exam 3- chronic pain Flashcards
Chronic pain definition
Uninterrupted persistent pain lasting for 3 months or more
Determination of source is not always clear
Things that go along with chronic pain
povrty, despair, suicide, divorce, interferes with ADLs, economic impact
Chronic pain classification
malignant or non malignant
Chronic pain treatment goal
improve ADLs, enhance function, multidisciplinary approach to treatment
Pathophysiology of chronic pain (4 steps)
- Afferent signals amplified
- descending modulation from dorsal horn pathway is decreased
- prolonged stimulation, inflammation and nerve injury can sensitize pain transmission fibers
- Death of inhibitory cells and/or cause structural neuroplastic changes
Central mechanisms of chronic pain (2)
- chronic inflammation
- hyper excitability of second order neurons in the dorsal horn
Primary neurotransmitter released by primary afferent in the dorsal horn
glutamate
Glutamate role in chronic pain
excites receptors, causing influx of calcium into cell –>increases second messengers such as protein kinase and phospholipase
Glutamate activates (2)
- NMDA receptor (among others)
- Substance P and CGRP to bind
Activation of secondary messengers from glutamate binding:
Up - regulation and hyperexcitability
Up-regulation and hyper excitability of NMDA receptors causes
Long term neuronal plasticity and eventually gene transcription changes = sensitization and chronic pain states
What is wind up
abnormal response and chronic pain sensation
What causes wind up
Repetitive stimulation from chronic inflammation or nerve damage
2 phases of windup:
- hyperalgesia (less and less stim required to initiate pain
- FIbers that don’t normally carry painful stimulation are recruited and start transmitting pain
Chronic pain can lead to
psychological dysfunction
Prevention of chronic pain and wind up
Treat underlying conditions
In windup, synchronous volleys of affarents produce
long lasting synaptic potentials
Windup is the repetitive activation of ______ which______
C-fibers, which increases magnitude of evoked responses
Windup leads to
central sensitization
Central sensitization is
enhanced excitability of dorsal horn neurons
Central sensitization contributes to
hyperalgesia
Types of chronic pain (4)
- neuropathic pain
- nociceptive pain
- somatic pain
- visceral pain
Neuropathic pain definition and manifestations
example
pain radiates from a damaged nerve along dermatome
manifestations: intense burning sensation, allodynia. (exaggerated pain repsonse)
ex. shingles
Complex regional pain syndrome s/sx
spontaneous pain, hyperalgesia, allodynia, trophic, sudomotor, vasomotor abnormalities, active/passive movement disorders
Complex regional pain syndrome treatment (3)
Sympathetic block,
meds,
spinal cord stimulator
Complex regional pain syndrome meds
gabapentin, ketamine infusion, memantine
Complex regional pain syndrome type 1 (including pathophys)
Reflex sympathetic dystrophy
cause: trauma, surgery, neck injury, female
Complex regional pain syndrome type II (including pathophys)
Causalgia
cause: nerve injury (i.e. nerve cut in surgery)
Somatic pain originates in
arms, legs, face, muscles, tendons, extrinsic areas of body
Somatic pain is triggered by
acute injury or chronic disease (cut, bruise, arthritis, joint injury)
Visceral pain and presentation
internal organs
recepted as referred pain
Presentation: N/V, jitteriness
Inflammatory nuerochemical substances and reason
Bradykinin, histamine, substance P
Serves to protect and prevent further damage
Chronic post-surgical pain risk factors:
- preoperative pain
- comorbidities/autoimmmune
- secondary gain
Chronic postsurgical pain treatment goal
reduce central sensitization
Methods to reduce central sensitization in postsurgical chronic pain
Pre-op treat (meds and block)
meds: NSAIDS/ketamine
Post op control of chronic postsurical pain (3)
- Antidepressants
- PO pain meds: ST opioids, anticonvulsants, topical agents, NMDA antagonists
- Topical agents
Chronic postsurgical pain nature
neuropathic without identifiable nerve injury. Still possible nerve compression/damage
Common Chronic postsurgical pain surery:
Thoracotamy or thoracic penetration of some sort)
Pharmaceuticals MOA in chronic pain (2)
- assist in returning body to normal function (reduce cycle)
- Treat pain perception only w/o reducing dysfunctional cycle of chronic pain
NSAIDS MOA
COX blocking–>reduces release of PGs
Best to reduce inflammation
COX-2 is better than nonselective COX inhibitor
Aspirin
nonselective COX inhibitor
Aspirin side effect
prolonged platelet aggregation
Multimodal treatment options for chronic pain (8)
- Meds
- Rehab
- Psychology
- Interventional pain management
- implantable therapies
- Complementary/alternative treatments
- Nutrition counseling
- Vocational Counseling
Opioids act in the
CNS, not periphery (not effective in chronic pain’s main source of pain)
can be used for short term releif
Opioid induced hyperalgesia
Sensitization to painful stimuli d/t opioid exposure (hyperalgesia)
May be same or different pain from original pain
Chronic opioid therapy and preoperative pain management (3)
- Know doses, don’t d/c or if you must, give adjunct
- Consider intrathecal or epidural infusion and continue perioperatively
- benzos
Methadone use
1.Preemptive analgesia for acute pain management
2. opioid addiction txmt
*need EKG - prolonged QT
Suboxone use
get off chronic opioids - prevents w/d and raving
Suboxone MOA
Blocks other opioids from binding
Suboxone caution
NEVER give versed or benzos: can throw them back into addiction
Chronic opioid therapy patients - perioperative pain management (5)
- Increase dose
- avoid opioid antagonist or agonist-antagonist (w/d)
- Nonopioid analgesic adjuncts (ketamine, clonidine, dex)
- Magnesium 2-3 g
- regional/local
Gabapentin (antivonvulsant) in chronic pain - MOA
blocks alpha 2 delta of Ca+ channels in CNS, prevents excitatory neurotransmitter release
overall decrease in neuronal excitation
Perioperative pain management in COT (4)
- Regional
- IV PCA (feeling of control)
3.pain specialist
4.Monitory for respiratory depression
Ketamine MOA
blocks NMDA = treatment and prevention of chronic pain
Pros of ketamine perioperatively
- lowers opioid requirement (even at low dose 0.25-0.5 mg/kg)
Ketamine should be used at a _____ because _____
low dose (0.5 mg/kg or less), because it minimizes N/V, hallucinations.
Cylobenzaprine (flexeril) result
Relief of muscle spasm
Cyclobenzaprine (flexeril) is chemically related to
amtriptyline (antidepressant)
NSAID topical agents pros (2)
- absorption better than PO
- Continuous deliver may. help reestablish a noral pathway
Sleep is important for
healing and cell regeneration
promote sleep in chronic pain!KAn
Issue with sleep aid meds
interrupt rapid eye movement, disrupting quality of sleep
Antidepressant and chronic pain MOA
Block reuptake of serotonin and NE = increase their availability
Improved mood = increased compliance, decreased opioid use
in chronic pain, Tricyclic antidepressants used for (3)
1.postherpetic neuralgia
2. HAs
3. fibromyalgia
SNRIs are preferred in
those with cardiac disease
Lidocaine patch MOA
local Na+ channel blockade
Capsaicin cream MOA
reduces nerve fiber density w/ daily application
Mexiletine is
PO lidocaine
lidocain IV helps with
resistant neuropathic pain syndrome
Lidocaine infusions show _____ in treatment with neuropathic pain
relief equal to morphine, gabapentin, amtriptyline
Dexmedetomidine MOA (3)
- Peripheral analgesia effect
- central analgesia effect
- Local analgesia effect
Dexmedetomidine peripheral analgesia effect MOA
inhibits A delta and C fibers
Dex central analgesic effect MOA
Depolarizes blue plaque in descending pathway in spinal cord in pre-synaptic pathway
inhibits release of substance P –>inhibit spinal cord transmission –> terminates pain signal
Dex local analgesia effect MOA
modulation of hyperalgesia - alpha2 receptor stimulator
*add to peripheral nerve block
SE of dex in peripheral nerve block
N/V, resp depression, itching
Corticosteroids in chronic pain
anti-inflammatory effect: inhibit phospholipase A2 = prevent release of arachiadonic acid
overall decrease in inflammatory cytokines