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(Physio) Clinical Assessment and Treatment > Pain and Management > Flashcards

Pain and Management Flashcards

1
Q

Describe the Gate Control Theory.

A

Possible brain modulation, not just a passive system• Includes descending pathways

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2
Q

What are endorphins?

A

Endogenous opioids released within the brain and spinal cord

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3
Q

What is referred pain? Why do we have it?

A

WHAT: an error in perception by the sensory cortex in the brain as to the source of the painful stimulus (i.e., felt elsewhere than its true site)

WHY: cutaneous, visceral, and skeletal muscle nociceptors converge on a common nerve root of the spinal cord, but brain interprets as cutaneous (higher proportion)

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4
Q

What is the difference between segmental and extrasegmental referred pain?

A

SEGMENTAL: pain referred to a structure within the same dermatome

EXTRASEGMENTAL: pain referred to >1 dermatome (multiple levelsàsevere)

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5
Q

In one sentence, what is a dermatome?

A

An area of skin in which sensory nerves derive from a single spinal nerve root

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6
Q

Where does the dermatome project? Where can pain refer along a dermatome?

A

Projects more distally than the key muscle (myotome)

Dermatome and key muscles develop from the same segment

Any structure within a particular segment can refer pain to the same dermatome of that segment

It may refer along the whole length of the dermatome or only part of it

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7
Q

What is root pain? Is all root pain referred? Is all referred pain root pain?

A

Irritation of nerves and nerve roots

Deep, sharp and well localized

All root (radicular) pain is referred, but not all referred pain is root pain

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8
Q

What is acute pain? Give examples. What is its role?

A

Results from injury or disease that causes, or can cause, tissue damage

E.g., infection, trauma, metabolic disorder progression, degenerative disease

Protects against further tissue damage

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9
Q
  • Results from injury or disease that causes, or can cause, tissue damage
  • E.g., infection, trauma, metabolic disorder progression, degenerative disease
  • Protects against further tissue damage.

What kind of pain is this?

A

Acute pain

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10
Q

What is subacute pain? What is its purpose?

A

Similar to acute pain occurring later in the process

Continues to protect against damage

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11
Q
  • Similar to acute pain occurring later in the process
  • Continues to protect against damage.

What kind of pain is this?

A

Subacute pain.

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12
Q

What is chronic pain? What is it associated with? Does it have a role?

A

Persists beyond the normal time expected for healing of injured tissue

Associated with structural and functional changes in the central nervous system

No longer a symptom or protective

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13
Q
  • Persists beyond the normal time expected for healing of injured tissue
  • Associated with structural and functional changes in the central nervous system
  • No longer a symptom or protective.

What kind if pain is this?

A

Chronic

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14
Q

Give two kinds of stimulus or source of pain, and one example for each.

A

Chemical Sources

• Substances that are released with tissue injury (space occupying)

Mechanical Sources

  • Normal Stress on Abnormal Tissue
  • Ex: movement with a patient just out of a cast
  • Abnormal Stress on Normal Tissue
  • Not necessary for pathology to be present for pain to be produced

•Ex: bend finger back and hold it

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15
Q

How can upregulation and sensitization happend?

A
  • Nociceptive system is usually very quiet
  • When injury activates the system, a relatively innocuous stimuli can trigger pain perception
  • Events that were not painful before become painful
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16
Q

What is nociceptive pain? What are its characteristics?

A

Nociceptive pain: normal pain response
• Usually aching or throbbing and well-localized, time limited (resolved once the tissue heals), responds well to analgesics

17
Q

What is neuropathic pain? What are its characteristics?

A
  • Neuropathic pain: nerve damage (e.g., abnormal firing, increased signal to brain). It is a direct consequence of a lesion or disease affecting the somatosensory system
  • Tingling, shock-like or burning pain, usually chronic and responds poorly to conventional analgesics
18
Q

What is hyperalgesia?

A

Hyperalgesia: increased pain from a stimulus that normally provokes pain

19
Q

What is allodynia?

A

Allodynia: pain due to stimulus that does not normally provoke pain

20
Q

What could cause neuropathic pain? Explain and give examples.

A

May result from various causes that affect the brain, spinal cord and peripheral nerves, including:

• Complex Regional Pain Syndrome (II)

  • Diabetic Neuropathy
  • Phantom Limb Pain
  • Post-Stroke

Often experienced in parts of the body that otherwise appear normal

Generally chronic, severe and resistant to over-the-counter analgesics

21
Q

How could neuropathic pain be desribed by the patient?

A

Pain may be spontaneous or evoked (e.g., allodynia, hyperalgesia, hyperpathia)

The quality of the pain is described as burning, electric shock, shooting and dysesthesia

**Often the stimulus/response relationship is unclear

22
Q

Name the three known mechanisms for neuropathic pain

A

Known mechanisms include:

  • Ectopic impulse generation
  • Response to activity in adjacent nerves
  • Changes in sensitivity
23
Q

Describe peripheral sensitization. What are the three ways in which the increase could happend?

A
  • Increased afferent nociceptor input to the CNS. Peripheral sensitization causes the amount of pain that you feel to be out of proportion to the extent of your injury
  • Increasing pain signals that could occur through:
  • Spontaneous firing, not requiring a signal• An easier threshold to reach
  • Increased firing frequency
24
Q

In peripheral sensitization, what is the role of the chemical mediators after a trauma?

A

Trauma

Inflammatory Response

Chemical Influence on Afferent Neuron Impulse

25
Q

Describe the reduced reponse threshold pathway of peripheral sensitization.

A
  • Chemicals released in response to tissue trauma will bind to ion channels in the membrane to alter permeability and excitability
  • Indirect influence through 2nd messenger system
  • (altered pH of the tissue)
  • Inhibition of after-hyperpolarization
26
Q

What is central sensitization? What is it initiated by?

A
  • An aspect of neuroplasticity (i.e., brain changes with experience)
  • Describes the changes at the cellular level which support neuroplastic changes in
  • • Spinal cord
  • • Supraspinal centres

• Initiated by high activity levels the in peripheral nociceptors leading to activity- dependent increases in excitability of nerves in the spinal cord

27
Q

What are the two mechanisms of central sensitization called?

A

Chemical property changes

Neuroanatomical reorganization

28
Q

Why as clinicians should we be aware of sensitization?

A

BAD NEWS

  • The nervous system changes in response to pain
  • It becomes more sensitive to pain
  • What may be considered “excessive” pain behaviours may actually reflect sensitization of the nociceptive system

GOOD NEWS

• The nervous system changes in response to experience or intervention

29
Q

What are the purposes of pain assessment?

A
  • Diagnosis
  • Prognosis
  • Track changes over time (numeric rating scale)
  • Assist in clinical decision making – quality and type of pain to determine Rx
30
Q

What are some things you could be looking for during a pain history assessment?

A

Pain Characteristics – onset, duration, location, quality, intensity, associated symptoms, exacerbating and relieving factors [OPEN ENDED QUESTIONS!]

Past and current management therapies

Relevant medical and family history

Psychosocial history

Impact of pain on daily life – work, daily activities, personal relationships, sleep,

appetite, emotional state

Patient (and family’s) expected goals for treatment

  • ASK the patient about their pain (consider the ICF model)
  • Asking about ADL’s and IADL’s
  • Asking about physical activity, mood, sleep, appetite, energy level
  • Identify THE PATIENT’S preferred pain terminology
  • Hurting, aching, stabbing, discomfort, soreness
  • Use a pain scale that works for the individual
  • Insure understanding of its use
  • Modify sensory deficits

(Physio) Clinical Assessment and Treatment (15 decks)

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