Pain Flashcards

(50 cards)

1
Q

describe nociceptive nerves

A

free unspecialised nerve endings with pain channels in the membrane

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2
Q

what is the most common pain receptor

A

transient receptor potential family of channels
sensitive to O2, pH, osmolarity, valinoids (capsicum), heat

allows calcium into the cell

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3
Q

what substances can sensitise pain receptors

A

substance P, bradykinins, serotonin, pH, ATP, NO, other chemicals.

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4
Q

what channels are opened when someone is exposed to extreme heat or cold

A

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

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5
Q

how are nociceptors activated when exposed to mechanical stimulation

A

unknown but presumed to be a form of insensitive mechanoreceptor which allows Na entry when activated

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6
Q

what effect does histamine have on pain sensation

A

histamine causes hyperalgesia through its effects on blood vessels

(causes fluid to leave blood vessels)

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7
Q

what effect does bradykinin have on pain fibres

A

activates pain fibres directly and causes an increase in prostaglandins

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8
Q

what ion is produced by tissue damage

A

H+ ions which give muscle ache

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9
Q

what enzyme is inhibited by NSAIDS

A

cyclooxegenase which makes prostaglandin E2

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10
Q

what effect does calcitonin gene related peptide have on pain (vasodilator neuropeptide)

A

recruits silent receptors which increase summation in the dorsal horn

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11
Q

describe A delta fibres

A

myelinated
sharp 1st pain
extreme temps
mechanical pinching

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12
Q

describe C fibres

A

unmyelinated
secondary slow pain
mechanical pinching, temp and chemical pain

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13
Q

what neurotransmitters are released by nociceptive fibres

A

glutamate, substance P, calcitonin gene release peptide

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14
Q

what cause calor and rubor

A

hyperaemia

mediated by substance P and CGRP

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15
Q

what causes tumour (swelling)

A

plasma extravasation

mediated by substance P and CGRP

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16
Q

what is the anterolateral system

A

ascending pain system

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17
Q

what is the function of periaqueductal gray

A

descending pain regulation

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18
Q

what is the function of the reticular formation

A

motor response to pain and ascending arousal

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19
Q

what is the neospinothalamic (anterior) route

A

fast/sharp pain to the VPL and primary somatosensory cortex

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20
Q

what is the paleospinothalamic tract

A

slow burning pain to the limbic association cortices

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21
Q

where do nociceptive fibres synapse

A

dorsal horn (quick to cross)

22
Q

what are nociceptive specific ascending axons

A

C and A delta only

23
Q

what are wide dynamic range neurons (WDR)

A

any sensory input can fire in a graded fashion based on C fibre frequency (higher pain = higher input)

24
Q

which pain fibres are polymodal

25
what are the 3 physiological signs of pain
heat, redness, swelling, mediated by histamine
26
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
27
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
28
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
29
summarise wind up
the intensity of signal from the C fibres is translated through WDR neurons into variation in pain sensitivity
30
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
31
what do A-beta fibers detect
non painful stimuli
32
name the endogenous opioids
endorphins, encephalins, and dinorphins sensitive to opiates and present at all levels of the pain pathway high efficacy for analgesia
33
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
34
describe three methods of pain modulation
gate theory wind up descending analgesia and endogenous opioids
35
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
36
what areas of the brain are involved in pain
``` cortex brainstem (saliency) opioid PAG limbic system amygdala hypothalamus dorsal horn ```
37
what happens if you electrically stimulate the PAG
strong analgesia but blocked by naloxone
38
what is nociceptive pain
normal pain from injury, inflammation etc | will go away when the injury goes
39
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
40
what is hyperalgesia
strong reaction to low intensity noxious stimuli
41
what is allodynia
painful reaction to a non noxious stimuli
42
what is summation
repeated low stimuli causes increasing intensity of response
43
what is parasthesia
tingling without stimulation or dysthesia which is burning or shooting pain without stimulation which can sometimes be associated with thalamic syndrome
44
why is persistent neuropathic pain hard to treat
caused by maladaptation of the dorsal horn wind up system
45
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
46
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
47
what causes migranes
unknown but may be due to vasoconstriction and vasodilation
48
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
49
and finally
pain can not be re-experienced from memory the fear of pain is very important for patients
50
describe a conceptual framework for pain
previous sensitising episodes (e.g. chlamydia) background factors mediators (sociocultural, family, economic) neurophysiology (e.g. central maladaption) pathology