Self Directed Study Flashcards

1
Q

What are the four stages of nocioception?

A

Transduction, transmission, perception and modulation

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2
Q

Perception, explain process etc.

A

Triggered by noxious stimuli
Intensity not related to tissue damage.
Nerve damage doesn’t respond to analgesic

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3
Q

What is suffering used for?

A

As a language to describe pain, not all suffering is pain

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4
Q

What are pain behaviours?

A

Result from pain and suffering, they are observable and quantified. Influenced by the environment

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5
Q

What is transient pain?

A

Pain that happens in every day life. Not a reason to seek medical treatment and not associated with tissue damage,

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6
Q

What is acute pain?

A

Substantial injury of body tissue, pain stops before healing is complete. Malignant pain can be continuous acute. Changes of nociceptors occur in acute stages.

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7
Q

What is chronic pain

A

Takes months/years to heal, unrelenting, intensity is out of proportion to original injury, exceeds body’s ability to heal

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8
Q

Who is the best girl in the whole world, starts with A and ends with B?

A

Anna Josefa Maria Scheib! πŸ˜€πŸ˜€πŸ˜€πŸ˜πŸ˜πŸ˜πŸ˜˜πŸ˜˜πŸ˜˜πŸ’πŸ’πŸ’πŸ“žπŸ“žπŸ“žβ˜ŽοΈπŸŽ‰πŸŽŽπŸš¨β¬†οΈβ¬†οΈβ¬†οΈβ¬†οΈβ¬†οΈβ¬†οΈβ¬†οΈβ¬†οΈβ¬†οΈβ¬†οΈβ¬†οΈβ¬†οΈ

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9
Q

What is nocioception?

A

Encoding and processing of noxious stimuli. Specialised transducers attached to a delta and c fibres which may be biased by inflammatory and neural changes

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10
Q

What is the most plasuible link for transition of acute to chronic pain?

A

Modification

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11
Q

What does prolonged firing of c fibres do?

A

Causes release of glutamate (major excitatory neurotransmitter within the cns )

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12
Q

What is wind up?

A

An increased in intensity and duration of response by a giving the nmda receptors. Normally nmda is blocked, continuous stimulation removes this.

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13
Q

Why is nmda receptor available after on going tissue injury? And what does this open receptor play a role in?

A

Through release of inflammatory chemicals from c fibres. Inflammatory and neuropathic pain States. Results in secondary hyperalgesia also

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14
Q

What is required for descending hibatory pathways? And wher?

A

Nmda receptors in the substantia gelantosa.

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15
Q

Why don’t anti inflammatorys work very well for neuropathic pain?

A

Injuries and diseases of the nervous system that result in neuropathic pain promote inflammatory mediators within the spinal cord. Blocking peripheral inflammation alone would not work

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16
Q

Explain the process of peripheral sensitization.

A

Tissue damage releases inflammatory cells and also causes neurogenic inflammatory response. Inflammatory cells release chemical mediators. An inflammatory chemical soup is created that sensizitize high threshold nociceptors.

17
Q

What changes occur with peripheral sensitization?

A

Increased responsiveness to thermal stimuli at site of injury (primary hyperalgesia).
Awakening of the silent nociceptors by chemical sensitization, randomly discharging.
Changes in receptive field.

18
Q

Primary afferent nociceptors terminate in different laminae levels on several classes of Neurons. What classes are they and why do they do this?

A

Projection Neurons that transmit information to supraspinal structures. One type is the wide dynamic range (noxious and non noxious). Third class is inter neutrons involved in excitatory and inhibitory Neurons.