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20005 > pain > Flashcards

pain Flashcards

1
Q

what are the 2 different sensor fibres

A

type c and delta fibres

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2
Q

what are type c fibres

A
  • small, non-myelinated fibres
  • slower passing of pain information
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3
Q

what type of pain do type c fibres detect

A

dull and aching

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4
Q

what type of pain do delta fibres detect

A

hit and sharp pain

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5
Q

how do sensors work under the skin

A
  1. there are free nerve ending receptors on the end of the fibres
  2. different receptors will respond to different stimuli eg heat, mechanical manipulation
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6
Q

how to TRP receptors work for sensation

A
  • they are receptors used to detect painful stimuli
  • they change shape to let different ions in when stimulated
  • this creates and action potential
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7
Q

stages of pain pathway to the brain

A
  1. receptors detect stimulus which travels through the spinothalamic tract to the thalamus
  2. information processed in the cortex
  3. pain information goes to the reticular formation
  4. pain is relayed to the limbic system from the reticular formation - where decision on what to do occurs
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8
Q

what happens with a broken cell membrane

A
  • platelet activation
  • phospholipase are free ready to degrade the phospholipids in an orderly fashion
  • leads to the arachidonic acid pathway
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9
Q

what are the stages of the arachidonic acid pathway

A
  1. tissue injury
  2. injury to phospholipid membrane
  3. arachidonic acid released
  4. Cyclooxygenase pathway and lipoxygenase pathway
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10
Q

what are the stages of the COX pathway

A
  1. COX pathway tiggered
  2. prostaglandin G2
  3. prostaglandin H2
  4. prostacyclin, prostaglandin, thromboxane
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11
Q

what is the lipoxygenase pathway broken into

A

leukotrienes - causing bronchoconstriction and smooth muscle contraction

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12
Q

what does prostaglandin production cause

A

pain and inflammation

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13
Q

what does thromboxane production cause

A

platelet aggregation

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14
Q

what is in cellular content

A
  • potassium ions from intracellular fluid
  • hydrogen ions needed for energy,
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15
Q

how are hydrogen ion part of pain sensitisation

A

they affect pain perception and are released from cells when damaged which cause pain

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16
Q

what molecules are involved in platelet activation

A
  • bradykinin - produced from the clotting cascade
  • 5HT (serotonin) - produced from activation of platelets and in the CNS its a neurotransmitter
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17
Q

is peripheral sensitization from cell injury and platelet activation what compounds accumulate

A
  • potassium
  • hydrogen
  • prostaglandins
  • bradykinin
  • 5HT
18
Q

how to increase nociceptor sensitization

A
  • increase the number of channels
  • need a lower threshold for the channels to respond to
19
Q

hyperalgesia

A

bigger response to sensitization

20
Q

allodynia

A

hyperalgesia to something that wasn’t painful

21
Q

stages of pain sensitsiation

A
  1. lesion to the cells
  2. releases H+, K+, Prostaglandin, 5-HT, bradykinin
  3. these sensitise the nerves which produce substance p
  4. substance p tiggers the mast cells to release histamine which acts of the nociceptors to send the pain signal
  5. substance p is also a vasodilator creating redness and warmth in injury
22
Q

what are the2 ways that bradykinin works in pain sensitisation

A

it both activates and causes pain in the pathway

23
Q

why do we get referred pain

A
  • there are non specific/ individualised nociceptors for organs so pain is directed to where there is better nociception eg the skin
  • the skin and organ also synapse at the same dermatome
24
Q

what do sensory neurones do

A

detect the pain

25
Q

what does the motor neurone do

A

responds to the pain and where withdrawal from the pain (reflex to spine)

26
Q

what is the pain gate

A
  • inside the dorsal horn
  • touch sense receptors from Abeta fibres which synapse onto our pain system
27
Q

stages of the pain gate working

A
  1. touch sensation enters
  2. stimulates the inhibitory interneuron in the dorsal horn
  3. A beta fibres fire
  4. these synapse on the inhibitory neurones
  5. reduced or weak activation of pain
28
Q

how does pain change with out the A beta fibres

A

the inhibitory neurone is not activated so the touch sensation travels in on the c fibre to the projection neurone causing strong activation

29
Q

what do projection neurons do

A

it is where the pain extends through to go to the brain stem and the reticular activation system

30
Q

what is the reticular activation system

A

contains grey matter in the brain - periaqueductal grey

31
Q

what is periaqueductal grey

A

the start of the descending pain pathway

32
Q

what are the stage of the descending pain pathway

A
  1. periaqueductal grey - this descends from the same level of the spine as where the pain started
  2. it releases encephalins and endorphines when it gets a pain trigger
  3. these synapse onto 2 lower neurone on the brain stem
  4. serotonergic and noradrenergic neurones secrete serotonin and noradrenaline
  5. these 4 inhibit the projection neurons in the descending pain pathway
33
Q

what are SSRI and SNRI

A
  • SSRI - selective serotonin reuptake inhibitor
  • SNRI - selective noradrenergic reuptake inhibitor
34
Q

how to the 2 serotonin descending pathways work

A

one inhibits and one facilitates pain modulation

35
Q

how does morphine work as pain management

A

it stimulated the release or serotonergic and noradrenergic neurones to inhibit pain

36
Q

how does aspirin work as as pain management treatment

A
  • decrease the production of prostaglandins
  • decreases nociceptor sensitivity
37
Q

how does local anaesthetic work as as pain management treatment

A
  • sodium channel blocker
  • stops pain as action potentials can’t travel
38
Q

how does spinal opioids/ ket work as as pain management treatment

A

bind to the dorsal horn and affect the serotonin pathway

39
Q

how do alpha 2 agonists work as as pain management treatment

A

have a greater activity on the descending inhibitory pain pathway

40
Q

how does inflammation change pain and central sensitisation

A
  • it makes the nociceptors to become more sensitive (COX2 inhibitor treatment)
  • damaged neurones can also become perpetually stimulated
41
Q

what occurs in central sensitisation

A
  • the CNS is more sensitive
  • projection neurones become more and more active
  • causes glutamate secretion to NMDA receptors
42
Q

why is there an increased response in central sensitisation

A

there is increased NMDA receptors causing long term potentiation and a decrease in inhibitory interneurons

20005 (29 decks)

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