*Pain Pathways (Exam II) Flashcards

1
Q

What are the 2 components of pain?

A
  1. Sensory-discriminative
  2. Motivational-affective

S3

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2
Q

Differentiate the sensory-discriminative & motivational-affective aspects of pain.

A
  • Sensory-discriminative - Ascending pathways and the perception of pain (location, intensity, sensation, etc.)
  • Motivational affective - responses to painful stimuli (Ex. arousal, reflexes, endocrine responses, and emotional changes)

S3

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3
Q

What is nociception?

A
  • The experience of pain through a series of complex neurophysiologic processes.

S4

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4
Q

Medication targets causes of pain through actions on 4 things

A
  1. transduction
  2. transmission
  3. modulation
  4. interpretation

in both PNS and CNS

S4

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5
Q

What is the % of Chronic pain in adult population

A

40 %

(8% - 37% low back pain)

S6

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6
Q

What are the four stages of pain perception?

A
  1. Transduction (tissue level)
  2. Transmission (via nerves)
  3. Modulation (via spinal cord)
  4. Perception (CNS)

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7
Q

What is Transduction?
What 3 types of stimuli turns into action potential?

A

Nerve/electrical impulses/signals start at the nerve endings

Type of stimuli:
- mechanical
- chemical
- thermal

S9 and S10

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8
Q

What is Transmission?
Which nerve fibers are involved?

A

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

  • A delta and C fibers

S9 and S10

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9
Q

What is Modulation?

A

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

S9

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10
Q

What is Perception?
What does it activate?

A

Thalamus acting as the central relay station for incoming pain signals & the primary somatosensory cortex serving for discrimination of specific sensory stimuli.

it activates descending inhibitory pain pathways and memory

S9 and S10

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11
Q

What drugs are used to affect the transduction of pain?
What specifically is being affected by these drugs?

A
  • Local anesthetics & NSAIDs
  • Peripheral nociceptors are affected

S10

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12
Q

What drugs are used to affect the transmission of pain?
What specifically is being affected by these drugs?

A
  • Local anesthetics
  • Αδ and C fibers
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13
Q

What drugs are used to affect the modulation of pain?
What specifically is being affected by these drugs?

A
  • LA’s, opioids, ketamine, α2 agonists
  • Afferent fibers of the dorsal horn

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14
Q

What drugs are used to affect the perception of pain?
What specifically is being affected by these drugs?

A
  • General anesthetics, opioids, α2 agonists
    -Brain

S10

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15
Q

Where does the modulation of pain impulses occur?

A

Dorsal horn of the spinal cord

S12

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16
Q

Where are nociceptors located?

A
  • Skin
  • Muscles
  • Joints
  • Viscera
  • Vasculature

S13

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17
Q

What characterizes afferent C-fibers?

A
  • Unmyelinated
  • Pain from heat (burning) & sustained pressure
  • Slow (less than 2 m/s)

S14

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18
Q

What characterizes A fibers?

A

-Myelinated
- Type I: Aβ & Aδ (heat,mechanical, chemical)
- Type II: Aδ (heat)
- Fast (>2 m/s)

S14

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19
Q

What chemical mediators of pain are targeted with spinal anesthetics?

A

Peptides

  • Bradykinin
  • Calcitonin
  • CGRP
  • Substance P

S15 NEED TO MEMORIZE THIS

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20
Q

Which chemical mediator is released first in response to injury?

A

Bradykinin

S15 NEED TO MEMORIZE THIS

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21
Q

What chemical mediators of pain are inhibited by NSAIDs?

A

Lipids
- Prostaglandins
- Thromboxanes

S15 NEED TO MEMORIZE THIS

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22
Q

What chemical mediators of pain are inhibited by cannabis?

A

Lipids
- Endocannabinoids

S15 NEED TO MEMORIZE THIS

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23
Q

What is sensitization?

A
  • Decreased pain threshold (likely due to upregulation of receptors)

S18

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24
Q

↑ pain sensations to normally painful stimuli.

A

Hyperalgesia

S18

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25
Q

perception of pain to normally non-painful stimuli

A

Allodynia

S18

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26
Q

What characterizes primary hyperalgesia?

A

Hyperalgesia at original site of injury.

  • Lower pain threshold
  • increased response to suprathreshold stimuli
  • Spontaneous pain
  • Expansion of receptive field

S19

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27
Q

What characterizes secondary hyperalgesia?

A
  • Sensitization of CNS → hyperalgesia from uninjured skin surrounding injury.

S19

28
Q

What is the relay center for nociceptive and sensory activity?
How does sensory activity travel from this area to the cerebrum?

A
  • Spinal Dorsal Horn
  • travels through Ascending pathways

S20

29
Q

What area of the brain accounts for the perception (location & intensity) of pain?

A
  • Somatosensory Cortex I & II (SI & SII)

S20

30
Q

Where are afferent C-fibers located in the spinal column?

A
  • Dorsal horn: Lamina I & II

S21

31
Q

What is another name for Lamina II?
What drugs work here?

A
  • Substantia gelatinosa
  • Opioids work here
  • also Alpha 2 Agonist (according to Castillo)

S21

32
Q

Where are mylinated fibers that innervate muscles and viscera located in the spinal column?

A

Laminae I, IV, & VII, and ventral horn

S21

33
Q

Whichlaminaes are NKI receptor and substance P located in the spinal column?

A

Laminae III & IV

S21

34
Q

What happens when pain is projected to supraspinal brain regions

A

Gate is OPEN

S22

35
Q

What happens when pain is not felt with simultaneous inhibitory impulses?

A

Gate is CLOSE

S22

36
Q

What nerve fibers are associated with an “open-gate” for pain?
What nerve fibers can shut this gate?

A
  • Aδ & C-fibers = open
  • Aβ fibers = closed

S22

37
Q

What parts of the brain are involved in the Perception of motivational-affective pain components?

A
  • Limbic cortex
  • Thalamus

S23

38
Q

What areas of the brain may depress or facilitate the integration of painful information in the spinal dorsal horn?

A
  • PAG - Peraqueductal Gray Matter
  • RVM - Rostral Ventral Medulla

S23

39
Q

What neurotransmitters propagate excitatory transmissions in the spinal column?

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

S28

40
Q

What neurotransmitters propagate inhibitory transmissions in the spinal column?

A
  • GABAA
  • Glycine
  • Enkephalins
  • NE
  • Dopamine

S28

41
Q

What are the four ascending pain pathways?

A
  • Spinothalamic
  • Spinomedullary
  • Spinobulbar
  • Spinohypothalamic

S29

42
Q

What information is carried by the spinothalamic pathway?
What laminae are used?

A
  • Pain, Temp, & Itch
  • Laminae I, VII, and VIII

S29

43
Q

What information is carried by the spinobulbar pathway?
What laminae are used?

A
  • Behavior towards pain
  • Laminae I, V, and VII

S29

44
Q

What information is carried by the spinohypothalamic pathway?
What laminae are used?

A
  • Autonomic, neuroendocrine & emotional aspects of pain
  • Laminae I, V, VII, & X.

S29

45
Q

What part of the suprapinal pathway differentiates where pain is coming from?

A

Forebrain S1 & S2 (Somatosensory cortex 1 & 2)

S30

46
Q

What supraspinal areas deal with the emotional/motivational aspects of pain?

A
  • Anterior cingulate cortex (ACC)
  • Insular Cortex (IC)

S30

47
Q

Where do the descending inhibitory tracts originate?
Where do they then synapse at?

A
  • PAG (periaqeueductal gray matter)
  • then synapse at dorsal horn

S31

48
Q

What neurotransmitters are increased with exercise?

A

-Serotonin
- Endorphins
- Enkephalins

S31

49
Q

How do inhibitory tracts inhibit the propagation of painful stimuli?

A

Hyperpolarizing Aδ & C fibers

  • ↓ release of substance P
  • ↑ pK⁺ and inhibiting Ca⁺⁺ channels

S31

50
Q

Descending pathways of pain modulation can be ____ or ____ ?

A

Inhibited or Faciliated

  • Descending Inhibition Pathway (DI)
  • Descending Facilitation Pathway (DF)

S32

51
Q

What are factors of Descending Pathways of pain modulation?

A
  • Other somatic stimuli
  • Psychological factors (arousal, attention, and expectation)

S32

52
Q

Where does the pain inhibiting impulse originate from in the descending inhibitory tracts?

A

PAG-RVM areas

S32 and 34

53
Q

When is pain considered chronic rather than acute?

A
  • If > 3 - 6 months
  • If pain persists beyond tissue healing

S36

54
Q

Type of pain that persists after the tissue has healed

A

Neuropathic pain

S37

55
Q

Who is at increased risk of neuropathic chronic pain?

A
  • Cancer patients
  • Diabetics

S37

56
Q

What is the treatment for chronic neuropathic pain?

A
  • Opioids
  • Gabapentin
  • Cannabis
  • Amitriptyline

All situation dependent

S37

57
Q

How is visceral pain characterized?

A

Diffuse and poorly localized

S37

58
Q

What is complex regional pain syndrome?

A

Variety of painful issues following an injury
(sponateous pain, hyperalgesia, edema, etc.)

S38

59
Q

When can babies begin to perceive pain?

A

23 weeks

they have lower pain threshold & exaggerated pain responses

S38

60
Q

How can the effects of pain in the cardiovascular system be summarized?

A
  • ↑ SNS
    (↑BP, HR, ↑ SVR, etc.)
  • Compromised LV

S40

61
Q

What are the pulmonary effects of chronic pain?

A
  • ↑ total body O2 consumption/CO2 production
  • Decreased movement of chest wall (Atelectasis & Intrapulmonary shunting)
  • Impaired coughing

S41

62
Q

How does pain affect the GI/GU system?

A
  • ↑ SNS = ↑ sphincter tone and ↓ peristalsis = N/V, ileus, distension, etc.
  • hypersecretion of acid
  • Stress ulcers

S42

63
Q

What hormones experience an increase in response to chronic pain?

A

catabolic hormones
*Catecholamines
*Cortisol
*Glucagon

S43

64
Q

What hormones experience a decrease in response to chronic pain?

A

Anabolic Hormones
- Insulin
- Testosterone

S43

65
Q

What are Hematologic Response to pain?

A

Stress Related

  • Platelet adhesiveness
  • Reduced fibrinolysis
  • Hypercoagulability

S44

66
Q

What are emotional responses to pain?

A
  • Anxiety
  • Sleep disturbance
  • Depression

S45

67
Q

What are immune responses to pain?

A
  • Stress related
    Leukocytosis
  • Depressed reticuloendothelial system
    Increased infection

S45