4 - Pain Flashcards
an unpleasant sensory and emotional experience associated with actual or potential tissue damage
pain
with pain withdrawal reflex, sensory neuron goes through _ root ganglion
motor neuron travels though _ root
dorsal
ventral
_ = the perception of pain
nociception
nociceptors respond to extreme temps, mechanical and chemical stimuli
they are _ receptors (type)
free nerve endings
the cells bodies of nociceptors are located in _ and _
spinal ganglia (body) and trigeminal ganglia (face)
nociceptors _ adapt to stimuli
DO NOT
continued stimulation of nociceptors _ threshold at which nociceptors respond, this is called _
decrease
sensitization
A(delta) fibers
(are/not) myelinated
_ type of pain
_ stimuli
are
localized, sharp
mechanical/thermal
(Anitial - bee sting)
C fibers
(are/not) myelinated
_ type of pain
_ stimuli
not
poorly localized, diffuse
mechanical, thermal, chemical
3 neurotransmitters used for pain:
glutamate, substance P, CGRP
NT are produced in _ and released _ or _
spinal ganglion
centrally (CNS) or peripherally (injury site)
peripherally, NT lead to redness, swelling, and tenderness
they inc activation of nociceptors and _ threshold (sensitization)
decrease
when “silent” nociceptors are activated, they _
expand receptive field area of painful stimulus
activation of nociceptors results in opening on _ channels, leading to depolarization
Na+
A(delta) and C fibers can be activated by heat:
_ - hot thermal stimulation
_ - cold thermal stimulation
TRPV1 (capsaicin)
TRPM8
A(delta) and C fibers can ALSO be activated by _
mechanical stimulation
A(delta) and C fibers can ALSO be activated by mechanical stimulation
-cannot be activated by _,
light touch
high threshold, only activated when potential for tissue damage
C fibers are also activate by _
wide range of Chemicals
chemicals that activate C fibers include:
external irritants and substances released during tissue damage by nociceptors and inflammation
peripheral sensitization:
tissue damage->release of _,
these sensitize _
bradykinin & prostaglandins
peripheral nociceptors
noxious stimulus is detected by nociceptor -> free nerve ending releases _ and _
substance P and CGRP
substance P and CGRP stimulate _ cells to release histamine and bradykinin, which induce _ and further sensitization
mast, vasodilation
heightened response to low-intensity painful stimulus (hot shower hurts)
hyperalgesia
pain experienced with normally non-painful stimulus (water hitting your back)
allodynia
when silent nociceptors are recruited, there is further amplification in posterior horn, _ temporal and spatial summation of incoming signal
increasing
silent nociceptors only respond to molecules secreted by _
activated nociceptors
synaptic targets in the spinal cord:
A(delta) and C fibers synapse with either _ or _
nociceptive-specific cells or Wide Dynamic Range (WDR)
nociceptive specific cells synapse with _
only A(delta) and C fibers
WDR cells synapse with _
ALL sensory fibers (including A(beta) nonpainful touch)
the synapse in the _ is EXCITATORY
posterior horn
AMPA and NMDA receptors of _
glutamate
NK1 receptors of _
substance P
CGRP receptors of _
CGRP
Wind Up and Central Sensitization:
WDR cells fire in _ fashion, intensity determined by _
graded; frequency of C fiber signaling
WDR amplify signal through _
windup
windup is: chronic bombardment of C fibers in dorsal horn leads to _
increased kinase production
inc kinase from windup causes:
- _ of NMDA receptors
- increased _ production
- “_” is dorsal horn
upregulation
glutamate
sprouting
chronic bombardment also leads to _ production in dorsal horn, which travels to periphery via _
substance P; C fibers
substance P travels via C fibers to periphery to _ threshold and _ receptive fields
decrease; increase
sensitization serves to _ pain signal to _ behavioral changes
amplify, evoke
sensitization mechanisms can become maladaptive and lead to _
permanent changes in wiring
pain modulation:
descending inhibition - _
descending facilitation - _
mind/matter, need to be able to function
we don’t want the pain to go away, it protects us
Gate Control Theory of Pain
1. balance between nociceptive input (Adelta and C) and touch input (Abeta): rubbing painful area shifts input towards _ and away from _
touch (abeta) pain (Adelta and C)
Gate Control Theory of Pain
2. inhibitory interneurons that synapse with WDR neurons in posterior horn:
they are inhibited by _, excited by _
nociceptive input, touch input
Gate Control Theory of Pain (2.)
Adelta and C -> inhibit inhibitory interneurons -> __
more signaling = pain
Gate Control Theory of Pain (2.)
Abeta - > excite inhibitory interneurons -> __
less signaling = less pain
descending influences on pain act as _
salience filter (how important is this pain)
reticular formation: locus coeruleus produces Norepi and modulates _ response to pain
physiological
Periaqueductal Gray (PAG) receives input from cortex and hypothalm and projects to superior colliculus to:
make you look where you feel the pain
opiod receptors are found at _ levels of pain system
all
opioid drugs influence _ pain processing
cortical
opioid receptors are physiologically active by _ molecules that act as NT including: enkephalins, endorphins, dynorphins
endogenous (our body makes them)
opioid receptors inhibit _ influx or facilitate _ efflux, hyperpolarizing the cell, less pain perceived
Ca++, K+
morphine blocks _
wound healing
chronic pain is experienced by chronic activation of nociceptors; therapy is to _
treat underlying inflammation
chronic neuropathic pain arises with a lesion to somatosensory system and _
persists after the injury has healed (Herpes Zoster)
spontaneous tingling
paresthesia
burning, electric, shooting pain
dysesthesia
increased pain to low intensity stimulus
hyperalgesia
painful reaction to innocuous stimuli
allodynia
repeat small pain = incr pain with brushing hair
summation
maladaptive peripheral sensitization:
overexpression of TRPV1 receptors = burning sensation
overexpression of Na+ channels=_
lower threshold for signaling, spontaneous discharge of signals
maladaptive central sensitization
changes _ receptor physiology, increases expression leading to spontaneous activity _ _
paresthesias, dysesthesias
maladaptive central sensitization
sprouting phenomenon: disruption of _ —-> _
spinal cord lamella; allodynia
