Pain Pathways (Exam II) Flashcards

1
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)
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2
Q

What is nociception?

A
  • The experience of pain through a series of complex neurophysiologic processes.
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3
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, thalamus)
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4
Q

Where does the modulation of pain impulses occur?

A
  • Dorsal horn of the spinal cord
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5
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
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6
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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7
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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8
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
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9
Q

Where are nociceptors located?

A
  • Skin
  • Muscles
  • Joints
  • Viscera
  • Vasculature
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10
Q

What characterizes afferent C-fibers?

A
  • Unmyelinated
  • Pain from heat (burning) & sustained pressure
  • Slow (less than 2 m/s)
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11
Q

What characterizes Aδ fibers?

A

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

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12
Q

What chemical mediators of pain are targeted with spinal anesthetics?

A

Peptides

  • Substance P
  • Calcitonin
  • Bradykinin
  • CGRP
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13
Q

Which chemical mediator is released first in response to injury?

A
  • Bradykinin
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14
Q

What chemical mediators of pain are inhibited by NSAIDs?

A

Lipids
- Prostaglandins
- Thromboxanes

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15
Q

What chemical mediators of pain are inhibited by cannabis?

A

Lipids
- Endocannabinoids

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16
Q

What is sensitization?

A
  • Decreased pain threshold (likely due to upregulation of receptors)
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17
Q

Differentiate hyperalgesia and allodynia.

A
  • Hyperalgesia - ↑ pain sensations to normally painful stimuli.
  • Allodynia - perception of pain to things that aren’t normally painful.
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18
Q

What characterizes primary hyperalgesia?

A

Hyperalgesia at original site of injury.

  • Lower pain threshold
  • Spontaneous pain
  • Expansion of receptive field
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19
Q

What characterizes secondary hyperalgesia?

A
  • Sensitization of CNS → hyperalgesia from uninjured skin surrounding injury.
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20
Q

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

A
  • Somatosensory Cortex I & II (SI & SII)
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21
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
  • Ascending pathways
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22
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
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23
Q

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

A
  • Dorsal horn: Lamina I & II
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24
Q

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

A
  • Substantia gelatinosa
  • Opioids
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25
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
26
Q

What receptors does ketamine target for pain modulation?

A
  • NMDA
27
Q

The excision of what structure would result in the complete loss of perception of pain?

A

Amygdala

Bonus points if you just said the whole brain you degenerate.

28
Q

What neurotransmitters propagate excitatory transmissions in the spinal column?

A
  • Glutamate
  • Calcitonin
  • Neuropeptide Y
  • Aspartate
  • Substance P
29
Q

What neurotransmitters propagate inhibitory transmissions in the spinal column?

A
  • GABAA
  • Glycine
  • Enkephalins
  • NE
  • Dopamine
30
Q

What are the four ascending pain pathways?

A
  • Spinothalamic
  • Spinomedullary
  • Spinobulbar
  • Spinohypothalamic
31
Q

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

A
  • Pain, Temp, & Itch
  • Laminae I, VII, and VIII
32
Q

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

A
  • Behavior towards pain
  • Laminae I, V, and VII
33
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.
34
Q

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

A

S1 & S2 (Somatosensory cortex 1 & 2)

35
Q

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

A
  • Anterior cingulate cortex (ACC)
  • Insular Cortex (IC)
  • Amygdala
36
Q

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

A
  • PAG (periaqeueductal gray matter)
  • Synapse at dorsal horn
37
Q

What neurotransmitters are increased with exercise?

A
  • Endorphins
  • Enkephalins
  • Serotonin
38
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
39
Q

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

A

PAG-RVM areas

40
Q

When is pain considered chronic rather than acute?

A
  • If > 3 - 6 months
  • If pain persists beyond tissue healing
41
Q

Who is at increased risk of neuropathic chronic pain?

A
  • Cancer patients
  • Diabetics
42
Q

What is the treatment for chronic neuropathic pain?

A
  • Opioids
  • Gabapentin
  • Amitriptyline
  • Cannabis

All situation dependent

43
Q

How is visceral pain characterized?
What examples were given in lecture?

A
  • Diffuse and poorly localized
44
Q

What is complex regional pain syndrome?

A
  • Variety of painful issues following an injury (sponateous pain, hyperalgesia, edema, etc.)
45
Q

When can babies begin to perceive pain?

A

23 weeks

46
Q

How does pain affect the GI/GU system?

A
  • ↑ SNS = ↑ sphincter tone and ↓ peristalsis = N/V, ileus, distension, etc.
  • Stress ulcers
47
Q

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

A

↑ SNS

↑BP, HR, etc.

48
Q

What hormones experience a decrease in response to chronic pain?

A

Anabolic Hormones
- Insulin
- Testosterone

49
Q

What are the pulmonary effects of chronic pain?

A
  • Shallow breathing → atelectasis and pneumonia.
50
Q

Pain

A
  • emphasizes the complex nature of pain as a physical, emotional, and psychological condition
  • Degree of tissue damage?
51
Q

What is Hyperalgesia

A

Increased pain sensations to normally painful stimuli.

52
Q

What is Allodynia

A

perception of pain sensations in response to normally non-painful stimuli.

53
Q

What are unmyelinated afferent fibers

A

C- fiber: burning pain from heat and pressure from sustained pressure.

54
Q

What are myelinated afferent fibers

A

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

55
Q

What are the cheical mediators of pain?

A
  • Peptides (Substance P, Calcitonin, Bradykinin [1st released], CGRP)
  • Eicosanoids
  • Lipids (Prostaglandins, Thromboxanes, Leukotrienes, Endocannabinoids)
  • Neutrophins
  • Cytokines
  • Chemokines
  • Extracellular proteases and protons
56
Q

What are the receptors ion Channels of peripheral nerve physiology of pain?

A
  • (Dorsal Root Ganglion & Peripheral Terminals)
  • Purinergic
  • Metabotropic
  • Glutamatergic
  • Tachykinin
  • TRPV I
  • Neurotrophic
  • Ion channels (Nav 1.8)
57
Q

What are the cardiovascular response to pain?

A
  • Prominent
  • Hypertension
  • Tachycardia
  • Myocardial irritability
    ↑ SVR
  • Compromised LV
    ↓ CO
  • Myocardial ischemia
58
Q

What is the pulmonary Response pain ?

A
  • ↑ total body O2 consumption/CO2 production
    ↑ Vm and work of breathing
  • Splinting
  • Decreased movement of chest wall
    Atelectasis
    Intrapulmonary shunting
    Impaired coughing
59
Q

What is the Gi/Gu Response

A
  • Enhanced sympathetic tone…↑ sphincter tone, and ↓ motility
    Ileus
    Urinary retention
  • Hypersecretion of acid
    Stress ulceration
    Aspiration
  • N/V
  • Abdominal distention
60
Q

What is the endocrine reponse to pain

A
  • ↑ catabolic hormones
    o Catecholamines
    o Cortisol
    o Glucagon
  • ↓ anabolic hormones
    o Insulin
    o Testosterone
  • Effects
    o Negative nitrogen balance
    o Carbohydrate intolerance
    o Increases renin, aldosterone, angiotensin
61
Q

What is the hematologic reponse to pain

A
  • Stress Related
    o Platelet adhesiveness
    o Reduced fibrinolysis
    o Hypercoagulability
62
Q
A