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Year 2 C&M symposia > Pain > Flashcards

Pain Flashcards

1
Q

What is nociception?

A

The sensory process that provides signals in the nervous system that trigger pain.

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2
Q

What is pain?

A

The feeling/perception of sensations from a part of the body.
-sore/stinging/ache

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3
Q

What controls pain sensations?

A

A specific part of the somatosensory system.

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4
Q

What is congenital analgesia?

A

Inability to feel pain from birth.

  • decreased lifespan as don’t learn from pain
  • rare: ~32 people
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5
Q

What is the structure of nociceptors found in peripheries?

A

Free nerve endings.

-Pacinian, Ruffini’s, etc

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6
Q

What happens to nociceptive nerve endings in the dermis?

A

They branch out to unmyelinated endings.

-leads to difficulties localising pain

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7
Q

Where are the cell bodies of normal sensory receptors located?

A

In the dorsal root ganglion.

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8
Q

What does tissue damage and inflammation trigger?

A

The release of peripheral chemical mediators.

-e.g. prostaglandins, bradykinin

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9
Q

What effect does substance P have on mast cells?

A

Substance P stimulates mast cells to release histamine and bradykinin
» chemical nociceptors.

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10
Q

What is the function of prostaglandins/bradykinin/histamines in pain?

A

They sensitise chemical nociceptors&raquo_space; easier for an AP to be generated.
-can induce hyperalgesia

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11
Q

What is hyperalgesia?

A

Abnormally heightened sensitivity to pain.

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12
Q

What are the main modalities of nociceptors? (3)

A
  • Mechanical (pressure)
  • Thermal (hot/cold)
  • Chemical (e.g. histamine)
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13
Q

Do most nociceptors only respond to one modality?

A

No, most are polymodal.

-respond to mechanical, thermal and chemical stimuli

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14
Q

Which types of free nerve endings does transduction of nociceptive stimuli occur in? (2)

A
  • Unmyelinated C fibres

- Thinly myelinated A-delta fibres

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15
Q

How do sensory fibres project to the brain?

A

Travel to dorsal horn, and project to brain via ascending pathways.

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16
Q

What sort of pain do TRPV receptors detect?

A

Thermal - heat.

TRPV1 also detects chemical

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17
Q

What sort of pain does a TRPM8 receptor detect?

A

Thermal - cold.

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18
Q

What sort of pain do TRPV1, ASIC and DRASIC recptors detect?

A

Chemical.

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19
Q

What sort of pain do MDEG, DRASIC and TREK-1 receptors detect?

A

Mechanical.

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20
Q

What is microneurography?

A

An experiment that records transcutaneous nerve signals and is used to discriminate sensory afferents.

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21
Q

What is the difference between detectors that sense warmth and pain from heat?

A

THERMORECEPTORS sense temperature, but no increase above a certain threshold
NOCICEPTOR transmission increases when temperature becomes painful (45*+)

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22
Q

What sort of fibres are associated with low threshold mechanoreceptors?

A

Large diameter, rapidly conducting afferents (I/II).

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23
Q

What sort of fibres are associated with nociceptors and thermoreceptors?

A

Small diameter, slow conducting afferents (III/IV).

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24
Q

What types of nociceptors have A-delta fibres?

A

Thermal and mechanical nociceptors.

20m/sec

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25
Q

What types of nociceptors have C fibres?

A

Polymodal nociceptors.

2m/sec

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26
Q

What are the 2 categories of pain perception?

A

1st and 2nd pain.

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27
Q

What sort of sensation is 1st pain, and which fibres carry it?

A
  • Sharp/prickling sensation

- Fast A-delta fibres

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28
Q

What sort of sensation is 2nd pain, and which fibres carry it?

A
  • Dull ache/burning

- Slow C fibres

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29
Q

What type of pain is more easily localised; 1st or 2nd?

A

1st pain is more easily localised.

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30
Q

What type of pain has slow onset; 1st or 2nd?

A

2nd pain has slow onset.

1st pain has rapid onset.

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31
Q

Which type of pain is more persistent; 1st or 2nd pain?

A

2nd pain is more persistent.

1st pain has a shorter duration.

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32
Q

What type of receptors produce 1st pain?

A
  • Mechanical nociceptors

- Thermal nociceptors

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33
Q

What type of receptors produce 2nd pain?

A

Polymodal nociceptors.

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34
Q

Summarise 1st pain.

A
  • Fast A-delta fibres
  • Sharp/prickling sensation
  • Easily located
  • Rapid onset
  • Short duration
  • Mechanical and thermal nociceptors
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35
Q

Summarise 2nd pain.

A
  • Slow C fibres
  • Dull ache/burning
  • Poorly localised
  • Slow onset
  • Persistent
  • Polymodal nociceptors
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36
Q

Is it possible to selectively anaethetise A-delta and C fibres?

A

Yes, but wouldn’t do it clinically.

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37
Q

Where are nociceptive fibre cell bodies located?

A

Within dorsal root ganglion.

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38
Q

Upon entering the dorsal horn, what happens to primary afferents?

A
  • They can ascend/descend on spinal cord level in the ZONE OF LISSAUER (dorsolateral)
  • Then synapse within superficial laminae
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39
Q

What effect does the fact that 1* fibres can ascend/descend before synapsing have?

A

Can lead to pain localisation issues.

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40
Q

What are the principle laminae that nociceptor afferents enter?

A

Laminae I and II.

substantia gelatinosa; most dorsal

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41
Q

Why does referred pain occur between viscera and cutaneous sources?

A

Nociceptive afferents from internal organs and the skin enter the spinal cord through common routes and synapse with the same 2* neurons.

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42
Q

Where is pain from angina often referred to?

A

Upper chest wall and left arm.

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43
Q

Where is pain from appendicitis often referred to?

A

Abdominal wall around the navel.

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44
Q

Where is pain from the oesophagus often referred to?

A

Chest wall.

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45
Q

Where is pain from the bladder often referred to?

A

Perineum.

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46
Q

Where is pain from the ureter often referred to?

A

Lower abdomen and back.

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47
Q

Where is pain from the prostate often referred to?

A

Lower trunk and legs.

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48
Q

What excitatory neurotransmitter do pain afferents release?

A

Glutamate.

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49
Q

What substances do vesicles at synaptic terminals of pain afferent contain?

A

Neuropeptides.

-e.g. substance P

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50
Q

What is the function of substance P?

A

Mediator of nociceptive synaptic transmission in the dorsal horn.
-helps to differentiate between different levels of pain

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51
Q

Where is substance P most dense?

A

In the superficial dorsal horn.

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52
Q

What type of pathway are ascending pain pathways?

A

Contralateral spinothalamic pathways.

-cross at level of spinal cord entry

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53
Q

What is the process of pain information travelling to the brain?

A

Stimulus&raquo_space; 1* neuron&raquo_space; dorsal horn of spinal cord&raquo_space; synapses&raquo_space; 2* neuron&raquo_space; ascends to thalamus&raquo_space; synapses&raquo_space; 3* neuron&raquo_space; somatosensory cortex (PCG).

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54
Q

What is the overall pathway for conveying pain/temperature called?

A

Anterolateral system.

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55
Q

What are the 3 components of the anterolateral system?

A
  • Lateral spinothalamic tract
  • Spinoreticulothalamic tract
  • Anterior spinothalamic tract
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56
Q

What is another name for the spinoreticulothalamic tract?

A

Paleospinothalamic tract.

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57
Q

Where does the anterior spinothalmic tract project to?

A
  • Reticular formation

- Periaqueductal grey matter

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58
Q

Which sensory afferents follow the same route to the sensory cortex as pain afferents?

A

Non-nociceptive temperature afferents.

-both spinothalamic pathway

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59
Q

What is dissociated sensory loss (Brown-Sequard syndrome)?

A

Unilateral spinal cord lesion.
» sensory loss of touch/proprioception on same side (DORSAL COLUMN PATHWAY)
» sensory loss of pain on opposite side (SPINOTHALAMIC PATHWAY)

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60
Q

What pathway carries pain and temperature sensations from the face/head?

A

Trigeminothalamic tract.

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61
Q

How do pain and temperature sensations from the face and head travel to the somatosensory cortex?

A

1* afferents travel in spinal trigeminal tract to brainstem&raquo_space; synapse in pars caudalis&raquo_space; 1* neurons&raquo_space; trigeminothalmic tract&raquo_space; thalamus&raquo_space; VPM&raquo_space; cortex.

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62
Q

How can pain be ‘visualised’?

A

Using a PET scan of regional cerebral blood flow.

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63
Q

Which areas of the brain light up on a PET scan when thermal pain is induced to the hand?

A
  • 1* somatosensory cortex

- Limbic cortex (insular and anterior cingulate)

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64
Q

What is ‘phantom pain’?

A

Pain and touch sensations with no sensory inputs.

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65
Q

What proportion of amputees suffer from phantom pain?

A

50-80%.

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66
Q

How is phantom pain treated?

A

Highly resistant to treatment.

-various drugs/treatments tried

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67
Q

What is the cause of phantom pain?

A

Aetiology is unclear.

  • may be due to cortical reorganisation (thalamus/cortex)
  • may be due to central sensitisation (change in synaptic structure of dorsal horn)
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68
Q

What are opiates?

A

Analgesic drugs derived from opium.

-relieve pain

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69
Q

What are the main opiate receptors in the brain? (3)

A
  • mu
  • kappa
  • sigma
70
Q

Where are mu opiate receptors found in higher concentrations in the brain?

A

Thalamus and cerebral cortex.

71
Q

Give 2 examples of commonly-used opiate drugs?

A
  • Morphine

- Heroine

72
Q

What are endorphins?

A

Endogenous opioids produced by the CNS and pituitary gland.

-control pain and immune responses

73
Q

Give examples of endorphins.

A
  • Met-enkephalin
  • Leu-enkephalin
  • Dynorphin
  • Peptides E and F
74
Q

Which propeptides are endogenous opioid peptides synthesised from?

A
  • Proenkephalin
  • Proopiomelanocortin
  • Prodynorphin
75
Q

What is the endocannabinoid system?

A

Endogenous cannabinoid receptors located in the brain and throughout the CNS/PNS.

76
Q

What endogenous ligands respond to cannabis? (2)

A
  • Anandamide

- 2-arachidonyl-glycerol

77
Q

How does cannabis affect the body?

A

Inhibits behavioural responses to noxious stimuli and limits hyperalgesia and neuropathic pain.
-acts at spinal and supraspinal sites

78
Q

What are the main higher brain centres involved in pain perception? (3)

A
  • Thalamus (perception)
  • Cortex (localisation)
  • Limbic (emotional)
79
Q

Where do descending endogenous analgesic pathways project from? (2)

A
  • Periaqueductal grey matter

- Reticular formation

80
Q

How do descending endogenous analgesic pathways decrease transmitter release from 1* afferent terminals?

A

They interact with opioid receptors.

-presynaptic inhibition

81
Q

What proportion of the adult population endure chronic pain?

82
Q

What is hyperalgesia?

A

Increased pain or touch sensations.

-usually due to inflammation

83
Q

What is allodynia?

A

Increased pain sensitisation (touch-evoked pain).

|&raquo_space; increased response

84
Q

What type of afferents cause hyperalgesia?

A

C-afferents.

85
Q

What type of afferents cause allodynia?

A

A-beta afferents.

86
Q

What are the 3 causes of hyperalgesia?

A
  • Reduced pain threshold
  • Increased stimulus intensity
  • Spontaneous pain
87
Q

What does the Gate Theory of Pain (Melzack and Wall) explain?

A

Why pain can be reduced by stimulating mechanoreptors (e.g. rubbing knee after falling over).

88
Q

How is pain classified?

A
  • DURATION (acute/chronic)

- PATHOPHYSIOLOGY (neuropathic/nociceptive)

89
Q

What are the main features of acute pain? (3)

A
  • Resolves with healing of injury
  • Protective function
  • Assists wound healing
90
Q

What are the main features of chronic pain? (2)

A
  • Extends beyond expected healing time

- Ceases to serve protective function

91
Q

What system regulates nociceptive pain?

A

Opioidergic system.

92
Q

Does a distal radius fracture cause acute or chronic pain?

A

Acute.

-resolves with healing

93
Q

Does osteoarthritis cause acute or chronic pain?

A

Chronic pain.

94
Q

What are possible adverse effects of acute pain? (3)

A
  • CVS stress
  • Respiratory compromise
  • Hypercoagulation
95
Q

What is the process of pain perception?

A

Transduction (stimulus)
» conduction (receptor)
» transmission (CNS)
» perception (pain/withdrawal)

96
Q

What are the main factors that affect changes in pain perception?

A
  • TISSUE DAMAGE
  • Anxiety/depression
  • Gender
  • Circadian variation
  • Climate
97
Q

What are the levels of the WHO analgesia ladder? (3)

A
  1. Freedom from cancer pain
  2. Pain persisting/increasing
  3. Pain persisting/increasing
98
Q

What pain relief is given for level 1 on the WHO analgesia ladder (freedom from cancer pain)?

A

Mrophine
Fentanyl
Methadone

99
Q

What pain relief is given for level 2 on the WHO analgesia ladder (pain persisting/increasing)?

A

Codeine
Tramadol
Dihydrocodeine

100
Q

What pain relief is given for level 3 on the WHO analgesia ladder (pain persisting/increasing)?

A

Aspirin
NSAIDs
COX-2 inhibitors

101
Q

Which non-opioid analgesics are used to treat acute pain?

A
  • NSAIDs
  • COX-2 inhibitors
  • Paracetamol
102
Q

What is the mode of action of NSAIDs?

A
  • Act peripherally
  • Inhibit cyclooxygenase
  • Decreases prostaglandin synthesis
103
Q

What are the main side effects of NSAIDs? (4)

A
  • GI irritation/bleeding
  • Renal toxicity
  • Drug interactions
  • CVS side effects (COX2)
104
Q

What is the mode of action of paracetamol?

A
  • Act centrally
  • Analgesic and antipyretic effects
  • Inhibit central prostagladin synthesis
105
Q

What is the main side effect of paracetamol?

A

Toxic liver damage risk.

106
Q

Which 2 sites in the spinal cord do opioid analgesics act at?

A
  • Presynaptically

- Postsynaptically

107
Q

How do opioid analgesics act pre-synaptically?

A

Reduce pain signal transmission.

108
Q

How do opioid analgesics act post-synaptically?

A

Hyperpolarise membrane&raquo_space; decrease the probability of AP generation.

109
Q

What do opioid analgesics mainly act on?

A

Nociceptive pain.

-only partially effective in neuropathic pain

110
Q

Give 2 examples of weak opioids.

A

Tramadol

Codeine

111
Q

Give 2 examples of strong opioids.

A

Morphine

Oxycodone

112
Q

What is the mode of action of opioid analgesics?

A
  • Activate endogenous analgesic system
  • Stimulate receptors in limbic system
  • Affect descending pathways that modulate pain
  • Reduce ascending pain transmission
113
Q

What are the main side effects of opioid analgesics?

A
  • Nausea/vomiting
  • Constipation
  • Dizziness
  • Somnolence
114
Q

What is a problem with large bolus opioid analgesics?

A

Large fluctuations between pain/analgesia/side effects.

115
Q

Why is patient-controlled analgesia beneficial?

A

Less fluctuations in concentration - stays in analgesic range.

116
Q

What is the dose for patient-controlled morphine?

A

1mg bolus, with a 5 minute lockout time.

117
Q

What is a serious side effect of systemic opioid analgesia?

A

Respiratory depression and hypoxia.

118
Q

What is the best early warning sign of respiratory depression?

A

Progressive sedation.

-not respiratory rate or SpO2

119
Q

Which opioids should be avoided if a patient is suffering from renal failure?

A

Morphine and codeine.

120
Q

What is epidural analgesia?

A

Drugs administered to epidural space (between dura mater and canal wall).

121
Q

What is epidural analgesia commonly used for? (3)

A
  • Post-operatively
  • Labour pain
  • Chronic pain
122
Q

What are the main benefits of epidural analgesia?

A
  • High quality pain relief
  • Improved pulmonary function
  • Reduced sepsis
  • Reduced cardiac morbidity
123
Q

Where is a high thoracic (T3-5) epidural analgesic delivered?

124
Q

Where is a low thoracic (T5-10) epidural analgesic delivered?

125
Q

Where is a low thoracic/high lumbar (T10-L3) epidural analgesic delivered?

126
Q

Where is a lumbar (L2-S3) epidural analgesic delivered?

127
Q

Where is a caudal (S2-5) epidural analgesic delivered?

128
Q

What proportion of patients with advanced cancer experience pain?

129
Q

What proportion of cancer pain is treated with opioids?

130
Q

What is oromorph?

A

Liquid morphine.

-fast release

131
Q

What is MST/MXL?

A

Sustained release morphine.

132
Q

Cancer treatment: What is the dose of morphine on day 1?

A
  • 10mg oromorph (4 hourly)
  • 3x10mg breakthrough

TOTAL - 90mg

133
Q

Cancer treatment: What is the dose of morphine on day 2?

A
  • 15mg oromorph (4 hourly)
  • 2x15mg breakthrough

TOTAL - 120mg

134
Q

Cancer treatment: What is the dose of morphine on day 3?

A
  • 20mg oromorph (4 hourly)
  • no breakthrough

TOTAL - 120mg

135
Q

Cancer treatment: What is the dose of morphine on day 4?

A
  • 60mg MST (12hourly)

- 20mg oromorph breakthrough

136
Q

What type of cancer is the celiac plexus block commonly used for?

A
  • Pancreatic carcinoma

- Upper abdominal neoplasia

137
Q

What nerves does a celiac plexus block affect?

A

Nerves surrounding the abdominal aorta.

138
Q

Which part of the spinal cord do spinal opioids act at?

A

The dorsal horn.

139
Q

Where does lipophobic spinal morphine go?

A

Reaches the brainstem.

140
Q

Where does lipophilic spinal fentanyl go?

A

Remains segmentally localised.

141
Q

What proportion of the population suffer from neuropathic pain?

142
Q

What is neuropathic pain?

A

Spontaneous pain / hypersensitivity to pain in association with damage to the nervous system.

143
Q

Give some examples of neuropathic pain.

A
  • Diabetic neuropathy
  • Post-operative neuropathy
  • Post herpetic neuropathy (shingles)
144
Q

What is the mechanism of neuropathic pain?

A

Trauma&raquo_space; hyperexcitable dorsal horn&raquo_space; nociceptive signals.

145
Q

What are supraspinal mechanisms of neuropathic pain?

A

Melzack’s neuromatrix; active generation.

146
Q

What are the main features of neuropathic pain? (6)

A
  • In absence of tissue damage
  • In area of sensory loss
  • Paroxysmal/spontaneous
  • Allodynia
  • Hyperalgesia
  • Dysaesthesias
147
Q

What does paroxysmal mean?

A

A sudden attack or increase in symptoms.

148
Q

What is allodynia?

A

Pain in response to a non-painful stimulus.

149
Q

What is dysaesthesias?

A

Unpleasant abnormal sensations.

-e.g. “ants crawling on skin”

150
Q

What are the main co-morbidities of neuropathic pain? (3)

A
  • Depression
  • Insomnia
  • Anxiety
151
Q

What does the McGill pain questionnaire measure?

A

Pain quality.

-78 ranked descriptors

152
Q

What are the advantages of the McGill pain questionnaire? (2)

A
  • Well validated

- Quality assessed

153
Q

What are the disadvantages of the McGill pain questionnaire? (2)

A
  • Time consuming

- Insensitive to small change

154
Q

What type of pain medication acts at the brain?

155
Q

Which types of pain medications act at the dorsal horn synapses? (4)

A
  • Opioids
  • Antidepressants
  • Anticonvulsants
  • Non-opioid analgesics
156
Q

Which types of pain medications act at peripheral nociceptors? (2)

A
  • Topical analgesics

- Non-opioid analgesics

157
Q

What drugs are used to treat neuropathic pain? (4)

A
  • NSAIDs (poor)
  • Antidepressants
  • Anticonvulsants
  • Opioids
158
Q

What is the efficacy of antidepressants? (3)

A
  • Neuropathic pain
  • Complex regional pain syndrome
  • Tension headache
159
Q

What is the mode of action of antidepressants?

A

Inhibit neuronal reuptake of noradrenaline and serotonin (5-HT).

160
Q

What are the main side effects of antidepressants?(4)

A
  • Constipation
  • Dry mouth
  • Somnolence
  • Abnormal HR
161
Q

What type of antidepressants are most effective for neuropathic pain?

A

Tri-cyclic agents (TCAs).

-serotonin uptake inhibitors relatively ineffective

162
Q

What is the efficacy of anticonvulsants?

A

Neuropathic pain.

163
Q

What are the main anticonvulsants used to treat neuropathic pain? (3)

A
  • Gabapentin
  • Pregabalin
  • Carbamazepine
164
Q

What is the mode of action of gabapentin?

A

Binds to presynaptic voltage-dependent calcium channels.

165
Q

What is the mode of action of pregabalin?

A

Interacts with special N-type calcium channels.

166
Q

What is the mode of action of carbamazepine?

A

Blocks sodium and calcium channels.

167
Q

What are the main side effects of anticonvulsants? (4)

A
  • Sedation
  • Dizziness
  • Ataxia
  • Peripheral oedema
168
Q

What is ataxia?

A

The loss of full control of bodily movements.

169
Q

Which anticonvulsants are GABA agonists? (2)

A
  • Valproate

- Clonazepam

170
Q

What sort of pain does gabapentin prevent?

A

Neuropathic, but not nociceptive.

171
Q

What are the 4 dimensions of pain conceptualised by Loeser?

A

Nociception
>Pain
>Suffering
>Pain behaviours

172
Q

What is operant conditioning?

A

If pain behaviour is reinforced, it’s more likely to occur.

Year 2 C&M symposia (11 decks)

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