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NSB Lectures > Physiology of pain > Flashcards

Physiology of pain Flashcards

1
Q

What is pain?

A

An unpleasant sensory and emotional experience, associated with, or resembling that associated with actual or potential tissue damage.

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2
Q

What is pain accompanied with?

A

An emotional reaction e.g. fear, anxiety, a negative effect.

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3
Q

What are the two main types of pain?

A

Adaptive
Pathological

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4
Q

What is adaptive pain?

A

Pain that we learn and adapt from - usually good protective pain.

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5
Q

Adaptive pain can be further divided into inflammatory and ____.

A

Nociceptive

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6
Q
A
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7
Q

How is somatic pain different from visceral?

A

Somatic felt in peripheral tissues e.g. skin, joints, muscles (superficial or deep). Visceral felt in organs.

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8
Q

What is nociceptive pain?

A

Pain that is causes by damage to tissue - somatic pain or visceral pain.

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9
Q

What are nociceptors?

A

Primary sensory afferent neurons that detect noxious information.
Found in nerve endings all over body.

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10
Q

Where does neuropathic pain originate?

A

In the CNS or PNS.
Usually caused by a chronic, progressive nerve disease. Can also occur due to injury or infection.

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11
Q

What is an example of central nerve damage?

A

Stroke
Parkinsons

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12
Q

Which types of sensations would suggest peripheral nerve damage?

A

Burning
Tingling
Pins + needles

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13
Q

What is dysfunctional pain?

A

Pain that has not been caused by any damage, therefore pain is the pathology.
There is a dysfunctional amplification of normal sensory signals.
Fibromyalgia, IBS.

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14
Q

What morphology are nociceptors?

A

Pesudo-unipolar - cell body is in the dorsal root ganglion.

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15
Q

What are free nerve endings?

A

Nerve endings in the periphery that are not encapsulated by anything (Non-encapsulated dendrites).
They are unique to nociceptors.
Alpha delta or C sensory fibres.

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16
Q

How are free nerve endings different to other nerve endings?

A

Other nerve endings (e.g. Merkel discs, Pacinian corpuscles) have a capsule around them and are also Alpha Beta sub types, whereas free nerve endings are A-delta/C.

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17
Q

The larger the diameter of sensory nerve fibres means the larger the what?

A

Myelination.

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18
Q

Which sub-type of nerve fibres have the largest and smallest diameter and what sensations do they transmit?

A
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19
Q

Are nociceptors first, second, or third order neurons?

A

First order neurons.

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20
Q

Which nociceptor fibres mediate a fast, sharp pricking pain? And which mediate a slow, dull ache?

A

Fast pricking - A delta (first response)
Slow ache - C (second response)

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21
Q

What is a reflex arc and what nerve fibre activates this?

A

A neural pathway that controls a reflex without the signal having to go to CNS first. Brain receives the input as the reflex is being carried out.
Activated by A-delta fibres.

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22
Q

Is there are first and second response with visceral pain?

A

No - only a first response, which is why visceral pain feels deep and dull as it’s only innervated by C fibres.

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23
Q

Can nociceptors only respond to one stimuli?

A

No - nociceptors are polymodal so are able to respond to different stimuli.

24
Q

Which four stimuli can activate nociceptive sensory afferent nerve fibres?

A

Pressure
Temperature
Chemical
Tissue damage

25
Q

How is pressure transmitted to the CNS?

A

Mechanically sensitive ion channels at nerve endings detect pressure, ions get activated, AP initiated at the free nerve ending + then propagated to the dorsal horn and carried up spinothalamic tract.
Precise channels not yet known.

26
Q

How is temperature transmitted through the body?

A

TRP (Transient Receptor Potential) Family of receptors transduce different temperatures.
Receptor opens ion pore, cations come in. Ion movement tiggers AP that travel from nerve endings of nociceptors to dorsal horn, then travels up spinothalamic tract.

27
Q

Which receptors detect hot, cold and very cold? And what are their agonists?

A
28
Q

How does inflammation affect nociceptors?

A

Chemicals released in tissue injury and inflammation excite nociceptors, causing depolarisation + an AP to be triggered from nerve ending to dorsal horn.

29
Q

What receptors do ATP, H+ and Serotonin bind to, which excites and activates nociceptors?

A
30
Q

What is hypersensitivity?

A

An over-reaction of the immune system to a substance.

31
Q

What is neurogenic inflammation?

A

A prolonged inflammatory response that can lead to hypersensitivity, sensitisation and can contribute to the pathophysiology of inflammatory diseases.
Activation of one branch of nociceptor by inflammation triggers the release of Substance P + CGRP (Calcitonin gene related peptide) –> These are released in the periphery + cause vasodilation –> Vasodilation triggers mast cell production + activation –> Mast cells release histamine and prostaglandins –> This causes more inflammation.
This can occur in both CNS + PNS.

32
Q

What are the two types of hypersensitivity reactions that are caused by inflammation modulating nociceptors?

A

Hyperalgesia - Noxious stimuli produce exaggerated pain response (only meant to be a bit painful).
Allodynia - Non-noxious stimuli produce a painful response (it’s not meant to be painful).

33
Q

How does hypersensitivity after an injury help healing?

A

Ensures contact with the injured tissue is minimised until the repair is complete.

34
Q

Peripheral sensitisation can lead to what type of hypersensitivity reaction?

A

Hyperalgesia.
Can be an adaptive mechanism to prevent further injury.

35
Q

Central sensitisation can lead to what type of hypersensitivity reaction?

A

Allodynia + Hyperalgesia.
This is pathological rather than adaptive.

36
Q

Which type of sensitisation is a major mechanism in neuropathic pain?

A

Central.

37
Q

What is peripheral sensitisation?

A

An increase in responsiveness of the peripheral ends of nociceptors that’s driven by tissue injury or inflammation.
Threshold for activation of channel is reduced, making it easier for AP to be triggered.

38
Q

How does bradykinin affect TRPV1?

A

Bradykinin binds to receptor (metabotropic G protein-coupled) –> Protein kinase activated –> TRPV1 phosphorylated (Reduces the channel’s threshold) causing sensitisation + increased firing.

39
Q

Prostaglandins reduce the threshold of which ion channel?

A

Na+

40
Q

In the spinothalamic tract, nociceptors (first order neurons) enter the dorsal horn and synapse with second order neurons where?

A

In the substantia gelantiosa (Rexed Laminae II in dorsal horn of grey matter).

41
Q

What substance do nociceptors release that excite second order neurons?

A

Glutamate
Substance P

42
Q

Why do people experience referred pain?

A

There is convergence of visceral and cutaneous nociceptors on the same second order neurons, so the brain perceives visceral pain as cutaneous.

Example - cutaneous nociceptors from skin on L arm synapses onto same second order neurons as visceral nociceptors from the heart. This creates a convergence of the cutaneous and visceral nociceptors on the second order neuron, and the brain perceives visceral pain as cutaneous as it follows the same pathway.

43
Q

All sensations are perceived by what sensory component in the brain?

A

Somatosensory cortex.
SSC divided into areas that correlate with specific parts of the body.
Homunculus enables the encoding of the stimuli by seeing where the pain is and understanding the modality of the stimuluses.

44
Q

Third order neurons project to the insula and cingulate cortex, and also activate other cortical regions of the limbic system. Why is the relevant for pain?

A

The activation of these areas enables us to process the emotional component of pain that gives us the unpleasantness and negative effect.

45
Q

How can pain be modulated in the Spinothalamic tract?

A

Inhibitory (reduce pain) and excitatory (increase pain) responses.

46
Q

Which two brain regions are important in pain modulation?

A

PAG (Periaqueductal grey matter) in midbrain (surrounds cerebral aquaduct).
RVM (Rostral Ventromedial Medulla)
Higher cortical regions project and modulate to PAG –> PAG projects and modulates to RVM –> RVM projects to the dorsal horn.

47
Q

How is pain inhibited by PAG?

A

PAG neurons excite serotonergic neurons –> 5HT neurons excite inhibitory interneurons in the dorsal horn of the spinal cord –> Inhibitory interneurons inhibit spinothalamic tract neurons (By inhibiting 2nd order neurons) –> Leads to decreased firing.

48
Q

5HT neurons excite inhibitory interneurons to inhibit pain. What else excites inhibitory interneurons?

A

Noradrenalin pathway via locus coeruleus.

49
Q

What do inhibitory interneurons release to inhibit second order neurons?

A

Endogenous opioids: Enkephalins, Endorphins + Dynorphins.

50
Q

What forms the endogenous opioid system?

A

Endogenous opioids + their receptors.
Endorphin - Mu receptor
Enkephalin - Delta receptor
Dynorphin - Kappa receptor

51
Q

What can activate the endogenous opioid system?

A

The spinothalamic tract by sending collaterals (Spinomesencephalic fibres).
Higher cortical brain regions (Limbic structures + sensory cortex).

52
Q

How do opioids reduce pain?

A

They act in the CNS by binding to opioid receptors.

53
Q

How do NSAIDS reduce pain?

A

They block COX which is important for producing prostaglandins.

54
Q

How does acetaminophen (Paracetamol) reduce pain?

A

No one’s figured it out yet.
Only used for nociceptive pain.

55
Q

What type of drugs are useful for neuropathic pain, and work in the CNS to block neurotransmission?

A

Adjuvants - Antidepressants, anti-epileptic medication.

56
Q

There is no specific analgesia for which type of pain?

A

Dysfunctional.

57
Q

In which parts of the pain pathway, do opioids and NSAIDS work?

A

NSB Lectures (48 decks)

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