78/81. Pain I/II Flashcards
What is the difference between nociception and pain?
Nociception: path of pain from nociceptor to brain (STOPS before perception)
Pain: unpleasant sensation/perception of noxious stimuli
Nociception without Pain: Surgery
Pain without Nociception: Phantom limb pain
Difference between acute and chronic pain
Acute: serves fx to protect body, resolves with tx of cause, recent onset and short duration
goal: tx sx until they resolve
Chronic: no biological fx, persists DESPITE resolved cause
goal: maximize fx independent of health system (manage not cure)
What fibers transmit pain? Where do they synapse in the spinal cord (what lamina)?
What tracts are involved in pain?
How is visceral pain sensed?
Ad: pain/temp (thin myelin) - withdrawal reflex (lamina I)
Ab: touch (lamina II)
C: pain/temp (no myelin) - sustained pain (lamina III)
Neospinalthalamic Tract: where pain processed
Paleospinothalamic Tract: where emotion attached (fear center)
Spinoreticular Tract: increases awareness of pain (wakes you up)
Visceral pain: follows sympathetics back to SC along spinal nerves far from original location - referred pain (cardiacs go with somatics from arm/jaw)
What is gate control theory?
Touch reduced pain in same area
Because Ab touch fibers synapse to interneurons in dorsal horn that inhibit pain neurons
(More complex interplay between Ab, C, Ad fibers and brain exist)
Define allodynia, hyperalgesia, secondary hyperalgesia
How does peripheral sensitization occur?
Allodynia: non-noxious stim now noxious
Hyperalgesia: noxious stim now MORE noxious
Secondary Hyperalgesia: hyperalgesia around injured area (non-burned skin around a burn)
Peripheral sensitization: allodynia in injured area
What are 3 mechanisms of Central Sensitization?
Why don’t opioids work on neuropathic pain?
How do PGs contribute to sensitization?
- Wind-Up: more NMDA receptors put up on 2o neurons in dorsal horns
- Neural Sprouting: Ab fibers branch to 2o pain neurons (touch = nociception)
- Phenotype Switching: Ab fibers produce Substance P/CGRP (pain NTs) - send to dorsal horn
Opiods: only act on 1o Neurons (less C fiber transmission and increase descending system activity)
- no effect on NMDA (windup)
- no effect on Ab Fibers (sprouting/phenotype switch)
PGs: sensitize pain nerve endings/CNS pain
tx: NSAIDs - relieve pain w/o inflammation due to less PGs = less sensitization
Why do different patients experience different amounts of pain?
What is the placebo effect?
Biologic variability in sensitivity and # NMDA receptors, more PG making capabilities, higher tendency of CNS neural sprouting, strength of descending system
Placebo: change in illness with symbolic tx (no physiologic/pharmacologic effect); NALOXONE REVERSIBLE (possibly endorphin mediated, not purely psych), never use to aid in Dx or tx
Goal and Approach to tx of acute pain in outpt and hospital setting
Goal: reduce pt baseline (not bring to 0/10)
Outpt: non-opiods, then weak opioids (tylenol/codeine/hydrocodone, tramadol), then stronger opiods (individualize by pt)
Hospital: IV (faster onset and pts NPO)
Pt Controlled Analgesia - push button for relief, less overuse
NSAIDS - ketorolac, ibuprofen
Tylenol
If opioids fail - try regional/neuraxial analgesia
What are 3 types of regional anesthesia?
What to do if all else fails?
- Epidural anesthesia - infuse opioids/local anesthetics in SC (abd/thoracic surgery, hip/knee replacement, C-section, intra/post op pain - reduce opioid need)
- Peripheral Nerve Blocks - profound pain relief w/o opioids, use peripheral nerve catheters, block sensory/motor fibers (can’t do rehab, higher injury risk with numb limbs)
- Wound Infiltration - local anesthetic - Targeted, no motor block, but limited area/duration/infection risk
If all else fails
KETAMINE: IV dissociative anesthetic via NMDA receptor antagonism (less glu to excite 2o pain neurons)
limited to OR/ICU/PACU use
What 5 groups of meds should you use for chronic pain mgmt?
- NSAIDs - good for mild pain (no role in neuropathic pain)
- Antidepressants: block 5HT/NE reuptake, enhance descending inhibition (NO TOLERANCE)
- Antiepileptics - BEST IN NEUROPATHIC PAIN (Gabapentin, Lyrica, Carbamazepine) - decrease excitation and increase inhibition (block V-gated Na Channels), block windup by preventing repetitive discharge to tx neuropathic pain
- Muscle Relaxants - GABA agonists (Baclofen, Metoxolone - have TOLERANCE), Tizanidine (a2 agonist - no tolerance)
- Chronic Daily Opioids (be careful! only if low-dose, stable, working pt with improvement) Hydrocodone - only available orally - must be prescribed in person
Interventional approaches to chronic pain mgmt
Nerve Blocks: establish site of pain, predict surgical outcome, sometimes therapeutic adjunct
Implantable Stimulators
Intrathecal Pumps
Neurosurgery: high risk, irreversible (trigeminal decompression)
Interdisciplinary Model: interaction of multiple services at one visit
