Pain Flashcards

1
Q

Define pain threshold.

A

It is the intensity of the stimulus before it is considered pain

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2
Q

Describe pain tolerance and what changes pain tolerance.

A

It is the intensity and duration of the stimulus before the patient complains.

Tolerance is reduced by anxiety, boredom, fatigue, repeated exposure
Tolerance is increased by alcohol, medication, hypnosis, warmth, distractions, strong beliefs.

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3
Q

What is hyperalgesia and allodynia?

A

Allodynia - pain due to a stimulus that is not normally painful

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4
Q

What is paresthesia and causalgia

A

Paresthesia - abnormal burning, tingling, numbness,

Causalgia - sustained burning and allodynia after a traumatic nerve lesion.

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5
Q

What are the nociceptors and what stimulates them?

A

Free nerve endings of A delta and C fibres. Stimulated by chemical, mechancal and thermal stimuli.

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6
Q

What are the four processes in pain pathway?

A

Transduction
Transmission
Perception
Modulatin

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7
Q

What are the types of pain fibres are there and what are their differences?

A

A delta fibres and C fibres.

A delta fibres:
Myelinated, fast 4-30 m/s
Respond to mechano-thermal stimuli
Pain is well localised, Sharp, stinging, pricking, (first pain)

C fibres
Non-myelinated, slow 0.5-2 m/s
Respond to chemical, thermal and mechanical stimuli.
Pain is diffuse, dull, burning, aching, second pain

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8
Q

What is the transduction of pain?

A

External painful stimuli is converted to electrical signal

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9
Q

What is the name of the two pathways that take pain to the brain?

A

The neo-spinothoracic tract that takes info from rexed lamina 1 tothe contralateral spinothalamic tract through the anterior commisure to the midbrain, thalamus and post-central gyus.

The paleo-spinothalamic tract takes infor from rexed lamina 2 to the contralateral spinothalamic tract through the anterior commisure and carries info to the reticular formation and the limbic system.

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10
Q

What structures in the brain preceive pain and what do the sense?

A

The limbic system - emotional and behavioural response
The reticular formation - Autonomic and motor response to pain
THe primory somatosensory cortex - percption and interperation of pain.

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11
Q

How and where is pain dampening occuring?

A

Segmental inhibition and descending inhibitory nerves.
Gate control theory - gate inthe dorsal hon that can blcok pain - A delta and C fibres open the gate and A beta fibres (light touch) close it. Messages fromthelso open or close the gate.

Segmental inhibition - there is an inhibitory neuron that contains the endogenous opioids enkephalins. These prevent neurotransmitter release from A delta and C fibres

Descending inhibitory neurons: descending inhibitory neurons stimulate the inhibitory interneuron

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12
Q

What upregulates pain (windup)?

A

Increased action potentials of second order neurons in the dorsal horn.
Continuous stimulation from the C fibres. This causes the receptors to be more sensitive, thus lowering it’s threshold for stimulation (central sensitization).
Caused by inflammation

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13
Q

There are two pathways for inflammatory pain, what are they?

A

Non-neurogenic - release of inflammatory mediators such as cytokines, chemokines and prostaglandins from the blood and connective tissue in response to damage.

Neurogenic - caused by the release of neuropeptides by neurons (substance P, nordrenaline) that act on inflammatory cells and make the recepors more sensiive causing primary hyperalgesia.

Both pathways lead to lowering the threshld of the receptor - hyperalgesia

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14
Q

What is peripheral sensitization?

A

When the inflammatory meiator produced by cells in the periphery cause the pain receptors to be more sensiive to the pain stimulus - this is primary hyperalgesia.

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15
Q

What is central sensitization?

A

Increased action potentials of second order neurons in the dorsal horn.
Continuous stimulation from the C fibres. This causes the receptors to be more sensitive, thus lowering it’s threshold for stimulation (central sensitization).

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16
Q

What is the difference between primary and secondary hyperalgesia?

A

Primary: When inflammation causes peripheral sensitization the are is primary hyperalgesia. This is within the damaged area.
Secondary: when the area surrounding the damaged tissue has increased sensitivity. Even touch f the damaged tissue cause pain. This is caused by central sensitization (windup) (reduced threshold).

17
Q

How does chronic pain develop?

A

After continued stimulation of pair receptors an the development of primary and central sensitization, eventually the CNS also changes and the glial cells in the dorsal horn begin producing cytokines to stimulate the C fiber from the periphery to release neurotransmitters that stiulates the second order neurons. The pain is now generated in the dorsal horn and not the periphery.