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PBL Y2 S3 > Case 2 - Pain > Flashcards

Case 2 - Pain Flashcards

1
Q

Define pain

A

Unpleasant sensory or emotional experience associated with, or resembling that associated with, actual or potential tissue damage

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2
Q

List the steps involved in pain processing

A

1- Detection - a noxious stimuli is detected by nociceptive fibres
2- Transduction - thermal / mechanical/ chemical signals changed into electrical signal
3- Conduction - along a peripheral nerve, i.e. sciatic
4- Transmission - lateral spinothalamic tract transmits pain
5- Perception - biopsychosocial model, i.e. effect of catrophising
6- Modulation - i.e. move foot away from pain

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3
Q

What are the 4 types of pain?

A

Nociceptive pain
Inflammatory pain
Neuropathic pain
Nociplastic pain

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4
Q

What is nociceptive pain?

Is it good or bad pain?

A

Pain from actual or threatened damage (noxious stimuli) due to direct activation of nociceptors by high-threshold stimuli. Pain is evoked in a graded response by high-intensity stimuli, and lasts longer if the pain is more severe (appropriate response).

Good pain - adaptive and serves a protective response

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5
Q

What is inflammatory pain?

Is it good or bad pain?

A

Associated with regions of acute inflammation and peripheral sensitisation. Inflammation leads to the release of histamine, prostaglandins, ATP and 5-HT, which leads to increased nociceptive excitability/ responsiveness. this can cause pain even with innocuous stimuli.
Normal signs = heat, redness, swelling

Good pain - adaptive and protective during healing, and is reversible

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6
Q

What is neuropathic pain?

Is it good or bad pain?

A

Pain caused from lesion or disease of the somatosensory nervous system. It is persistent and has maladaptive amplification. Pain can be spontaneous, i.e. evoked from both low-intensity and high-intensity stimuli

Bad pain - no useful purpose

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7
Q

What are some features of neuropathic pain?

A

Sensitisation - either peripheral (increased responsiveness of nociceptors) or central (increased excitability of CNS neurons).
- Hyperalgesia = abnormal increased sensitivity to painful stimuli
- Allodynia = lower threshold of nociceptors, so stimuli that don’t normally cause pain do - example is tactile allodynia (pain of brushing the skin, central sensitisation)

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8
Q

What is nociplastic pain?

Is it good or bad pain?

A

Altered nociception despite no evidence of tissue damage or disease/ lesions. Activates peripheral nociceptors. E.g. fibryomyalgia

Bad pain - not useful

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9
Q

Name the two ascending sensory tracts

A

Spinothalamic
Dorsal columns

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10
Q

What information do spinothalamic tracts transmit?

A

Lateral spinothalamic = pain and temperature
Ventral spinothalamic = crude touch and pressure

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11
Q

Describe where neurons synapse within the spinothalamic tract

A

Receptor is in periphery, axon in spinal cord
1- First order neurone = dorsal horn of grey matter
2- Second order neurone = decussates and ascends to the thalamus
3- Third order neurone = synapses in ventral posterior nucleus of thalamus, which then goes to somatosensory cortex (S1 and S2)

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12
Q

What information do the dorsal columns transmit?

A

Information from discriminative touch, fine touch, vibration and proprioception

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13
Q

Describe where neurons synapse within the dorsal columns

A

1- First order neurone = from periphery, moves ipsilaterally and ascends up towards the medulla.
- Fasciculus Gracilis tract - info from lower limbs, synapses in the nucleus gracilis
- Fasciculus Cuneatus tract- info from upper limbs, synapses in the nucleus cuneatus
2 - Second order neurone = decussates in the medulla (forms the medial lemniscus) which ascends to the thalamus
3- Third order neurone = goes to the somatosensory cortex

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14
Q

Name the descending tract and where the neurons synapse

A

Corticospinal tract
1- Precentral gyrus, through internal capsule
2- In the medulla, 85-90% decussate (lateral corticospinal tract), and 10-15% continue ipsilateral (ventral corticospinal tract) before decussating in the sispinalnal cord
3- Synapse with a lower motor neurone

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15
Q

What is acute pain? Give some of its characteristics

A

Provoked by disease or injury (damage) and serves a useful biologic purpose (protective).
- Intensity correlates with the triggering stimulus
- Can be clearly located

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16
Q

What is chronic pain? Give some of its characteristics

A

Pain that outlasts the normal time of healing, due to altered nerve signals. It can be considered a disease state and is persistent. Includes neuropathic and nociplastic pain. .
- Uncoupled from causative agent (intensity doesn’t correlate)
- Lasts 3-6 months +
- No adaptive or protective function

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17
Q

What is the basis behind chronic pain?

A

Neuronal plasticity:
- Peripheral sensitisation: lower threshold and increased responsiveness of peripheral ends of nociceptors
- Central sensitisation: Increased excitability of neurons in the CNS to normal inputs, so abnormal responses (i.e. hyperalgesia)

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18
Q

What are the characteristics of AA and AB fibres?

A

Large cell body (40-80 um)
Myelinated axons
Fast nerve conduction velocity (40-120 m/s)

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19
Q

What is the function of AA and AB fibres?

A

AA= Proprioception
AB= mechanoreceptors

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20
Q

What are the characteristics of A-delta fibres?

A
  • Small to medium cell body (15-50 um)
  • Thinly myelinated
  • medium nerve conduction velocity (10-30 m/s)
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21
Q

What is the function of A-delta fibres?

A

Respond to mechanical and thermal stimuli

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22
Q

What are the characteristics of C fibres?

A

Small cell body (10-25 um)
Not myelinated
Slow nerve conduction velocity (0.2-2 m/s)

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23
Q

What is the function of C fibres?

A

Responds to thermal, mechanical and chemical stimuli

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24
Q

Which fibres transmit fast and slow pain, and hot and cold temperatures? What neurotransmitter do these fibres use?

A

A delta = fast pain, cold - use glutamate
C fibres = slow pain, heat - use substance P

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25
What are the differences between slow vs fast pain?
Slow pain = aching, burning - poorly localised Fast pain = rapid onset (like a pin prick) - precisely localised
26
What is a silent polymodal nociceptor?
Type of C fibre that is only activated if inflammation is present
27
What Rexed laminae do A delta and C fibres send branches to innervate?
A delta = rexed laminae I and III-V C fibres = rexed laminae I - II
28
How do A delta fibres transmit pain?
A delta = first order neurone, synapses in the dorsal horn then decussates Terminates in the thalamus Goes to somatosensory cortices to interpret pain quality and localisation
29
How do C fibres transmit pain?
C fibre = first order neurone, synapses in the dorsal horn then decussates Terminates in the thalamus Goes to reticular formation and the periaqueductal grey (PAG) area, this is less precise but important for pain perception
30
What is the role of the reticular formation?
Keeps you alert
31
What is the role of the PAG?
Pain relief - releases endogenous opioids
32
What are Rexed laminae?
Grey matter of the spinal cord is characterised into different parallel laminae by the size of the neurons present and the packing density.
33
Describe the changes beween the superficial dorsal horn, mid dorsal horn and then ventral horn of the rexed laminae?
Superficial dorsal = packed and small sensory neurons Further down the dorsal horn = sensory neurons get bigger and are less packed Vental horn = motor neurons so are bigger cell bodied, and less tightly packed
34
What is the pain gate theory?
Suggests inhibitory interneurons are inhibited by AB fibres. Therefore, can get pain relief by increasing AB input ('rubbing it better') - this is theorised to shut the pain gate that was opened by C-fibres, as rubbing floods the hurt area with tactile AB encoded stimulation = reduces pain
35
What are 4 receptors involved in pain?
TRPM8 - activated by a decrease in temperature TRPV1 - activated by an increase in temperature ASIC - activated by an increase in H+ P2X and P2Y - activated by ATP
36
Why do mints feel cold and hot chilli peppers feel hot when you eat them?
Mints feel cold because menthol activates TRPM8, the receptor activated by a decrease in temp (percieved as cold) Peppers feel hot because capsaicin activates TRPV1, the receptor activated by an increase in temp
37
What are the mechanisms behind neuropathic pain?
- Increased inflammatory cells and mediator response: resident mast cells release histmaine and cytokines, causing release of action potential. this increases vascular permeability= inflammatory soup - Altered nociceptors activity: increased ectopic firing, altered receptor/ ion channel expression (peripheral sensitisation) - Altered spinal processing, central sensitisation and synaptic reorganisation: increased nociceptor activity, leads to central sensitisation (spinal hyperexcitability) - Altered central processing and descending inhibition
38
What are the effects of spinal hyperexcitability?
Increased activity of C fibres Increased neuropeptides, i.e. substance P and glutamate Glutamate activates NMDA receptors and second order neurons
39
What are some biopsychosocial factors that influence pain perception?
Biological: injury, abnormalities in CNS function, problem with immune system, symptoms Psychological: emotional, cogntiive, behavioural responses to pain Social: support from others, reaction of others, cultural norms for expressing pain
40
How can mood, expectation and hypervigilance affect pain perception?
Mood: depression and anxiety activate pain pathways so can increase perception of pain severity Hypervigilance: being aware of pain can make it feel more painful Expectation: expecting pain can make it feel more painful
41
What are the features of a catastophising personality type?
Rumination: repetitive negative thinking of the same event Magnification: negatively exaggerating the importance of a situation (making it a bigger deal than it is) Helplessness: sensing a lack of control of outcomes
42
What is a pain management programme (PMP)?
A psychologically-based rehabilitation programme delivered in a group setting by a psychologist, physiotherapist and medical practitioner
43
What are the aims of a PMP?
- Help patients move from medical model of pain to a biopsychosocial model - Build self-management skills and reduce reliance on HCPs - Educate about physiological effects of pain - Positive lifestyle changes, improve mood and reduce emotional distress
44
Give examples of structural and functional imaging techniques
Structural: CT scan, MRI scan Functional: SPECT, PET
45
How does a CT scan produce an image? Gives its pros and cons
X-ray beam is rotated around a patient and reconstructed to give a detailed image - Pros = quick, cheap, convenient - Cons = involves radiation, poor quality
46
How does a MRI scan produce an image? Give its pros and cons
Uses a large magnet and creates high contrast images Pros = Good quality (can distinguish white and grey matter of the spinal cord) and no radiation Cons= slow, expensive, more effort
47
When would a CT or MRI scan be used?
CT scan - for viewing bone and freshly clotted blood, i.e. trauma or suspected haemorrhage MRI scan - MS, spinal cord compression, brainstem lesions
48
What are the 2 types of weighted images on an MRI scan?
T1-weighted: water appears dark (i.e. CSF, grey matter) and fatty tissues appear bright (i.e. white matter). has high detail T2-weighted: water appears bright and lipid appears dark. Brain abnormalities are bright and easier to see than T1
49
When would T1 and T2-weighted MRI scans be opted for?
T1 = used for assessing the cortex, focal liver lesions T2 = oedema, white matter lesions
50
How does a SPECT scan produce an image? Give its pros/ cons
Gamma-mitting radioisotope; inject into blood and then use a gamma camera Pros = cheap, convenient Cons= poor spatial resolution
51
How does a PET scan produce an image? Give its pros/ cons
Positron-emitting radioisotopes; 2 gamma rays emitted at 180 degrees and then detected by a ring of detectors Pros = good spatial resolution Cons= expensive, more effort, harmful radiation
52
When would a SPECT and PET scan be used?
SPECT - blood flow, i.e. in Alzheimers PET - research tool
53
What is the multi-modal anaesthesia approach to treating pain?
Aims to target all 4 steps of perception: 1: transduction - local anaesthetics, NSAIDs, opioids 2: transmission - local anaesthetics, opioids 3: perception - physical and psychological therapies 4- Modulation - physical and psychological therapies, opioids
54
How might chronic pain be treated?
- Antidepressants, anti-convulsants, opioids - Interventional pain medicine, i.e. spinal cord stimulation - Pain management programmes
55
When might spinal cord stimulation be opted for?
If pain persists > 6 months, despite conventional medicine
56
Describe the stepwise management protocol for pain
1: Anti-convulsants OR tricyclic anti-depressants 2: SSRIs, SNRIs or lidocaine 3: Opioids (weaker) 4: Stronger opioids, cannabinoids or lamotrigine
57
Give an example of anti-convulsants
Gabapentin Pregabalin
58
Give an example of a tricyclic anti-depressant
Amytriptyline Duloxetine
59
Give an example of an SSRI used in pain
Paroxetine
60
How do NSAIDs work?
Inhibit prostagnaldins, reducing inflammation and nociception. they mainly act on the periphery and are mostly non-selective (inhibit both COX-1 and COX-2)
61
What are some side effects of NSAIDs?
GI irritation, risk of GI bleeds, renal toxicity
62
How do local anaesthetics work?
Dissociate once they are past the cell membrane (i.e. gain H+ ion) and then block sodium ion channels. this stops neural transmission
63
How do nerve fibres differ in sensitivity to local anaesthetics?
Small nerve fibres are more sensitive than larger ones Myelinated fibres are blocked before non-myelinated fibres (of the same size)
64
How do opioids lead to pain relief?
2 mechanisms. The first: 1- activates opioid receptors causing a decrease in intracellular cAMP concentration 2- Decreases calcium ion influx so less NT is released (glutamate and substance P) 3- at postsynaptic membrane, K+ channels open which causes hyperpolarisation 4- Decreased probability of an action potential (by preventing Ca2+ influx) = Prevents pain signal transmission 2nd mechanism - inhibits descending inhibitory pathway, affects the thalamus and limbic system to alter the emotional assessment of pain
65
What receptors and neurotransmitters does morphine affect?
u-receptors = inhibits ACh, glutamate and substance P
66
What are some side effects of opioids?
Addiction Respiratory depression Decreased level of consciousness
67
What is the mode of action of ketamine? When might it be used for pain relief?
Binds to and blocks the NMDA receptor, preventing spinal transmission to the spinal cord Used post-surgery for pain
68
How does gabapentin work for pain relief?
Blocks calcium channels, reduces the excitability of the NS. Given to help reduce opioid requirements
69
How is addiction diagnosed?
It is diagnosed as a 'substance misuse disorder', using a checklist which grades the disorder from mild (2-3 present), moderate (4-5 present) to severe (6-7 present). Examples: - Tolerance - Physical withdrawal state - Difficulties controlling use - Strong desire to take the substance - Progressive neglect of other interests - Persistence with substance despite detrimental effects
70
What is the pathophysiology behind addiction?
Main area: medial forebrain bundle - from the ventral tegmental area to the medial prefrontal cortex, where the brain processes pleasure and reward. >> There is increased dopamine in the nucleus accumbens.
71
How can opiates increase dopamine?
Indirectly by binding to GABA mu receptor
72
What is tolerance?
Diminished response to a substance, i.e. decreased effect or needing more to have the same effect
73
How can tolerance be caused?
Over time using the same drug, there is a decreased number of post-synaptic receptors (or receptor desensitisation to the drug). This means more dopamine is needed to have the same effect
74
What receptor is involved in tolerance?
U1 receptor - has a role in analgesia but also physical dependence
75
What are some symptoms of withdrawal?
Anxiety, shaking, lower appetite, headache, vomiting
76
What is a big risk when patients attempt to withstand drugs of abuse?
Accidental overdose following a detox - the detox removes the tolerance, so when they relapse they often go to the pre-detox dose which is fatal
77
How do gradual dose reduction regimens work?
Allows endogenous dopamine to increase as you slowly taper off exogenous dopamine, which combats withdrawal symptoms.
78
What is the recommended dose reduction when tapering off a drug?
5-20% dose reduction every 4 weeks - the slower tapers are tolerated better
79
How is opiate dependence treated?
1: detoxification - will experience withdrawal symptoms during (especially severe symptoms at 1-3 days after last usage) 2: relapse prevention using substitution pharmacotherapy, i.e. give a drug that has some pleasurable effects but limited side effects 3: lifestyle and behaviour change - i.e. community reinforcement, motivational interviewing, CBT
80
Compare symptoms on day 3 to day 10 of abstinence from a drug
day 3: severe anxiety, moderate depression, high craving, abdominal pain, vomiting day 10: moderate anxiety, subclinical depression, moderate craving
81
Give examples of drugs (and their mode of action) used for substitute pharmacotherapy for opiates
Methadone = agonist, inhibits GABA to increase dopamine. Has some risk but a lot less than opiates Buprenophine = partial agonist, also inhibits GABA. This has less risk but also less pleasurable Naltrexone = antaxonist, no pleasure but is thought to block mu opiate receptor and reduce dopaminergic activity, which reduces cravings
82
What is sciatica? Give example of symptoms
Symptoms associated with irritation of the sciatic nerve (L4-S3), i.e. unilateral pain radiating from the buttock, down the thigh and possibly to ankle or foot. - Sharp, stabbing, burning pain - Parasthesia (pins and needles) - Numbness and weakness
83
Where does the sciatic nerve provide motor and sensory innervation?
Sensation (sensory)= lateral lower leg and foot Motor = posterior thigh, lower leg and foot
84
What are some causes of sciatica?
Herniated disc, spondylolisthesis (anterior displacement of vertebrae out of line with the one below), spinal stenosis
85
What is a red flag in terms of sciatica symptoms?
If the pain was bilateral - red flag as could indicate cauda equina syndrome
86
How is sciatica diagnosed?
- Sciatic stretch test: lie on back, 1 leg extended till limit of hip flexion reached, then dorsi flex the ankle. If sciatica pain- indicates nerve irritation - Xray: reveal overgrowth of bone pressing on the nerve - MRI: may reveal herniated discs
87
How is sciatica treated?
Anti-inflammatories, i.e. NSAIDs Muscle relaxants Tricyclic antidepressants, i.e. amytriptyline Surgery to remove the pressure on the nerve
88
What is a dermatome?
Strip of skin innervated by a single spinal nerve
89
How is a dermatome formed during development?
In the 3rd week, paroxial mesoderm differentiates into somites Ventral portion - sclerotome, becomes bones of vertebral column Dorsal portion - dermomyotome, becomes the dermis (skin) Creates dermatomes of nerves - map overlaps
90
How can sensation be lost in a dermatome?
3 adjacent dorsal roots must be cut due to the signficiant overlap between roots
91
What type neurons does the dorsal, lateral and ventral horn contain?
Dorsal = sensory Lateral = autonomic Ventral = motor
92
What are the nerve roots of the sciatic nerve?
L4-S3
93
Which nerve is the only one that can be traced back to the lumbar plexus?
Femoral nerve
94
What is the 52 week linking rule?
Benefits are protected for the first year after a person with a disability starts work
95
What is diffuse noxious inhibitory control?
Endogenous pain modulation phenomenon where activity of pain-signalling neurons in the spinal dorsal horn and trigeminal nuclei is reduced in response to noxious stimuli applied to other areas of the body (i.e. acupuncture needle).

PBL Y2 S3 (10 decks)

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