Pain Flashcards

1
Q

what is pain?

A

pain is an unpleasant sensory experience associated with actual or potential tissue damage or described in terms of such damage. it is also an intensely personal experience with biological, psychological and social components existing where and when the person says it exists. it is a subjective experience and is the most common reason for people seeking medical advice

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2
Q

what is the original biomedical definition of pain and why is it wrong?

A

biomedical definition = a response to a painful stimulation.
however this model implies that the individual is passive in the pain experience. there is also evidence to dispute this interpretation for example:
- for the same pain, 80% of civilians requested medication whereas only 20% of soldiers did
- 5-10% of amputees experience phantom limb pain
- placebos - 30% of chronic pain patients reported the same pain reduction from sugar pills as morphine
clearly there are psychological factors involved in pain perception

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3
Q

what is the biopsychosocial approach to pain?

A

pain is a dynamic interaction between the biological, psychological and social factors unique to the individual. the model is multimodal and assumes the individual to be active in their pain experience

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4
Q

what factors contribute to the experience of pain?

A

biological:
- stimulus intensity
- physical health
- injury
- sleep
- medication use
psychological:
- pain perception
- coping skills
- catastrophizing
- fear/pain avoidance
- depression
- previous experience
social:
- work/disability
- culture/norms
- economic factors
- environmental factors

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5
Q

describe the psychological aspect of the pain gate theory

A

there is a neural gate at the spinal level that modifies pain perception. it receives signals from peripheral nerve fibres, descending central influences and large and small fibres. when the pain gate opens, there is more pain perception, when it closes, there is less. factors such as injury, anxiety, boredom etc open the pain gate. factors such as medication, relaxation and distraction close the pain gate

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6
Q

describe the fear avoidance model

A

injury causes a pain experience, in healthy individuals there is no fear, and so the pain is confronted and the individual eventually recovers. in unhealthy individuals they catastrophize pain, experience pain related fear, demonstrate avoidance and as a result depression, disuse or disability, this then leads to a greater pain experience (this element of the model is cyclical)

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7
Q

what is pain catastrophizing?

A

irrationally negative reactions and forecast of events relating to pain

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8
Q

what is appraisal theory?

A

a persons evaluative judgement of a situation determines their emotional response to it

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9
Q

how can pain be measured?

A

numerical scales
validated measures of pain and functioning
observation
physiological measures

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10
Q

how can pain be managed?

A

surgery
medication
physical activity
holistic approaches (CBT, attention diversion, physical activity etc)
pain toolkits for chronic pain

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11
Q

why is it important to experience pain?

A
  • early warning system that alerts us to danger or warns us of actual/potential risks or damage
  • elicits changes in behaviour to try and avoid danger or harm
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12
Q

what are the different types of pain?

A

superficial –> somatic –> visceral
insignificant –> severe –> life changing
acute –> chronic

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13
Q

what are some potential causes of congenital absence of pain disorder?

A
  • issues with central perception mechanisms (brain or spinal cord)
  • issues with peripheral transmission: mutation of the SCN9A molecule which sits on nociceptive nerve endings, it creates non functional voltage gated sodium channels at nociceptive nerve endings meaning that no action potentials are generated at these nerve endings so no pain signals are sent to the brain
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14
Q

what is the definition of nociception?

A

the neural process of encoding noxious stimuli

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15
Q

What are nociceptors?

A

complex free nerve endings that register information about noxious stimuli

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16
Q

what chemicals/early activators trigger nociceptors?

A
  • bradykinin
  • serotonin
  • histamine (released by mast cells)
  • prostoglandin
  • H+
  • K+
17
Q

define peripheral sensitisation?

A

sensitisation of free nerve endings at an injury site, making the nociceptive neuron more sensitive to noxious stimuli.

18
Q

describe the process of peripheral sensitisation of a free nerve ending?

A

when long term damage is experienced, the nociceptive neuron produces substance p. Substance p causes neurogenic inflammation and vasodilation at the site of injury. it also causes mast cells to produce more histamine, which in turn activates the nociceptive neuron, creating a pain feedback loop.

19
Q

how does nociceptive information get from the site of damage to the brain?

A

damage occurs –> free nerve ending registers damage –> sensory axons (C and A delta fibres) –> spinothalamic pathway –> brain

20
Q

which two nerve fibres carry nociceptive information to the spine?

A

C fibres = polymodal fibres which carry slower, deeper pain sensations
A delta fibres = thermal or mechanothermal fibres which carry sharp, pricking, hot or cold pain sensations

21
Q

describe the process of central sensitisation/spinal hyperexcitability

A

this is the same principle as long-term potentiation:
small stimuli causes glutamate to bind to AMPA receptors and triggers an action potential
large stimuli frees up NMDA receptors so that glutamate can bind to them. this leads to an influx of Ca2+. this starts an intracellular cascade which sensitises the post-synaptic cell to smaller stimuli.

22
Q

how does nociceptive information ascend the spine?

A

indirect spinothalamic tract: slower C fibres send information to the limbic system, hypothalamus, reticular formation and reticular activating system. this information has much poorer spatial discrimination
direct spinothalamic tract: faster A delta fibres send information to cortical areas. this information has better spatial discrimination and discrimination of type of pain sensation.

23
Q

what is referred pain and why does it happen?

A

referred pain: pain in one area of the body is also experienced in other areas as well. it occurs because when the body is developing in the womb, the nervous system begins to develop when body parts are not necessarily in the same place they end up.

24
Q

describe the pain gate theory (physiologically)

A

In the spine, an inhibitory neuron sits next to nociceptor neurons. its job is to inhibit second order neurons by releasing GABA.
when the nociceptor sends a signal, it inhibits this inhibitory neuron, allowing the pain signal through to the spine.
but the interneuron is also flanked by a mechanoreceptor, when this sends a signal it turns the inhibitory neuron on, which means that the pain/nociceptor signals are once again blocked/inhibited.
it illustrates the key concept of ‘rub it better’

25
Q

what is the neuromatrix of pain theory?

A

the perception of pain does not come from the brains passive registration of tissue trauma but from its active generation of subjective experiences through a network of neurons known as the neuromatrix.

26
Q

what are the two descending pathways which control the pain gate?

A

these are pathways from the brain to the pain gate which can reduce pain sensations.
1. the serotonergic pathway. this stems from the periaqueductal grey in the midbrain and releases serotonin
2. noradrenergic pathway. this stems from the pons and releases noradrenaline
these pathways are the connection between conscious pain perception and nociceptive signals. overactivity from these pathways can result in loss of pain sensation.

27
Q

what is neuropathic pain?

A

damage to the somatosensory system resulting in pain perception without current physical cause.

28
Q

what is hyperalgesia?

A

increased sensitivity following tissue injury.
primary = local to the site of damage
secondary = extending to the surrounding ‘undamaged’ areas.

29
Q

what is allodynia?

A

increased sensitivity to non-noxious stimuli following tissue injury. caused by a central mechanism whereby microglia which are activated during inflammation switch inhibitory input to excitatory

30
Q

What are the main differences between A-delta and C fibres?

A

A-delta fibres are myelinated, C fibres are not.
A-delta fibres are 1-5 micrometers in diameter, C fibres are 0.2-1.5 micrometers in diameter (C fibres are much thinner)
A-delta fibres have a conduction velocity of 5-40m/s. C fibres have a conduction velocity of 0.5-2m/s (C fibres are much slower)
A-delta fibres pain (mechanical and thermal) information. C fibres carry pain (mechanical, thermal and chemical) information

31
Q

describe how descending modulatory pain pathways function

A

descending pathways stem from the periaqueductal gray in the brain stem. this area receives nociceptive information from the spinothalamic tract and sends descending signals down the spinal cord.
these pathways release endogenous enkephalins which bind to delta opioid receptors within the dorsal horn. this process stops the release of neurotransmitters so nociceptive signals are not sent.
two descending pathways exist, the serotonergic pathway which release serotonin and the noradrenergic pathway which releases noradrenaline.

32
Q

what type of pain is associated with A-delta fibres?

A

fast, sharp pain

33
Q

what type of pain is associated with C fibres?

A

slow, deep pain