Sensory system and pain Flashcards

1
Q

mechanoreceptors

A

tough, auction vesitbular

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2
Q

touch

A

pacinain corpuslce

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3
Q

audition

A

hair cell

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4
Q

vesitbular

A

hair cell

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5
Q

photoreceptors

A

vision

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6
Q

vision

A

rods and cones

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7
Q

chemoreceptors

A

olfaction, taste, arterial pO2, pH of CSF

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8
Q

thermoreceptors

A

temp

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9
Q

olfaction

A

olfactory receptors

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10
Q

taste

A

taste budsy

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11
Q

temperature

A

warm/ cold receptors

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12
Q

nocicpetors

A

extreme pain and temp

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13
Q

extreme pain and temps

A
  • thermal nociceptors

- polmodal nocicpetors

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14
Q

when are arterial Po2 found

A

carotid and aortic bodies

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15
Q

where are vestibular hair cells found

A

macula, semicircular canal

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16
Q

where are audition hair cells found

A

organ of Corti

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17
Q

where are pH of CSH receptors found

A

ventrolateral medulla

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18
Q

where are nociceptor and thermal receptors found

A

the skin

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19
Q

neurophathic

A

’ pain which originates from the pathology of the NS)pain caused by damage or disease affecting the somatosensensory NS

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20
Q

somatosensor NS

A

part of the sensory system concerned with conscious perception of touch, pressure, pain, temp, position, movement and vibration
- arising from muscles, joints skin and fascia

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21
Q

sensitisation

A

typically results form a cellular receptors becoming more likely to respond to a stimulus e.g. repetition of a painful stimuli makes one more responsive to a loud noise

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22
Q

an enhancement in response to a stimuli

A

sensitisation

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23
Q

mechanism of peripheral sensistiasation

A

sensory neurone expression of alpha-adrenoreceptors causes over expression of voltage gated Na+ channels
- afferent neurones start expressing adrenooreceptors

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24
Q

adrenoreceptors are not usually expressed

A

in afferent nerves-but in chronic pain states, they become over epxressed

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25
Q

in chronic pain states, any kind of stress that stimulates sympathetic nervous system can lead to

A

more pain- thats how perception of pain can be changed

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26
Q

where nerves no longer listen to stimulus of nociepection-

A

sensitisation

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27
Q

and increase in voltage gates sodium channels

A

more sensitive- smaller stimuli will evoke a large response

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28
Q

neuropathic pain can also occur in

A

afferent synapses in reflect arc

  • peripheral nerve at the spinal cord goes up into the brain
  • pain then goes to the thalamus and cortex
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29
Q

cortex

A

where emotion and reasoning happens- therefore neuropathic pain can change emotions

30
Q

fear and pain are interlinked

A

because peripheral nerves relaying a painful stimuli goes up into the brain and into the cortex where emotion and reasoning occur

31
Q

Pain is all in

A

the CNS

32
Q

inflammatory mediators are released

A

at sites of injury

33
Q

inflammatory mediators

A

released in response to injury from leaky blood vessels and damaged tissues: ATP, histamine, prostaglandin, substance P, protons, 5-HT, bradykinin

34
Q

pain pathway

A

1) nociceptive stimuli
2) impulse foes to the CBS via afferent neurone to the spine
3) synapse in dorsal horne of the spin- releases main eciatory NT- glutamate and ATP
4) binds to receptors (AMDA and NMDA)
5) impulse carried up to the hypothalamus which simulates the cortex- where we perceive pain

35
Q

AMPA

A

fast

36
Q

NMDA

A

slow due to prolonged membrane depolarisation being needed to remove magnesium block

  • long term processes
  • LTP (chronic pain states)
37
Q

summary of sensitisation

A

Adrenoceptors are not usually expressed in afferent nerves- but in chronic pain states, they can become over expressed
Any kind of stress that stimulates sympathetic nervous system can lead to even more pain- that’s how perception of pain can be changed e.g. phantom limb injury
Peripheral sensitization- where nerves no longer listen to stimulus of nociception from the stump, also responding to the sympathetic nervous system e.g. levels of stress and fear
Also increase in expression of voltage gated sodium channels- more sensitive- smaller stimuli will evoke a large response

38
Q

phantom limb

A

the perception of pain in absent body parts

-experienced by most amputee patients

39
Q

perisperhal mechanisms involved in phantom limb

A

these pains are attributed to abnormal growth of injured nerve fares coming neuromas, which fire abnormal APs at the stump

40
Q

spinal mechanism involved in phantom limb

A

peripheral nerve injury can lead to the degeneration of C fibres in the dorsal horn of the spinal cord, therefore A fibres may branch into some limning

  • A fibre input could be reported as noxious
  • expressing substance P
41
Q

simple explanation for phantom limb

A

phantom pains can be attributed to abnormal goeth of injured nerve fibres at the stump site

42
Q

capsaicin

A

the active compound in chillies acts on vanillin receptors and causes released of Substance P from the nociceptors, which is what causes the pain
-TRPV1

43
Q

vanilliod receptors

A

trance noxious that stimuli

44
Q

two types of pain conductance

A

fast response (Aδ fibres) and slow response (C fibres)

45
Q

fast response Aδ fibres

A
  • large
  • myelinated
  • up to 10m.sec
  • sharpe stabbing pain
46
Q

slow response C fibres

A
  • small
  • unmyelinated
  • up o 1.2 m/sec
  • acing budning
47
Q

receptors for fast response Aδ fibres

A
Thermal or mechanical:
Mechanically gated
TRPV1- temp gated >42 degrees, pH<5.5 (gated by protons)
Also vanilloids- e..g capsaicin
TRPM8- cold and menthol
48
Q

receptors for slow response C fibres

A
Polymodal
High intensity
Mechanical
Chemical
Hot/cold
49
Q

inflammatory mediators can cause

A

hyperalgesia

50
Q

hyperlgesia

A

is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves.

51
Q

inflammatory mediators and hyperalgesia

A

directly excited nociceptors making them more sensitive to other agents

52
Q

inflammatory mediators

A

increase rate of opening of TRP channels

53
Q

thermoreceptors are made up of

A

fast response Aδ fibres and slow response C fibres

54
Q

each TRp has

A

a unique thrshold

55
Q

TRPV2

A

extreme hot

56
Q

TRPA1

A

extreme cold

57
Q

thermal nociceptors sue

A

C fibres and response to extreme col/hot

58
Q

withdrawal reflex

A

1) stimulus (pain) detected by receptors in the skin
2) impulse sent via sensory neurone to synapse with the relay neurone in the dorsal horn
3) relay neurone synapses with motor neurone which sends an impulse to the effectors
4) muscle moves limb away from noxious stimuli

59
Q

recycling of ACH at the NMJ

A

ACH i converted by to choline and acetate by acetylcholinesterase
-co transported with sodium back to the pre-synaptic bouton

60
Q

Each is made by

A

acetylcholinesterase

61
Q

ionotropic

A

transmembran

  • binding site and channel combines
  • channels opena nd close letting ions in and out
  • post synaptic in general
  • rapid response
62
Q

Metabotropic

A
  • no channels
  • linked to G proteins
  • wen a ligand binds G proteins ar euactivated
  • once activated 2nd messengers tole beings
  • slow
  • pre and post syanptic
63
Q

long term potentiation definiton

A

-an increasee in efficacy of a synapse with repetitive stimulation

64
Q

LTP - a repeated depolarisation of the post synaptic men results in

A

alterations in the NMDA glutamate receptor- allowing ore calcium to enter

65
Q

LTP involves changes in

A

both the pre and post synaptic membrane

  • a given response to any stimuli will increase
  • can also cause new neurones to form from existing ones
66
Q

calcium and LTp

A

-causes AMPA receptors in post synaptic vesicles to come to the surface- therefore depolarisation of pst synaptic neurone is increased for any given stimuli

67
Q

memory

A

the ability to recall knowledge and skills learned in the past
- how info is encoded, stored and retrieved

68
Q

two categories of meory

A

declarative and procedural

69
Q

declarative

A
  • the recall of new facts
  • recall of events
  • verbal reasoning
  • personal experience
  • short and long term (Hippocampus)
70
Q

procedural

A
  • applies memory to motor skills
  • learning new motor skills
  • once learned, rarely forgotten
  • cerebellum has key role