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Pathophysiology of ill-health > Pain > Flashcards

Pain Flashcards

1
Q

British Pain Society 2018

Relevance - surveys?

Effective pain management founded on…? BPS 2018

A 
Repeated surveys within the UK and
Europe show poor management of pain
and there is plentiful evidence of the
personal and economic costs of acute
and chronic pain.

Effective pain management must be
founded on excellent pain education
(British Pain Society 2018)

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2
Q

British Pain Society 2018:

Undergraduate Healthcare Professional Should be able to…

A

Describe and critique commonly proposed theories of pain

Be aware of the main structures involved in pain transmission, transduction, perception and modulation

Understand the principles of the Gate Control Theory

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3
Q

What are the 5 x processed involved in pain

A

Transduction, Conduction, Transmission, Perception, Modulation

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4
Q

Widely accepted that the ability to assess pain is….

A

…the foundation of effective treatment

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5
Q

QAA - Quality Assurance Agency for Higher Education

A

Develop an understanding of a complex body
of knowledge, some of it at the current
boundaries of the discipline

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6
Q

McCaffrey (1968) - definition (seminal)

A

“Pain is whatever the person experiencing it says it is, existing whenever they say it does”

  • regularly quoted in the literature, from ‘Clinical Manual For Nursing Practice’ - McCaffrey, 1968
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7
Q

British Pain Society 2018 - definition of pain

A

Unpleasant Sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”

  • BPS 2018
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8
Q

Chronic Pain Def

A

Persistent pain which continues after healing or is the result of ongoing damage - chronic pain is recognised as a long term condition in its own right.

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9
Q

Acute Pain

A

Relates to pain occurring during tissue damage and repair for example during sudden illness, surgery, trauma and burns. The pain typically improves with tissue healing

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10
Q

3 x definitions ?

A

Pain, Chronic pain and Acute pain.

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11
Q

British Pain Society 2014 - relevance

How many Brits suffer pain daily resulting in ?

Add in more facts please rel. to MH

A

Approximately 10 million Britons suffer pain daily resulting in a major impact on their quality of life and more days off work

Consider Muscoskeletal injury in HC workers

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12
Q

The British Pain Society- relevance

How many people have chronic pain?

What %?

When in life stage?

A

8 Million people have chronic pain of moderate intensity. A further 6 million have chronic pain.

6-8% of the population have severe pain that prevents some or most activities.

Prevalence of chronic pain doubles over the age of 65

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13
Q

What is pain (for)?

A

Pain is a natural consequence of many situations of ill-health, normal processes e.g. traumatic injury, nociceptor mediated pain

Warning system - Protective - in attempt to prevent further injury

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14
Q

Physiologically

Amplitude =

What type of pain does this module cover?

What are afferent vs efferent nerves?

A

Nociceptor Mediated Pain

Amplitude relates to intensity

Afferent nerves encode aspects of stimulus

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15
Q

Types of pain?

Cutaneous
Somatic
Visceral
Referred Pain
Neuropathic Pain
A

Cutaneous - skin
Somatic - deeper connective tissue
Visceral - Internal Organs
Referred Pain - perceived as away from the site of origin
Neuropathic Pain - resulting from damage to nerves or nerve endings e.g. phantom limb pain

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16
Q

Rene Decartes - theory of pain?

A

Straight line channel from skin to brain

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17
Q

Von Frey - theory of pain?

A

Pain pathways move from specialised receptors in body tissue to a pain centre in the brain

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18
Q

Critique of pain theories generally?

A

A LOT of pain psychology and physiology remains a mystery

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19
Q

3 x physiological Causes:

A
  • Nociception (caused by actual or potential injury - covered in this module)
  • Inflammatory Pain (e.g. release inflam. mediators, those allow water in, can be experienced as pain)
  • Neuropathic pain (damage to nerves e.g. burns)
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20
Q

Ascending Pain Pathway - overview

A

Pain stimulus -> Nociceptor -> Spinal Cord -> Brain (via spinothalamic tract)

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21
Q

5 x classic stages

A 
Transduction
Conduction
Transmission
Modulation
Perception
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22
Q

Nervous System comprises of…

Central -?
Peripheral-?
Motor -?

A

Central -BRAIN AND SPINAL CORD
Peripheral- SENSORY AFFERENT NERVES
Motor - EFFERENT NERVES

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23
Q

Neurones - what do they do?

Dendrites -?
Cell body (soma) -?
Axon - ?

A

Dendrites - Receive info from the body
Cell body (soma) - Organises information
Axon - Transmit information to other parts of the NS

Where two nerves meet : synapse

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24
Q

Nociceptor pain - how is it triggered?

A

Any trauma e.g. a cut, biological hazard, bacterial/viral/parasitic infection, hypoxia, burn etc

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25
Q

Nociceptors - what are they?

A

Highly specialised primary sensory neurones mainly located in skin, joints and walls of organs

Contain special protein receptors within their membrane

Once stimulated by noxious stimuli, the protein receptors reshape to create ion channels causing ions to flow through stimulating an action potential

Noxious stimuli -> Action Potential

But ….

Cold receptors -> Pain
Heat Receptors -> Pain
Touch receptor -> Pain

26
Q
  1. Transduction
A

Nociceptor detects noxious stimuli - This is translated to electrical activity at the sensory endings of nerves.

This is done via the release of CHEMICAL MEDIATORYS from the damaged cells leading to an electrical impulse being fired off (action potential)

  • Mechanoreceptor - pinch and prick
  • Silent Nociceptors - inflammation
  • Polymodal mechanoheat receptors - heat / cold

& NOCICEPTORS (free afferent nerve endings bringing info from body to brain)

This happens via the sodium potassium - move through diffusion - impulse fired, ATP to move electrolytes back to original position

27
Q

Free Nerve Endings

A

Nociceptors - designed to detect pain

28
Q

Mediators released following injury?

A

Mediators;

SUBSTANCE P
Protaglandin - reduce threshold of pain receptors, subsequently increasing the sensation of pain
Bradykinin - reduce threshold of pain receptors, subsequently increasing the sensation of pain.
Seretonin
Potassium
Histamine - binding to receptor sites on nociceptors, thereby directly stimulating nociceptors to cause pain

-> These produce a variety of reactions e.g. vasodilation / constriction, cellular permeability***, inflammation

29
Q

What is the consequence of mediator activity?

A

Conversion of cell trauma to an electrical impulse AP - Transduction

IF chemical mediators stimulate nociceptor above ‘pain threshold’, we experience PAIN

30
Q

Protaglandin / Bradykinin - action following injury?

A

reduce threshold of pain receptors, subsequently increasing the sensation of pain

31
Q

Histmamine - action following injury?

A

Binds to receptor sites on nociceptors - direct activation causing pain (smaller amounts - itching, irritation)

32
Q

Lactic Acid Production - what does it do?

anaerobic cell respiration

A
  • Lowers pain threshold
33
Q

Hydrogen and Potassium - what do they do?

A
  • Sensitise pain receptors making them more sensitive to low intensity stimuli
  • Critical for de-polarisation and repolarisation required for making an AP and subsequent pain impulse
34
Q

Oedema - what does it do re. pain?

A

Stimulates nociceptors - stretched cells

35
Q

Example of medicine which acts at TRANSDUCTION level

A

e.g. Lignocaine

Interferes with the movement of sodium in/ out of cells

Therefore you do not generate electricity - essentially blocks the generation of AP’s and transduction

36
Q
  1. Conduction
A

= Propagation of the impulse through the sensory nervous system. Along the ‘first order’ neurones

Primary Afferant neurones project the electrical pan impulse to the DORSAL HORN of the spinal cord

Ascending relay neurons project the impulse from the spinal cord up to the brain stem and thalamus via Thalamo-cortical projections

37
Q

DORSAL HORN (of the spinal cord)

A

Where there is the synaptic junction of FIRST ORDER and SECOND ORDER neurones

38
Q

FIRST ORDER NEURONES

where are they?

A

Long neurones in the peripheral nervous system, ending at dorsal horn

Tranduction to conduction, and then at the DORSAL HORN, CONDUCTION ends and TRANSMISSION begins (electricity -> chemical)

39
Q

SECOND ORDER NEURONES

where are they?

A

Relays impulses via the spinothalamic tract in the spinal cord OR spinoparabrachial pathway up to the brain (there is synaptic junction here)

TRANSMISSION and then at synaptic junction, pain impulse then CONDUCTED

40
Q

THIRD ORDER NEURONES

where are they?

A

In the brain, the thalamus

41
Q

A-delta fibres

  • what are they?
  • characteristics
  • function
A

Sensory Afferent Nerve with:

Large myelinated sheath

FAST impulses, produces sharp pain

Relatively thick size nerve fibre allowing very rapid transmission of pain stimulus (5-30 metres per second)

This is to make the body withdraw rapidly from the painful and harmful stimulus, to avoid further damage

42
Q

C-nerve fibres

A

Sensory Afferent Nerve with:

Small, narrow fibre with non-myelinated sheath 0.2-1 thousandth of a milimeter!

SLOW - less than 2m per second

Throbbing, burning, more chronic-type pain, starts immediately after fast

Body response - immobilisation (guarding, spasm, rigidity) so that healing can take place

43
Q

Fast vs Slow pain

A

Fast - quick, sharp pain assoc with A-fibres

Slow - dull / burning sensation associated with C fibres

44
Q
  1. Transmission
A

In order for pain impulses to be transmitted across the synaptic cleft = ‘transmission’, requiring CHEMICALS

ATP, glutamate, bradykinin, nitrous oxide, SUBSTANCE P

45
Q
  1. Modulation
A

Sensory / discriminative aspects of pain

Beliefs / emotions - psychological aspects

46
Q

Melzack and Wall, 1965

A

GATE CONTOL THEORY

47
Q

What is GATE CONTROL THEORY ?

A

Stimulation of the fibres that transmit non-painful stimuli can block pain impulses at the GATE of the dorsal horn of the dorsal horn

e.g if A beta fibres (touch receptors) are stimulated, they dominate and close the gate

Brain perceives touch instead of

Explains tendency to grab and rub a stubbed toe

Descending fibres of the CNS (B fibres - pain sensattion inhibition) have the ability to exciteinhibitory neurons which then release endorphins, enkepalins and dynorphins which INHIBIT SUBSTANCE P RELEASE -

48
Q

Which substances inhibit substance P release?

A
  • endorphins
  • enkepalins
  • dynorphins
49
Q

What do B fibres do?

A

Inhibit pain sensation

50
Q

What stimuli can ‘close the gate’/

A

e.g. cold / heat, / touch

51
Q

Why do we apply ice?

A

Cooling slows the rate of transmission of nerve impulses reducing the number of pain signals transmitted to the brain,

52
Q

Modulation - ‘Referred Pain’ also relevant - what is it?

A

Due to close proximity of nerves in spinal cord, brain can struggle to perceive location of injury

e. g. heart and skin converge at same point in spinal cord
e. g. heart attack - pain radiating into arm

53
Q

Which 2 x theories are relevant to MODULATION

A

Gate Control Theory (Melzack and Wall, 1965)

‘Referred pain’ also relevant

54
Q
  1. Perception
A

Unique psychology of the individual is relevant and the conscious experience of the pain

From the THALAMUS, pain signals are sent out to higher brain areas including the

  • Anterior Cingulate Cortex (esp. chronic pain, region is activated during pain perception Kuner et al 2017)
  • Somatosensory Cortex (locate and describe pain)
  • Limbic system (Thalamus part of this)- pain pleasure, affection, anger, evaluates seriousness of pain, helps remember why
55
Q

Pain - physiological changes…? / consequences

A

Elevation in hormone production and the sympathetic nervous system response, individuals in pain will experience increases in HEART RATE, BLOOD PRESSURE elevating both CARDIAC OUTPUT and OXYGEN CONSUMPTION

Instigates STRESS RESPONSE, increasing circulating catecholamines which can cause vasoconstricton and impairing tissue perfusion

Adverse effect on cardiovascular, gastrointestinal, respiratory, neuroendocrine and musculoskeletal system & is associated with anxiety and sleeplessness (MacIntyre and Schug 2015)

Associated hyper metabolism, hyperglycaemia, lipolysis, breakdown of muscle mass

Suppresses natural killer cell activity, critical for immune system function

56
Q

catecholamines

A

Cause vasoconstriction and impairs tissue perfusion

57
Q

Catecholamines

A

Can cause vasoconstriction and impairs tissue perfusion

Catecholamines are hormones made by your adrenal glands, which are located on top of your kidneys. Examples include dopamine; norepinephrine; and epinephrine (this used to be called adrenalin or adrenaline). Your adrenal glands send catecholamines into your blood when you’re physically or emotionally stressed.

58
Q

Pain and Vomitting (mega principle) - how?

others:
pH fall -> resp rate up
hypoxia -> cyanosis
damaged cell -> pyrogen -> up temp
BP fall -> HR goes up
BP fall - ? Loss of conscious
BP fall - >Reduced Urine output
A

Area of the brain = base of fourth ventricle

AKA Emetic Centre
Chemoreceptors numerous in this area, including:

Seretonin
Substance P

If you release substance P, you are at risk of vomiting (as Subs P stimulates emetic centre)

Lactic acid can lower pain threshold
Pain = substance p release
ANYONE who is in pain
Hypoxic - produce lactic acid

Asthma - in pain due to hypoxia? could vomit
Pneumonia - green/ yellow in mouth, also could be vomit
Anaphalyatic shock - cyanosis, swellng…hypoxia? -> vomit?

ALWAYS SAY WHY

PAIN &/OR LOW BP

59
Q

Low BP - poor perfusion to GI system? could cause

A

= Vomit

60
Q

Gastric fluid contains:

Na+ (Sodium)
K+ (Potassium)
Cl- (Chloride)
H+ (hydrogen)

A

20-60mmol NA+/l
14 mmol K+ / l
140mmol Cl-/l
60-80 mmol H+/l

61
Q

Excessive vomitting can cause:

A

Cardiac arrest potentially
Seizures
Low potassium / Sodium

Due to electrolyte imbalance

62
Q

Assessing Pain:

HOW in MH setting?

Acute Care

A

considered the ‘fifth vital sign’

Acute Care - OPQRST (Hudak 1998) (especially in cardiac world)

Onset - what were you doing when the pain began? Sudden or gradual?
Precipitating factors - what provokes the pain / makes it better?
Qualitative data - describe the pain e.g. burning, stabbing
Radiation - area?
Severity - rate on scale 0-10 none - worst imaginable
Timing - what were they doing at onset? Come/go? Change over time? Has it happened before?

Pathophysiology of ill-health (16 decks)

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