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Year 2 Medicine > Physiology of Pain 2 > Flashcards

Physiology of Pain 2 Flashcards

1
Q

Clinical pain

  • Clinical pain, as the name suggests, is seen in clinics
  • Associated with damage to tissues, including the nervous system
  • Mechanisms can be nociceptive and/or neuropathic
    • … - normal functioning of nociceptors in response to tissue injury
    • … - Pain in response to injury to the nervous system
A
  • Clinical pain, as the name suggests, is seen in clinics
  • Associated with damage to tissues, including the nervous system
  • Mechanisms can be nociceptive and/or neuropathic
    • Nociceptive - normal functioning of nociceptors in response to tissue injury
    • Neuropathic - Pain in response to injury to the nervous system
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2
Q

Clinical pain

  • Clinical pain, as the name suggests, is seen in clinics
  • Associated with damage to tissues, including the nervous system
  • Mechanisms can be nociceptive and/or neuropathic
    • Nociceptive - normal functioning of nociceptors in response to tissue …
    • Neuropathic - Pain in response to injury to the … …
A
  • Clinical pain, as the name suggests, is seen in clinics
  • Associated with damage to tissues, including the nervous system
  • Mechanisms can be nociceptive and/or neuropathic
    • Nociceptive - normal functioning of nociceptors in response to tissue injury
    • Neuropathic - Pain in response to injury to the nervous system
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3
Q

Pain < 3 months = …

A

Pain < 3 months = acute

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4
Q

Pain > 3 months = …

A

Pain > 3 months = chronic

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5
Q

Acute pain

  • Due to tissue … or …
    • E.g. following surgery, musculoskeletal injury, burn, headache, visceral pain
  • … mechanism - when injury site recovers - pain stops
A
  • Due to tissue injury or inflammation
    • E.g. following surgery, musculoskeletal injury, burn, headache, visceral pain
  • Nociceptive mechanism - when injury site recovers - pain stops
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6
Q

Acute pain

  • Due to tissue injury or inflammation
    • E.g. following surgery, musculoskeletal injury, …, headache, … pain
  • Nociceptive mechanism - when injury site … - pain …
A
  • Due to tissue injury or inflammation
    • E.g. following surgery, musculoskeletal injury, burn, headache, visceral pain
  • Nociceptive mechanism - when injury site recovers - pain stops
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7
Q

Acute pain mechanisms

  • Acute pain is due to the excitation of nociceptors
    • E.g. … activation via:
      • ATP - binds to purinergic receptors sitting at the peripheral terminals of nociceptors
      • Proton/acid binding to acid sensing ion channels
      • serotonin binding to the 5-HT3 receptor sitting on the terminals of nociceptors
  • Overall - Compounds bind to receptor - switches on nociceptor - triggers spinothalamic tract - pain
  • OR: Mechanisms of acute pain may also be due to … sensitisation - leads to hyperalgesia:
    • … -reduces threshold for activation, opens more easy
    • … - reduce threshold of firing of these channels
A
  • Acute pain is due to the excitation of nociceptors
    • E.g. Direct activation via:
      • ATP - binds to purinergic receptors sitting at the peripheral terminals of nociceptors
      • Proton/acid binding to acid sensing ion channels
      • serotonin binding to the 5-HT3 receptor sitting on the terminals of nociceptors
  • Overall - Compounds bind to receptor - switches on nociceptor - triggers spinothalamic tract - pain
  • OR: Mechanisms of acute pain may also be due to peripheral sensitisation - leads to hyperalgesia:
    • Bradykinin -reduces threshold for activation, opens more easy
    • Prostaglandins - reduce threshold of firing of these channels
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8
Q

Acute pain mechanisms

  • Acute pain is due to the … of nociceptors
    • E.g. Direct activation via:
      • ATP - binds to purinergic receptors sitting at the peripheral terminals of nociceptors
      • …/… binding to … sensing ion channels
      • … binding to the 5-HT3 receptor sitting on the terminals of nociceptors
  • Overall - Compounds bind to receptor - switches on nociceptor - triggers spinothalamic tract - pain
  • OR: Mechanisms of acute pain may also be due to peripheral sensitisation - leads to …:
    • Bradykinin -reduces threshold for activation, opens more easy
    • Prostaglandins - reduce threshold of firing of these channels
A
  • Acute pain is due to the excitation of nociceptors
    • E.g. Direct activation via:
      • ATP - binds to purinergic receptors sitting at the peripheral terminals of nociceptors
      • Proton/acid binding to acid sensing ion channels
      • serotonin binding to the 5-HT3 receptor sitting on the terminals of nociceptors
  • Overall - Compounds bind to receptor - switches on nociceptor - triggers spinothalamic tract - pain
  • OR: Mechanisms of acute pain may also be due to peripheral sensitisation - leads to hyperalgesia:
    • Bradykinin -reduces threshold for activation, opens more easy
    • Prostaglandins - reduce threshold of firing of these channels
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9
Q

Acute pain treatments

  • Lots of acute pain treatments
  • Very effective
  • Sites of action are:
      1. … (i.e. at the site of injury)
      1. …
      1. Or both
A
  • Lots of acute pain treatments
  • Very effective
  • Sites of action are:
      1. PNS (i.e. at the site of injury)
      1. CNS
      1. Or both
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10
Q

Local anaesthetics

  • Examples include …, …
    • Act in periphery
    • … applied to skin
  • Mechanism of action:
    • Prevents nociceptor firing by … sodium channels
A
  • Examples include lidocaine, lignocaine
    • Act in periphery
    • Topically applied to skin
  • Mechanism of action:
    • Prevents nociceptor firing by blocking sodium channels
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11
Q

Local anaesthetics

  • Examples include lidocaine, lignocaine
    • Act in …
    • Topically applied to skin
  • Mechanism of action:
    • Prevents … firing by blocking … channels
A
  • Examples include lidocaine, lignocaine
    • Act in periphery
    • Topically applied to skin
  • Mechanism of action:
    • Prevents nociceptor firing by blocking sodium channels
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12
Q

NSAIDs

  • Examples include …, ibuprofen
  • Act in periphery
  • Mechanism of action:
    • Reduce the inflammatory response by inhibiting … synthesis
    • Reduce peripheral sensitisation
  • Cyclooxygenase (…) inhibited -> … synthesis reduced - > Prevents decrease in Na+ channel threshold
A
  • Examples include aspirin, ibuprofen
  • Act in periphery
  • Mechanism of action:
    • Reduce the inflammatory response by inhibiting prostaglandin synthesis
    • Reduce peripheral sensitisation
  • Cyclooxygenase (COX) inhibited -> Prostaglandin synthesis reduced - > Prevents decrease in Na+ channel threshold
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13
Q

Paracetamol/Acetaminophen

  • Paracetamol is not a … (no anti-… properties)
  • Acts …
  • Mechanism of action:
    • Exact mechanism not known
    • Inhibits cyclooxygenase enzymes in …NS
    • Acts on … serotonergic pathway
A
  • Paracetamol is not a NSAID (no anti-inflammatory properties)
  • Acts centrally
  • Mechanism of action:
    • Exact mechanism not known
    • Inhibits cyclooxygenase enzymes in CNS
    • Acts on descending serotonergic pathway
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14
Q

Topical capsaicin treatment

  • Component of … …
  • Acts in … - Topically applied to skin
  • Mechanism of action:
    • TRP… agonist - Persistent opening of TRP… -> Calcium overload -> … stops working
A
  • Component of chili peppers
  • Acts in periphery - Topically applied to skin
  • Mechanism of action:
    • TRPV1 agonist - Persistent opening of TRPV1 -> Calcium overload -> Nociceptor stops working
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15
Q

Opioids

  • Examples include …, …, tramadol
  • Most … pain relief but numerous side effects
  • Act … and …
  • Mechanism of action - … of the endogenous opioid system:
    • Brainstem (disinhibition)
    • Spinal Cord
    • Peripheral (inhibits channels on nociceptors)
A
  • Examples include morphine, codeine, tramadol
  • Most effective pain relief but numerous side effects
  • Act centrally and peripherally
  • Mechanism of action - agonists of the endogenous opioid system:
    • Brainstem (disinhibition)
    • Spinal Cord
    • Peripheral (inhibits channels on nociceptors)
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16
Q

Gate control theory

  • Pain evoked by nociceptors can be reduced by the simultaneous activation of low threshold … (Aβfibres)
  • Simply put, … or blowing on the painful area can … the pain
  • … of pain at the spinal cord level
A
  • Pain evoked by nociceptors can be reduced by the simultaneous activation of low threshold mechanoreceptors (Aβfibres)
  • Simply put, rubbing or blowing on the painful area can reduce the pain
  • Modulation of pain at the spinal cord level
    *
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17
Q

Mechanisms of gate control

  • Stimulation of … fibres at injury site activates interneurons in dorsal horn, which … spinothalamic neurons
  • Rubbing/blowing - activates … fibres
    • C fibres inhibit inhibitory interneurons – opens gate
    • … fibres activate inhibitory interneurons – closes gate
A
  • Stimulation of Ab fibres at injury site activates interneurons in dorsal horn, which inhibit spinothalamic neurons
  • Rubbing/blowing - activates Ab fibres
    • C fibres inhibit inhibitory interneurons – opens gate
    • Aβ fibres activate inhibitory interneurons – closes gate
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18
Q

Mechanisms of gate control

  • Stimulation of Ab fibres at injury site activates interneurons in dorsal horn, which inhibit spinothalamic neurons
  • Rubbing/blowing - activates Ab fibres
    • C fibres … inhibitory interneurons – … gate
    • Aβ fibres … inhibitory interneurons – … gate
A
  • Stimulation of Ab fibres at injury site activates interneurons in dorsal horn, which inhibit spinothalamic neurons
  • Rubbing/blowing - activates Ab fibres
    • C fibres inhibit inhibitory interneurons – opens gate
    • Aβ fibres activate inhibitory interneurons – closes gate
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19
Q

Chronic pain is pain that persists for over … months - it is very common

A

over 3 months

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20
Q

chronic pain is very common -affects …-…% of population

A

20-50chronic pain is very common -affects 20-50% of population

21
Q

Examples leading to chronic pain:

A

Chronic back pain, cancer, carpal tunnel syndrome, arthritis, fibromyalgia, diabetes, migraine, post-surgery, postherpetic neuralgia (shingles), phantom limb pain, multiple sclerosis, trigeminal neuralgia

22
Q

Chronic pain can be … or …

A

Chronic pain can be nociceptive or neuropathic

23
Q

Neuropathic pain

  • Nerve injury may be a compression, traction, sever, h…, demyelination, t… or n…
  • Affects …% of the population
  • However, a nerve injury may not always be obvious on … examination
A
  • Nerve injury may be a compression, traction, sever, hypoxia, demyelination, tumour or neuroinflammation
  • Affects 8% of the population
  • However, a nerve injury may not always be obvious on clinical examination
24
Q

Neuropathic pain

  • Nerve injury may be a c…, traction, s…, hypoxia, d…, tumour or neuroinflammation
  • Affects 8% of the population
  • However, a nerve injury may not always be obvious on clinical …
A
  • Nerve injury may be a compression, traction, sever, hypoxia, demyelination, tumour or neuroinflammation
  • Affects 8% of the population
  • However, a nerve injury may not always be obvious on clinical examination
25
Q

Symptoms of neuropathic pain

A
26
Q

Neuropathic pain mechanisms

  • Mechanisms are complex, involving both peripheral and central nervous systems
  • Main peripheral mechanisms:
      1. Peripheral …
      1. Increased … of primary …
  • Main central mechanisms:
      1. Central … - within spinal cord
      1. Changes in activation patterns/cortical … - within brain
A
  • Mechanisms are complex, involving both peripheral and central nervous systems
  • Main peripheral mechanisms:
      1. Peripheral sensitization
      1. Increased firing of primary afferents
  • Main central mechanisms:
      1. Central sensitization - within spinal cord
      1. Changes in activation patterns/cortical remapping - within brain
27
Q

Neuropathic pain mechanisms

  • Mechanisms are complex, involving both peripheral and central nervous systems
  • Main peripheral mechanisms:
      1. Peripheral sensitization
      1. … firing of primary afferents
  • Main central mechanisms:
      1. Central sensitization - within … …
      1. Changes in … patterns/… remapping - within brain
A
  • Mechanisms are complex, involving both peripheral and central nervous systems
  • Main peripheral mechanisms:
      1. Peripheral sensitization
      1. Increased firing of primary afferents
  • Main central mechanisms:
      1. Central sensitization - within spinal cord
      1. Changes in activation patterns/cortical remapping - within brain
28
Q

Increased firing of primary afferents

  • At nerve injury sites, the damaged tips of nociceptors fire spontaneously
  • … nociceptor - ion channels formed still but … at site of injury - tips of nociceptors more … and send pain impulses up the … tract - site swells to form … at the injury site
  • Responsible for spontaneous pain and also phantom limb pain
  • Underlies … … pain mechanisms
A
  • At nerve injury sites, the damaged tips of nociceptors fire spontaneously
  • Severed nociceptor - ion channels formed still but accumulate at site of injury - tips of nociceptors more excitable and send pain impulses up the spinothalamic tract - site swells to form neuroma at the injury site
  • Responsible for spontaneous pain and also phantom limb pain
  • Underlies central neuropathic pain mechanisms
29
Q

Increased firing of primary afferents

  • At nerve injury sites, the damaged tips of nociceptors fire …
  • Severed nociceptor - ion channels formed still but accumulate at site of … - tips of nociceptors more excitable and send pain impulses … the spinothalamic tract - site … to form neuroma at the injury site
  • Responsible for … pain and also … … pain
  • Underlies central neuropathic pain mechanisms
A
  • At nerve injury sites, the damaged tips of nociceptors fire spontaneously
  • Severed nociceptor - ion channels formed still but accumulate at site of injury - tips of nociceptors more excitable and send pain impulses up the spinothalamic tract - site swells to form neuroma at the injury site
  • Responsible for spontaneous pain and also phantom limb pain
  • Underlies central neuropathic pain mechanisms
30
Q

Central sensitization

  • Increase in the responsiveness of … neurons within the … … system
  • Normal inputs begin to produce … responses
  • Signal amplified due to the reduced threshold for activation (similar to …)
A
  • Increase in the responsiveness of nociceptive neurons within the central nervous system
  • Normal inputs begin to produce abnormal responses
  • Signal amplified due to the reduced threshold for activation (similar to LTP)
31
Q

Central sensitization

  • … in the responsiveness of nociceptive neurons within the central nervous system
  • Normal inputs begin to produce … responses
  • Signal … due to the … threshold for activation (similar to LTP)
A
  • Increase in the responsiveness of nociceptive neurons within the central nervous system
  • Normal inputs begin to produce abnormal responses
  • Signal amplified due to the reduced threshold for activation (similar to LTP)
32
Q

Reduced threshold for activation - central sensitization

  • Constant firing of axons from the periphery (following injury)
  • Sustained release of …
  • Prolonged depolarisation of the postsynaptic membrane
  • Massive influx of calcium ions through … receptors
  • Activation of …
  • … of NMDA/AMPA receptors - alters kinetics of channels and causes insertion of more channels - neurons fire more easily - also channel protein …
A
  • Constant firing of axons from the periphery (following injury)
  • Sustained release of glutamate
  • Prolonged depolarisation of the postsynaptic membrane
  • Massive influx of calcium ions through NMDA receptors
  • Activation of kinases
  • Phosphorylation of NMDA/AMPA receptors - alters kinetics of channels and causes insertion of more channels - neurons fire more easily - also channel protein synthesis
33
Q

Reduced threshold for activation - central sensitization

  • Constant firing of axons from the periphery (following injury)
  • Sustained release of glutamate
  • Prolonged … of the postsynaptic membrane
  • … influx of calcium ions through NMDA receptors
  • Activation of kinases
  • Phosphorylation of NMDA/… receptors - alters … of channels and causes insertion of more channels - neurons fire more easily - also channel protein …
A
  • Constant firing of axons from the periphery (following injury)
  • Sustained release of glutamate
  • Prolonged depolarisation of the postsynaptic membrane
  • Massive influx of calcium ions through NMDA receptors
  • Activation of kinases
  • Phosphorylation of NMDA/AMPA receptors - alters kinetics of channels and causes insertion of more channels - neurons fire more easily - also channel protein synthesis
34
Q

Central hyperalgesia mechanism

  • Following central …:
    • Activation of nociceptors results in … spinal cord activation leading to …
A
  • Following central sensitization:
    • Activation of nociceptors results in amplified spinal cord activation leading to hyperalgesia
35
Q

Central allodynia mechanism

  • Non-noxious A… fibres also synapse onto … order spinothalamic neurons
    • Normally these are non-…
  • Following central sensitization:
    • Non-noxious afferents activate sensitized 2nd order neurons
A
  • Non-noxious Aβ fibres also synapse onto 2nd order spinothalamic neurons
    • Normally these are non-functional
  • Following central sensitization:
    • Non-noxious afferents activate sensitized 2nd order neurons
36
Q

Central allodynia mechanism

  • Non-… … fibres also synapse onto 2nd order spinothalamic neurons
    • Normally these are non-functional
  • Following central …:
    • Non-… afferents activate sensitized 2nd order neurons
A
  • Non-noxious Aβ fibres also synapse onto 2nd order spinothalamic neurons
    • Normally these are non-functional
  • Following central sensitization:
    • Non-noxious afferents activate sensitized 2nd order neurons
37
Q

Problem with central changes (pain) = not easily …

A

Problem with central changes (pain) = not easily reversible

38
Q

Chronic pain - treatments

  • Difficult to treat - … pain treatments often do not work
  • Good individual patient … is critical
  • Important to manage primary condition as well as other associated symptoms
    • Depression
    • … disturbances
    • …
A
  • Difficult to treat - Acute pain treatments often do not work
  • Good individual patient management is critical
  • Important to manage primary condition as well as other associated symptoms
    • Depression
    • Sleep disturbances
    • Fatigue
39
Q

Chronic pain - treatments

  • … to treat - Acute pain treatments often do not work
  • Good individual patient management is critical
  • Important to manage primary condition as well as other associated symptoms
    • …
    • Sleep …
    • …
A
  • Difficult to treat - Acute pain treatments often do not work
  • Good individual patient management is critical
  • Important to manage primary condition as well as other associated symptoms
    • Depression
    • Sleep disturbances
    • Fatigue
40
Q

Current neuropathic pain treatments

  • Drugs:
    • … antidepressants
    • Anti…
    • Topical … or …
  • …puncture
  • Physical therapies – e.g. manipulation of tissues, pacing
  • Psychological therapies – e.g. … … therapy
  • Surgery – e.g. spinal cord stimulator (activate a-beta fibres as they enter spinal cord - activate inhibitory interneurons which act on our second-order neurons - same as gate control)
A
  • Drugs:
    • Tricyclic antidepressants
    • Anticonvulsants
    • Topical capsaicin or lidocaine
  • Acupuncture
  • Physical therapies – e.g. manipulation of tissues, pacing
  • Psychological therapies – e.g. cognitive behavior therapy
  • Surgery – e.g. spinal cord stimulator (activate a-beta fibres as they enter spinal cord - activate inhibitory interneurons which act on our second-order neurons - same as gate control)
41
Q

Current neuropathic pain treatments

  • Drugs:
    • Tricyclic …
    • …
    • Topical capsaicin or …
  • …
  • Physical therapies – e.g. manipulation of tissues, pacing
  • Psychological therapies – e.g. cognitive behavior therapy
  • Surgery – e.g. spinal cord … (activate a-beta fibres as they enter spinal cord - activate inhibitory interneurons which act on our second-order neurons - same as gate control)
A
  • Drugs:
    • Tricyclic antidepressants
    • Anticonvulsants
    • Topical capsaicin or lidocaine
  • Acupuncture
  • Physical therapies – e.g. manipulation of tissues, pacing
  • Psychological therapies – e.g. cognitive behavior therapy
  • Surgery – e.g. spinal cord stimulator (activate a-beta fibres as they enter spinal cord - activate inhibitory interneurons which act on our second-order neurons - same as gate control)
42
Q

Tricyclic antidepressants

  • Examples include … and duloxetine
  • Act centrally
  • Mechanism of action:
    • Act on … … pathways
    • Inhibits reuptake of … (and noradrenalin)
A
  • Examples include amitriptyline and duloxetine
  • Act centrally
  • Mechanism of action:
    • Act on descending inhibitory pathways
    • Inhibits reuptake of serotonin (and noradrenalin)
43
Q

Anticonvulsants

  • Examples include … - fewer side effects, gabapentin and carbamazepine
  • Act centrally
  • Mechanism of action: (proposed)
    • Act in spinal cord to reduce …
    • Blocks calcium (…) and … (carbomazepine) channels
  • … blocks presynaptic voltage-gated Ca2+ channels - Prevent release of glutamate
A
  • Examples include pregabalin - fewer side effects, gabapentin and carbamazepine
  • Act centrally
  • Mechanism of action: (proposed)
    • Act in spinal cord to reduce excitability
    • Blocks calcium (pregabalin) and sodium (carbomazepine) channels
  • Pregabalin blocks presynaptic voltage-gated Ca2+ channels - Prevent release of glutamate
44
Q

Anticonvulsants

  • Examples include pregabalin - fewer side effects, gabapentin and …
  • Act centrally
  • Mechanism of action: (proposed)
    • Act in … … to reduce excitability
    • Blocks calcium (pregabalin) and sodium (…) channels
  • Pregabalin blocks presynaptic voltage-gated Ca2+ channels - Prevent release of …
A
  • Examples include pregabalin - fewer side effects, gabapentin and carbamazepine
  • Act centrally
  • Mechanism of action: (proposed)
    • Act in spinal cord to reduce excitability
    • Blocks calcium (pregabalin) and sodium (carbomazepine) channels
  • Pregabalin blocks presynaptic voltage-gated Ca2+ channels - Prevent release of glutamate
45
Q

NICE guidelines on treatment of neuropathic pain

  • First-line of treatment:
    • …, duloxetine, P… or gabapentin
  • Second-line of treatment:
    • … drugs or …
  • Third-line of treatment:
    • Refer patient to a … pain service and consider oral tramadol (opioid) or in combination with the second-line treatment consider topical lidocaine
A
  • First-line of treatment:
    • Amitriptyline, duloxetine, pregabalin or gabapentin
  • Second-line of treatment:
    • Switch drugs or combine
  • Third-line of treatment:
    • Refer patient to a specialist pain service and consider oral tramadol (opioid) or in combination with the second-line treatment consider topical lidocaine
46
Q

NICE guidelines on treatment of neuropathic pain

  • First-line of treatment:
    • …, duloxetine, pregabalin or gabapentin
  • Second-line of treatment:
    • Switch drugs or combine
  • Third-line of treatment:
    • … patient to a specialist pain service and consider oral … (opioid) or in combination with the second-line treatment consider topical …
A
  • First-line of treatment:
    • Amitriptyline, duloxetine, pregabalin or gabapentin
  • Second-line of treatment:
    • Switch drugs or combine
  • Third-line of treatment:
    • Refer patient to a specialist pain service and consider oral tramadol (opioid) or in combination with the second-line treatment consider topical lidocaine
47
Q

Placebo and complimentary alternative medicines

  • Important to consider the … effect
    • … analgesia has been demonstrated (in well controlled studies) for the treatment of neuropathic pain - Due to activation of descending inhibitory pathways
  • Many Complementary Alternative Medicines
    • Examples include …, massage therapy, homeopathy, hypnosis, reiki
  • BUT - ‘Very few forms of CAM reduce pain in a clinically relevant way’
  • Exceptions include … -trigger release of endorphins
A
  • Important to consider the placebo effect
    • Placebo analgesia has been demonstrated (in well controlled studies) for the treatment of neuropathic pain - Due to activation of descending inhibitory pathways
  • Many Complementary Alternative Medicines
    • Examples include acupuncture, massage therapy, homeopathy, hypnosis, reiki
  • BUT - ‘Very few forms of CAM reduce pain in a clinically relevant way’
  • Exceptions include acupuncture -trigger release of endorphins
48
Q

Placebo and complimentary alternative medicines

  • Important to consider the placebo effect
    • Placebo analgesia has been demonstrated (in well controlled studies) for the treatment of neuropathic pain - Due to activation of … … pathways
  • Many … Alternative Medicines
    • Examples include acupuncture, massage therapy, homeopathy, hypnosis, reiki
  • BUT - ‘Very few forms of CAM reduce pain in a clinically relevant way’
  • Exceptions include acupuncture -trigger release of …
A
  • Important to consider the placebo effect
    • Placebo analgesia has been demonstrated (in well controlled studies) for the treatment of neuropathic pain - Due to activation of descending inhibitory pathways
  • Many Complementary Alternative Medicines
    • Examples include acupuncture, massage therapy, homeopathy, hypnosis, reiki
  • BUT - ‘Very few forms of CAM reduce pain in a clinically relevant way’
  • Exceptions include acupuncture -trigger release of endorphins
49
Q

What’s gone wrong in chronic pain?

A

Year 2 Medicine (162 decks)

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