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21 Cards in this Set

  • Front
  • Back
what are some examples of subst released in response to tissue damage?
ATP, bradykinin, 5HT (serotonin), prostaglandins
what is the main stimulus for pain?
tissue injury; activates free nerve endings
what is the most important synapse in the detection and modification of pain?
1st synpase b/w AD(elta)/ C fiber central afferents and the dorsal horn projection neuron (DHPN)
what activates the DHPN?
substance P rel by A(Delta)/ C fibers
what is the ATP receptor on the free nerve ending?
P2X
3 categories of pain
physiologic (normal)
inflammatory (pain)
neuropathic pain
what is neurogenic inflammation?
a process by which nociceptor neurons aplify and extend the inflammatory process
what are conditions under which pain is perceived? what can cause pain?
nociceptor activity can cause pain
you can have activation of nociceptors w/o the perception of pain
you can have pain w/o the activation of nociceptors
what is allodynia?
when a formerly non-painful stimulus (below pain threshold) is perceived as pain
what is hyperalgesia?
when stimuli that were normally perceived as painful are now perceived as MORE painful
what causes hyperalgesia?
sensitization of nociceptor endings-> incr in reactivity to a stimulus
often due to local inflamm which lowers the threshold of the nociceptor
what are 3 types of nociceptors?
mechanical nociceptors: localized, rapid onset (ex: sharp obj)
thermal nociceptors: heat above 45C (heat pain)
polymodal nociceptors: resp to several stimuli; mediated by C fibers; delayed, poorly localized; dull aching pain
what are some ex of receptors on the free nerve ending?
TRPVs
P2X (binds ATP)
TrkA (binds NGF)
what are TRP channels?
family of receptors on free nerve endings
TRPV1- AD(elta) and C fibers; detects moderate heat (45C) and Capsaicin (chilis)
TRPV2- higher temps (52); AD(elta) fibers only
what is the process that leads to allodynia? why do mechanoreceptors lead to the perception of pain?
A(Beta), A(Delta), and C fibers all terminate on DHPN
however, normally, DHPN has no R for NT rel by A(Beta). w/ inflamm, R for mechanoR form and so the DHNP becomes sensitized to all kinds of stimuli
what is the mxn of hyperalgesia?
lower threshold/sensitization- upregulate expression of R on free n. ending (ex: P2X)-> incr firing rate of DHPN
explain referred pain in a MI
nociceptors in heart and L arm both synapse on same DHPN
DHNP is used to being stimulated by free n. ending from L arm so when nociceptors from heart activate the DHPN, the signal is misinterpreted as coming from the L arm
what is the descending control of pain perception?
mediated by ALS fibers (spinomesencephalic) that synapse at periaqueducal gray; stimulates descending inputs that synapse in nucleus raphe magnus and rel serotonin on serotonergic neurons; synapse on inhibitory enkephalinergic interneurons that rel enkephalin on C fiber terminals, preventing NT rel from pain fiber into DHPN
what are enkephalinergic nerurons?
inhibitory interneurons; rel enkephalin to prevent transmission of pain from C fibers to DHPN
what is the gate theory of pain? what does it explain?
explains why we rub areas that hurt
transmission of ascending pain info is blocked by concurrent stimulation of A(Beta)s
mxn of gate theory of pain
when bump your knee, C fibers rel glutamate onto DHPNs causing them to fire and transmit pain
by rubbing your knee, you activate mechanoR A(Beta) fibers which activate INHIBITORY neurons that synapse and prevent activation/firing of DHPN