Pain Flashcards

1
Q

Number of people with chronic pain in UK

A

7.8 million

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2
Q

Amount spent of incapacity benifits due to chronic pain

A

£3.8 billion

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3
Q

Nociceptive pain

A

response to tissue or inflammatory pathology with noxious stimuli

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4
Q

Neuropathic pain

A

non functioning in the nervous system, such as nerve damage or ion channel changes

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5
Q

Idiopathic pain

A

Brain areas causing pain

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6
Q

Fibres associated with pain

A

C and A delta.

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7
Q

How is nociception felt

A

Sensory endings in tissue activated by stimuli such as chemical, thermal, mechanical

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8
Q

Where do pain fibres end

A

Grey matter of spinal chord, lamina 1 and II in superficial dorsal horn

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9
Q

Name of superficial dorsal horn

A

substantia gelatinosa

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10
Q

What NTs + Receptors do pain fibres release to next neurons in spinal chord

A

Glutamate and ATP.
Act on AMPA for immediate pain
NMDA for slower wind up of pain

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11
Q

Name of tract from spinal chord to thalamus

A

Spinothalamic tract

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12
Q

Where thalamus projects to

A

Cortex. Gives location and intensity

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13
Q

Key area of decending control of pain

A

Periaqueductal grey in midbrain. Collects info from amny brain areas such as cortex, hypothalamus, amygdala

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14
Q

Where does PAG project to

A

Rostroventral medulla, which then projects to dorsal horn.

Release 5HT which is excitatory and promotes pain throught 5HT 2/3 R

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15
Q

Where does NA noicipetice pathway descend from

A

Locus coerulus. Limbic and RVM connect into it.

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16
Q

What receptros are common in descending pathways

A

Endogenous opioid

17
Q

Central causes of pain sensitisation (4 - full names)

A

Substance P
NGF (Nerve growth factor)
BDNF (Brain derived neurotrophic factor)
CGRP

18
Q

How is NGF made

A

Made in peripheral tissues when tissues are damaged

19
Q

How does NGF work

A

Binds to TrkA receptor. This is a kinase linked receptor

20
Q

Activated TrkA downstream effects (4)

A

Increase in electrical activity
Chemosensitivity
Acts on genome in DRG cell body to release SP, CGRP, BDNF
Increase in ion channel expression - Na, P2X, TRPV1

21
Q

Antibody to TrkA receptor

22
Q

Tanezumab uses

A

Effective in lower back pain
Good for OA
Causes joint damage

23
Q

BDNF receptor + location

A

TrkB on postsynaptic dorsal horn

24
Q

TrkB action

A

Phosphorylates NMDA subunit GluN1, sensitising the receptor for glutamate

25
Lidocaine action
Blocks Na channels
26
Na v 1.7 mutation problem
Can't feel pain
27
What is inherited erythromyalgia
Na v 1.7 mutation Low threshold and enhanced response Causes attacks of burning and redness in extremites
28
What is familial episodic pain syndrome
Mutation in TRPV1, Enhanced response to pain. Causes episodic upper body pain
29
TRPV1 actions
Allows Na and Ca into the axons, increasing excitation
30
Direct activators of TRPV1 (4)
Heat Capsasin Protons Endovanilloids
31
Bradykinin release and receptor
Released by tissues in damage, acts on B2 receptor
32
Bradykinin receptor action
Couples to PKC. | PKC phosphylates TRPV1, facilitating its opening
33
Prostaglandins action
Bind to prostanoid receptor Activates PKA PKA inhinits K channels and keeps Na channels open
34
TNF and IL1 in pain action
sensitise nociceptors
35
ATP action in pain
Comes from damaged cells, | Acts on P2X 2 or 3 ion channels, which lets ions in
36
What does the LC do?
Descending control over pain. NA acting at the alpha 2 adrenoreceptor gives inhibitory control
37
Tapentadol mechanism of action (2)
Mu agonist | NA reuptake inhibitor