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Mar: Sem 6 - Principles B > Acute and Chronic Pain > Flashcards

Acute and Chronic Pain Flashcards

1
Q

What are the different ways to classify pain?

A
  • Length (Acute/Chronic)
  • Physiology (Nocicpetic/Neuropathic)
  • Etiology
  • Affected Area
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2
Q

What is acute pain primarily due to?

A

Nociception

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3
Q

What is chronic pain primarily due to?

A
  • Neuropathic
  • Physiological and behavior factors
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4
Q

What are the four major processes of pain?

A
  • Transduction
  • Transmission
  • Modulation
  • Perception
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5
Q

What is transduction?

A
  • Noxious stimuli are converted to nerve impulses by nociceptors.
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6
Q

Fibers that transmit “fast pain” that is sharp and well localized.

A

A-δ fibers

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7
Q

Fibers that transmit “slow pain” that is dull and poorly localized.

A

C fibers

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8
Q

How will inflammation contribute to the threshold of pain stimulus?

A

Reduce threshold to pain stimulus (allodynia)

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9
Q

How will inflammation contribute to the response to pain stimulus?

A

Increase response to pain stimulus (hyperalgesia)

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10
Q

What are the inflammatory mediators involved in Transduction?

A
  • Prostaglandin
  • Bradykinin
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11
Q

What are the excitatory mediators involved in Transduction?

A
  • Glutamate
  • CGRP
  • NGF
  • SP
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12
Q

What are the inhibitory mediators involved in Transduction?

A
  • Opioids
  • SST
  • Cannabinoids
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13
Q

What is transmission?

A

Pain signals are relayed from the afferent pathway along the spinothalamic tract to the brain.

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14
Q

What is the first-order neuron?

A
  • Pain signal from periphery to dorsal horn (cell body in dorsal root ganglion)
  • Pain source to spine
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15
Q

What is the second-order neuron?

A
  • Signal from dorsal horn to thalamus (cell body in dorsal horn)
  • Spine to brain
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16
Q

What is the third-order neuron?

A
  • Thalamus to the cerebral cortex (cell body in the thalamus)
  • Brain to cerebral cortex
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17
Q

What is Modulation?

A

The process where the pain signal is amplified or dampened as it advances toward the cerebral cortex.

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18
Q

What is the most important site of modulation?

A

Substantia Gelatinosa in the Dorsal Horn (Lamina II and Lamina III)

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19
Q

Where does the descending inhibitory pathway begin before it is projected to the Substantial Gelatinosa?

A
  • Periaqueductal Gray
  • Rostroventral Medulla
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20
Q

How is pain inhibited?

A
  • Spinal neurons release GABA and glycine (inhibitory NT)
  • Descending pathway release NE, 5HT, and endorphins
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21
Q

How is pain augmented?

A
  • Central sensitization
  • Wind-up
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22
Q

Where does modulation occur?

A
  • Nociceptor in the spinal cord
  • Nociceptor in the supraspinal structures
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23
Q

How is peripheral modulation of pain facilitated?

A

Nociceptors and neurons display sensitization from repeated stimulation

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24
Q

How is peripheral modulation of pain inhibited?

A

Peripheral exogenous opioid release

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25
Q

How is central modulation of pain facilitated?

A
  • Wind-up and sensitization of second-order neurons
  • Receptive field expansion
  • Hyperexcitability of flexion reflexes
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26
Q

How is central modulation of pain inhibited?

A
  • Segmental inhibition (signal stops in second-order neuron and spinothalamic tract)
  • Supraspinal inhibition (signal sent down the spinal cord to inhibit pain at the dorsal horn)
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27
Q

What is perception?

A

How we process afferent pain signals in the cerebral cortex and limbic system

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28
Q

What drugs can prevent pain Transduction?

A
  • NSAIDs
  • Antihistamine
  • Opioids
  • LA
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29
Q

What drugs can prevent pain Transmission?

A
  • LA
  • Opioids
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30
Q

What drugs can prevent pain Modulation?

A
  • Opioids
  • Alpha-2 agonist
  • NMDA receptor antagonists
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31
Q

What drugs can prevent pain Perception?

A
  • Opioids
  • Alpha-2 agonist
  • General Anesthesia
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32
Q

What are the two types of Neuropathic Pain?

A
  • Central
  • Peripheral
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33
Q

What are the two types of Nociceptive Pain?

A
  • Visceral
  • Somatic
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34
Q

What are the two types of Visceral Pain?

A
  • True
  • Parietal
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35
Q

What are the two types of Somatic Pain?

A
  • Superficial
  • Deep
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36
Q

What is the most common cause of acute pain?

A

Nociceptive Pain

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37
Q

What is the benefit of having acute pain?

A

Serves to detect, localize, and limit tissue damage (ie: hot stove)

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38
Q

How is somatic superficial pain characterized?

A
  • Well localized
  • Sharp
  • Pricking, Throbbing, Burning
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39
Q

How is somatic deep pain characterized?

A
  • Less well-localized
  • Dull, aching
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40
Q

What is the cause of visceral pain?

A

D/t disease process or abnormal organ function

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41
Q

How is true visceral pain characterized?

A
  • Can be localized or referred
  • Dull, diffused, usually midline
42
Q

How is parietal visceral pain characterized?

A
  • Can be localized or referred
  • Sharp, stabbing localized to the organ or distant site
43
Q

How is chronic pain categorized?

A
  • Malignant (R/t CA and its treatment)
  • Nonmalignant (Neuropathic, musculoskeletal, inflammatory)
44
Q

What are the different types of Chronic Pain Syndromes?

A
  • Somatic (low back pain, degen. disc sx, failed back sx.)
  • Visceral (abdominal CA, pancreatitis)
  • Neuropathic (CRPS, trigem. neuralgia, phantom pain)
45
Q

This type of pain is caused by injury to the Nervous System.

A

Neuropathic Pain

  • Result of tumor compressing nerve or spinal cord
  • Cancer actually infiltrating into nerves or spinal cord
  • Diabetic neuropathy
46
Q

How is chronic pain developed?

A
  • Peripheral sensitization: Injury → chemical release → sensitizing area. ↓ Threshold and ↑ response to nociception.
  • Central sensitization: Membrane excitability, synaptic recruitment, and ↓ inhibition. Uncoupling of pain from peripheral stimuli.
47
Q

What is sensitization?

A

The process where repeated stimuli reduce the threshold of primary afferent nociceptors.

48
Q

What is Complex Regional Pain Syndrome (CRPS)

A

Neuropathic pain disorder (chronic pain condition) usually affecting a limb after an injury or surgery,

49
Q

What are the risk factors to developing CRPS?

A
  • Previous trauma or surgery
  • Nerve injury (Causalgia, Type II)
  • Work-related injury
  • Female
50
Q

What are the two types of CRPS?

A
  • Reflex sympathetic dystrophy (Type I)
  • Causalgia (Type II) - documentation of a prior nerve injury
51
Q

Signs and Symptoms of CRPS?

A
  • Spontaneous pain
  • Hyperalgesia
  • Allodynia
  • Active and passive movement disorders
52
Q

What is Reflex sympathetic dystrophy (Type I)?

A
  • Pain disproportionate to injury.
  • Pain persists beyond the time the tissue-damaging process has ended.
53
Q

How does the sympathetic nervous system play a major role in Reflex Sympathetic Dystrophy?

A

Sympathetic outflow can induce the discharge of primary afferent nociceptors

Selective blockade of the sympathetic outflow provides relief.

54
Q

What will continuous sympathetic outflow cause to the muscle?

A

Nociceptor activity will cause muscle contractions (sometimes sustained)

Use of Skeletal Muscle Relaxants will provide relief

55
Q

What is Causalgia (Type II)?

A

Causalgia arises after an injury or trauma to a peripheral nerve.

56
Q

The most common site of CRPS II pain is the ____________.

A

Brachial Plexus

57
Q

Where is CRPS Type II pain generally localized?

A

Around the injured nerve

58
Q

What are the symptoms of Type II pain?

A
  • Similar to Type I (burning, aching)
  • Pain exceeds 6 months
59
Q

Complex Post Surgical Pain (CPSP) affects what percentage of patients?

A

10%

  • Begins as “difficult to control” acute postoperative pain
  • Becomes persistent pain with neuropathic features and unresponsive to opioids
60
Q

What is considered Complex Post Surgical Pain (CPSP)?

A
  • Pain that persists longer than expected
  • 3-6 months post-op
  • D/t possible nerve damage during the procedure

Described as hyperalgesia, dysaesthesia, allodynia

61
Q

What is the first-line treatment for neuropathic pain?

A
  • TCA
  • SNRI
  • Gabapentanoids
  • Topicals

4-6 week time line for drugs to reach therapeutic levels and assess effectiveness.

62
Q

What is the third-line treatment for neuropathic pain?

A
  • Referred to Pain Specialist
  • SSRIs/ Anticonvulsants/ NMDA Antagonist
  • Interventional Therapies
63
Q

What is the fourth-line treatment for neuropathic pain?

A

Neuromodulation (Stimulator Trial)

Will need >50% pain relief w/ trial before implant

64
Q

What is the fifth-line treatment for neuropathic pain?

A

Low Dose Opioids

4-6 week time line for drugs to reach therapeutic levels and assess effectiveness.

65
Q

What is the sixth-line treatment for neuropathic pain?

A

Targeted Drug Therapy (Implantable Pain Pump Trial)

Will need >50% pain relief w/ trial before implant

66
Q

When will Interdisciplinary Management of Chronic Pain be the most helpful?

A

Helpful in Chronic Non-malignant Pain

Psychologist, PT, OT, Anesthesia combo

67
Q

What is the most studied antidepressant for tx of neuropathic pain?

A
  • Tricyclic Antidepressant (TCA)
  • First-line treatment of neuropathic pain
68
Q

MOA of TCA

A
  • Inhibition of serotonin and norepinephrine re-uptake
  • Blocks histamine, adrenaline, ACh, and Na Channels
  • Pain relief at 20-30% of effective antidepressant dose
69
Q

What are the most commonly studied SNRIs for tx of neuropathic pain?

A
  • Duloxetine (Cymbalta)
  • Venlafaxine (Effexor)
70
Q

MOA of SNRIs

A

Facilitate descending inhibition by blocking serotonin and noradrenaline (NE) reuptake.

71
Q

SNRIs will be most helpful in these patients dealing with neuropathic pain.

A
  • Peripheral diabetic neuropathy
  • Peripheral neuropathy
  • Osteoarthritis
  • Chronic low back pain
  • Fibromyalgia
  • Depression
72
Q

What anticonvulsant drugs are most commonly used to treat neuropathic pain?

A
  • Gabapentin (Gralise, Neurotin, Horizant)
  • Pregabalin (Lyrica)
  • Carbamazepine
73
Q

Dose of Gabapentin.
MAX dose.

A
  • 600 mg TID
  • MAX daily dose: 3600 mg
74
Q

Dose of Pregabalin.
MAX dose.

A
  • 150 mg BID or TID
  • MAX daily dose: 600 mg
75
Q

When will lidocaine patches be ineffective?

A
  • Post-surgical neuropathic pain
  • Diabetic neuropathy w/ allodynia or hyperalgesia
76
Q

MOA of Topical Capsaicin

A
  • Binds to TRPV1 receptor located on Aδ and C-nerve fibers
  • Release Sub-P and depolarize the nerve
  • Long term exposure → overstimulation, ↓ Sub-P = Desensitization of nerve and reversible nerve degeneration
77
Q

What concentration of Topical Capsaicin is recommended for neuropathic pain?

A

8%

78
Q

MOA of Tramadol

A
  • Weak mu-opioid agonist
  • Inhibitor of serotonin and NE reuptake

Effective in Tx of Neuropathy in Diabetics, postherpetic, and CA related pain

79
Q

What are possible procedural therapies for neuropathic pain?

A
  • Somatic blocks (Trigeminal nerve block)
  • Sympathetic blocks (Celiac plexus block)
  • Epidurals/ Radiofrequency ablation
  • Implantable stimulators (Spinal orDeep Brain)
80
Q

MOA of Ketamine

A
  • NMDA Antagonist
  • Astrocyte activation may stop the progression of neuropathic pain at its source
81
Q

Cells involved in neuralgia at the central level

A
  • Ependymal cells
  • Oligodendrocytes
  • Astrocytes
  • Microglia
82
Q

Cells involved in neuralgia at the peripheral level

A
  • Satellite cells
  • Schwann cells
83
Q

What is the hallmark sign of neuropathic pain?

A
  • Elevated extracellular levels of glutamate
  • This results in the presynaptic release of more glutamate
  • Impairs glutamate reuptake from glial cells
  • Increase pain sensation and transmission
84
Q

What β-lactam can be used to treat neuropathic pain?

A

Ceftriaxone

85
Q

What β-lactamase inhibitor can be used to treat neuropathic pain?

A

Clavulanic Acid

86
Q

What is Targeted Drug Delivery?

A
  • Delivery of medication to the site of action at the dorsal horn
  • Increases potency of medication
87
Q

What does Targeted Drug Delivery bypass?

A
  • First-pass metabolism
  • Blood-brain barrier
88
Q

What medications are usually used in Targeted Drug Delivery?

A
  • Morphine
  • Ziconotide (N-type calcium channel blocker)
89
Q

Benefits of Physical Activity for Pain

A
  • 30% improvement in low back pain
  • Extremely effective for centralized pain conditions
  • Cheap
90
Q

What supplements can be used to aid sleep?

A
  • Melatonin 3-10 mg qHS
  • L-theanine 200 mg qHS
  • Magnesium 200-600 mg (titrate to SE of loose stools)
91
Q

What medications can be used to aid sleep?

A
  • Cyclobenzaprine 5-10 mg (2 hr before bed)
  • Amitriptyline 25-50 mg qHS
  • Duloxetine 30-60 mg qHS
  • Gabapentin 300-600 mg qHS
92
Q

What lab is an accepted marker of chronic inflammation?

A
  • CRP
  • Obese patients are prone to chronic non-resolving inflammation
  • Elevated CRP → increase rates of low back pain
93
Q

What diets can decrease inflammation?

A
  • Fruits
  • Vegetables
  • Omega 3 Fatty Acids
94
Q

What diets are anti-inflammatory?

A
  • Fruits
  • Vegetables
  • Legumes
  • Healthy oils/ Omega
95
Q

What items are involved in the Mediterranean diet?

A
  • Vegetables
  • Fish
  • Olive oil as main fat
96
Q

What are the two non-essential amino acids?

A
  • Glutamate
  • Asparate
  • Both act as excitatory NT
97
Q

What is the most common negative emotion with chronic pain?

A

Anxiety

Education surrounding the cause of pain found to reduce pain in patients with fibromyalgia

98
Q

What is Tension Myositis Syndrome

A

A condition characterized by chronic muscle pain d/t psychological stress, emotional triggers, and tension rather than physical injury.

99
Q

Integrated Chronic Pain Management

A

Integrated Chronic Pain Management

100
Q

What is the second-line treatment for neuropathic pain?

A
  • Tramadol
  • Combo 1st line therapies

4-6 week time line for drugs to reach therapeutic levels and assess effectiveness.

Mar: Sem 6 - Principles B (14 decks)

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