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Sophie - The Nervous System - Year 2 > 20.2 Pain > Flashcards

20.2 Pain Flashcards

1
Q

What is the normal function of pain?

A

To protect the body - by alerting about potential damage

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2
Q

What is the long-term function of pain?

A

To provide learning and behavioural changes that ensure dangerous behaviours are avoided in the future - and prolong survival

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3
Q

Which type of pain do A-delta fibres transmit?

A

Sharp ‘first’ pain

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4
Q

Which type of pain do C fibres transmit?

A

Slower, longer-lasting, burning ‘second’ pain

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5
Q

What do P2X channels respond to?

A

An increase in ATP in the tissue

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6
Q

What does an increase in ATP in the tissue indicate?

A

That there is cellular damage, as intracellular ATP is leaking out into the extracellular matrix

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7
Q

What does P2X receptor activation lead to influx of?

A

Sodium, potassium, calcium

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8
Q

What do TRPV1 channels respond to?

A

Noxious heat, vanilloids (e.g. capsaisin), low pH (protons)

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9
Q

What does TRPV1 channel activation mainly lead to influx of?

A

Calcium

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10
Q

What do ASIC channels respond to?

A

Increased proton conc

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11
Q

What does increased proton conc indicate?

A

Heartburn, ischaemia, acid placed on skin

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12
Q

What is the role of K+ in pain?

A

It directly stimulates C-fibre depolarisation through K+ channels

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13
Q

What is the role of Na+ in pain?

A

Voltage-gated Na channels activation leads to sodium influx –> triggers excitability of nociceptors

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14
Q

Which receptor does bradykinin activate?

A

B2 receptor (metabotropic)

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15
Q

What does bradykinin activating the B2 receptor lead to?

A

Gq pathway activation –> PKC activation –> ionotropic channels are phosphorylated –> HYPERalgesia

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16
Q

Which receptor do prostaglandins activate?

A

Prostanoid receptor (metabotropic)

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17
Q

What does prostaglandin activating the prostanoid receptor lead to?

A

Gs pathway –> PKA activation –> ionotropic channels are phosphorylated –> increased depolarisation of nociceptor

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18
Q

What is the effect of nerve growth factor (NGF) on the nociceptor?

A

Increases expression of ionotropic receptors on nociceptor surface - makes depolarisation more likely

19
Q

Through which tract do nociceptive fibres enter the dorsal horn of the spinal cord?

A

Lissauer’s tract

20
Q

Which Rexed laminae do the A-delta and C fibres mainly synapse in?

A

I and II
Some in V

21
Q

Which receptors do enkephalins act on?

A

δ-opioid receptors

22
Q

What is the intracelluar pathway stimulated by enkephalins?

A

Gi pathway –> reduce intracellular cAMP –> dephosphorylation of postsynaptic receptors so that second-order neurons in the pain pathway are desensitized

23
Q

What is hyperalgesia?

A

Lowered threshold and excessive response to noxious stimuli (i.e. heightened pain).

24
Q

Give an example of hyperalgesia.

A

Pressure sensitivity of bruised tissue

25
Q

What are the two main types of pain (based on their origin)?

A
  • Peripheral pain -> Due to activation of nociceptors in the skin or soft tissue by tissue injury.
  • Neuropathic pain -> Not due to nociceptor activation, but due to damage of peripheral and/or central nerves. (Chronic pain caused by a lesion or disease to the somatosensory nervous system)
26
Q

What is meant by psychological modulation of pain?

A

Cognitive, attentional and emotional variations can modulate pain perception and make it more or less intense

27
Q

What is referred pain?

A

Pain perceived at a different location to the original painful stimulus

28
Q

Where can cardiac pain be referred to?

A

Central chest, up neck, left arm, shoulder

29
Q

Where can foregut pain be referred to?

A

Epigastric region

30
Q

Where can midgut pain be referred to?

A

Periumbilical region

31
Q

Where can hindgut pain be referred to?

A

Pelvic region

32
Q

Give examples of some pains associated with cranial nerves.

A

trigeminal neuralgia and migraine

33
Q

What is the main cause of trigeminal neuralgia?

A

Blood vessel pressing against the trigeminal nerve

34
Q

What are the symptoms of trigeminal neuralgia?

A

Stabbing, lancinating or electrical pain sensation in the face
Can be episodic or sustained

35
Q

What is migraine and what is the pathophysiology?

A
  • A headache disorder characterized by cluster of symptoms including nausea, sensory sensitivity, aura, severe headache and vertigo.
  • Pathophysiology likely involves changes in cerebrovasculature, inflammation and neural networks (including the hypothalamus, cerebral cortex and trigeminal nucleus)
  • Changes in circulating 5-HT and peptides are thought to play a role.
36
Q

What are the peripherally acting analgesics?

A

Aspirin and other NSAIDS, local anaesthetics, ibuprofen

37
Q

What are some centrally-acting analgesics?

A

Opioids and their receptors (codeine, tramadol),

38
Q

What are examples of NSAIDs?

A

Aspirin, ibuprofen

39
Q

What is the mechanism of local anaesthetics reducing pain?

A

They block voltage-gated Na channels –> signals cannot propagate along the smallest nociceptive fibres

40
Q

What is the mechanism of centrally-acting analgesics?

A

Act on on δ, κ, and (for codeine and tramadol) µ-opioid receptors
–> Gi pathway, reduction of cAMP, desphosphorylation of ionotropic receptors needed for second-order nerve stimulation

41
Q

What is the mechanism of anxiolytics?

A

Serotonergic agonists - mimic descending supply from raphe nuclei, stimulating enkephalin release and pain inhibition

42
Q

What can be used to treat migraines?

A

sumatriptan

43
Q

What is the mechanism of sumatriptan?

A

5-HT inhibitor that reduces peripheral vasodilation in the head, preventing GCRP/neuropeptide release that increase sensitisation of pain fibres

Sophie - The Nervous System - Year 2 (46 decks)

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