Pain management Flashcards
Transduction
- pain stimulus converted into nerve impulse
- impulses travel from nerve endings toward the CNS
Transmission
-impulse is carried to brain via Neospinothalamic or Paleospinothalamic pathways
Perception
- messages from periphery are interpreted by brain
- influenced by neural circuitry and psychosocial factors
Modulation
- brain sends signals to suppress or amplify pain signals
- gate control theory of pain
Fast pain receptors
- felt within 0.1 secs of stimulus
- sharp, prickling, acute, electric
- not felt in deeper tissues
- associated with tissue destruction
- to stimulate brain to remove tissue from injurious agent
- Delta A fibers
slow pain receptors
- felt >1 sec of stim
- increases slowly over many seconds
- burning, aching, throbbing, nauseous
- to remind you to allow the area to recoup
Types of pain stimuli
- mechanical
- thermal
- chemical
What substances are released from damaged tissue that stimulate pain receptors?
- Bradykinin
- Serotonin
- Histamine
- K+ ions
- Acids
- Prostaglandins
- Substance P
Neospinothalamic tract
- Type A delta pain fibers (fast pain receptors)
- mechanical and thermal pain
- nerve fibers travel all the way to thalamus
- pain can be localized precisely
Paleospinothalamic tract
- Type C pain fibers (slow pain receptors)
- Terminates widely in brainstem (pons)- signal must pass thru additional short fibers
- chemical pain
- not well localized, important for suffering
What impact does reticular formation have?
strong arousal on nervous activity in the brain when in severe pain- hard to sleep
what are the primary neurotransmitters involved in pain suppression?
Enkephalin and Serotonin
Name NSAIDs
Aspirin Diclofenac Diflunisal Etodolac Fenoproten Ibuprofen Celecoxib Ketorolac Nabumetone Naproxen Piroxicam Salsalate Sulindoac Tolmetin
What is the mechanism of action of NSAIDs
- Covalently modifies COX1 and COX2 pathways => inhibits prostaglandin synthesis => interrupts transduction of pain
- COX1 is found in blood vessels, stomach, kidneys, plts, and intestines (physiologic stimulation)
- COX2 is induced by cytokines and mediators during inflammation
When are NSAIDs indicated?
- musculoskeletal disorders
- chronic post op pain d/t inflammation
- pain d/t inflammation
Side effects of NSAIDs
- d/t COX-1 inhibition
- GI intolerance/ulcers
- blockage of plt aggregation- stroke & MI
- inhibited renal function- Na & H2O retention, HTN, AKI
- prolonged gestation
- vasomotor rhinitis
NSAID drug interactions
- potentiates anticoagulation
- increased lithium and methotrexate toxicity
- decreased effectiveness of antihypertensives
What lab is important to monitor for NSAIDs
K+ (hyperkalemia d/t decreased renal perfusion)
Acetaminophen
- COX inhibitor (perhaps COX3 or very selective COX2)
- better for kidneys
- works well for fever
What is the mechanism of action for opioids?
- binds to mu receptors => inhibits nociceptive (pain) receptors in CNS
- acts as synthetic enkaphlins
What are other effects of opioids beyond pain management?
- directly suppresses resp. and cough centers
- stimulates chemoreceptor trigger zone (CTZ)
- decreases HCl secretion in stomach
- decreases biliary, pancreatic, and intestinal secretions
- enhances nonpropulsive contractions and inhibits propulsive contractions in sm intest.
- augments anal sphincter tone
Side effects of opioids
- N/V
- constipation
- urinary retention
- mental clouding
- dizziness
- hypotension
Tapentadol (Nucynta)
- synthetic mu-agonist and norepi reuptake inhibitor
- for neuropathic pain
- ER version- for diabetic periph neuropathy
Tramadol (Ultram)
- very selective, weak mu-opioid receptor agonist
- norepi reuptake inhibition
- poteniates serotonin release
- can produce physical addiction
- risk of seizure with recreational use
