lecture 15 & 16: Pain - Mechanisms, Signs,& Therapy (Exam 2) Flashcards
(76 cards)
1
Q
______ were the first drug class to break the billion dollar market in vet med
A
NSAIDS
2
Q
pain plasticity
A
The ability of the nervous system responsible for pain transmission to change, usually resulting in increased pain sensitivity
3
Q
what is the current major focus in pain research
A
Dorsal root ganglion
4
Q
GABA
A
Inhibitory neurotransmitter that helps regulate pain signals
5
Q
macrophages
A
play a key role in pain and can be either pain-promoting or pain-reducing.
6
Q
Secondary Hyperalgesia
A
Increased pain sensitivity in areas surrounding the injury site
7
Q
Silent Nociceptors
A
Pain receptors that are normally inactive but can be awakened by tissue damage or inflammation
8
Q
Chronic Pain
A
Persistent pain that continues beyond normal healing time
9
Q
____________ can help treat pain by reducing sympathetic nervous system activation.
A
beta blockers
10
Q
Specialized facilities for studying and treating pain, with few remaining in veterinary schools
A
Pain Centers
11
Q
The ________ at MGH is a major pain research facility with ______ floors dedicated to pain studies.
A
Wang Center; 6
12
Q
Medication that mimics GABA, used to treat neuropathic pain
A
gabapentin
13
Q
What is pain defined as in modern veterinary medicine?
A
An unpleasant sensory and emotional experience associated with actual or potential tissue damage
14
Q
pain definition
A
An unpleasant sensory and emotional experience associated with actual or potential tissue damage
15
Q
primary hyperalgesia
A
Increased pain sensitivity at the site of injury
16
Q
Allodynia
A
Condition where non-painful stimuli become painful
17
Q
A-delta fibers
A
Partially myelinated nerve fibers that carry pain signals
18
Q
_____ is one of the simplest therapies for pain as it slows nerve conduction.
A
ICE
19
Q
neural inflammation
A
Inflammatory response in nervous tissue that can enhance pain sensitivity
20
Q
What type of receptors are activated when pain becomes potentially tissue-damaging?
A
NMDA receptors
21
Q
Central Sensitization
A
Increased responsiveness of pain neurons in the central nervous system
22
Q
NMDA Receptors
A
Neural receptors activated during intense pain that contribute to central sensitization
23
Q
Local anesthetics
A
Drugs that block nerve conduction to prevent pain transmission
24
Q
c-fibers
A
Unmyelinated nerve fibers that transmit pain signals
25
nociceptors
High-threshold pain receptors that respond to potentially tissue-damaging stimuli
26
Pain receptors have than touch receptors.
higher thresholds
27
disinhibition
Loss of inhibitory control that can lead to increased pain sensitivity
28
peripheral Sensitization
Process where injury site becomes more sensitive due to inflammatory cell invasion
29
glutamate
Main neurotransmitter involved in pain signal transmission
30
The _______ and _________ are brain regions important in emotional aspects of pain.
limbic system; amygdala
31
sympathetic tone
Level of activation of the sympathetic nervous system that can influence pain perception
32
Sympathetic Nervous System
System that can amplify pain when activated during stress
33
substance P
Neurotransmitter involved in central pain sensitization
34
Beta Blockers
Medications that can help manage pain by reducing sympathetic nervous system activity
35
Where is the largest pain center in the United States located?
MGH (Massachusetts General Hospital)
36
What are the two main types of nerve fibers that carry pain signals?
A-delta and C fibers
37
____ are one of the best indicators of pain in animals.
behavioral changes
38
Central Sensitization
Increased responsiveness of pain-transmitting neurons in the central nervous system
39
______ is one of the most common painful conditions in veterinary medicine.
osteoarthritis
40
_______ is located in the top layers of the dorsal horn
substantia gelatinosa
41
What is peripheral sensitization caused by?
Infiltration of inflammatory cells
42
primary vs secondary Hyperalgesia
primary-Increased pain sensitivity at the site of injury
secondary-Increased pain sensitivity in surrounding uninjured areas
43
Unmyelinated nerve fibers that transmit pain signals
C fibers
44
What condition is associated with genetic defects in sodium channels?
Congenital inability to feel pain
45
collateral sprouting
Growth of new nerve fibers, contributing to chronic pain.
46
What protective function does pain serve?
Pain serves as a protective mechanism to prevent further tissue damage.
47
sensory phys pathways
Transduction
Transmission
Modulation
Projection
Perception
48
know this
49
wide dynamic range neuron (WDR)
respond to a range of
innocuous and noxious mechanical stimuli
50
Pathologic Pain Processe
1. Amplify the response to non-painful stimuli
2. Create and Amplify the response to pain stimuli
3. Create a chronic pain state
51
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
Glial Cell Activation
6. Stress and Pain (PTSD)
7. Collateral Sprouting
52
Neuroinflammation
**CNS and Peripheral Glial Cell Activation**
Schwann cells insulate axons, and satellite cells support neuron bodies in peripheral ganglia.
53
maladaptive pain
pain that doesn't promote healing and repair
54
which pain state is this
nociceptive
55
which pain state is this
inflammatory
56
which pain state is this
neuropathic
57
which pain state is this
nociplastic
58
these are examples of
NSAIDS
59
____________ a nonsteroidal, non-cyclooxygenase inhibitor of prostaglandin E2
(PGE2) EP4 receptor antagonist It is administered to treat canine osteoarthritis
pain and inflammation.
galiprant
60
describe opioids
Inhibition of adenylyl cyclase
Closure of voltage-gated calcium channels
Opening of potassium channels and membrane hyperpolarization
61
opioid agonists
morphine
hydromorphone
methadone
fentanyl
62
opioid partial agonist
Butorphanol
buprenorphine
nalbuphine
63
opioid antagonists
naloxone
naltrexone
64
alpha 2 agonists
Xylazine
Clonidine
Detomidine
Romifidine
Medetomidine
Dexmedtomidine
65
alpha 2 antagonist
Yohimbine
Tolazoline
Atipamazole
66
Block NMDA receptors
Decrease perception
ketamine and magnesium
67
Define Pain
An unpleasant sensory & emotional experience associated w/ actual or potential tissue damage
68
Explain pain transmission
* Start - pain receptors detect noxious stimuli
* Nerve fibers - Two fiber types (alpha delta & C fibers); higher threshold than touch receptors; facilitate pain signal transmission
* CNS pathway - signals first travel to the dorsal horn of the spinal cord; signals then project to the brain for conscious pain perception
* Immune system involvement - Plays a crucial role in pain modulation; inflammatory mediators can sensitize pain receptors
69
What are the pain pathways
1. initiation (nociceptors): Specialized sensory receptors, detect noxious stimuli, & have higher activation thresholds
2. Nerve transmission: alpha delta are partially myelinated & c fibers that are unmyelinated
* Myelin helps facilitate rapid impulse transmission, provide protective nerve sheath, & supplies nutrients to nerves
3. CNS relay: goes to the dorsal horn of the SC then projects to the brain
4. Brain processing: the limbic system, amygdala, & locus coeruleus process emotional & sensory pain components
5. Neurotransmitter involvement: Primary neurotransmitter is glutamate; receptor activation is either AMPA receptors if there is low glutamate or NMDA receptors if there is high amounts glutamate (potential tissue damage)
70
List the mechanisms for physiologic & pathologic pain
* Physiologic: Protective function, req a noxious stimulus, carried by A-delta & c fibers, primary neurotransmitter is glutamate
* Pathologic: Promotes/intensifies/ & prolongs pain, lowers the pain threshold, creates neurologic memory, & can lead to chronic pain, peripheral sensitization, central sensitization, activation of silent nociceptors, disinhibition neural inflammation, stress activation, & collateral sprouting
71
What is the diff btw/ adaptive & maladaptive pain
* Adaptive pain: a normal pain response to tissue damage, involves norm pain receptors, associated w/ the healing process, typically resolves w/in 3 to 10 D, & even w/ severe injuries usually returns to norm w/in 4 to 6 M
* Maladaptive: pain that is out of proportion to the tissue damage, persists beyond the expected healing time, does not support healing, & becomes a chronic pain cycle ("pain chronification")
72
Describe the classification
* Somatic: originates from musculoskeletal system
* Visceral pain: originates from internal organs & considered the most severe type of pain
* Superficial pain
* Deep Pain: Generally more painful
* Nociceptive: normal pain response to tissue damage & high threshold pain receptors
* Inflammatory pain: assoc w/ the release of inflammatory substance
* Neuropathic pain: caused by nerve pain
* Nocyplastic pain (dysfunctional pain): persistent pain w/ changes in CNS & occurs w/out clear tissue damage
* Can be classified by severity: mild, moderate, & severe
73
Identify & understand pain assessment (scoring & methods)
* Visual analog scales (VAS): subjective scales & potential inconsistency btw/ practitioners
* Categorical descriptive scales: uses descriptive terms like mild, mod, & severe
* Behavioral numerical scale: assigns numerical values to specific pain behaviors
* Time activity analysis: measures time spent in different activities & indicates potential pain levels
* Composite pain scale: Combines multi pain indicators
* Grimace scales: Assesses facial expressions & is considered less reliable
* Recommendations: Quantitative methods are preferred, behavioral observation is crucial, PE is most effective, & req practice wide consensus on pain assessment
* The glasgow composite pain score is one of the best methods
74
What are the pharmacologic methods for treating pain? what are their MoAs?
* Local Anesthetics: Examples are Lidocaine, Bupivacaine, Ropivacaine; Mechanism: Block nerve conduction; Specific uses: Wound treatment, nerve blocks
* NSAIDs (Non-Steroidal Anti-Inflammatory Drugs): Examples are Carprofen, Robenacoxib, Deracoxib, Pyroxicam; Mechanism: Inhibit prostaglandin E2 (PGE2); Block inflammatory cytokines
* Opioids: Examples are Morphine, Fentanyl; Mechanism: Bind to opioid receptors in CNS; Produce analgesia and euphoria
* Alpha-2 Agonists: Examples are Xylazine, Detomidine, Medetomidine; Mechanism: Bind to alpha-2 adrenergic receptors; Produce sedation and analgesia
75
What are the complimentary methods for treating pain? what are their MoAs?
* Physical Therapy
* Electrical Therapy (e.g., TENS)
* Complementary Therapies: Acupuncture, Herbal/Nutraceutical treatments, & Environmental modifications
76
What is the multimodal therapy approach
* Combines multiple treatment strategies
* Typically involves drugs
* Aims to provide comprehensive pain management
