Pain Flashcards
describe nociceptive nerves
free unspecialised nerve endings with pain channels in the membrane
what is the most common pain receptor
transient receptor potential family of channels
sensitive to O2, pH, osmolarity, valinoids (capsicum), heat
allows calcium into the cell
what substances can sensitise pain receptors
substance P, bradykinins, serotonin, pH, ATP, NO, other chemicals.
what channels are opened when someone is exposed to extreme heat or cold
transient receptor potential vanilloid channels (TRPV)
Depolarises the cell by allowing sodium and calcium entry to give an action potential
can be regulated to change its sensitivity
how are nociceptors activated when exposed to mechanical stimulation
unknown but presumed to be a form of insensitive mechanoreceptor which allows Na entry when activated
what effect does histamine have on pain sensation
histamine causes hyperalgesia through its effects on blood vessels
(causes fluid to leave blood vessels)
what effect does bradykinin have on pain fibres
activates pain fibres directly and causes an increase in prostaglandins
what ion is produced by tissue damage
H+ ions which give muscle ache
what enzyme is inhibited by NSAIDS
cyclooxegenase which makes prostaglandin E2
what effect does calcitonin gene related peptide have on pain (vasodilator neuropeptide)
recruits silent receptors which increase summation in the dorsal horn
describe A delta fibres
myelinated
sharp 1st pain
extreme temps
mechanical pinching
describe C fibres
unmyelinated
secondary slow pain
mechanical pinching, temp and chemical pain
what neurotransmitters are released by nociceptive fibres
glutamate, substance P, calcitonin gene release peptide
what cause calor and rubor
hyperaemia
mediated by substance P and CGRP
what causes tumour (swelling)
plasma extravasation
mediated by substance P and CGRP
what is the anterolateral system
ascending pain system
what is the function of periaqueductal gray
descending pain regulation
what is the function of the reticular formation
motor response to pain and ascending arousal
what is the neospinothalamic (anterior) route
fast/sharp pain to the VPL and primary somatosensory cortex
what is the paleospinothalamic tract
slow burning pain to the limbic association cortices
where do nociceptive fibres synapse
dorsal horn (quick to cross)
what are nociceptive specific ascending axons
C and A delta only
what are wide dynamic range neurons (WDR)
any sensory input can fire in a graded fashion based on C fibre frequency (higher pain = higher input)
which pain fibres are polymodal
C fibres
what are the 3 physiological signs of pain
heat, redness, swelling, mediated by histamine
what is wind up (dorsal horn sensitisation)
long term sensitization of post synaptic neurons in the dorsal horn
mediated by WDR neurons which open NMDA channels
the inrush of calcium causes nuclear expression resulting n increased Na blockade of K channels
the net result is a resting potential closer to the threshold and a more sensitive cell
this amplifies the pain signal
what is the function of wind up
priority salience in the cortex (you notice it more)
protection from further injury
memory- increased duration of stimulation increases the chance of consolidation
what is the mechanism of wind up
based on the special characteristics of the NMDA receptor and Ca ion flow
induces changes in nuclear expression and membrane channel activity
the stronger the C fibre pain signal the more the dorsal horn post synaptic fibres become sensitive to input
summarise wind up
the intensity of signal from the C fibres is translated through WDR neurons into variation in pain sensitivity
what is the gate theory of pain
if you rub a painful area it activates A-beta fibres which inhibits pain
similar theory behind TENS and capsaicin
what do A-beta fibers detect
non painful stimuli
name the endogenous opioids
endorphins, encephalins, and dinorphins
sensitive to opiates and present at all levels of the pain pathway
high efficacy for analgesia
describe descending analgesia systems in the spinal cord
inhibition of incoming pain signals at the cord level and presence of encephalin secreting neurons that suppress pain signals in the cord
this can be used by the CNS to increase or decrease salience of selected signals
describe three methods of pain modulation
gate theory
wind up
descending analgesia and endogenous opioids
describe the cortical pain matrix
there is no single pain centre in the brain
somatosensory topographical discrimination
limbic system including the cingulate gyrus
saliency- relative potentiation of a specific input
what areas of the brain are involved in pain
cortex brainstem (saliency) opioid PAG limbic system amygdala hypothalamus dorsal horn
what happens if you electrically stimulate the PAG
strong analgesia but blocked by naloxone
what is nociceptive pain
normal pain from injury, inflammation etc
will go away when the injury goes
what is neuropathic pain
causalgia (peripheral nerve trauma) phantom limb pain entrapment neuropathy (carpal tunnel) peripheral neuropathy nociceptive pathway damage
pain persists beyond the healing process
what is hyperalgesia
strong reaction to low intensity noxious stimuli
what is allodynia
painful reaction to a non noxious stimuli
what is summation
repeated low stimuli causes increasing intensity of response
what is parasthesia
tingling without stimulation or dysthesia which is burning or shooting pain without stimulation which can sometimes be associated with thalamic syndrome
why is persistent neuropathic pain hard to treat
caused by maladaptation of the dorsal horn wind up system
what is central maladaptation
long term sensitisation in the structure of the synapses in the dorsal horn
increased ionotropic glutamate receptors (NMDA) causes a sensitivity in second order neurons which then send more pain signals to the thalamus
descending modulation of inhibitory interneurons becomes maladapted
what are headaches caused by
irritation of venous sinuses, the dura at the base of the skull or meninges and blood capillaries
dehydration causes low CSF causing the brain to settle onto the base of the skull causing deformation of the dura at the base of the skull and meninges
what causes migranes
unknown but may be due to vasoconstriction and vasodilation
what is the mechanism of referred pain
the brain localises pain by were is arises in the cortex
skin and visceral sensory fibres travel together
and finally
pain can not be re-experienced from memory
the fear of pain is very important for patients
describe a conceptual framework for pain
previous sensitising episodes (e.g. chlamydia)
background factors
mediators (sociocultural, family, economic)
neurophysiology (e.g. central maladaption)
pathology
