Pain Pathway (2) Flashcards

1
Q

What are the 2 components of pain?

A

Sensory (discriminative)

Motivational (affective)

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2
Q

What are the ascending pain pathways?

A

Spinothalamic and Tigemino-thalamic tracts

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3
Q

What part of the brain does pain transmit to?

A

Cerebral cortex for perception of pain

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4
Q

Responses to painful stimuli include:

A

Attention and arousal
Somatic and autonomic reflexes
Endocrine responses
Emotional changes

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5
Q

Why is pain described as having complex nature?

A

emphasizes the complex nature of pain as a physical, emotional, and psychological condition

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6
Q

What is nociception? What do medications target?

A

The experience of pain with a series of complex neurophysiologic processes

Meds target causes of pain by actions on transduction, transmission, interpretation, and modulation in both PNS and CNS.

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7
Q

Hyperalgesia:

A

Increased pain sensations to normally painful stimuli

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8
Q

Allodynia:

A

Perception of pain sensations in response to normally non-painful stimuli

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9
Q

Chronic pain in ___% of the population

A

40%

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10
Q

Annual cost related to pain:

A

$40 billion (not including surgery and lost workdays)

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11
Q

Most common reason for people seeking medical care:

A

Pain

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12
Q

Low back pain __% - ___% in people 45-60y/o

A

8-37

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13
Q

What is the pathway after nociception stimulation?

A
  • Transduction
  • Transmission
  • Modulation
  • Perception
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14
Q

Nerve/electrical impulses/signals start at the nerve endings:

A

Transduction

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15
Q

Travel of nerve/electrical impulses to the nerve body connecting to the dorsal horn of the spinal cord:

A

Transmission

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16
Q

Process of altering (inhibitory/excitatory) pain transmission mechanisms at the dorsal horm to the PNS and CNS:

A

Modulation

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17
Q

Thalamus acting as the central relay station from incoming pain signal and the primary somatosensory cortex serving for discrimination of specific sensory stimuli:

A

Perception

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18
Q

What is the central relay station for incoming pain signals?

A

Thalamus

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19
Q

Where is the primary discrimination area for specific sensory stimuli?

A

Somatosensory Cortex

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20
Q

Where does modulation of pain transmission occur?

A

Dorsal horn

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21
Q

Where does transduction of nerve impulses start?

A

Nerve endings

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22
Q

What meds affect transduction of pain from mechanical, chemical, and thermal stimuli into action potentials?

A

LA, NSAIDS (peripheral nociceptors)

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23
Q

What med modulates transmission of pain action potentials via A delta and C fibers?

A

Local Anesthetics

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24
Q

What meds modulate afferent signals of pain in the dorsal horn of spinal cord?

A

LA, opioids, ketamine, A2 agonist

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25
Q

What meds alter perception of pain by activating descending inhibitory pain pathway and memory?

A

Opioids, A2 agonists, General Anesthetics

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26
Q

Where does the modulation of pain impulses occur?

A

Dorsal horn

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27
Q

Where are nociceptors located?

A
  • Skin
  • Muscles
  • Joints
  • Viscera
  • Vasculature
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28
Q

How does pain pathway progress from peripheral nerve?

A

Stimulus→ nociceptor→ resting threshold → transmission→modulation→interpretation

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29
Q

What type of fibers are afferent unmyelinated fibers? What type of pain is transmitted on these fibers?

A

C fibers: burning pain from heat and pressure from sustained pressure

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30
Q

What type fibers (I and II) are afferent myelinated fibers?

A

Type I fibers ( Aβ & Aδ fibers): heat, mechanical, chemical
Type II fibers (Aδ fibers): heat

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31
Q

What are the chemical mediators for pain in the periphery?

A

Peptides (substance P, Calcitonin, bradykinin, CGRP)

Eicosanoids

Lipids (PGs, TXA, leukotrienes, endocannabinoids)

Neutrophins

Cytokines

Chemokines

Extracellular Proteases and protons

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32
Q

What chemical mediator is released first in response to pain?

A

Bradykinin

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32
Q

What do chemical mediators of pain cause?

A

Vasodilation, Inflammation, expansion of pain

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33
Q

Decreased pain threshold at the original site of injury from heat and mechanical injury:

A

Primary hyperalgesia

33
Q

What happens as a result of Primary hyperalgesia?

A

Decreased pain threshold
Increased response to suprathreshold stimuli
Spontaneous pain
Expansion of receptive field

34
Q

Uninjured skin surrounding the injury (only mechanical stimuli):

A

Secondary Hyperalgesia

35
Q

What happens with secondary hyperalgesia?

A

Sensitization of central neuronal circuits

36
Q

What is the relay center for nociceptive and other sensory activity in the CNS?

A

Spinal dorsal horn

37
Q

What is the path for the ascending pain pathway?

A

Goes to brainstem and forebrain→perception of pain location and intensity

38
Q

What is another term for lamina I? What fibers synapse here?

A

Lamina marginalis

Afferent C fibers

39
Q

What is another term for lamina II? What fibers synapse here?

A

Substantia Gelatinosa

Afferent C fibers

40
Q

Where do myelinated fibers synapse? What are they innervating?

A

Lamina I, IV, VII and ventral horn (A fibers)

Innervating muscles and viscera

41
Q

Which lamina do opioids work to inhibit pain transmission?

42
Q

Which lamina affect NKI receptor with substance P?

A

Lamina III and IV

43
Q

When did the gate control theory of pain come about?

44
Q

What does the “gate open” indicate? What fibers are involved when gate is open?

A

Pain is projected to supraspinal brain regions

A delta fibers (small, myelinated) and C fibers (unmyelinated)

45
Q

What does “gate closed” indicate? What fibers are involved?

A

Pain is not felt with simultaneous inhibitor impulses (EX: rubbing bumped elbow)

A beta fibers (larger diameter and myelinated)

46
Q

Which fibers deliver info about pressure and touch?

A

A beta fibers→large, myelinated

47
Q

Where is perception of motivational-affective pain components sent?

A

Limbic cortex and thalamus

48
Q

Area in the brain that depresses or facilitates the integration of pain info in the spinal dorsal horn:

A

Periaqueductal gray (PAG) / Rostral Ventromedial Medulla (RVM)

49
Q

Neuromodulators of the CNS:

A
  • Substance P
  • Glutamate
  • CGRP
  • NMDA
  • AMPA
  • BDNF
  • Cytokines
50
Q

Tissue injury releases _______ and ________ to the nociceptor.

A
  • Substance P
  • Glutamate
51
Q

What mediators do damaged cells, mast cells, and platelets release?

A
  • Bradykinin
  • Histamine
  • PGs
  • Serotonin
  • H+ ions
  • Lactic Acid
52
Q

A excitatory impulse mediator:

53
Q

Excitatory impulse modulation in the spinal cord:

A
  • Glutamate
  • Calcitonin
  • Neuropeptide Y
  • Aspartate
  • Substance P
54
Q

Inhibitory impulse modulation in the spinal cord:

A
  • GABA
  • Glycine
  • Enkephalins
  • Norepinephrine
  • Dopamine
55
Q

What are the different ascending pathways of nociceptive info?

A
  • Spinothalamic
  • Spinomedullary
  • Spinobulbar
  • Spinohypothalamic
56
Q

Which ascending pathway is responsible for pain, temp, and itch?

A

Spintothalamic (lamina I, VII, VIII) all afferent fibers

57
Q

Which ascending pathway involves the behavior toward pain?

A

Spinobulbar (laminae I, V, VII)

58
Q

Which ascending pathway involves autonomic, neuroendocrine, and emotional aspects of pain?

A

Spinohypothalamic (Laminae I, V, VII, and X)

59
Q

What part of the forebrain is involved with identifying pain location?

A

SI: primary somatosensory cortex

60
Q

What part of the forebrain is involved with intensity of pain?

61
Q

Where does supraspinal modulation of nociception occur?

A
  • Forebrain (SI and SII)
  • Anterior cingulate cortex ()ACC
  • Insular cortex: ACC and IC: emotional/motivational aspects
  • Prefrontal Cortex
  • Thalamus
  • Cerebellum
62
Q

Where does the descending inhibitory tract originate? Where does the signal travel through and then synpase?

A

Periaqueductal gray (PAG) → Travels through rostral ventromedial medulla (RVM) → dorsolateral funiculus → Synpase in dorsal horn

63
Q

What neurotransmitters are involves in descending inhibitory tract?

A

Endorphins, Enkephalins, Serotonin

64
Q

What is the MOA of descending inhibitory tract?

A

Hyperpolarize: uses A delta and C fibers

Decrease release of substance P→ opening of K+ channels/ inhibition of Ca++ channels

65
Q

What factors affect the descending inhibition/facilitation pathways?

A

Other somatic stimuli: lack of sleep, stress, prior experiences, etc

Psychosocial factors: arousal, attention, and expectation

66
Q

Which receptors are part of the the PAG-RVM system?

A

Mu, Kappa, Delta

(hyperalgesia and allodynia)

67
Q

Where does the pain impulse originate if it is pertaining to the descending inhibitory tract?

68
Q

How long does pain have to last to classify as chronic?

A

> 3-6 months→ persists beyond tissue healing

69
Q

Unpleasant emotional experiences use the same pathways as ________ __________.

A

Chronic pain

anxiety, depression, cognitive deficits, emotional distress

70
Q

Type of pain that persists after the tissue has healed:

A

Neuropathic pain→ allodynia and hyperalgesia

71
Q

Who is at increased risk for neuropathic pain?

A

Cancer patients d/t chemo and radiation therapy

72
Q

What is the treatment for neuropathic pain?

A

Treat based on symptoms (opioids, gabapentin, amitryptiline, cannabis)

73
Q

Diffuse, poorly localized pain: What are causes of this?

A

Visceral Pain

Ischemia, Stretching of ligament attachments , spasms, distention

74
Q

Complex Regional Pain Syndromes:

A

A variety of painful conditions following injury in a region with impairment of sensory, motor, and autonomic systems

Spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, active and passive movement disorders, and trophic changes of skin & SQ tissues

75
Q

How does the CV system respond to pain?

A

↑BP
↑HR
↑SVR
↑ myocardial irritability

↓CO
↓Myocardial ischemia

76
Q

How does pulmonary system respond to pain?

A

↑ total body O2 consumption/CO2 production
↑ Vm and work of breathing

Splinting

Decreased movement of chest wall
Atelectasis
Intrapulmonary shunting

Impaired coughing

77
Q

How does GI/GU respond to pain?

A

Increased sphincter tone
Decreased mobility (ileus, urinary retention)

Hyper secretion of acid (stress ulcers, aspiration)

N/V

ABD distention (decrease peristalsis)

78
Q

Endocrine system response to pain:

A

↑ catabolic hormones
* Catecholamines
* Cortisol
* Glucagon

↓ anabolic hormones
* Insulin
* Testosterone

Effects
* Negative nitrogen balance
*Carbohydrate intolerance
*Increases renin, aldosterone, and angiotensin

79
Q

What are hematologic responses to pain?

A

Stress related:

  • Platelet Adhesiveness
  • Reduced fibrinolysis
  • Hyper-coagulability
80
Q

How does the immune system respond to pain?

A

Stress related

  • Leukocytosis
  • Depressed reticuloendothelial system (increased infection)
81
Q

What are some emotional responses to pain?

A
  • Anxiety
  • Sleep disturbance
  • Depression