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Anatomy & Physiology > E3 Nociception > Flashcards

E3 Nociception Flashcards

1
Q

true or false
pain is subjective and conscious

A

true

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2
Q

what is not very accurate because of pain being subjective

A

the 1-10 scale

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3
Q

what is the fancy term for pain

A

algesia / nociception

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4
Q

What does anticipated pain do to the response

A

makes it worse

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5
Q

examples of pain without damage

A

emotional stress
phantom pain

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6
Q

what is nociception

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage

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7
Q

what is the precentral gyrus

A

before the central sulcus
motor

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8
Q

what is the postcentral gyrus

A

after the central sulcus
somatosensory / sensations

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9
Q

what controls / inhibits the ascending pathway

A

descending pathway

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10
Q

what sends the signal to the brain and is operational first before the descending pathway

A

ascending pathway

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11
Q

describe the ascending pathway

A
  1. immune cell / any cell is damaged
    -releases cytokines (prostaglandin)
  2. 1st order neuron through the dorsal root
    -release substance P
  3. 2nd order neuron decussates to spinothalamic tract
    -goes up through the medulla, pons, midbrain, and ends in the thalamus
  4. 3rd order neuron relays info to post central gyrus
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12
Q

what is PG generated from

A

arachidonic pathway

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13
Q

what is substance P

A

chemical that transmits signal

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14
Q

where does the scond order neuron terminate

A

thalamus

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15
Q

what is the thalamus

A

relay station

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16
Q

what part of the brain is the precentral gyrus

A

frontal

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17
Q

what part of the brain is the postcentral gyrus

A

parietal

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18
Q

true or false
sensation one the left side of the body goes up the left side and down the right

A

false
sensation is on opposite side of site of stimulation

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19
Q

what is a response to inflammation

A

PG

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20
Q

where does the nerve go in and out

A

goes in the dorsal root
goes out the ventral root

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21
Q

what makes up the brainstem

A

midbrain
pons
medulla

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22
Q

what is the perception of pain received in an area corresponding to

A

sensory/motor homunculus

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23
Q

what nuclei is norepinephrine

A

locus aeroli

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24
Q

what nuclei is serotonin

A

raphae magnus of medulla

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25
Q

describe the descending pathway

A
  1. 1st order neurons goes from periaquaductal gray matter of midbrain to nucleus raphae magnus of medulla
  2. meets second neuron that goes to the the same area of that the 1st and 2nd order neurons of the ascending pathway meet
  3. releases either serotonin or norepinephrine
    -binds to presynaptic neuron and inhibits substance P by stimulating interneuron
    -interneuron releases enkephalin (opioid)
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26
Q

where do the 1st and second motor neuron meet

A

substantia gelatinosa

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27
Q

where does the spinothalamic tract extend

A

goes from spine to thalamus

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28
Q

“decussates”

A

crosses over so the perception is on the opposite side of the brain

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29
Q

where are the intraneurons located

A

substantia gelatinosa

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30
Q

what does the interneuron do?

A

releases enkephalins (opioid)
-inhibits presynaptic neuron from releasing substance P
- inhibit post synaptic neuron from depolarizing

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31
Q

what does inhibiting the post synaptic neuron from depolarizing do

A

stops stimulus from continuing to thalamus

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32
Q

what is the biologically important function of pain

A

protective function
-normal response to injury or disease

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33
Q

what are manifestations of pain related to tissue injury

A

hyperalgesia
allodynia

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34
Q

hyperalgesia

A

exaggerated response to a noxious(harmful) stimulus

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35
Q

allodynia

A

perception of pain from normally innocuous(not harmful) stimuli

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36
Q

innocuous

A

not harmful

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37
Q

noxious

A

harmful

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38
Q

what are hyperalgesia and allodynia the result from

A

changes in peripheral/central nervous system referred to as peripheral or central sensitization

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39
Q

what can happen even after healing has taken place in some individuals

A

persistent (chronic) pain

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40
Q

what contributes to sensitization resulting in persistent (chronic) pain

A

genetic and environmental factors

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41
Q

what is chronic pain seen in a result from and examples

A

autoimmune disorders

lupus
rheumatoid arthritis

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42
Q

what do nociceptors signal and contribute to?

A

signal acute pain

contribute to persistent pathological pain disorders from previous injury or ongoing disease when chronically sensitized

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43
Q

characteristics of acute pain

A

begins suddenly, usually sharp
warning to disease/injury
disappears when underlying cause is treated

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44
Q

characteristics of subacute pain

A

lasts 6-12 weeks
improves with nonsurgical treatment

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45
Q

characteristics of pain

A

more difficult to treat
persists for months or years
may cause depression, anxiety, and sleep problem

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46
Q

what is chronic pain characterized by?

A

the abnormal state and function of the spinal cord neurons which become hyperactive

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47
Q

what does hyperactivity result from?

A

increased transmitter release

by spontaneously active primary afferent neurons
and
by increase responsiveness of postsynaptic receptors
- in part due to phosphorylation

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48
Q

How is a hyperexcitable state maintained?

A

by release of biologically active factors from activated glia

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49
Q

what are the activated glia normally that maintain a hyperexcitable state?

A

astrocytes and microglia

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50
Q

where does a hyperexcitable state occur?

A

dorsal horn

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51
Q

How is a hyperexcitable state aggravated?

A

by the loss of inhibitory interneurons involved in pain modulation

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52
Q

where is the substantia gelatinosa located?

A

dorsal horn of gray area

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53
Q

PTN

A

pain transmission neuron

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54
Q

PG

A

prostoglandins

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55
Q

EAA

A

exhibitory amino acids

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56
Q

what releases pro-inflammatory mediators

A

activated glia

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57
Q

what activated glia cells

A

Viruses and Bacteria

PTN
-NO
-PG

Primary Afferent
-Substance P
-EAA’s
-ATP

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58
Q

what does the activated glia then produce

A

pro inflammatory mediators
IL-1
TNF
ROS
NO
PG
EAA
ATP

59
Q

what does the release of the substances form the activated glia enhance

A

enhance PTN excitability
enhance primary afferent, substance P and EAA release

60
Q

when does the does nociceptive sensory systemreturn to normal function

A

as soon as healing takes place

61
Q

when do many features of sensitization persist and manifest as chronic pain and hyperalgesia

A

system itself is injured, leading to chronic neuropathic pain

62
Q

what is chronic pain accompanied according to imaging studies?

A

permanent structural alteration in specific brain areas that play a critical role in nociception

63
Q

common types of pain

A

nociceptive
neuropathic
inflammatory

64
Q

true or false
there are many ways to classify pain and classifications may overlap

A

true

65
Q

nociceptive pain

A

normal response to noxious insult or injury of tissues such as skin, muscles, visceral organs, joints, tendons, or bones

66
Q

examples of nociceptive pain

A

somatic
visceral

67
Q

what is somatic nociceptive pain

A

musculoskeletal (joint pain, myofascial pain), cutaneous

often well localized

68
Q

what is visceral nociceptive pain

A

hollow organs and smooth muscle

usually referred

69
Q

neuropathic pain

A

pain initiated or caused by a primary lesion or disease in the somatosensory nervous system

70
Q

where does neuropathic pain occur

A

anywhere on spinal cord up to brain

71
Q

what do sensory abnormalities range from for neuropathic pain

A

deficits perceived as numbness to hypersensitivity (hyperalgesia and allodynia)
and
deficits perceived as paresthesias

72
Q

what does paresthesias feel like

A

tingling, burning, prickling
(usually felt in appendages)

73
Q

examples of neuropathic pain

A

diabetic neuropathy
postherpeutic neuralgia
spinal cord injury pain
phantom limb pain
post-stroke central pain

74
Q

inflammatory pain

A

activation and sensitization of the nociceptive pain pathway by a variety of mediators released at a site of tissue inflammation

75
Q

what mediators have been implicated as key players in inflammation ?
they do this by infiltrating what cells?

A

proionflammatory cytokine

leukocytes, vascular endothelial cells, or tissue resident mast cells

76
Q

what are some examples of pro-inflammatory cytokines

A

IL‐1‐alpha
IL‐1‐beta
IL‐6
TNF‐alpha
chemokines
reactive oxygen species
vasoactive amines
lipids
ATP
acid

77
Q

examples of inflammatory pain

A

appendicitis
rheumatoid arthritis
inflammatory bowel disease
herpes zoster (shingles)

78
Q

true or false
pathological processes occur in isolation

A

false
never occur in isolation

79
Q

characteristics of pathological processes

A

> 1 mechanism may be present
1 type of pain may be detected in a single patient

80
Q

example of pathological processes as a clinical implication of pain

A

inflammatory mechanisms are involved in neuropathic pain

81
Q

are all well-recognized pain disorders easily classifiable?

A

no

82
Q

what are the treatments from pain disorders that are well recognized but not classified easy?

A

specific therapies are well known

83
Q

examples of pain disorders that are well recognized but not classified easy

A

cancer pain
migraine
primary headaches
wide spread pain of the fibromyalgia type

84
Q

how does phantom pain mirror therapy work

A

mirror neuron in our pre motor cortex
-fires when acts and observes by another

decreases pain by resolving conflict between motor intention proprioceptor and visual system

85
Q

what fiber sensory afferent nerve fibers are involved in pain sensation

A

C-fiber
A-delta

86
Q

c-fiber

A

non-myelinated (slow

aching pain later

mechanical
thermal
chemical

87
Q

A-delta fiber

A

large, myelinated (fast)

sharp, immediate pain

mechanical
thermal

88
Q

how does neuroplasticity relate to pain

A

strengthen or inhibit a pathway
-chronic continues to trigger/reinforce pathway
-so continues to change

can be desensitized

89
Q

example of nerve damage

A

root canal
-nerve goes wild is what causes pain

90
Q

enhanced pain from stimulus that does not usually produce that much

A

hyperalgesia

91
Q

what type of pain is fibromyalgia

A

allodynia
-touch arm or certain clothing causes pain

92
Q

refers to central pain sensitization following normally nonpainful, often repetitive, stimulation

A

allodynia

93
Q

describe the simulus intensity and pain intensity graph

A
94
Q

where does transduction happen

A

peripheral nerve (PNS)

95
Q

where can transmission happen

A

central transmission
synaptic transmission
peripheral transmission

96
Q

where are the A and C fibers located

A

dorsal root ganglion

97
Q

what are the primary sensory neurons

A

EAA - excitatory amino acid
CGRP - calcitonin gene-related peptide
SP - substance P
Gal - galatin
NPY - neuropeptide Y

98
Q

what is glutamate

A

excitatory amino acid (EAA)

99
Q

what is galatin

A

neuropeptide g-couple receptor for K channels
hyperpolarizing effect

100
Q

tranduction

A

conversion of stimulus into action potential

101
Q

transmission

A

impulse travels to synapses in dorsal horn
secondary euron decussates

102
Q

perception (where occurs)

A

cerebral cortex

103
Q

modulation

A

facilitation or inhibition via descending efferent pathways/neurotransmitters

104
Q

nociceptive nerve fiber Aα

A

efferent motor
fast, sharp pain
myelinated

105
Q

nociceptive nerve fiber Aβ

A

afferent sensory
fast, sharp pain
myelinated

106
Q

nociceptive nerve fiber δ (delta)

A

afferent sensory
5-30 m/s
fast, sharp pain
myelinated

107
Q

nociceptive nerve fiber C

A

afferent sensory
0.5-2 m/s
slow, aching, throbbing pain
unmyelinated

108
Q

what are the cells involve in tissue damage and inflammation and what do they specifically do?

A

mast cell & macrophage & platelets
-produce PAF (platelet activating factor)
-activates H1 (GCPR)

platlets
-produce bradykinins
-activates P2X2

damage (maybe platelets)
-activates A2 & ASIC

eosinophil & keratinocytes
-produce β endorphin (opioid)
-activate µ opioid

109
Q

what modulators of tissue damage and inflammation are inhibitory

A

µ opioid
GIRK
M2
GABAa

110
Q

what modulators of tissue damage and inflammation are GPCRs

A

SHT
H1 - histamine
EP - epinephrine
B1/2 - bradykinins 1&2
µ opioid
A2 - autoreceptor
M2
TRPV1 - transient receptor protein voltage

111
Q

what modulators of tissue damage and inflammation are cytokine receptors (JAK kinase)

A

IL-1R
TRKA - capsalcin

112
Q

what modulators of tissue damage and inflammation are ion channels

A

P2X2
ASIC - acid sensing ion channel
GIRK - g-protein inward rectifying K+
GABAa

113
Q

what does A2 deal with

A

alpha 2
autoreceptor

dampening of signals

114
Q

what does ASIC deal with

A

acid sensing ion channel
-activated when pH in body decreases
-injury = acidic environment

115
Q

what does P2X2 deal with

A

ATP signaling

116
Q

what does GIRK deal with

A

hyperpolarizing membrane

117
Q

what does TRPV1 deal with

A

capsalcin

in peppers and icy hot
-rubbing injury / only used topically

open ion channels to respond to pain

118
Q

is interneuron part or ascending or descending?

A

descending

119
Q

gate theory of pain

A

pain reduced by activating a nonpainful sensation

rubbing can close the gate by inhibiting pain by going to the thalamus
-deep pressure activates pascinian corpuscles

120
Q

what activates nociceptors

A

noxious stimuli (H+ / temp / etc. ) applied to endoorgans

121
Q

what prostoglandins are released from injury (and from what)

A

released from damaged cells
PG E2
serotonin (5-HT)
nerve growth factor (NGF)

released from blood vessels
bradykinin (BK)

released from nociceptors
substance p (SP)

122
Q

what do the prostoglandins etc. do once released from injury

A

activate nociceptors directly or sensitize them to subsequent stimuli

123
Q

how do the nociceptors get sensitized to stimuli

A

parallel activation of intracellular kinases by GPCR and tyrosine kinase receptors

124
Q

what are the primary nociceptive afferents what do they synapse with

A

C-fibers
A delta fibers

synapse to second motor neuron in substantia gelatinosa

125
Q

what is released from the primary afferent terminals (A)

A

glutamate (Glu)
substance P

126
Q

what does the release of glutamate do

A

activates glutamate receptors
- NMDA R
- AMPA R
- mGluRs

activates neurokinin receptors
- NK-1

located post synaptically on the spinal neurons

127
Q

how are these synapses negatively modulated

A

by spinal inhibitory interneurons (I)
-employ enkephalins (Enk) or gamma-aminobutyric acid (GABA) as neurotransmitter

128
Q

how does antinociception occur

A

activated noradrenergic or seotonergic systems activate inhibitory interneurons

129
Q

what are depressive disorders from

A

exaggerated hyperalgesic effect
-level of neurotransmitters is lower / higher response

130
Q

where is the gating of pain

A

substantia gelatinosa

131
Q
A
132
Q

what are the cannabinoid receptors in the endocannabinoid system

A

CB1 and CB2
GPCRs

133
Q

what is the endocannabinoid system and receptors involved in

A

appetite, pain sensation, mood, memories

inflammatory pathways ? (potential)

134
Q

what does CB1 do

A

reduce substance P being released

(presynaptic)

135
Q

what do CB1 and CB2 mostly bind to?

A

anandamide (endogenous cannabinoid)

136
Q

what does CB2 do?

A

suppresses reactive microglia behavior and central neuroinflammation

on glia (microglia)

137
Q

antagonist

A

blocks

138
Q

agonist

A

stimulates

139
Q

what does alpha 2 do

A

stimulates the autoreceptor to reduce further neurotransmitter release

140
Q

what acts on the brain

A

opioids
alpha2 agonists
centrally acting analgesics
NSAIDS
COX-2 inhibitors

141
Q

what acts on the dorsal root

A

local anesthetics
opioids
alpha2 agonists

142
Q

what acts on the peripheral nerve

A

local anesthetics

143
Q

what acts on the peripheral nociceptors

A

local anesthetics
anti-inflammatory drugs
NSAIDS
COX-2 inhibitors

Anatomy & Physiology (5 decks)

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