Exam 2: Lecture 15/16: Pain Mechanisms and Targets Flashcards
(112 cards)
1
Q
what is the definition of pain
A
an unpleasant sensory and emotional experience associated with or resembling that associated with actual or potential tissue damage
2
Q
T/F: An inability to communicate does not negate the possibility that a human or nonhuman animal experiences pain
A
TRUE!!
3
Q
what is sensory physiology
A
detection mechanisms for specific stimuli
4
Q
what are the pathways of sensory physiology
A
transduction, transmission, modulation, projection, and perception
5
Q
what is nociception
A
the sensory nervous systems process of encoding noxious stimuli
6
Q
what nerve fibers carry pain
A
A-delta and C fibers
7
Q
are A-delta myelinated or unmyelinated
A
myelinated
8
Q
are c fibers myelinated or unmyelinated
A
unmyelinated
9
Q
what pain information specifically do A-delta fibers carry
A
mechanical and thermal
10
Q
what pain information specifically do C fibers carry
A
mechanical, thermal, and chemical
11
Q
T/F: Nociceptors have a very high threshold compared to touch fibers
A
TRUE!
12
Q
where are nociceptors found
A
in the skin, muscle, and all inner organs
13
Q
what are the stimuli nociceptors specialized at in detecting
A
changes in the environment like mechanical forces and chemical changes like inflammatory cytokines, pH, and temp
14
Q
What type of receptors do nociceptors activate
A
either a g-protein coupled receptor or a specialized ion channel
15
Q
what is plasticity
A
changes at the nervous tissue which amplifies pain signal transmission to the brain
16
Q
Where are highly plastic neurons found
A
in the spinal dorsal horn
17
Q
what are wide dynamic range neurons
A
neurons that respond to a range of innocuous and noxious mechanical stimuli and exhibit a frequency-dependent, progressive increase in neuronal excitability and ectopic activity
18
Q
what sensory are wide dynamic range neurons responsible for
A
touch, itch, pain
19
Q
what are the 2 biggest players for perception of pain in the brain
A
amygdala and locus coeruleus
20
Q
what does the limbic cortex control
A
behavior
21
Q
what does the hippocampus control
A
fear and behavior
22
Q
what does the septal area control
A
emotion
23
Q
what does the hypothalamus control
A
homeostasis, sympathetic modulation
24
Q
what does the locus coeruleus control
A
primary source of NE which is inhibitory
25
T/F: nociceptors are a protective warning system
true!
26
Why are stimuli sensed by nociceptors perceived as a warning system to the body
glutamate in increased concentrations activate NMDA receptors to perceive the stimuli as potential tissue damage/painful
27
What are the 3 things that can happen from prolonged pain
1. amplified response to non-painful stimuli
2. create and amplify the response to pain stimuli
3. create a chronic pain state
28
what are the 7 pain processes that promote, intensify, and prolong pain
1. peripheral sensitization
2. central sensitization (activation of NMDA-R)
3. activation of silent nociceptors
4. disinhibition
5. neuroinflammation via glial cell activation
6. stress and pain (PTSD)
7. collateral sprouting
29
what is peripheral sensitization
an increased sensitivity of fibers at the site of tissue injury or inflammation which causes a low threshold for pain and greater response to stimuli
30
WBCs are involved in peripheral sensitization. How?
when there is an injury, WBCs flood the site to clean up the injury but all of the things that WBCs release activates the nociceptors which lowers the threshold
31
T/F: Macrophages have 3 different types so they are considered plastic
true!
32
T/F: because macrophages are "plastic" they can increase or decrease pain depending on the surrounding
true!!!!
33
What cells are involved in pro-inflammatory mediators
T-cells, mast cells, macrophages, and neutrophils
34
how does central sensitization happen
an increased tissue damage = increased input to CNS = decreased threshold = decreased amount of stimuli to activate
35
T/F: Central sensitization can not be in a chronic hypersensitized state
False, it can be put into a hypersensitized state due to chronic or prolonged injury
36
what is the definition of central sensitization
an enhancement neuronal function and nociceptive pathways caused by increased in excitability, synaptic efficacy and reduced inhibition
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T/F: Central sensitization is a manifestation of somatosensory plasticity in response to activity, inflammation, and neural injury
true
38
T/F: central sensitization is linked to acute pain
false, it is linked to development of CHRONIC pain
39
What are silent nociceptors
receptors that are normally unresponsive to noxious mechanical stimulation but become active to mechanical stimulation during inflammation and tissue injury
40
where are silent nociceptors located
in the skin and deep tissues with nociceptors
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what are the targets of silent nociceptors
TRPV1, TRPV3, TRPV4, TRPV8
42
What is disinhibition
a temporary loss of normal function/inhibition due to anesthetic medications. The patient is not in full control of their actions
43
Where do peripheral glial cells live
surround the cell bodies of the neurons and along the axons
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what are the main type of cells in neuro-inflammation
schwann cells and satellite cells
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If you have acute pain or acute glial activation, what cells respond to the pain intensity
microglia cells are activated
46
If you have chronic pain or chronic glial activation, what cells respond to the pain intensity
astrocyte activation
47
T/F: Stress alters the CNS microenvironment and disinhibits the immunoregulatory mechanisms
True!!
48
what does stress cause when it alters the CNS
it constrains microglial and neuro-inflammatory processes to produce a primed state of activation
49
what are alarmins
danger signals
50
what are DAMPs
damage-associated molecular pattern molecules
51
what is HMBG1
a stress protein and cytokine mediator of inflammation
52
Do we know a lot about collateral sprouting
we sure dont... it is a topic that is not that studied
53
what is collateral sprouting for fibers
sprouting of collateral A-beta fibers from sensory axons into superficial dorsal horn laminae
54
T/F: T and B cells are lymphocytes but have a small job in the activation of nociceptors
false! They are a key component of the adaptive immune system for activating nociceptors
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T/F: T and B cells contribute to the inflammatory response and influence the transition from acute to chronic pain
TRUE!! Pain chronification
56
T/F: T cells attack infected cells but do not increase pain
false, they attack infected cells and increase pain by releasing pro-inflammatory cytokines
57
T/F: B cells produce antibodies to fight pathogens which causes nociceptor sensitization and altered membrane trafficking
true!!
58
When does acute pain become chronic
when we do not properly treat the pain when it happens
59
why does persistent post surgical pain happen
because we are not the best at treating pain when it happens :(
60
what the definition of pain chronification
a maladaptive form of neuropathic pain involving peripheral and central sensitization, CNS plasticity, and a loss of inhibition
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what can pain chronification also be called
transient pain progressing to persistent pain
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what is maladaptive pain
pain that doesn't promote healing and repair
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what is the evidence of nociceptive pain state
evidence of noxious insult
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what are the symptoms of nociceptive pain state
pain localized to area of stimulus/joint damage
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what are the signs of nociceptive pain state
on imaging will see mechanical pathology/altered joint architecture such that normal movements will likely produce excessive forces sufficient to activate nociceptors
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what is the evidence of inflammatory pain state
sterile or infectious inflammation
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what are the symptoms of inflammatory pain state
redness, warmth, or swelling of infected area
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what are the signs of the inflammatory pain state
on imaging will see signs of inflammatory changes
will also detect pathogens/response to abx
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what is the evidence of neuropathic pain state
evidence of sensory nerve damage
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what are the symptoms of neuropathic pain state
decreased pinprick pr vibration sense, straight leg raise, and mechanical and cold allodynia
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what is the evidence of dysfunctional/nociplastic pain state
pain the the absence of detectable pathology
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what are the signs/symptoms of dysfunctional/nociplastic pain state
no identifiable noxious stimulus, inflammation, or neural damage, evidence of increased amplification or reduced inhibition with abnormal excitability and connectivity
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what is hyperalgesia
increased pain from a stimulus that normally produces pain
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what is hyperpathia
an abnormal reaction to repetitive painful stimulus
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what is allodynia
pain due to a stimulus that does NOT normally produce pain
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what is adaptive pain
pain that produces behavior that promotes healing and recovery
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what is maladaptive pain
pain that is out of proportion to tissue damage or which persists after tissue healing
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T/F: Maladaptive pain promotes and supports healing and repair
FALSE it does not
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what is pain chronification
the process of transient pain progressing into persisten pain
80
what are the classifications of pain
location, severity, and mechanism
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how can you describe pain location
is it somatic or visceral
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how can you describe severity of pain
mild, moderate, or severe
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what are the different mechanisms of pain
inflammatory, neuropathic, and idiopathic
84
what are the 6 ways we can assess pain
1. visual analogue scales (behavior)
2. simple categorical descriptive scales
3. numerical rating scales
4. time/activity analysis
5. compositie pain scales
6. grimace scale (the WORST WAY in muirs opinion)
85
what are the routes of pain therapy
1. pharmacologic
2. Physical therapy
3. electrical
4. complimentary
5. herbal/nutraceutical
6. environmental
86
what are the goals of multimodal analgesia
additive or synergistic analgesic effects
87
what is synergism
the interaction or cooperation of two or more substances to produce a combined effect greater than the sum of their separate effects
88
list some of the routes of drug administration
1. oral (PO)
2. IV
3. IM
4. SQ
5. topical (transdermal, TD)
6. intra-articular (IART)
89
what are the names of local anesthetics we use
lidocaine, mepivacaine, bupivacaine, ropivacaine
90
what is this a picture of
lidocaine patch
91
what NSAIDs are salicylic acid
aspirin
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what NSAIDs are para-aminophenol
acetominiphen
93
what NSAIDs are fenamic acids
flunixin megulamine
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what NSAIDs are pyrazolones
dipyrone
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what NSAIDs are acetic acids
ketorolac
96
what NSAIDs are proprionic acids
carprofen, ketoprofen, naprozen
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what NSAIDs are oxicams
piroxicam and meloxicam
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what NSAIDs are coxibs
deracoxib, firocoxib, robenacoxib
99
What type of drug is galliprant
a non-steriodal, non-cyclooxygenase inhibitor of PGE2 EP4 receptor antagonist
100
what is galliprant used for
pain and inflammation
101
how do opioids cause sedation
inhibition of adenylyl cyclase, closure of voltage-gated Ca channels, and opening of K channels and membrane hyperpolarization
102
what is opioid induced neurotoxicity
euphoria or excitement
103
what drugs are opioid agonists
morphine, hydromorphone, methadone, and fentanyl
104
what drugs are partial opioid agonists
butorphanol, buprenorphine, nalbuphine
105
what drugs are opioid antagonists
naloxone, naltrexone
106
what drugs are alpha-2 agonists
xylazine, clonidine, detomidine, romifidine, medetomidine, dexmedtomidine, zenalpha
107
what are alpha-2 antagonists
yohimbine, tolazoline, atipamazole
108
what is zenalpha made up of
medetomidine and vatinoxan
109
how do ketamine and magnesium work
block NDMA receptors to decrease perception
110
is there any evidence that homeopathic meds work? What are 2 examples
traumeel and cannabis....no evidence
111
what are some nutraceuticals used for osteoarthritis (supplements)
hyaluronic acid, ascorbic acid, chondroitin sulfate, collagen hydrolysate, vitamin D, vitamin E
112
what is hyperesthesia
increased sensitivity to stimulation
