E3 Nociception Flashcards
(143 cards)
1
Q
true or false
pain is subjective and conscious
A
true
2
Q
what is not very accurate because of pain being subjective
A
the 1-10 scale
3
Q
what is the fancy term for pain
A
algesia / nociception
4
Q
What does anticipated pain do to the response
A
makes it worse
5
Q
examples of pain without damage
A
emotional stress
phantom pain
6
Q
what is nociception
A
an unpleasant sensory and emotional experience associated with actual or potential tissue damage
7
Q
what is the precentral gyrus
A
before the central sulcus
motor
8
Q
what is the postcentral gyrus
A
after the central sulcus
somatosensory / sensations
9
Q
what controls / inhibits the ascending pathway
A
descending pathway
10
Q
what sends the signal to the brain and is operational first before the descending pathway
A
ascending pathway
11
Q
describe the ascending pathway
A
- immune cell / any cell is damaged
-releases cytokines (prostaglandin) - 1st order neuron through the dorsal root
-release substance P - 2nd order neuron decussates to spinothalamic tract
-goes up through the medulla, pons, midbrain, and ends in the thalamus - 3rd order neuron relays info to post central gyrus
12
Q
what is PG generated from
A
arachidonic pathway
13
Q
what is substance P
A
chemical that transmits signal
14
Q
where does the scond order neuron terminate
A
thalamus
15
Q
what is the thalamus
A
relay station
16
Q
what part of the brain is the precentral gyrus
A
frontal
17
Q
what part of the brain is the postcentral gyrus
A
parietal
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
19
Q
what is a response to inflammation
A
PG
20
Q
where does the nerve go in and out
A
goes in the dorsal root
goes out the ventral root
21
Q
what makes up the brainstem
A
midbrain
pons
medulla
22
Q
what is the perception of pain received in an area corresponding to
A
sensory/motor homunculus
23
Q
what nuclei is norepinephrine
A
locus aeroli
24
Q
what nuclei is serotonin
A
raphae magnus of medulla
25
describe the descending pathway
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)
26
where do the 1st and second motor neuron meet
substantia gelatinosa
27
where does the spinothalamic tract extend
goes from spine to thalamus
28
"decussates"
crosses over so the perception is on the opposite side of the brain
29
where are the intraneurons located
substantia gelatinosa
30
what does the interneuron do?
releases enkephalins (opioid)
-inhibits presynaptic neuron from releasing substance P
- inhibit post synaptic neuron from depolarizing
31
what does inhibiting the post synaptic neuron from depolarizing do
stops stimulus from continuing to thalamus
32
what is the biologically important function of pain
protective function
-normal response to injury or disease
33
what are manifestations of pain related to tissue injury
hyperalgesia
allodynia
34
hyperalgesia
exaggerated response to a noxious(harmful) stimulus
35
allodynia
perception of pain from normally innocuous(not harmful) stimuli
36
innocuous
not harmful
37
noxious
harmful
38
what are hyperalgesia and allodynia the result from
changes in peripheral/central nervous system referred to as peripheral or central sensitization
39
what can happen even after healing has taken place in some individuals
persistent (chronic) pain
40
what contributes to sensitization resulting in persistent (chronic) pain
genetic and environmental factors
41
what is chronic pain seen in a result from and examples
autoimmune disorders
lupus
rheumatoid arthritis
42
what do nociceptors signal and contribute to?
signal acute pain
contribute to persistent pathological pain disorders from previous injury or ongoing disease *when chronically sensitized*
43
characteristics of acute pain
begins suddenly, usually sharp
warning to disease/injury
disappears when underlying cause is treated
44
characteristics of subacute pain
lasts 6-12 weeks
improves with nonsurgical treatment
45
characteristics of pain
more difficult to treat
persists for months or years
may cause depression, anxiety, and sleep problem
46
what is chronic pain characterized by?
the abnormal state and function of the spinal cord neurons which become hyperactive
47
what does hyperactivity result from?
increased transmitter release
by spontaneously active primary afferent neurons
and
by increase responsiveness of postsynaptic receptors
- in part due to phosphorylation
48
How is a hyperexcitable state maintained?
by release of biologically active factors from activated glia
49
what are the activated glia normally that maintain a hyperexcitable state?
astrocytes and microglia
50
where does a hyperexcitable state occur?
dorsal horn
51
How is a hyperexcitable state aggravated?
by the loss of inhibitory interneurons involved in pain modulation
52
where is the substantia gelatinosa located?
dorsal horn of gray area
53
PTN
pain transmission neuron
54
PG
prostoglandins
55
EAA
exhibitory amino acids
56
what releases pro-inflammatory mediators
activated glia
57
what activated glia cells
Viruses and Bacteria
PTN
-NO
-PG
Primary Afferent
-Substance P
-EAA's
-ATP
58
what does the activated glia then produce
pro inflammatory mediators
IL-1
TNF
ROS
NO
PG
EAA
ATP
59
what does the release of the substances form the activated glia enhance
enhance PTN excitability
enhance primary afferent, substance P and EAA release
60
when does the does nociceptive sensory systemreturn to normal function
as soon as healing takes place
61
when do many features of sensitization persist and manifest as chronic pain and hyperalgesia
system itself is injured, leading to chronic neuropathic pain
62
what is chronic pain accompanied according to imaging studies?
permanent structural alteration in specific brain areas that play a critical role in nociception
63
common types of pain
nociceptive
neuropathic
inflammatory
64
true or false
there are many ways to classify pain and classifications may overlap
true
65
nociceptive pain
normal response to noxious insult or injury of tissues such as skin, muscles, visceral organs, joints, tendons, or bones
66
examples of nociceptive pain
somatic
visceral
67
what is somatic nociceptive pain
musculoskeletal (joint pain, myofascial pain), cutaneous
*often well localized*
68
what is visceral nociceptive pain
hollow organs and smooth muscle
*usually referred*
69
neuropathic pain
pain initiated or caused by a primary lesion or disease in the somatosensory nervous system
70
where does neuropathic pain occur
anywhere on spinal cord up to brain
71
what do sensory abnormalities range from for neuropathic pain
deficits perceived as numbness to hypersensitivity (hyperalgesia and allodynia)
and
deficits perceived as paresthesias
72
what does paresthesias feel like
tingling, burning, prickling
(usually felt in appendages)
73
examples of neuropathic pain
diabetic neuropathy
postherpeutic neuralgia
spinal cord injury pain
phantom limb pain
post-stroke central pain
74
inflammatory pain
activation and sensitization of the nociceptive pain pathway by a variety of mediators released at a site of tissue inflammation
75
what mediators have been implicated as key players in inflammation ?
they do this by infiltrating what cells?
proionflammatory cytokine
leukocytes, vascular endothelial cells, or tissue resident mast cells
76
what are some examples of pro-inflammatory cytokines
IL‐1‐alpha
IL‐1‐beta
IL‐6
TNF‐alpha
chemokines
reactive oxygen species
vasoactive amines
lipids
ATP
acid
77
examples of inflammatory pain
appendicitis
rheumatoid arthritis
inflammatory bowel disease
herpes zoster (shingles)
78
true or false
pathological processes occur in isolation
false
never occur in isolation
79
characteristics of pathological processes
>1 mechanism may be present
>1 type of pain may be detected in a single patient
80
example of pathological processes as a clinical implication of pain
inflammatory mechanisms are involved in neuropathic pain
81
are all well-recognized pain disorders easily classifiable?
no
82
what are the treatments from pain disorders that are well recognized but not classified easy?
specific therapies are well known
83
examples of pain disorders that are well recognized but not classified easy
cancer pain
migraine
primary headaches
wide spread pain of the fibromyalgia type
84
how does phantom pain mirror therapy work
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
what fiber sensory afferent nerve fibers are involved in pain sensation
C-fiber
A-delta
86
c-fiber
non-myelinated (slow
aching pain later
mechanical
thermal
chemical
87
A-delta fiber
large, myelinated (fast)
sharp, immediate pain
mechanical
thermal
88
how does neuroplasticity relate to pain
strengthen or inhibit a pathway
-chronic continues to trigger/reinforce pathway
-so continues to change
can be desensitized
89
example of nerve damage
root canal
-nerve goes wild is what causes pain
90
enhanced pain from stimulus that does not usually produce that much
hyperalgesia
91
what type of pain is fibromyalgia
allodynia
-touch arm or certain clothing causes pain
92
refers to central pain sensitization following normally nonpainful, often repetitive, stimulation
allodynia
93
describe the simulus intensity and pain intensity graph
94
where does transduction happen
peripheral nerve (PNS)
95
where can transmission happen
central transmission
synaptic transmission
peripheral transmission
96
where are the A and C fibers located
dorsal root ganglion
97
what are the primary sensory neurons
EAA - excitatory amino acid
CGRP - calcitonin gene-related peptide
SP - substance P
Gal - galatin
NPY - neuropeptide Y
98
what is glutamate
excitatory amino acid (EAA)
99
what is galatin
neuropeptide g-couple receptor for K channels
hyperpolarizing effect
100
tranduction
conversion of stimulus into action potential
101
transmission
impulse travels to synapses in dorsal horn
secondary euron decussates
102
perception (where occurs)
cerebral cortex
103
modulation
facilitation or inhibition via descending efferent pathways/neurotransmitters
104
nociceptive nerve fiber Aα
efferent motor
fast, sharp pain
myelinated
105
nociceptive nerve fiber Aβ
afferent sensory
fast, sharp pain
myelinated
106
nociceptive nerve fiber δ (delta)
afferent sensory
5-30 m/s
fast, sharp pain
myelinated
107
nociceptive nerve fiber C
afferent sensory
0.5-2 m/s
slow, aching, throbbing pain
unmyelinated
108
what are the cells involve in tissue damage and inflammation and what do they specifically do?
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
what modulators of tissue damage and inflammation are inhibitory
µ opioid
GIRK
M2
GABAa
110
what modulators of tissue damage and inflammation are GPCRs
SHT
H1 - histamine
EP - epinephrine
B1/2 - bradykinins 1&2
µ opioid
A2 - autoreceptor
M2
TRPV1 - transient receptor protein voltage
111
what modulators of tissue damage and inflammation are cytokine receptors (JAK kinase)
IL-1R
TRKA - capsalcin
112
what modulators of tissue damage and inflammation are ion channels
P2X2
ASIC - acid sensing ion channel
GIRK - g-protein inward rectifying K+
GABAa
113
what does A2 deal with
alpha 2
autoreceptor
dampening of signals
114
what does ASIC deal with
acid sensing ion channel
-activated when pH in body decreases
-injury = acidic environment
115
what does P2X2 deal with
ATP signaling
116
what does GIRK deal with
hyperpolarizing membrane
117
what does TRPV1 deal with
capsalcin
in peppers and icy hot
-rubbing injury / only used topically
open ion channels to respond to pain
118
is interneuron part or ascending or descending?
descending
119
gate theory of pain
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
what activates nociceptors
noxious stimuli (H+ / temp / etc. ) applied to endoorgans
121
what prostoglandins are released from injury (and from what)
*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
what do the prostoglandins etc. do once released from injury
activate nociceptors directly or sensitize them to subsequent stimuli
123
how do the nociceptors get sensitized to stimuli
parallel activation of intracellular kinases by GPCR and tyrosine kinase receptors
124
what are the primary nociceptive afferents what do they synapse with
C-fibers
A delta fibers
synapse to second motor neuron in substantia gelatinosa
125
what is released from the primary afferent terminals (A)
glutamate (Glu)
substance P
126
what does the release of glutamate do
activates glutamate receptors
- NMDA R
- AMPA R
- mGluRs
activates neurokinin receptors
- NK-1
*located post synaptically on the spinal neurons*
127
how are these synapses negatively modulated
by spinal inhibitory interneurons (I)
-employ enkephalins (Enk) or gamma-aminobutyric acid (GABA) as neurotransmitter
128
how does antinociception occur
activated noradrenergic or seotonergic systems activate inhibitory interneurons
129
what are depressive disorders from
exaggerated hyperalgesic effect
-level of neurotransmitters is lower / higher response
130
where is the gating of pain
substantia gelatinosa
131
132
what are the cannabinoid receptors in the endocannabinoid system
CB1 and CB2
GPCRs
133
what is the endocannabinoid system and receptors involved in
appetite, pain sensation, mood, memories
inflammatory pathways ? (potential)
134
what does CB1 do
reduce substance P being released
(presynaptic)
135
what do CB1 and CB2 mostly bind to?
anandamide (endogenous cannabinoid)
136
what does CB2 do?
suppresses reactive microglia behavior and central neuroinflammation
on glia (microglia)
137
antagonist
blocks
138
agonist
stimulates
139
what does alpha 2 do
stimulates the autoreceptor to reduce further neurotransmitter release
140
what acts on the brain
opioids
alpha2 agonists
centrally acting analgesics
NSAIDS
COX-2 inhibitors
141
what acts on the dorsal root
local anesthetics
opioids
alpha2 agonists
142
what acts on the peripheral nerve
local anesthetics
143
what acts on the peripheral nociceptors
local anesthetics
anti-inflammatory drugs
NSAIDS
COX-2 inhibitors
