PAIN HYPERSENSITIVITY - BIO&PHYSIOLOGY Flashcards

1
Q

how does the nervous system act to protect and preserve to avoid furthur contact with noxious stimuli

A

threshold is lowered so nervous system is more sesitive
pain response to stimuli is enhanced and prolonged

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2
Q

what can cause hypersensitivity

A

chemotherapy, diabeties, tumours, stroke

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3
Q

what is hyperalgesia

A

pain in response to noxious stimuli with an exaggerated response

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4
Q

describe the prostoglandin sensitisation pathway

A

PG’s produced from AA activae Gs G proteins
activates adenylyl cyclase - this converts ATP to cyclic AMP
cAMP activates protein kinase A
- facilitates VG Na+ channels
changes nociceptor excitability

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5
Q

what activates acid sensitive ion channels

A

protons

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6
Q

how does ATP become preswnt outside the cell

A

cell rupture

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7
Q

when ATP enters extracellular fluid, what are the two receptors it can bind to and ehat type of receptors are these

A

P2 receptors
1) P2Y - G protein coupled receptor
2)P2X - ligand gated ion channel (P2X3 is the receptor involved i pain sensigtisiation

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8
Q

what is bradykinin generated from

A

kininogen

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9
Q

what receptor is involved in heat response

A

TrpV1 - Ca2+ ion channel

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10
Q

how does bradykinin form

A

tissue damage leads to kininogen leaking from blood cells which bradykinin is generated from

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11
Q

how does bradykinin increase sensitivity to heat

A

1) binds to bradykinin receptor 2
2) G G-protein activated
3) phospholipase C-beta activated
4) phospholipid PIP2 converted to diacylglycerol
5) protein kinase C-E form activated
6) TrpV1 phosphylated
the phosphorylated Ca2+ channel is more sensitive to heat stimuli as the thermal activation threshold has been lowered = inc response to heat

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12
Q

what is peripheral sensitisation

A

reduction in threshold and an amplification in responsiveness of nociceptors

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13
Q

when does peripheral sensitisation occour

A

when peripheral terminals are exposed to inflammatory mediators = hypersensitivity at sites of inflammation

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14
Q

what is secondary hyperalgesia

A

spread of tension beyond lesion sites - ie PAIN EVERYWHERE

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15
Q

what is central sensitisation

A

functional shift in the somatosensory system from high to low threshold pain hypersinsitivity in nociceptors

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16
Q

what do the AMPA and NMDA receptor do

A

on postsynaptic terminal of projection neuron
glutamate (NT) receptors - when glutamatee binds they become permeable to cations such as Na+ andd Ca2+

17
Q

which receptor does ketamine block

A

NMDA