6.2 Pain Flashcards

1
Q

What is pain

A

Pain is an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage. It is a warning sign for dangerous stimuli.

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2
Q

Describe congenital pain insensitivity

A

Congenital pain insensitivity is a rare genetic condition where patients do not feel pain.The individuals often do not learn that certain activities are dangerous. Those with congenital pain insensitivity have lower lifespans. It can be due to various inherited conditions

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3
Q

What are the 3 main types of pain

A

normal (nociceptive) pain, inflammatory pain and neuropathic pain

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4
Q

What is normal (nociceptive) pain

A

A short lived pain, warning you not to do a certain action again

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5
Q

What is inflammatory pain

A

When there is some kind of ongoing injury/infection in a peripheral tissue, the nerves supplying the tissue let you know about the damage.

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6
Q

What is neuropathtic pain.

A

Pain caused by some kind of pathology in the nervous system, mainly in the peripheral nervous system. It s difficult to treat as it is resistant to analgesics. It often serves no useful purpose as it is not protective of any damage.

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7
Q

What is hyperalgesia

A

When a normally mildly painful stimulus has elevated pain levels more than usual. It is an increased response to suprathreshold stimuli.

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8
Q

What is allodynia

A

When a normally non painful stimulus becomes painful. It is a lowered threshold for activation

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9
Q

What type of pain does hyperalgesia and allodynia occur in

A

inflammatory and neuropathic pain

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10
Q

Describe how hyperalgesia/allodynia can be caused

A

Due to increased sensitisation of the nociceptors, this can be due to the release of inflammatory peripheral mediators of pain from tissues or from changes in the CNS

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11
Q

Describe nociceptors

A

They are free nerve endings that respond to intense (noxious) stimuli that can be mechanical, thermal or chemical. They are primary afferent neurons that signal painful stimuli.

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12
Q

Describe the pain pathway

A

The pain pathway involves the spinothalamic tract. The 1st order primary afferents (nociceptors) synapse onto 2nd order spinothalamic tract neurons in the dorsal horn of the spinal cord. The axons of these 2nd order neurons then decussate and travel up to thalamus, where they synapse on 3rd order neurons. These neurons then project to the cerebral cortex

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13
Q

What is the key difference between nociceptive primary afferent axons and most other receptors.

A

They have a smaller axon diameter, therefore they conduct impulses more slowly

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14
Q

Describe the 2 types of nociceptive primary afferent axons

A

Fine myelinated axons (A§ fibres), these have 2-5 μm diameter and conduct at 5-30 metres/sec.

Unmyelinated axons (C fibres), these have less than 1 μm diameter and conduct at around 1 metres/sec.

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15
Q

Describe how the 2 types of nociceptive primary afferent axons can cause different pain types.

A

A§ axon nociceptors cause the first pain after the noxious stimuli which is fast and sharp.

C axon nociceptors then cause the second pain which is slower and not as intense (e.g pain from maintained pressure).

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16
Q

Describe some inflammatory peripheral mediators of pain from tissues.

A

bradykinin- released from damaged tissues It acts on bradykinin receptors on nociceptor terminals to activate and/or sensitise them

substance P- released from peripheral terminals of nociceptors, it dilates blood vessels and may activate mast cells

prostaglandins- synthesised by damaged lipid membranes, it sensitises nociceptors, rather than activating them directly

17
Q

How does aspirin act

A

It prevents prostaglandin synthesis, thus reducing nociceptor sensitisation

18
Q

Describe visceral (internal organ) nociception

A

Visceral (from internal organs) nociceptors terminate diffusely in the spinal cord and converge onto the same 2nd order neurons as cutaneous (skin) nociceptors, following the spinothalamic pathway. Visceral pain is poorly localised and and feels hard to pin point, ofter just feeling like the body surface.

19
Q

What do fMRIs indicate about pain pathways

A

Shows that the cortex is activated following noxious stimuli. The pain involves areas other than sensory perception like aversion, emotion and fear from different cortical areas.

20
Q

Which areas of the cortex are involved in pain detection

A

The primary somatosensory cortex (S1) and secondary somatosensory cortex (S2) in the parietal lobe. Also the anterior cingulate cortex and insular cortex.

21
Q

Describe the different parts of pain detection that the different parts of the cortex are involved in.

A

The primary and secondary somatosensory cortexes show the sensory-discriminative aspects of part such as the location, duration, intensity and nature of the stimulus.

The anterior cingulate and insular cortexes show the affective-motivational aspects of pain. The anterior cingulate cortex activity indicates the unpleasantness of pain and the insula cortex activity causes the aversion to pain.

22
Q

Describe some problems with the traditional pain pathway and what they suggest

A

-that severe injuries do not always cause pain,

-that pain can occur without obvious injury or disease

-that pain is affected by psychological factors

-that acupuncture can reduce pain

-cutting the pain pathway (the spinothalamic tract) via an anterolateral cordotomy procedure may not reduce pain permanently

They all suggest that pain pathways are more complex than the simple pathway and have considerable plasticity

23
Q

Describe the gate control theory

A

The gate control theory suggests hat components in the pain pathway can suppress pain. The stimulation of low threshold mechanoreceptive (Aβ) afferents reduces pain (equivalent to massaging skin around injured area), they may be acting through local spinal cord mechanisms activating inhibitory interneurons

24
Q

Describe stimulation produced analgesia

A

Electrical stimulation of spinal cord via electrodes in vertebral can provide effective pain relief.

Additionally, stimulation of periaqueductal grey matter in the midbrain gives strong and selective analgesia. However, the periaqueductal grey matter does not project directly to the spinal cord, insteas its thought that neurons in the raphe nuclei of the medulla that release 5-HT in the spinal cord. Opiates like morphine act on opiod receptors in this pathway to act as analgesics.