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Semester 2 FS Exam 1 > Pathways and Mechanisms of Pain > Flashcards

Pathways and Mechanisms of Pain Flashcards

(68 cards)

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1
Q

Nociception

A

the sensory response to a noxious stimulus

unconscious activity due to noxious stimulus - physiological mechanisms

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2
Q

Pain

A

the perception of nociceptive sensory information - need brain to interpret

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3
Q

Sensory - discrimination

A

perception of exteroceptive or enteroceptive noxious information and localization of the site

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4
Q

Motivation - affective

A

emotional and sympathetic responses and associated (learning) behaviors

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5
Q

Types of pain by characteristic

A
  1. Physical
  2. Inflammatory
  3. Neuropathic
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6
Q

Physical Pain

A

AKA physiological pain
Transient
Localized
Minimal tissue damage (warning)

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7
Q

Inflammatory Pain

A

Acute and chronic
Tissue damage
Mediated by the inflammatory process
Hypersensitivity (hyperalgesia) - protective, promotes healing

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8
Q

Neuropathic Pain

A

Damage/alteration to the nervous system (CNS or PNS), Chronic and maladaptive

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9
Q

Types of Pain by Site of Origin

A
  1. Somatic (sup and deep)

2. Visceral

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10
Q

Somatic - superficial

A

Discrete localization
Initial (sharp A Delta fiber)
Delayed burning, C fibers

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11
Q

Somatic Deep

A

Diffuse localization

CT, bones, joints, muscles

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12
Q

Visceral

A 
primarily conveyed by C fibers
Poorly localized
Often "referred" to somatic area along dermatome pattern 
Often described as achy
appendicitis, renal stones, ulcer
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13
Q

Physiological Pain Processing

A

Transduction
Transmission
Modulation
Perception

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14
Q

Transduction - Nociceptors

A

Free nerve endings
Body = spinal ganglia
Face = trigeminal ganglia

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15
Q

Transduction - TRP

A

Transient receptor potential family
similar to voltage gated channel –> influx of Na and Ca
Some TRPs are invovled in theramal regualtion

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16
Q

Nociceptors have a ___ threshold

A

High threshold so that we dont feel pain all the time

They are slowly adapting so they stay activated for a while

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17
Q

Stimuli for nociceptors

A
  1. Mechanical - only noxious stimuli (hammer to hand)
  2. Thermal - TRP family
    CMR-1 = 52 TRPV2 - noxious heat
    VR-1 = >42 TRPV2 - noxious heat, capsaicin
  3. Chemical
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18
Q

Chemical activators for nociceptors

A

K
H (pH)
Substance P
Bradykinin

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19
Q

Chemical sensitizers for nociceptors

A

Prostaglanding
Leukotrienes
ATP
Other chemical mediators of inflammation

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20
Q

Peripheral analgesics

A

NSAIDs non steroid anti inflammatory drugs (aspirin) produce most of their effect by reducing prostaglandin production

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21
Q

Silent Nociceptors

A

Unresponsive to non-noxious and high intensity noxious mechanical and thermal stimuli unless previously activated
Responsive to inflammation (chemical) stimuli
Once activated by inflammatory stimulus the silent receptors will respond to other modalities (pressure, temp)
Silent nociceptors are found mainly in viscera

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22
Q

Sensitization

A

an alteration of the membrane that brings the resting potential closer to threshold (more easily excited)

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23
Q

Primary Hyperalgesia

A

increased sensitivity to noxious and non-noxious stimuli in the area immediately surrounding the the primary site of damage due to a sensitization of the peripheral nociceptors

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24
Q

Hyperalgesia

A

an increased response to a stimulus that is normally painful

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25
Peripheral sensitization
Spreading of APs over other areas where membrane is at resting state - inc sensitivity - inc receptive field size - inflammatory mediators and sub P produced - activation of silent nociceptors (only with certain level of stimulus)
26
Axon Reflex - Sympathetic Sensory Coupling
signal from nociceptos activates sympathetic neurons and ganglia that innervate BVs - this induces axon reflex and contributes to signs of inflammation Flare response due to activation of peripheral nerves Release of Sub P and movement of AP Activation of sympathetic reflex response (coupling of sensory with autonomic systems) Triple response of Lewis (red, edema, flare)
27
Transmission - A delta fibers
myelinated responsible for localized, sharp "first" pain Respond to intense mechaincal (pinching) and thermal stimuli
28
Transmission - C fibers
Unmyelinated mediate poorly localized, diffuse second pain Polymodal - respond to mechanical, thermal and chemical stimulus
29
Afferent Fibers
Nociceptors are terminal portions of afferent fibers wth cell bodies in the DRG
30
A alpha and Beta
myelinated mechanical stimuli low threshold proprioception and light touch
31
Cutaneous - nociceptors
``` A delta (mechanical and heat) C (polymodal) ```
32
Muscle - nociceptors
mechanical, thermal, chemical and ischemia
33
Articular (joint) - nociceptors
2x as many unmyelinated as myelinated Adelta Cfibers Mechanical stimulus and inflammation
34
Viscera - nociceptors
Mainly C fibers | mechanical distention and chemcial
35
Lamina I
A delta fibers | Fast, acute pain
36
Lamina II and III
C fibers | slow, chronic pain
37
Lamina V
Wide dynamic range neurons --> both nociceptive A delta and C fibers but also innervated by A Beta (prop and light touch) Noxious and non-noxious signals
38
Nociceptive specific neurons
Spinothalamic neurons in lamina I II and III are termed nociceptive specific as they receive only noxious stimulus input
39
Wide Dynamic Range neurons
Spinothalamic neurons in lamina V because they receive both non-noxious (A alpha and A beta) and noxious (A delta and C) input
40
NTs for primary afferent input (A delta and C fibers)
Substance P Glutamate Neurokinin A
41
What does glutamate do
activateds AMPA receptor to produce rapid depolarizaton of spinal neuron
42
Co release of Sub P and glutamate produces...
complex set of responses allowing glutamate to also act on NMDA receptor - producing long lasting depolarization of post synaptic membrane THis makes neuron more easily excited and causes opening of Ca channels --> influx of Ca --> wind up phenomenon Contributes to secondary or central hyperalgesia
43
Secondary Hyperalgesia
PNS and CNS events Prolonged and increased activation of nociceptors in periphery and projection pathways at spinal cord Wider somatic area than primary and slower in developing
44
Allodynia
pain resulting from a non-nocious stimulus (sunburn when put shirt on) predominately produced by a facilitation of second order spinal neuron responsiveness to non-noxious stimulus through the wind up or a similar intense noxious input
45
Preemptive analgesia
lessening the secondary hyperalgesia by reducing the activation of the spinothalamic neuron `
46
Neuronal plasticity
modulation of intracellular signaling and changes in gene expression
47
Memories of pain - pathophysiogy
Lasting effects --> chronic pain
48
Acute sensitization
protective
49
Chronic sensitization
maladaptive no function Change in gene expression and proeins Inc the release of glutamate and sub P
50
Dorsal COlumn
Medial Lemniscus - discriminitve touch - proprioception A Beta fibers
51
Anterolateral System
Temperature Pain Crude touch C fibers and A delta
52
Neospinalthalamic tract
Fast type A delta fibers - machanical and acute thermal Projections from lamina I IV and V Anterolateral columns Thalamus - VPL Primary sensory cortex - sensory, location, modality, and intensity Sharp pain in my left arm associated with smaller receptive fields
53
Paleospinothalamic Tract
``` more medially located Slow type C fibers Lamina II III and V Anterolateral columns Thalamus (DM) Limbic System - affective and emotional aspect Ouch that hurts - i dont like it Associated with larger receptive fields ```
54
Spinoreticular Tract
Reticular formation Motor response to pain Descending pain control
55
Spinomesencephalic tract
midbrain - PAG Regulation and modulation of pain experience Descending pain control Superior colliculus - eye movements and regulation of gaze to the site of injury
56
Brain regions involved in pain percepton
amygdala - fear hippocampus - memory attention to pain - limbic system Anterior cingulate gyrus and insular cortex
57
Cerebral response to pain
``` threatening visual and auditory cues memory of pain - hippo anticipation of pain attention to pain - ACC empathy with pain of others ```
58
Anterior cingulate cortex
active during perception of pain, imagining pain and observation of pain in others attention to pain Initiation of behavioral reactions to pain
59
Insula
relay station to the limbic system (learning and pain memory) and to the hypothalamus
60
Gate Control Theory
Changing brain attention to something else (shake hand) gating mechanism within spinal cord that closes response to normal stimulation of fast conductivity large nerve fibers like ABeta (touch and proprio) Opens when slow conduction fibers (Adelta and C) transmit high volume of sensory signals ABeta wins initially cuz is bigger and faster - shaking hand activates these proprioceptive changes - so activate interneuron and shut down secondary afferent
61
Descending pathways of pain
shut down or reduce the pain | activation of periaqueductal grey matter
62
Pain modulation - therapeutic strategies
``` relief of pain by blocking signal from going up and activate the descenign motor pathways delay or arrest of disease process typical pharacological approaches - opioid analgesics (morophine) - NSAIDs (aspirin) - Glucocorticoids - DMARDS (used mainly for arthritis) ```
63
Common pain types
Chronic Referred Projected Neuropathic
64
Reflective Pain
perceived at a location other than the site of the painful stimulus
65
Convergence
of somatic and visceral pain fibers on secondary afferents in the dorsal horn (dermatomes) Nerves converge in psinal cord and send these signals to brain and it doesnt differentiate btw them (heart and arm)
66
Projected Pain
provides support of labeled line theory | Funny bone - feel it all the way in "labeled line"
67
Phantom pain
has to do with plasticity and reorganziation of brain
68
Sympathetic Mediated Pain
Reflex sympathetic dystrophy - causalgia = continuous burning pain long after seemingly trivial injuries Treatment = sympathectomy or nerve block

Semester 2 FS Exam 1 (3 decks)

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