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AHMB1 > 10: Pain > Flashcards

10: Pain Flashcards

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1
Q

Define pain.

A

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage

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2
Q

How does pain lead to modification of behaviour?

A

Pain signals can drive rapid spinal withdrawal reflexes
Activates higher centres in the brain that cause an unpleasant sensation and dominate attention

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3
Q

What are nociceptors?

A

Specialised sensory receptors that detect signals from damaged tissue or potential tissue damage

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4
Q

What are primary afferent fibres?

A

Nerve fibres that carry sensory information from receptors into the central nervous system. These are the first neurones in the sensory pathway and transmit signals like pain and temperature

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5
Q

What are action potentials?

A

Rapid, temporary changes in the electrical charge across a cell’s membrane that allow neurones and muscle cells to send signals

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6
Q

Why does increased myelination of a nerve fibre increase transmission speed of action potentials?

A

Because myelin is an insulating layer around the axon and prevents ion leakage and allows electrical signals to move more efficiently
Myelination enables saltatory conduction, where one action potential jumps from one node of Ranvier to the next, instead of travelling continuously along the axon, which is must faster than a smooth propagation

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7
Q

What are the three times of primary afferent fibre?

A

Aβ, Aδ, C

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8
Q

Compare the three types of primary afferent fibre.

A

Aβ
Large diameter
Heavily myelinated
Carries non-painful info (e.g. touch)
Fastest transmission speed

Aδ
Intermediate diameter
Light myelination
Carry pain and temperature information
Intermediate transmission speed
Fast, sharp pain

C
Narrow diameter
Unmyelinated
Carries temperature, pain, and itch sensations
Slowest transmission speed
Slow, dull pain

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9
Q

Describe the nerve endings that detect pain and compare them to those that detect touch.

A

Pain nerve endings:
Free nerve endings
Branch in the epidermal layer of the skin

Touch nerve endings:
Found deeper in the dermis, associated with particular receptor structures (i.e. corpuscles)

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10
Q

What is sensory transduction?

A

Mechanical, thermal, and chemical stimuli converted into electrical signals

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11
Q

What do TRPV1 receptors respond to?

A

Heat
Environmental irritants (nicotine)

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12
Q

What do TRPV2 receptors respond to?

A

Heat

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13
Q

What do TRPM8 receptors respond to?

A

Cold

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14
Q

What do TRPA1 receptors respond to?

A

Irritants

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15
Q

What do ASIC receptors respond to?

A

Acidic irritants

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16
Q

What is capsaicin?

A

A chemical found in chillis that activates the noxious heat receptor TRPV1
This is why spicy foods cause a burning sensation

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17
Q

What is menthol?

A

A compound found in mint plants that activates the TRPM8 cold receptor, which is why toothpaste is cooling

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18
Q

How do transducer receptors (e.g. TRPV1 and TRPV2) generate signals?

A

Transducer receptors are ion channels
When activated they cause an influx of ions into the nerve ending, causing a generator potential
If the generator potential is sufficient, it triggers an action potential which can be transmitted all the way along the nerve process to the spinal cord
Stronger stimulus = stronger action potential

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19
Q

Describe the pathway of a pain signal to the spinal cord.

A

Pain signal is interpreted via the free nerve endings of nociceptors in the epidermal layer of the skin
Primary afferent fibres transmit the signal (usually Aδ or C fibres) to the spinal cord
Signals enter through the dorsal root of the spinal cord
The fibres synapse with dorsal horn neurones

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20
Q

What happens when an action potential reaches the dorsal horn synapse?

A

Nociceptor endings contain glutamate (neurotransmitter) as well as neuropeptides
Dorsal horn neurone has different receptors for glutamate and neuropeptides
When an action potential reaches the nociceptor ending before the synapse, it drives a release of glutamate and neuropeptides
These diffuse across the synaptic cleft and activate receptors on the spinal cord neurone

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21
Q

What are local excitatory neurones?

A

These are neurones that receive pain signals from primary afferent fibres, amplify and spread the signal to increase the pain response locally within the spinal cord

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22
Q

What are local inhibitory neurones?

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A

Inhibitory neurones suppress the pain signals from primary afferent fibres by releasing inhibitory neurotransmitters and dampening the activity of excitatory neurones to reduce pain information passed to the brain

23
Q

Describe the ascending pain pathways.

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A

Aδ and C fibres carry the pain signal to the spinal cord
Some projections target the thalamus, then project to the somatosensory cortex, which helps process location and intensity of pain
Other projections may target the parabrachial nucleus, leading to amygdala, insular and cingulate cortex, important for emotional aspects of pain

24
Q

Describe the descending pain pathways

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A

Pariaqueductal gray (PAG) and rostral ventromedial medulla (RVM) in the brainstem send projections down to the spinal cord
These pathways involve neurotransmitters like serotonin and noradrenaline which can amplify or inhibit pain signals

25
What is congenital analgesia?
A condition in which patients are born without the ability to sense pain Individuals can suffer serious injuries and infections Often leads to fatality at young ages
26
What mutation causes congenital analgesia?
The SCN9A gene: encodes a sodium ion channel required to amplify generator potentials to the threshold necessary for an action potential SCN9A mutation makes the ion channel non-functional Therefore pain signals cannot be transmitted to the spinal cord and brain
27
How can expectations influence pain?
Cognitive factors such as expectations can influence pain by acting on the prefrontal cortex which then communicates to pain-related brain regions, modulating pain perception by activating the descending pain modulatory system
28
What is hyperalgesia?
When a painful stimulus is exaggerated
29
What is allodynia?
When a non-painful stimulus is perceived as painful
30
What is chronic pain?
Persistent pain beyond injury, causes the pain pathways to become sensitised, leading to an amplified pain response Characterised by hyperalgesia, allodynia, and spontaneous pain Can result following tissue damage (inflammatory pain) or nerve damage (neuropathic pain)
31
What are the two types of pain?
Inflammatory Neuropathic
32
Describe inflammatory pain.
Results from tissue damage/infection Promotes recovery by limiting contact with damaged peripheral tissue and therefore reducing change of further infection
33
Describe neuropathic pain.
Results from nerve damage Symptoms provide no positive role as there is no peripheral injured tissue to protect or repair
34
What is peripheral sensitisation?
A decrease in the threshold for activation and enhanced response to a given stimulus Means that a receptor is more receptive to a stimulus and will generate a larger response
35
What is central sensitisation?
Enhanced sensory input increases local excitatory control, decreases local inhibitory control, and a change in descending control fromt he brain Results in easier activation of motor outputs and reflexes and increased signals in ascending pathways
36
What is peripheral sensitisation?
A process by which nociceptors in the peripheral tissues (i.e. skin, muscles, organs) become more sensitive to stimuli and increase pain perception Occurs when inflammatory mediators such as bradykinin and serotonin are released at the site of injury and make nociceptors more responsive
by causing post-transcriptional and translational changes Peripheral sensitisation can cause hyperalgesia
37
What is central sensitisation?
A process by which the CNS becomes hyper-responsive to stimuli leading to increased pain sensitivity Occurs when nociceptors in the spinal cord and brain become overactive Causes allodynia Long-term pain can lead to central sensitisation where the pain threshold is lowered
38
What is an NSAID?
Non-steroidal anti-inflammatory drug E.g. aspirin, paracetamol, ibuprofen
39
What are opioids?
Pain-relieving drugs that work by binding to receptors in the brain, spinal cord, and other areas Work to block pain signals and alter perception of pain
40
Describe how opioids limit pain response.
Opioids bind to opioid receptors on the central terminals of nociceptors and on spinal cord neurones If receptors are activated on the central terminal of the nociceptor, causes reduction in neurotransmitter release If receptors are activated on the spinal cord neurones, reduces sensitivity to pain input (causes both pre-synaptic and post-synaptic inhibition)
41
How do opioids promote descending inhibition of pain?
Opioids act on the pariaqueductal gray (PAG) and rostral ventromedial medulla (RVM) These areas are at the origin of descending modulation pathways Opioids act on them to increase release of serotonin and noradrenaline
42
Are opioids better for inflammatory or neuropathic pain?
Inflammatory pain
43
What are some side effects of opioids?
Confusion, sedation, lethargy, addiction, tolerance, and dependence
44
How do NSAIDs limit pain?
NSAIDs act as inhibitors to Cox1 and Cox2 Prevents production of PGH2, and therefore prevents production of prostaglandin E2, which normally acts on receptors on pain nerve endings and drives intra-cellular signalling to promote inflammatory hyperalgesia Prostaglandin E2 inhibition increases pain inhibition in the spinal cord
45
Give two examples of anti-depressants.
Tri-cyclic antidepressants (TCAs) Serotonin-noradrenaline reuptake inhibitors (SNRIs)
46
How do SNRIs worK?
Inhibit reuptake of serotonin and noradrenaline back through the presynaptic neurone This increases the concentration of serotonin and noradrenaline in the synaptic cleft, enhancing their effects on post-synaptic receptors This helps to improve moods and manage pain
47
How do TCAs work?
Similarly to SNRis, they block serotonin and noradrenaline reuptake into presynaptic neurones This increases availability of neurotransmitter in the presynaptic neurones to improve mood and alleviate depression Unlike SNRis, TCAs block variety of other receptors: e.g. histamine and alpha-adrenergic receptors
48
How do anticonvulsants work?
They modulate ion channels to reduce likelihood of excessive firing (e.g. increasing activity of voltage gated calcium channels) Some enhance the effects of GABA to decrease neuronal excitability Block glutamate receptors, further inhibiting excitatory signalling
49
How do local anesthetics work?
Blocking voltage-gated Na+ channels Limits action potentials
50
How do NMDA receptor antagonists limit pain?
NMDA antagonists block NMDA receptors which are involved in central sensitisation and pain amplification By inhibiting calcium influx, they prevent the activation of PKC and CaMK2 kinases Reduces phosphorylation of NMDA receptors and therefore reduces their activity Prevents pain amplification
51
What are some examples of psychological therapies and how do they limit pain?
Assessment and formulation by a clinical psychologist Aiming to foster self-management using a range of techniques:
Cognitive behavioural therapy (CBT)
Motivational interviewing Relaxation/meditation/hypnotherapy Interpersonal therapy Acceptance and commitment therapy (ACT) Cognitive factors may activate the prefrontal cortex to promote descending pain inhibition
52
Why is it difficult to treat chronic pain?
Relies on subjective self-reporting Often using visual or numerical pain scales
53
Describe the pathway of translational pain research.
Chronic pain model -> helps to understand neurobiological mechanisms --> identify potential targets --> assess target utility in behavioural studies of chronic pain --> clinical trials
54
Why do so many chronic pain drugs fail at the clinical trial stage?
Labs focus on surgical nerve injury model rather than clinical disease model Pain assessment can differ between lab and clinic Sex differences in pain sensitivity and analgesic sensitivity Increasing evidence for sex differences in pain mechanisms

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