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PHTY2101 > Pain > Flashcards

Pain Flashcards

1
Q

Definition of pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

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2
Q

Nociception is:

A

The neural process of encoding noxious stimuli

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3
Q

What is a nociceptive stimulus?

A

An actual or potentially tissue damaging event transduced and encoded by nociceptors

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4
Q

What is a nociceptor?

A

A high-threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli

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5
Q

Describe the difference between nociception and pain.

A

Pain is felt, nociception occurs.

We often fear pain but we cannot fear nociception because it is neither seen nor felt.

A painful stimulus triggers pain, a nociceptive stimulus triggers nociceptors.

Pain can only occur in a live animal, nociception can occur in a removed neuron.

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6
Q

What are the three types of pain?

A

Nociceptive, neuropathic and neuroplastic.

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7
Q

Describe nociceptive pain.

A

Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors

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8
Q

Describe neuropathic pain.

A

Pain caused by a lesion or disease of the somatosensory nervous system

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9
Q

Describe neuroplastic pain.

A

Pain that arises from altered nociception, despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors, or evidence for disease or lesion of the somatosensory system causing the pain

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10
Q

What is the gate control theory of pain? What are the limitations of this theory?

A

Pain is modulated (gated) in the spinal cord. Large fibre signals (A beta) reduce small fibre signals (C).

Doesn’t explain chronic pain or phantom pain. Doesn’t consider tissue inflammation or psychosocial factors.

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11
Q

What are the two processess of neuroplastic pain?

A

Peripheral (inflammation & nerve injury) and central (receptor changes & plasticity).

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12
Q

What happens during acute inflammation?

A

influx of inflammatory cells

histamine release –blood vessels release plasma –oedema

nerves can also release inflammatory chemicals

creates inflammatory soup

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13
Q

What does inflammatory soup do?

A

Creates an acidic environment around the injury site

Increases sensitivity of nociceptors (peripheral sensitisation):

  • decrease in threshold for nociceptor activation
  • increase in responsiveness at nerve endings
  • activation of silent nociceptors
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14
Q

What are the two afferent nociceptor fibre types?

A

A-delta and C.

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15
Q

Describe A-delta fibres.

A 
specific to: mechanical & thermal stimuli
medium diameter
fast conduction rate (5-30 m/s)
first input to be received
small receptive field 
myelinated
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16
Q

Describe C fibres.

A 
specific to: mechanical, thermal & chemical stimuli 
unmyelinated
small diameter
slow conducting rate (0.5-2 m/s)
2nd input to be received 
large receptive field (non-specific)

may be silent nociceptors waiting for activation during sensitisation.

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17
Q

Explain neurogenic inflammation.

A

Inflammation caused by the release of neuropeptides from C fibers after a noxious stimulus.

Neuropeptides include:

  • Substance P
  • Glutamate
  • Calcitonin Gene-Related Peptide (CGRP)

These stimulate mast cells to release histamines and cause dilation of blood vessels.

18
Q

What fibre responds to touch stimulus?

A

A-beta.

19
Q

How do afferent fibres travel to the brain?

A

Via the dorsal horn (primary afferent) to the thalamus (secondary afferent).

20
Q

What are some clinical features of acute inflammation?

A

Pain:

  • ‘normal’
  • associated with recent onset and identifiable relationship to injury or disease
  • associated with tissue healing
  • 0-12 weeks
  • stimulus intensity and sensation are reasonably related
  • primary hyperalgesia

Inflammation:

  • redness, oedema, heat
  • may be diurnal pattern of pain and stiffness
21
Q

What is hyperalgesia?

A

increased pain from a stimulus that normally provokes pain

this is due to sensitisation of nociceptors (decreased threshold, greater response or expansion of receptor field)

22
Q

What is the difference between primary and secondary hyperalgesia?

A

Primary occurs at the site of injury, secondary occurs away from the site of injury.

23
Q

What is allodynia?

A

Pain response from stimuli that is not normally pain provoking.

24
Q

What is ischemia?

A

nociceptive input without inflammation

associated with:

  • prolonged or unusual posture
  • rapid ease of symptoms with postural change (opposite direction)
  • may be no evidence of trauma
  • may be worse at the end of the day, or with accumulation of activities
25
Q

What is the significance of the dorsal root ganglia in the peripheral nervous system?

A

it contains the cell bodies of afferent neurones of peripheral nerves (approx. 15,000 of them)

it is the first location of modulation & evaluation of messages from the tissues

modulates synthesis of receptors, ion channels & neurotransmitters

26
Q

What are the two mechanisms of neural tissue injury?

A

Mechanical irritation: repetitive compressive, tensile, friction, vibration forces

Chemical irritation: inflammatory soup after tissue injury

can go on to affect vascular, connective tissue and impulse conducting tissue components of the nervous system

27
Q

What is the process that leads to sensitisation of neural connective tissue nociceptors post nerve irritation?

A

venous congestion > impeded flow of blood and axoplasm > hypoxia & tissue injury > inflammatory response in the nerve trunk & DRG > oedema in nerve > increased fluid pressure in the nerve trunk

oedema in the nerve can lead to fibrosis within the nerve fascicle which compromises viscoelastic properties which puts greater mechanical stimulation on sensitised nociceptors

28
Q

What are abnormal impulse generating sites (AIGS)?

A

Also known as ectopic impulse generation sites.

Demyelination of nerve axons leading to abnormal nociceptive input and action potentials.

Due to impairment of axoplasmic flow, new ion channels accumulate in the unmyelinated areas.

29
Q

How does peripheral neurogenic pain present clinically?

A

Hyperactivity: pain, burning, feelings of cold, crawling, tightness, zings, prickling, “crawling ants”

Hypoactivity: sensory loss, weakness

May be motor involvement
May have night pain

Often in neural zone, along nerve trunk.

30
Q

What is referred pain?

A

Pain perceived at a location other than the site of the painful stimulus/origin

Pain perceived as arising or occurring in a region of the body innervated by nerves or branches of nerves other than those that innervate the actual source of pain

Can occur in a region that is either remote from or next to the source of pain, but the two locations are distinguishable based on their different nerve supply

Can be thought of as an error in the brain’s processes that determine exactly where the nociceptive input is from

31
Q

What is the physiological basis of referred pain?

A

Convergence of nociceptive pathways (multiple primary afferent neurones converge on secondary neurones in the dorsal horn)

32
Q

How may pain be referred from the upper spine to the forehead?

A

Convergence of afferent nerves from the 3rd cervical spine nerve and the trigeminal nerve from the forehead in the trigeminocervical nucleus.

33
Q

How does referred pain present clinically?

A

deep aching pain without anatomical borders

rarely distal to the knee or elbow

34
Q

What is somatic referred pain?

A

Pain referred from musculoskeletal tissues

35
Q

What is visceral referred pain?

A

pain referred from organs

36
Q

What is radicular pain?

A

peripheral neurogenic pain where the site of injury is at the level of the spinal nerve root

often follows dermatomal pattern

37
Q

How does radicular pain present clinically?

A

sharp shooting pain in a relatively narrow band which may correspond with the dermatome

may have pins & needles, numbness or weakness

38
Q

What are some reasons for persistant pain?

A

Ongoing or recurrent tissue damage

  • exacerbation of acute inflammation
  • nociceptive pain

Chronic inflammation (e.g. OA, RA)

  • disease process results in persistent or recurrent inflammation
  • nociceptive pain

Peripheral sensitisation

  • changes in peripheral nociceptors
  • nociceptive painCentral sensitisation
  • changes in the spinal cord and brain
  • nociplastic pain
Red flags (e.g. cancer)
-Pain may not be neuromusculoskeletal in origin
39
Q

What is the difference between central and peripheral sensitisation?

A

Peripheral:

  • decreased threshold for nociceptive neurones
  • increased responsiveness of nociceptive neurones
  • increased receptive fields of nociceptive neurones

Central:

  • increased responsiveness of the CNS to input coming from the periphery
  • inputs from non-nociceptive neurones now perceived as pain
40
Q

How does nociplastic pain present clinically?

A

Area & description:

  • Symptoms may not have a neat anatomical or dermatomal boundary
  • Any original pain may have spread (secondary hyperalgesia)
  • Multiple areas of pain may occur together or separately
  • May experience pain on the contralateral side
  • May have mechanical hyperalgesia at a location away from the injury site
  • May report sudden stabs of pain

Behaviour:

  • Ongoing pain beyond expected healing time
  • Summation
  • Distortion of the stimulus/response relationship
  • Unpredictable or inconsistent responses to input and treatment
  • May report pain with all movements
  • May report pain when they think about it
  • Can be highly irritable or unstable
  • Sensitivity to cold but not heat
  • pain may be seasonal/cyclical
  • may see symptoms in other systems (immune, GI etc)
41
Q

How can the endocrine system affect pain?

A

via the hypothalamus-pituitary-adrenal axis (HPA)

anterior pituitary gland secretes ACTH > adrenal cortex secretes cortisol > under stress the hypothalamus secretes CRH which stimulates the anterior pituitary to secrete ACTH and therefore the adrenal cortex to secrete cortisol (feedback loop)

42
Q

Why is cortisol important in the endocrine system? And why would chronic high levels in the bloodstream be harmful?

A

it maintains cardiovascular and metabolic homeostasis, stimulates protein catabolism and glycogen synthesis, regulates inflammatory & immune response

shuts down non-essential body systems in an emergency

long term high levels start interfering with other systems (i.e. immune, GI).

PHTY2101 (10 decks)

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