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Neuropharm > Pain > Flashcards

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

A

Tanezumab

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
Q

Lidocaine action

A

Blocks Na channels

26
Q

Na v 1.7 mutation problem

A

Can’t feel pain

27
Q

What is inherited erythromyalgia

A

Na v 1.7 mutation
Low threshold and enhanced response
Causes attacks of burning and redness in extremites

28
Q

What is familial episodic pain syndrome

A

Mutation in TRPV1, Enhanced response to pain. Causes episodic upper body pain

29
Q

TRPV1 actions

A

Allows Na and Ca into the axons, increasing excitation

30
Q

Direct activators of TRPV1 (4)

A

Heat
Capsasin
Protons
Endovanilloids

31
Q

Bradykinin release and receptor

A

Released by tissues in damage, acts on B2 receptor

32
Q

Bradykinin receptor action

A

Couples to PKC.

PKC phosphylates TRPV1, facilitating its opening

33
Q

Prostaglandins action

A

Bind to prostanoid receptor
Activates PKA
PKA inhinits K channels and keeps Na channels open

34
Q

TNF and IL1 in pain action

A

sensitise nociceptors

35
Q

ATP action in pain

A

Comes from damaged cells,

Acts on P2X 2 or 3 ion channels, which lets ions in

36
Q

What does the LC do?

A

Descending control over pain. NA acting at the alpha 2 adrenoreceptor gives inhibitory control

37
Q

Tapentadol mechanism of action (2)

A

Mu agonist

NA reuptake inhibitor

Neuropharm (15 decks)

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