Pain Flashcards

1
Q

What are the different responses to pain?

A

Autonomic - increased heart rate, pupil dilation
Somatic - eg withdrawal from pain source
Endocrine - eg cortisol from adrenal glands
Emotional

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2
Q

What is meant by pain being subjective?

A

It affects thinking and behavioural processes eg response to pain

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3
Q

What can pain, in general, be modified by?

A

Experience
Expectation
Immediate context ef playing sport, won’t feel pain as much

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4
Q

What is the difference between pain threshold and tolerance?

A

Stimulus threshold is the same in everybody - the amount of sensation required to feel pain

Tolerance is our variable reaction to a pain stimulus

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5
Q

What can affect pain tolerance?

A
Environmental situation
Physiological or emotional factors
Age
Ongoing pain
Placebo effect
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6
Q

What is nociception?

A

The non-conscious neural traffic originating with trauma or potential trauma to tissue

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7
Q

What are the stages of nociception?

A

Transduction - activation of nociceptors by a stimulus

Transmission - relay of action potentials along nociceptive fibres to the CNS

Modulation - by other peripheral nerve or CNS mechanisms

Perception - interpretation of the brain of the sensation as painful

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8
Q

What are nociceptors?

A

Specialised receptors for painful stimuli

They are free nerve endings

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9
Q

What are the types of nociceptors and what do they respond to?

A

Aδ: mechanical stimuli eg cut to skin

C fibres: respond to mechanical, thermal and chemical stimuli

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10
Q

What activates a nociceptor?

A

Cell damage which increases potassium, prostaglandin, serotonin and bradykinin levels to activate the nociceptor

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11
Q

What happens when a nociceptor is activated?

A

Depolarises the membrane over the threshold allowing generation of an action potential
Substance P is released by nociceptors

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12
Q

What does substance P do?

A

Increases capillary permeability

Contributes to inflammation by causing mast cells to release histamine - makes the receptor even more sensitive to stimuli as a protective mechanism to avoid further damage

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13
Q

How can analgesics have an effect at the site of injury and give examples

A

Reduce inflammation

  • NSAIDs which are COX inhibitors
  • steroids
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14
Q

Differences between Aδ and C fibres?

  • type of pain
  • localisation
  • threshold
  • purpose
  • velocity
A

Aδ: sharp and stabbing
C: dull, throbbing

Aδ well localised, C is poorly and often does visceral organ pain

Aδ fibres have lower threshold

Aδ: initiates withdrawal reflex
C: shows that tissue damage is occurring

Aδ: myelinated and small so conduction velocity is quicker

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15
Q

Which tract does pain travel up?

A

Lateral spinothalamic tract

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16
Q

What is analgesia?

A

The inability to perceive pain when tissue damage is occurring

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17
Q

How can analgesia be induced?

A
Drugs
Hypnosis
TENS (transcutaneous electrical nerve stimulation)
Natural childbirth techniques
Placebos
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18
Q

How does the body naturally ‘close the gate’ in pain?

A

Descending inhibitory neurones inhibit laminae I and V directly and indirectly (via SG) by using endogenous opioids and other neurotransmitters.

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19
Q

Name some endogenous analgesics

A

Enkephalins
Endorphins
Dynorphins
Endomorphins

20
Q

What are the opiate receptors?

A

μ mop
δ dop
κ kop
Nociceptin

21
Q

What are some antagonists of opiate receptors?

A

Naloxone

22
Q

What are some agonists of opiate receptors?

A

Morphine
Codeine
Heroin

23
Q

How do local anaesthetics work?

A

Inhibit voltage-dependent sodium channel activity which stops transmission to the CNS
Sit inside sodium channels, stopping transmission of the action potential and stabilising the membrane

24
Q

What do thalamocortical projections carry?

A

Information on location, intensity and nature of pain

25
Q

Via which system is the emotional response to pain?

A

The limbic system

26
Q

What does the stress response to pain travel via?

A

The hypothalamus

27
Q

Where does the lateral spinothalamic tract decussate? Where does it travel?

A

At the level of the spinal cord it enters

Up through the midbrain and thalamus to the post-central gyrus of the cerebral cortex

28
Q

Where do Aδ and C fibres enter the spinal cord?

A

At the apex of the dorsal horn

29
Q

Which fibres go through the substantia gelatinosa?

A

C fibres

30
Q

What do visceral fibres do when they enter the spinal cord and what is the consequence?

A

Visceral fibres coverage on the spinal cord second order neurones shared by somatic nociceptive fibres and feel the pain in that dermatome

31
Q

Which neurotransmitters are involved in the transmission of pain through the spinal cord?

A

Glutamate and substance P which excite second order neurones

32
Q

Where are opiate receptors found?

A

On terminals of the central processes of first-order nociceptive dorsal root ganglion neurones (pre-synaptic opiate receptors)

On dendrites of second order spinothalamic neurones (post-synaptic)

33
Q

What analgesics can be used in morphine-tolerant patients?

A

Baclofen (GABA) antagonist
Anti-depressants
Anti-convulsants

Somatostatin

34
Q

What is pain?

A

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

35
Q

What is the difference between the direct and indirect pathway of pain?

A

Direct is the main pain pathway

Indirect is the pathway involved in the affective aspect of pain ie the response. It is much slower

36
Q

What are the four main pathways involved in the indirect pathway?

A

Spinoreticular: arousal and wakefulness

Spinomesencephalic: activation of descending inhibition and emotional

Spinotectal: reflexes of eyes, upper body and head

Spinohypothalamic: autonomic and endocrine responses

37
Q

What happens to pain fibres when they enter spinal cord?

A

Enter laminae I, II and V

I and V synapse with second-order neurones

Fibres in II (the substantia gelatinosa) will be involved in modulation of the pain stimulus

They then decussate to other side

38
Q

Where do pain fibres of the face go?

A

They enter the trigeminothalamic system

39
Q

How is pain modulated by the substantia gelatinosa?

A

Acts negatively on laminae I and V to inhibit nociceptive impulses

40
Q

How can the effect of the substantia gelatinosa itself be modulated?

A

Aδ and C fibres can act on the SG to inhibit its inhibitory signal on I and V, resulting in positive effect of the pain impulse

Mechanoreceptors, via Aβ fibres, can increase its inhibitory effect, so rubbing the damaged area can reduce the pain felt

41
Q

Where do the descending inhibitory neurones arise from?

Where do they receive their stimulus from?

A

Periaqueductal grey matter (PAG) of the brain

Stimulated by the cortex and hypothalamus

42
Q

How does the PAG activate inhibitory neurones?

A

PAG consists of cells sensitive to opioid neuropeptides and stimulation of this area will have an analgesic effect

PAG stimulates the nucleus raphe magnus, sending inhibitory neurones down to laminae I and V

43
Q

What is a mixed nerve?

A

Contains a variety of different nerve fibres, which can vary in diameter, myelinated or demyelinated, different modalities

44
Q

What does a compound action potential show and how?

A

The different nerves present in a mixed cell by showing the varying conduction speeds

Fastest nerves appear in A waves (larger or myelinated or both)
C wave is smaller, unmyelinated neurones

45
Q

What can a compound action potential be used to highlight?

A

Conditions such as MS where there is demyelination of neurones, affecting their conduction velocities