pain Flashcards
(33 cards)
JCAHO changed pain management
mandation: need to document pain, tx
mech of pain management: #1
remove cause
mech of pain management: dec. inflammation, irritation, sensitivity of nerve endings
aspirin (prototype NSAID), NSAIDs
mech of pain management: block conduction of impulses by pain fibers
local anesthetics (lidocaine)
mech of pain management: modify processing of pain info in CNS
opioids: morphine
others: aspirin, acetominophen, NSAIDS
aspirin, ibuprofen, NSAIDs work via
- inhib. prostaglandin synthesis (COX-1, COX-2)
- alleviate pain by acting at nerve endings and in CNS
- antiinflammatory effects contribute to pain relief
- pain relieving dose is less than anti-inflammatory dose*
aspirin, ibuprofen, NSAIDs side effects
GI: irritation, bleeding
CV: HTN, MI, stroke
pain pathway
nociceptors–>afferent fibers–>DRG–>substantia gelatinosa–>STT–>thalamus–>TO BOTH: sensory cortex (feel the pain) and limbic system (emotional response)
pain mediators
endorphins, enkephalins, serotonin, NE, substance P, prostaglandins
opioids work primarily on the…
limbic system; pain does not cause as much distress
acetaminophen works via
inhib. PG syn. in CNS nerve endings (not in periphery)
also alleviates pain at nerve endings in CNS (unclear mech)
acetaminophen does NOT
affect inflammation
cause GI irritation
acetaminophen risks
hepatotoxicity at high doses (4 g/day)
*not only a problem with OD, ALSO with moderate doses if other risk factors (hepatitis, etOH) (2.5-3 g/day)
NSAIDs also have
anti-pyretic activity (lower fever)
Ketorolac (Toradol)
ACUTE pain management (not as much for anti inflammatory)
musculoskeletal, post-op, visceral (kidney stone, gall bladder stones)
injectable NSAID
-alt. to opioid for pain
selective COX-2 inhibs action
prev. anti-inflammatory affects w/out red. in COX-1 activity (important prostaglandins in upper GI “good guys” that inhib. acid prod. and is mucus producing)
selective COX-2 inhibs
celocoxib (Celebrex) -not as bad SE as other 2
rofecoxib (Vioxx)
valdecoxib (Bextra)
COX-2 is not always bad
maintain renal perfusion (COX-1)
produce prostacyclin:
vasodilate coronary vessels & inhibit plateled aggretation
even selective COX-2 inhibitor use can cause
inc. renin–>inc. aldosterone–>inc. Na retention–>HTN (COX-1 as well)
prostacyclin prod. prevented–>coronary
constriction and uninhibited platelet aggregation–>coronary HTN, heart attack, stroke
NSAIDs and etOH
contribute to HTN
problems with Ketorolac (Toradol)
causes GI irritation one of the worst!
ok for short term (1-2 days) not chronic
local anesthetics
-block sodium channels in nerve endings and axons and stop gen/cond of APs
small unmyelinated neurons are most sensitive
(type C pain fibers)
high enough conc. can affect motor neurons: spinal, regional, nerve block techniques
invasive procedures–>affect motor function and sensory modalities
newer low dose protocols of local anesthetics
more selective pain relief withough affecting other functions (+influsion pumps)
opioids
most effective drugs for sev. pain
under-utilized bc of legal issues and fear of addiction
-this should not prevent use for app. pain management
