pathophys of pain (wk9) Flashcards
pain definitions
Dysesthesia
Any abnormal sensation described by a patient as unpleasant
Paresthesia
A sensation that is typically described as “pins-and-needles” or “prickling”, but is not notably unpleasant
Analgesia
Reduction or loss of pain perception
Anaesthesia
Reduced perception of all touch & pain sensation
Hypoalgesia
Decreased sensation and raised threshold to painful stimuli
Hyperalgesia
Exaggerated pain response from a normally painful stimulus
Allodynia
Abnormal perception of pain from a normally non-painful mechanical or thermal stimulus
Hyperesthesia
Exaggerated perception of a touch stimulus
Causalgia
Burning pain in the distribution of a peripheral nerve
how does pain differ from other perceptions like touch, taste, and smell
doest exhibit adaptation
what type of pain is dermal pain
sharp or burning
where are nociceptors distributed
many depths of skin and visceral organs
- Nociceptors are widely distributed through multiple depths in the skin
▪ “Dermal pain” tends to be described as sharp or burning - Nociceptors are also widely distributed through many
visceral organs
▪ Skeletal/cardiac muscle – dull, pressure-like pain
▪ Joints (synovium) and bones (periosteum) – many different characteristics (sharp, dull, aching)
▪ Blood vessels – usually dull
▪ Nerve roots and meninges
▪ Hollow viscera – often dull, cramping but can be sharp
▪ Mesothelial linings (peritoneum, pleura, pericardium) – often sharp
▪ Many organs can cause a dull pain due to stretching of the capsule
4 types of nocicpetors
thermal
mechanincal
polymodal
silent nociceptors
thermal nociceptors
activated by temperatures > 45 C or less than 5 C
mechanical nocicpertors
activated by intense pressure applied to a structure (i.e. skin)
polymodal nociceptors
activated by high intensity mechanical, chemical, or thermal stimuli
silent nociceptors
receptors that are widely distributed through viscera (but can also be found in the skin) that do not normally transmit pain information
▪ Only “awakened” in a setting of continuous damage or inflammation
c fibers
unmyelinated
slow velocity
slow pain and thermopreception and itching
dull, poorly localized
A delta fibers
myelinated
fast
pricking pain and thermoception, localized
C fibers vs A delta
C: unmyelinated, slow, poorly localized
AD: myelinated, fast, localized
2 receptors type for nocicpetors?
transient receptor potential receptors (TRP) and acid sensing ion channels (ASIC)
what other receptors for molecules do noccicpetors express in inflammatory process
prostaglandins, bradykinin, histmaine, substance P, serotonin, Ach, ATP
▪ Prostaglandins – most are G-protein-coupled receptors that block potassium channels (leading to depolarization)
▪ Bradykinin – activated by pro-inflammatory, pro- coagulant processes
* protein that circulates in the bloodstream (kininogen) is activated to form bradykinin in situations involving tissue damage
example of activation of some receptors in found in nociceptive neurons can increase the activation of other receptors
bradykinin increases and sensitizes TRP receptors
major nociceptive sensory pathway?
spinothalamic tract
spinothalamic tractg
afferent
a delta and C fibers (cell bodies in dorsal root ganglion)
tract of lissauer= thinnest fibers (C fibers) bundle
contralateral; cross over
4 other ascending pain pathways
- spinothalamic tract
- paleospinothalamic pathway
- anterior spinothalamic tract
- lateral spinothalamic tract
spinothalamic tract cross over vibe
The fibres of the spinothalamic tract usually cross over (2nd order neurons) two or three levels superior to where the 1st-order neurons enter the spinal cord
▪ The fibres of 1st order neurons tend to ascend in a small fibre bundle (the tract of Lissauer) before crossing over and synapsing
paleospinothalamic pathway
-more medial that spinothalamic tract
-ascneding
▪ Project through the medulla and synapse within a different set of
thalamic nuclei (the intralaminar nuclei)
▪ Also synapse in a wide variety of other brainstem areas:
* Midbrainreticularformation,peri-aqueductalgraymatter, hypothalamus
* Mayberesponsibleformuchoftheemotionaldistressandmood impacts of pain
anterior spinothalamic tract for»
visceral pain
makes sense bc visceral organs are in front of spine
lateral spinothalamic tract
localized skin associate pain
makes sense bc lots of skin ie love handles on lateral side of spinal cord
fast pain vs slow pain
- Fast pain – well- localized, sharp pain carried by A-delta fibres
- Slow pain – poorer- localized, duller
▪ Carried by C- fibres
▪ Tends to last longer
first pain vs second pain
first: high intensity and quick via A delta fibers (myelinated)
second pain is less intense and last way longer via c fibers (unmyelianted)
top down modulation of pain- analgesia system
which brain area
which receptor and which fibers is it in more
periaqeudutal gray matter
opiate/ opiod MU receptors
release enkephalins, endorphins and dynorphins
c fibers have high [] of my opioid receptors bc
gate theory of pain control
what is the nonnociceptive fiber
non nociceptive fiber at similar spinal level reduce pain by rubbing area bc activates inhibitory interneuron that inhibits the projection interneuron
pain sensitivity and hyperalgesia from peripheral tissue damage and repetitive exposure to noxious stimuli
which chemicals?
bradykinin
histamine
prostaglandins
ATP, acetylcholine, serotonin
peripheral vs central sensitization
peripheral: molecules released at the site of tissue damage or inflammation increase the effectiveness of nociception
central: synaptic remodelling in dorsal horns- increased effectiveness of pain transmission
what fibers ar more Lilly to exhibit central sensitiization
C fibers
pro inflammatory cytokines in central sensitization release what
nerve growth factor which increases BDNF from C fibers
molecules released at the site of tissue damage or inflammation increase the effectiveness of nociception
antidromic vs orthodromic
▪ From periphery → spinal cord = orthodromic
▪ From spinal cord → periphery = antidromic
what substances can C fibers release and what do they cause?
Substance P and CGRP
▪ Substance P can cause mast cell degranulation, vasodilation, and edema
▪ CGRP can cause vasodilation
neurogenic inflammation
makes things hurt more
may seen maladaptive but if it hurts so much that you cant use it any more ift will protect against further tissue damage
recruit leukocytes for repair
and limit use to protect
substance P
from which fibers
which receptor does it bind
C fibers
▪ Augmenting inflammation ▪ Learning & neurogenesis ▪ Mood disorders
▪ Nausea and vomiting
▪ Cell growth and angiogenesis
Nk-1 (neurokinin-1) receptor
what makes c fibers transmit impulse for long periods of time (second pain0
substance P
- Substance P release→long-lasting depolarization of projection
neurons via modulation of other cation channels
▪ A-delta fibres don’t release substance P – therefore their EPSPs from release of glutamate tend to last less time
why does nerve injury sometimes cause pain instead of analgesia
pain gate theory
non nociciceptive (A-beta) vs nociceptive (c fibers)
- Injury to nerves tends to reduce the stimuli to the inhibitory interneurons→excessive activation of excitatory interneurons and nociceptive projection neurons
▪ A-beta fibres from “regular sensations” (vibration, touch) tend to stimulate inhibitory interneurons that reduce transmission of pain from projection interneurons
▪ C fibres that carry painful stimuli tend to inhibit the inhibitory interneurons
▪ Therefore, whether we feel pain or not depends on where the balance “sits” between nociceptive and non-nociceptive inputs
pain and mood disorders
same brain area, inflammation, central sensitization
referred pain
effect distant organs via dermatomes i.e. heart does T1-T4 in arms
