Pain Flashcards

1
Q

Define the term hyperalgesia.

A

An increased sensitivity to feeling pain and an extreme response to pain.

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2
Q

Define the term allodynia.

A

Pain due to a stimulus that does not normally provoke pain.

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3
Q

Describe the differences between C and A-delta fibres.

A

Unlike A-delta fibres, C fibres are smaller in diameter, and are unmeylinated. A-delta fibres respond to mechanical (pressure) stimulus and produce the sensation of sharp, localised, fast pain (faster action potential velocity), whereas C fibres respond to thermal, mechanical, and chemical stimuli and produce the sensation of dull, aching, burning, and delayed pain (slower action potential velocity).

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4
Q

Explain why pain is multi-factorial.

A

Pain is a multi-factorial phenomenon because it is an intensely personal experience with biological, psychological and social components, existing where and when a person says it exists. For example, biologically, pain receptors are not uniformly distributed across the body. Psychological states have been proved to impact pain perception, making it subjective. Socially, humans can learn and copy others’ behaviours, and if someone describes something being painful, it may then be experienced worse than what it would have been without this.

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5
Q

Outline the concept of referred pain and anatomical basis for its occurrence.

A

Referred pain is pain felt in a part of the body other than the actual source of the pain signals. The nervous system develops very early on, and as humans grow, tissues that were once in close proximity, move apart, but the nervous system stays in one place, hence why pain perception is confused.

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6
Q

List the psychosocial factors that lead to opening and closing of the pain gate.

A

Opening - stress, tension, depression, worry, boredom, lack of activity.
Closing - relaxation, contentment, optimism, happiness, distraction, pro-activity.

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7
Q

Outline the IASP definition of pain.

A

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

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8
Q

Describe the course and the nature of the information transmitted by Aδ and C fibres from the periphery to the cortex.

A

A delta fibres have a fast conduction velocity and carry information mainly from the nociceptive-mechanical or mechanothermal-specific nociceptors. However, C fibres have a slow conduction velocity and are activated by a variety of high-intensity mechanical, chemical and thermal stimulation and carry information from polymodal nociceptors. In general, C fibres release neuropeptides such as substance P whereas the A delta fibres release glutamate.

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9
Q

Describe the indirect spinothalamic tract.

A

Information is typically carried by slow, C fibres within the medial system. The areas that are reached are the limbic system, hypothalamus, reticular formation and reticular activating system. It has poor spatial discrimination of sense of pain sensations.

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10
Q

Describe the direct spinothalamic tract.

A

Information is carried by fast A-delta fibres within the lateral system. The areas that are reached are the cortical areas (primary somatosensory cortex) and can easily discriminate location and make sense of pain sensations.

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11
Q

Describe the pain gate theory.

A

Physiologically, the pain gate theory is the interaction between mechanosensory and nociceptive pathways. They act in opposite ways on the inhibitory neuron. For example, the the mechanoreceptor turns on the inhibitory neuron to bring down neuronal excitability (less pain, rubbing injury better), and the nociceptor turns this inhibition off to allow the signal to flow through the 2nd order neuron to turn up excitability to understand the pain when it first occurs e.g., when you first hurt yourself. However, psychological differences impact the gate theory too.

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12
Q

Describe the process of peripheral sensitisation.

A

This occurs at the 1st order sensory neuron, so the presynaptic neurons are sensitised. If there is continuous/inflammatory damage, substance P is produced which causes vasodilation, causing more symptoms of inflammation. In a positive feedback loop manner, mast cells and histamine are activated/released which activate free nerve endings to send up larger signals to the CNS. The longer the damage/inflammation persists, everything described above will continue to amplify.

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13
Q

Describe the process of central sensitisation.

A

This occurs at the 2nd order sensory neuron, so the post-synaptic neurons are sensitised. Within the dorsal horn of the spinal cord, after glutamate is released across the chemical synapse, NMDA and AMPA receptors are activated depending on the type of stimulation. AMPA receptors are activated if there is transient stimulation, and sodium voltage-gated channels are activated, and NMDA receptors are activated if there is strong stimulation, where calcium voltage-gated channels are activated. Information is sent through the spinothalamic tract, and this is the same process for memory, and how acute pain can develop into chronic pain.

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14
Q

Outline some real world applications of pain gate theory.

A

The overall application to relieve pain is by rubbing it better. This could be with hands such as a massage, but also, the use of a tens machine and acupunture. C-fibres can be activated by light stroking, providing relieving sensations and changes in brain activity that are similar to topical anaesthetic.

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15
Q

Describe the descending modulatory pain pathways.

A

There are two main pathways. The serotonergic pathway releases serotonin, starting from the periaqueductal grey and moving to the medulla and then the dorsal horn. The noradrenergic pathway releases noradrenaline/norepinephrine from the pons, through the medulla, into the dorsal horn. Both pathways activate the inhibitory neuron containing/releasing enkephalin to close the pain gate/relieve pain.

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16
Q

Describe the difference between pain perception and nociception.

A

While nociception refers to neural encoding of impending or actual tissue damage (i.e., noxious stimulation), pain refers to the subjective experience of actual or impending harm.

17
Q

Define nociception.

A

The neural process of encoding noxious stimuli.

18
Q

Define a nociceptor.

A

A sensory receptor that response to pain/tissue damage.

19
Q

Outline the role of free nerve endings in the reception of painful stimuli.

A

They are functionally used to detect potentially damaging chemical, mechanical and thermal stimuli which activate a number of receptors that are inflammatory mediators (substance P, prostaglandin, histamine) in order to activate and sensitise the free nerve endings. If the damage is significant enough, action potentials will be sent up the spinothalamic tract.

20
Q

Why is pain an important sensory modality?

A

Pain is very important because it is an early warning system to danger, potential or actual harm to tissues. It elicits changes in behaviour, it alerts you when your body is being damaged and it helps to avoid and prevent danger/harm.