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MD4001 Physiology > Pain > Flashcards

Pain Flashcards

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

A

C fibres

25
Q

what are the 3 physiological signs of pain

A

heat, redness, swelling, mediated by histamine

26
Q

what is wind up (dorsal horn sensitisation)

A

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
Q

what is the function of wind up

A

priority salience in the cortex (you notice it more)
protection from further injury
memory- increased duration of stimulation increases the chance of consolidation

28
Q

what is the mechanism of wind up

A

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
Q

summarise wind up

A

the intensity of signal from the C fibres is translated through WDR neurons into variation in pain sensitivity

30
Q

what is the gate theory of pain

A

if you rub a painful area it activates A-beta fibres which inhibits pain
similar theory behind TENS and capsaicin

31
Q

what do A-beta fibers detect

A

non painful stimuli

32
Q

name the endogenous opioids

A

endorphins, encephalins, and dinorphins
sensitive to opiates and present at all levels of the pain pathway
high efficacy for analgesia

33
Q

describe descending analgesia systems in the spinal cord

A

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
Q

describe three methods of pain modulation

A

gate theory
wind up
descending analgesia and endogenous opioids

35
Q

describe the cortical pain matrix

A

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
Q

what areas of the brain are involved in pain

A 
cortex
brainstem (saliency)
opioid PAG
limbic system
amygdala
hypothalamus
dorsal horn
37
Q

what happens if you electrically stimulate the PAG

A

strong analgesia but blocked by naloxone

38
Q

what is nociceptive pain

A

normal pain from injury, inflammation etc

will go away when the injury goes

39
Q

what is neuropathic pain

A 
causalgia (peripheral nerve trauma)
phantom limb pain 
entrapment neuropathy (carpal tunnel) 
peripheral neuropathy 
nociceptive pathway damage

pain persists beyond the healing process

40
Q

what is hyperalgesia

A

strong reaction to low intensity noxious stimuli

41
Q

what is allodynia

A

painful reaction to a non noxious stimuli

42
Q

what is summation

A

repeated low stimuli causes increasing intensity of response

43
Q

what is parasthesia

A

tingling without stimulation or dysthesia which is burning or shooting pain without stimulation which can sometimes be associated with thalamic syndrome

44
Q

why is persistent neuropathic pain hard to treat

A

caused by maladaptation of the dorsal horn wind up system

45
Q

what is central maladaptation

A

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
Q

what are headaches caused by

A

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
Q

what causes migranes

A

unknown but may be due to vasoconstriction and vasodilation

48
Q

what is the mechanism of referred pain

A

the brain localises pain by were is arises in the cortex

skin and visceral sensory fibres travel together

49
Q

and finally

A

pain can not be re-experienced from memory

the fear of pain is very important for patients

50
Q

describe a conceptual framework for pain

A

previous sensitising episodes (e.g. chlamydia)
background factors
mediators (sociocultural, family, economic)
neurophysiology (e.g. central maladaption)
pathology

MD4001 Physiology (19 decks)

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