the the spinal level may involve spinal reflexes in which afferent signals directly evoke motor reflexes or sympathetic reflexes- both operate on a positive feedback loop.
Modulation of Nociception - Supraspinal:
how does supraspinal inhibitory modulation work?
Descending inhibitory tracts originate from cell bodies in periaqueductal gray, retic formation, nucleus raphe magnus and descend into the dorsolateral fasciculus and synapse in dorsal horn. NT act presynaptically on FON and post synaptically on SON in spinothalamic tract
Modulation of Nociception - Supraspinal: What are the two groups of nerve fibers identified in inhibitory modulation?
Opioid and alpha 2. Opioids modulate transmission of afferent impulses in dorsal horn presynaptically at the FON.the NT b-endorphins & enkephalins hyperpolarize A delta & C fibers to block NT release (sub P etc). Opioids exert a direct inhibitory effect on postsynaptic membrane potential. Monoamine inhibitory pathways act similarly. fibers descend into dorsolateral fasiculus and synapse in substantia gelatinosa in dorsal horn. NE is released to hyperpolarize FON and wide dynamic range neurons in spinothalamic tract
Modulation of Nociception - Supraspinal: What is the common mechanism of action of inhibitory pathways
they are G proteins who functions via 2nd messengers (agonist) to convert GTP to GDP. opening of K channels and inhibition of Ca hyperpolarizes the nerve resulting in decreased nerve transmission of NT (pain).
How is the sensitization /intensification of painful stimuli mediated?
Via PGs- they lower the threshold for further activation of nociceptors. K, PG, bradykinin, sub P is released from damaged tissue and excite nociceptors (hyperalgesia). Sub P induces vasodilation, mast cell degran, histamine and serotonin release. This sensitizes damaged tissue and surrounding nociceptors causing hypersensitivity state (2ndary hyperalgesia)