Week 3 - Nociception Flashcards
what is the difference between pain and nociception?
pain is a conscious, emotional, psychological perception associated with noxious stimuli
nociception is any process in PNS or CNS associated with noxious or highly-unplesant stimulus
both pathways rely on different sets of structures
what are nociceptors? what are they activated by?
peripheral endings of primary sensory neurons whose cell bodies are located in dorsal root and trigeminal ganglia (like somatosensory receptors)
-harmful stimuli applied to skin or subcutaneous tissue
how do nociceptors differ from mechanoreceptors and other sensory receptors on skin?
least differentiated sensory receptors on skin
-exist as free nerve endings that don’t have peripheral structures that transduce and filter peripheral stimuli
what are the 2 types of nociceptors that mediate pain? what kind of fibers do they have? what are they activated by?
thermal/mechanical - small diameter, thinly myelinated A-delta fibers that conduct at 5-30 m/s
-activation associated with sharp, pricking pain
polymodal - small-diameter, unmyelinated C fibers that conduct at 0.5-2 m/s
-activated by high-intensity mechanical, chemical, and hot (over 45 C) or cold stimuli
how does a noxious stimulus activate a nociceptor?
depolarizing membrane of a sensory ending
- mechanisms of which are unknown
- nociceptors discharge only when stimulus is intense enough to cause damage
what does “noxious” mean?
high intensity and potentially tissue damaging or life threatening
what is the “first and second” pain? what happens if stimulation is intense enough?
stimulus intensity has to be raised to a level to activate corresponding fibers
1st: A-delta fibers in peripheral nerve = tingling
- if stimulation is intense enough, there is sharp pain
2nd: C fiber axons activated if stimulus intensity is increased further = duller, longer-lasting sensation of pain
can A-delta and C-fibers be separated?
yes, by anesthetic blocking experiments
-can selective anesthetize C and A-delta fibers
what is the receptor on both C and A-delta fibers? what is it activated by? how are APs triggered?
vanilloid receptor TrpV1
- activated by stimuli like capsaicin, head, acids, and anandamine (endogenous cannabanoid receptor stimulus)
- respond to endogenous chemicals similar to capsaicin that are released with peripheral injury
- AP Na+ voltage gated channels
what is hyperalgesia?
enhanced sensitivity and responsivity to stimulation of area in and around damaged tissue
- so if burn point A, near point B and C, all 3 of them will have decreased threshold sensitivity
- AKA if peripheral tissues are damaged, sensation of pain in response to subsequent stimuli is enhanced
what causes hyperalgesia?
sensitization of nociceptors by various substances released when tissue is damaged
- release of bradykinin, histamine, prostaglandins, and other agents from site of injury enhances responsiveness of nociceptive endings
- electrical activity in nociceptors stimulates local release of chemical substances that cause vasodilation, swelling, and release of histamine from mast cells
how do aspirin and other NSAIDs act?
inhibit cyclooxygenase (for biosynthesis of prostaglandins)
can pain be sensed if nociceptive pathways are damaged?
yes, pain can arise spontaneously in absence of activity in nociceptors
-pain due to peripheral nerves is important clinical problem with several etiologies
what is brachial plexus avulsion an example of? what is the pain from?
referred pain when nociceptive pathways are damaged; patients feel burning pain in dermatomes corresponding to denervated area (dorsal roots have been torn away)
-pain is from hyperactivity of dorsal horn neurons in deafferented region of cord
where do most nociceptive fibers terminate?
superficial dorsal horn (lamina I and II) projection neurons
-some A-delta nociceptive fibers project more deeply into lamina V
what do lamina I neurons contain? what are they called?
high density of projection neurons that process pain information
-excited solely by A-delta and C nociceptive fibers, thus called nociceptive specific (NS) projection neurons
what kind of input do lamina V neurons receive?
both mechanoreceptors and nociceptors, thus called wide dynamic range neurons (WDR)
- respond to both somatosensory and noxious stimuli
- have much larger receptive fields than NS neurons
in general, where do mechanoreceptor A-alpha, A-beta fibers, and nociceptor A-delta and C fibers synapse?
A-alpha/beta = lamina IV A-delta = lamina I and V C = lamina II
what is referred pain?
displacement of pain from visceral structure (organ) to a somatic area of the body b/c fo convergence of visceral and cutaneous cociceptors onto same dorsal horn projection neurons
where is anginal pain referred to?
upper chest wall and radiation of arm
where is esophageal pain referred to?
chest wall
where is ureteral pain referred to?
lower abdomen and back (happens if passing a kidney stone)
where is bladder pain referred to?
perineum
where is prostate pain referred to?
characteristic distribution above and below affected side
