Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 BB > 7. Anatomy and physiology of pain > Flashcards

7. Anatomy and physiology of pain Flashcards

1
Q

Define pain

A

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

Pain is a perception - not always associated with tissue damaging stimuli

“It is what the patient says it is” - open to interpretation due to different levels of pain thresholds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the four different mechanisms of pain?

A

Transduction - noxious stimuli translated into action potentials
Transmission - action potentials propagate along pain pathways
Perception - discrimination of the type of pain
Modulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a nociceptor?

A

A primary afferent i.e. a sensory receptor for painful stimuli
Brings informtion to the nervous system from peripheral axons in the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the different types of axons in the nociceptive system?

A

C fibres - unmyelinated - slow conducting (<1m/s-5m/s)

A delta fibres - very thin myelinating fibres - fast conducting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain the idea of first pain and second pain

A

E.g. touching a hot stove
First pain - transmitted via the a delta fibres - fast response to the pain to allow you to move your hand away from the hot stove
Second pain - slower response - more visceral, intense, emotional pain - the burning of your hand a while after touching the stove

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is transduction in the nociceptive system?

A

The transmission of pain sensation to action potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does transduction occur from noxious stimuli?

A

Nociceptors have free nerve endings within the tissues i.e. are not surrounded by capsules
Within the terminals, there are different ion channels which open in response to different stimuli e.g. TRPV1 opens in response to noxious heat and thermal stimuli and TRPM8 in response to cold stimuli

The stimuli must first reach the threshold before an action potential can be generated and reach the spinal cord - graded stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which fibres are damaged in diabetic neuropathy and how does this result in the symptoms of the disease?

A

C-fibres are damaged
There is no impulse to move the legs during e.g. sleep when uncomfortable
This can result in pressure sores, gangrenes, loss of blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the two main classes of C-fibres and how do they differ?

A
  1. Peptidergic c-fibres
    These release peptides peripherally and centrally
    Promote inflammation in the peripheral release - increased inflammatory cells to aid clear up of injury
  2. Peptide-poor c-fibres
    Have distinct receptors to allow the release of ATP into the injured skin
    More involved in mechanical stimuli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

To which lamina do the nociceptor fibres project to?

A

C fibres project to lamina I and II (and V)
A delta fibres project to lamina I and V

Lamina I - where all nociceptors project to
Lamina II - where interneurones are found (can be excitatory or inhibitory)
Lamina V - mixing of information occurs here - not just from nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where does the spinothalamic tract project to to mediate the majority of the sensation of pain?

A

Projects to the limbic system of the forebrain via the brainstem and the posterior medial thalamus

Nb. the pain also stimulates general arousal and focussing of attention on the painful region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are projection neurones?

A

These are second order neurones - carry the pain message onward from the primary afferent neurone
These decussate close to where the nociceptors enter the spinal cord and form the spinothalamic tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the two parts of the spinothalamic tract?

A

Anterior spinothalamic tract

Lateral spinothalamic tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the function of the anterior spinothalamic tract?

A

The anterior spinothalamic tract is the one carrying the majority of the adelta neurones going to lamina V

Innervates the ventral posterior lateral (VPL) and the ventral posterior medial (VPM) (these are nuclei of the somatosensory thalamus) i.e. the lateral portion of the thalamus
VPL is very important for touch stimuli

Conveys first, discriminative aspects of pain e.g. ‘move hand’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the function of the lateral spinothalamic tract?

A

This is the tract carrying the majority of the c fibres (also carries some a delta fibres) and these mainly project to lamina I

Innervates the more posterior/medial parts of the thalamus and also some part of the cortex

Conveys second, punishing aspects of pain e.g. ‘ouch, that hurts!’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the amygdala?

A

This is a region of the brain important for the memory of pain - the association of pain to a particular event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the difference between fast and slow pain?

A

Fast pain - sharp pain conveyed by adelta elicits reflexive withdrawal to prevent further injury
Slow pain - burning, lingering, emotionally changing pain

18
Q

How is our response to stimuli altered when there has been an injury and what is this known as?

A

When there has been an injury and slow pain has occurred, there is inflammation
This drops the threshold of pain of the nociceptors - something that was not painful in this region is now conveyed as painful

SO there is a reduced activation threshold and an increased responsiveness to the noxious stimuli

This is ‘Peripheral sensitisation’

19
Q

What are the four signs of inflammation?

How can the reduced threshold of pain be remediated?

A

Calor (heat)
Rubor (redness)
Dolor (pain)
Tumour (swelling)

Via anti-inflammatory drugs i.e. NSAIDs
These target prostaglandins

20
Q

What is central sensitisation?

A

This is where there is a prolonged nociceptor input to the CNS into the dorsal horn - the projection neurones become more active
The CNS is regulated in a persistent state of high reactivity
Low threshold pain stimuli can now activate the pain pathway

21
Q

What is the neurotransmitter involved in central sensitisation?

A

The nociceptor afferents release glutamate which acts of NMDA receptors - leads to changes in the secondary messenger systems and reduces the pain threshold due to increased excitation

22
Q

What are the hallmark presentations of sensitisation?

A

Hyperalgesia - increased sensitisation to noxious stimuli
Allodynia - increased sensitisation to all stimuli
Spontaneous pain

23
Q

How do peripheral sensitisation and central sensitisation differ to each other?

A

Peripheral - involves increased inflammation and nociceptors and sensory afferents
Central - involves nociceptive input into the dorsal horn and CNS and projection neurones - occurs due to peripheral tissue damage or inflammation

24
Q

What is chronic pain?

What is maladaptive pain?

A

Chronic pain arises from nociceptive pain and is adaptive, reversible and can heal
It is pain of more than 12 weeks usually associated with an underlying condition

Chronic pain can develop into maladaptive pain
This is a continued state of suffering - pain that persists past the healing phase following an injury

25
Q

What are the different types of maladaptive pain?

A

Neuropathic pain - due to injury/dysfunction in PNS or CNS
Dysfunctional pain - no known lesion or inflammation

NB. normal analgesics are not effective

26
Q

What causes maladaptive pain?

A

Anything that injures the CNS e.g. stroke, infection, drug treatments, diabetes

27
Q

What is pain modulation?

A

The modulation of the level of pain - whether the stimuli is perceived as more or less painful

28
Q

Where does pain modulation occur?

A

Occurs at all levels - cortex, brain/brainstem, spinal cord (central sensitisation), periphery (inflammation)

29
Q

What is endogenous modulation?

A

This is at the level of the spinal cord e.g. acupuncture
Some other input stimulus (innocuous) to the same area can dampen down the pain (like if you wack your hand and then rub it to make it feel better)
The innocuous pain would normally act to dampen down the pain transmission - this is known as the gate control theory

30
Q

Which neurones are responsible for pain modulation?

A

The interneurones located in lamina II

31
Q

How does acupuncture work as endogenous modulation?

A

Thought to activate adelta fibres via Diffuse Noxious Inhibitory Control (DNIC) of pain
Thought to work via the gate control theory

32
Q

What projections do neurones from the lateral spinothalamic tract have, other than to the cortex?

A

Has some extra projections:
Spinal circuitry - reflexes
Reticular formation - arousal and alerting cortex
Periaqueductal grey (PAG) in midbrain - descending pain modulation
Parabrachial nucleus in pons - limbic activation

33
Q

Briefly describe the periaqueductal grey (PAG) pathway?

A

This is one of the pain pathways which can result in the sensation of neuropathic pain
Via the usage of serotonin and noradrenaline

34
Q

What is the use of enkephaline in the PAG pathway?

A

The PAG contains enkephaline producing cells which suppresses pain

35
Q

What are enkephalines?

A

These are endogenous opioid peptides and these bind to opioid receptors

36
Q

How are prostaglandins produced in the body?

A

From arachidonic acid via COX-1 or COX-2

37
Q

When is COX-1 present in tissues?

A

Normally always present in the tissues at low levels

38
Q

When is COX-2 present in tissues?

A

COX-2 is induced during inflammation

39
Q

What is the role of prostaglandins on c-fibres?

A

PGs sensitise the c-fibres by increasing the numbers of other receptors and opening a greater number of these

40
Q

Which drugs target prostaglandins?

A

Analgesics

Anti-inflammatory drugs e.g. NSAIDs

41
Q

SO what is the role of prostaglandins in the body?

A

These are producing during times of pain/damage and these mediate inflammation

42
Q

What releases arachidonic acid?

A

Phospholipase A2

Year 2 BB (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions