lecture 15 & 16: Pain - Mechanisms, Signs,& Therapy (Exam 2) Flashcards
______ were the first drug class to break the billion dollar market in vet med
NSAIDS
pain plasticity
The ability of the nervous system responsible for pain transmission to change, usually resulting in increased pain sensitivity
what is the current major focus in pain research
Dorsal root ganglion
GABA
Inhibitory neurotransmitter that helps regulate pain signals
macrophages
play a key role in pain and can be either pain-promoting or pain-reducing.
Secondary Hyperalgesia
Increased pain sensitivity in areas surrounding the injury site
Silent Nociceptors
Pain receptors that are normally inactive but can be awakened by tissue damage or inflammation
Chronic Pain
Persistent pain that continues beyond normal healing time
____________ can help treat pain by reducing sympathetic nervous system activation.
beta blockers
Specialized facilities for studying and treating pain, with few remaining in veterinary schools
Pain Centers
The ________ at MGH is a major pain research facility with ______ floors dedicated to pain studies.
Wang Center; 6
Medication that mimics GABA, used to treat neuropathic pain
gabapentin
What is pain defined as in modern veterinary medicine?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage
pain definition
An unpleasant sensory and emotional experience associated with actual or potential tissue damage
primary hyperalgesia
Increased pain sensitivity at the site of injury
Allodynia
Condition where non-painful stimuli become painful
A-delta fibers
Partially myelinated nerve fibers that carry pain signals
_____ is one of the simplest therapies for pain as it slows nerve conduction.
ICE
neural inflammation
Inflammatory response in nervous tissue that can enhance pain sensitivity
What type of receptors are activated when pain becomes potentially tissue-damaging?
NMDA receptors
Central Sensitization
Increased responsiveness of pain neurons in the central nervous system
NMDA Receptors
Neural receptors activated during intense pain that contribute to central sensitization
Local anesthetics
Drugs that block nerve conduction to prevent pain transmission
c-fibers
Unmyelinated nerve fibers that transmit pain signals
nociceptors
High-threshold pain receptors that respond to potentially tissue-damaging stimuli
Pain receptors have than touch receptors.
higher thresholds
disinhibition
Loss of inhibitory control that can lead to increased pain sensitivity
peripheral Sensitization
Process where injury site becomes more sensitive due to inflammatory cell invasion
glutamate
Main neurotransmitter involved in pain signal transmission
The _______ and _________ are brain regions important in emotional aspects of pain.
limbic system; amygdala
sympathetic tone
Level of activation of the sympathetic nervous system that can influence pain perception
Sympathetic Nervous System
System that can amplify pain when activated during stress
substance P
Neurotransmitter involved in central pain sensitization
Beta Blockers
Medications that can help manage pain by reducing sympathetic nervous system activity
Where is the largest pain center in the United States located?
MGH (Massachusetts General Hospital)
What are the two main types of nerve fibers that carry pain signals?
A-delta and C fibers
____ are one of the best indicators of pain in animals.
behavioral changes
Central Sensitization
Increased responsiveness of pain-transmitting neurons in the central nervous system
______ is one of the most common painful conditions in veterinary medicine.
osteoarthritis
_______ is located in the top layers of the dorsal horn
substantia gelatinosa
What is peripheral sensitization caused by?
Infiltration of inflammatory cells
primary vs secondary Hyperalgesia
primary-Increased pain sensitivity at the site of injury
secondary-Increased pain sensitivity in surrounding uninjured areas
Unmyelinated nerve fibers that transmit pain signals
C fibers
What condition is associated with genetic defects in sodium channels?
Congenital inability to feel pain
collateral sprouting
Growth of new nerve fibers, contributing to chronic pain.
What protective function does pain serve?
Pain serves as a protective mechanism to prevent further tissue damage.
sensory phys pathways
Transduction
Transmission
Modulation
Projection
Perception
know this
wide dynamic range neuron (WDR)
respond to a range of
innocuous and noxious mechanical stimuli
Pathologic Pain Processe
- Amplify the response to non-painful stimuli
- Create and Amplify the response to pain stimuli
- Create a chronic pain state
Pain Processes that
Promote, Intensify and Prolong Pain
- Peripheral Sensitization
- Central Sensitization
Activation of NMDA-R - Activation of Silent Nociceptors
- Disinhibition
- Neuroinflammation
Glial Cell Activation - Stress and Pain (PTSD)
- Collateral Sprouting
Neuroinflammation
CNS and Peripheral Glial Cell Activation
Schwann cells insulate axons, and satellite cells support neuron bodies in peripheral ganglia.
maladaptive pain
pain that doesn’t promote healing and repair
which pain state is this
nociceptive
which pain state is this
inflammatory
which pain state is this
neuropathic
which pain state is this
nociplastic
these are examples of
NSAIDS
____________ a nonsteroidal, non-cyclooxygenase inhibitor of prostaglandin E2
(PGE2) EP4 receptor antagonist It is administered to treat canine osteoarthritis
pain and inflammation.
galiprant
describe opioids
Inhibition of adenylyl cyclase
Closure of voltage-gated calcium channels
Opening of potassium channels and membrane hyperpolarization
opioid agonists
morphine
hydromorphone
methadone
fentanyl
opioid partial agonist
Butorphanol
buprenorphine
nalbuphine
opioid antagonists
naloxone
naltrexone
alpha 2 agonists
Xylazine
Clonidine
Detomidine
Romifidine
Medetomidine
Dexmedtomidine
alpha 2 antagonist
Yohimbine
Tolazoline
Atipamazole
Block NMDA receptors
Decrease perception
ketamine and magnesium
Define Pain
An unpleasant sensory & emotional experience associated w/ actual or potential tissue damage
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
What are the pain pathways
- initiation (nociceptors): Specialized sensory receptors, detect noxious stimuli, & have higher activation thresholds
- 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 - CNS relay: goes to the dorsal horn of the SC then projects to the brain
- Brain processing: the limbic system, amygdala, & locus coeruleus process emotional & sensory pain components
- 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)
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
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”)
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
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
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
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
What is the multimodal therapy approach
- Combines multiple treatment strategies
- Typically involves drugs
- Aims to provide comprehensive pain management
