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147 - Exercise for health > Week 10 - Anatomy and Physiology and Pain > Flashcards

Week 10 - Anatomy and Physiology and Pain Flashcards

1
Q

What is 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

Why is pain important?

A
  • Necessary
  • Warning system
  • Symptom of injury or disease
  • Complex
  • Subjective/personal experience
  • Sensory experience (physical)
  • Emotional experience (psychological)
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3
Q

What is a noxious stimuli?

A

A stimulus that is actually or potentially damaging to tissue (Thermal/Mechanical/Chemical)

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4
Q

What is a pain perception threshold?

A

The minimum intensity of noxious stimulation that must be reached prior to pain being felt.

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5
Q

What is pain tolerance level?

A

The maximum amount of pain an individual can tolerate.

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6
Q

What is analgesia?

A

Lessening or absence of pain in response to a painful stimulus.

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7
Q

Hyperalgesia definition?

A

Increased sensitivity and response to a painful stimulus.

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8
Q

Hypoalgesia definition?

A

Decreased sensitivity to a painful stimulus.

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9
Q

Allodynia definition?

A

Pain resulting from a stimulus that would not usually provoke pain.
e.g. light touch applied to the skin

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10
Q

What is nociception?

A

The process by which information is conveyed to the Central Nervous System (CNS) as a result of the stimulation of specialised sensory receptors in the peripheral nervous system (PNS).

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11
Q

What are nociceptors?

A

Free nerve endings located throughout the body, which are sensitive to tissue trauma and detect potentially damaging noxious stimuli, ultimately leading to the sensation of pain.

When nociceptors are stimulated, they send information about the pain to the spinal cord and then the brain.

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12
Q

Where are nociceptors located in the body?

A

In the skin, bones, muscles, connective tissue, blood and viscera (internal organs).

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13
Q

Key points about nociceptive pain?

A
  • Normal, warning response to tissue damage.
  • Pain corresponds to the extent or severity of the tissue trauma or injury.
  • Fast, rapid onset, sudden sharp, pricking pain. Followed by a dull, aching or burning pain (depending on the stimulus responsible).
  • Acute or sub-acute (short-term).
  • Results from a specific injury.
  • Pain will resolve but can be recurrent.
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14
Q

What is acute/sub-acute pain?

A

Short-term pain and therefore persists for less than 3 months in duration.

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14
Q

What is chronic pain?

A

Pain persists for more than 6 months.
(nociceptive pain resolves)

Chronic pain no longer related to initial tissue injury.

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15
Q

What 3 types of noxious stimuli do nociceptors respond to?

A

THERMAL
MECHANICAL
CHEMICAL

When these stimuli exceed their normal parameters, causing rapid increased firing of these sensory receptors, that we begin to experience pain.

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16
Q

Examples of thermal stimuli?

A

Placing your hand under a very hot water tap
Accidentally grabbing a very hot panhandle

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17
Q

Examples of mechanical stimuli?

A

Tissues overstretched or under strain or pressure from a force.

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18
Q

Examples of chemical stimuli?

A

Experience pH changes at the site of injury.

As a result of the chemicals that are released during the local inflammatory process.

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19
Q

What is important to note about nociceptors?

A

Some are polymodal and respond to more than one of these stimuli.

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20
Q

What are the 3 main types of nociceptors?

A

1) High-threshold Aδ mechanosensitive mechanoreceptors: Respond to intense mechanical deformation:
- Type I A delta

2) Aδ mechanothermal nociceptors: Respond to intense heat stimuli
- Type II A delta

3) Polymodal nociceptors (PMN): Respond to a variety of tissue-damaging inputs:
- C fibre
- Noxious: Mechanical, thermal, chemical

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21
Q

What are mechanothermal nociceptors responsible for and structure?

A

→ Tend to initiate the protective reflex response to pain e.g. rapidly moving hand from hot pan handle.

→ Fast transmitting, small diameter myelinated nerve fibres

→ Produce the fast well-localised pain associated. with acute injury. e.g. sharp, stabbing pain if you stubbed toe.

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22
Q

What are the polymodal C nociceptors responsible for and structure?

A

→ Smaller, unmyelinated fibres - therefore slower in their transmission.
→ Tend to produce slow, poorly localised pain
→ Typically originate in fat layers of skin, muscles and joints
→ Respond to a wide variety of high-intensity noxious stimuli (mechanical, thermal and chemical)
→ Throbbing or burning pain that persists after initial tissue injury - pain is dull and lasts longer than the initial first pain.

23
Q

What is a key note about the polymodal C nociceptors ?

A

More likely to be effected by emotions or by the automatic nervous system as the pain persists for longer.

24
Q

Where are alpha delta fibres found?

A

In the Laminae I & V of Dorsal horn

25
Q

Where are C-fibres located?

A

Lamina II of Dorsal Horn (Substantia Gelatinosa)

26
Q

What are the 4 phases of nociceptive pain?

A
  1. Transduction (Ascending pathway)
  2. Transmission (Ascending pathway)
  3. Perception (Ascending pathway)
  4. Modulation (Descending pathway)

referred to as pain matrix

27
Q

What do the first 3 stages involve?

A

Ascending pathways where the pain signal coming from the site of injury travels up to the brain and the pain is perceived.

28
Q

What does the final stage of pain modulation represent?

A

The descending pathways

29
Q

What is the process leading up to transduction?

A
  • Noxious stimulus resulting in tissue damage
  • Chemical mediators released (substance P, Bradykinin, serotonin, histamine and PROSTAGLANDINS)
  • Nociceptors activated (all over body)
  • Leads to transduction
30
Q

Why are prostaglandins of most importance in ascending pathway?

A

Produced by nearly all cells, typically as a response to inflammation.

31
Q

What is transduction?

A

Generation of an action potential where a chemical signal is converted into an electrical signal.

This AP is then transmitted along afferent peripheral nerve fibres via first-order neurons from the site of injury to the dorsal horn of the spinal cord.

Additional second order nociceptors and are waiting to receive signal

32
Q

Relation of Dorsal horn to primary nociceptive Aδ and C fibres?

A

The dorsal horn is where the primary nociceptive Aδ (lamina I) and C fibres (lamina II) terminate and release chemicals.

  • Substance P released in order to synapse with the second-order afferent neurons.
33
Q

What happens to A delta fibres after they synapse with second-order neurons?

A

Many cross the midline at the spinal cord and then travel up the spinothalamic tract towards the brain.

As they ascend they reach the midbrain of the brainstem where some fibres branch into periaqueductal gray matter however most will continue on to the thalamus.

TRANSMISSION (2)

34
Q

What is the periaqueductal gray matter responsible for?

A
  • Integration of behavioural responses to pain.
  • Key structure involved in the modulation of pain
35
Q

What occurs once the A delta fibres have reached the thalamus?

A

These second-order neurons will synapse with a third order neuron which then projects the signal onwards to the somatosensory cortex in the parietal lobe.

This determines the location, intensity and quality of pain.

At this point, pain is perceievd.
PERCEPTION (3)

36
Q

What happens to C-fibres after they terminate in the dorsal horn (lamina II)?

A

Synapse with an interneuron which transmits the signal across to lamina V(5) .

Upon synapsing, the second order neuron travels across midline of spinal cord, transmits signal to brainstem but via spinoreticular tract.

37
Q

What happens to C fibres after going up the spinoreticular tract?

A

Fibres then terminate in one of 2 areas:
- reticular formation of brainstem
- thalamus → different part to where A delta fibres terminated

38
Q

What is the reticular formation responsible for?

A
  • Consciousness and sleep/wake cycles
  • Stimulated by projections from the ascending tracts
  • Explains why we may not sleep if we are in pain
  • Also sends descending signals to help control pain
  • Closely related to limbic system
39
Q

What happens to C fibres if they reach the thalamus?

A
  • Synapse with a third-order neuron
  • Projects to frontal lobe instead of parietal
  • This area concerned with psychosocial aspects of pain and emotions that pain evokes.
40
Q

What happens once A delta fibres have reached somatosensory cortex?

A

Triggers descending pain modulation pathway

41
Q

What areas in brainstem are involved in pain modulation?

A

Periaqueductal gray matter of midbrain - receives signals from thalamus, hypothalamus and cortex - processes nocioceptive info and relays it to rostral ventromedial medulla

Rostral ventromedial medulla (Nucleus raphe) - synapses with second order neuron (serotonergic noradrenergic neuron) - sends signal down to dorsal horn

41
Q

What is the goal of modulation (4)?

A

To respond to the pain source by reducing/altering the pain signal through neuronal inhibition of this ascending pathway.

42
Q

What does the second order neuron do once it reaches the dorsal horn?

A

Inhibit/control communication between first and second-order neurons of ascending pathways to control pain signals travelling up towards brain.

In dorsal horn: synapse with third-order neurons and release serotonin and noradrenaline.

43
Q

What do serotonin and noradrenaline do?

A

→ They bind on to the receptors of the first order neuron in ascending pathway - inhibits release of substance P - meaning it cannot then synapse with second order neuron.

→ They stimulate the inhibitory interneurons at the substantia gelatinosa (within lamina of dorsal horn) to release endogenous opioids which will inhibit pre-synaptic neuron from releasing substance P and thus no action potential is sent.

This prevents the continuation of the impulse up to the thalamus via the ascending pathway.

44
Q

What is the pain gate theory?

A

Hypothetical gateway in the spinal cord, which helps to control pain.

Suggests pain can be modulated at level of spinal cord, by not only descending signals but also non painful inputs which will typically close the gate to painful stim, inhibiting the ascending pathways.

45
Q

Where is the pain gate mechanism thought to take place?

A

In the substantia gelatinosa of the dorsal horn and spinal cord.

46
Q

When may the pain gate be open?

A

When activated in response to normal noxious stimuli, nociceptors stimulate the first, then second order neurons and at the same time, through the release of chemicals, impede the inhibitory interneurons in SG thus opening pain gate and allowing for pain transmission onwards.

47
Q

How can the pain gate be closed?

A

If the site of the injury is also subsequently stimulated by additional non-noxious stimuli such as touch or pressure, a different type of nerve fibre is activated (Large diameter A beta fibres).

Reactivate the inhibitory interneurons in SG to release encephalon, blocking the release of substance P, stopping or reducing the transmission of pain signals.

48
Q

Why do tens machines help to close the pain gate?

A
  • Electrical signals to skin
  • Trigger non-nociceptive A beta fibres
  • These fibres travel from site of application to the dorsal horn and activate the inhibitory interneurons, helping to close the pain gate.
49
Q

Factors that may influence individual differences in pain?

A
  • Duration and intensity of the noxious stimulus
  • Biopsychosocial implications which may be present at the time
50
Q

Two types of sensitisation?

A
  1. Peripheral sensitisation
  2. Central sensitisation
50
Q

What is peripheral sensitisation?

A
  • normal acute inflammatory response
    acting as a protective process
  • prolonged noxious stimuli sensitise first order nociceptors making them more
    excitable
  • lower threshold for activation ; activate more easily
  • hypersensitivity to non-noxious, not normally painful stimuli (Alloydnia) e.g. touching arm
  • if prolonged, can lead to abnormal pain state
51
Q

What is central sensitisation?

A
  • Basis for chronic pain
  • Increased sensitivity of the CNS, relative to the presence and intensity of noxious peripheral stimuli
  • Hyperalgesia
  • Pain outlives pathology
  • Pain perceives more tissue damage than there is
  • Physiological changes to CNS; repeated stimulation of C fibres→gradually increases the frequency of the dorsal horn neuron firing → lowers the threshold for activation → amplification of our response to a stimulus → increased sensitivity

Explains pain may not be pathological, but a result of physiological changes in CNS, explaining pain long after physiological effects at tissue have been resolved.

52
Q

What is exercise-induced hypoalgesia (EIH)

A
  • One form of endogenous pain modulatory processes
  • EIH dependent on multiple analgesic mechanisms that contribute to changes in pain sensitivity
  • Endogenous opiod system (descending pathways) is triggered by exercise induced cardiovascular changes in HR and BP
  • Exercise thought to stimulate the release of beta-endorphins from pituitary gland and hypothalamus, subsequently triggering the endogenous opioid system.
  • Hypothalamus projects onwards to periaqueductal gray matter resulting in further endogenous analgesic effects
52
Q

Challenges of using exercise to modulate pain?

A
  • Understanding the parameters of therapeutic exercise for pain relief e.g. mode, frequency, duration, intensity
  • Ability to modify exercise parameters to take into account patient factors e.g. age, condition, pain levels, health status, biopsychosocial factors
  • Additional barriers/considerations e.g. fear avoidance, catastrophising, CBT
  • Patient education
  • Motivation
53
Q
A

147 - Exercise for health (8 decks)

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