Management of Acute Post-operative Pain Flashcards
(50 cards)
what did pain used to be believed to be?
-punishment from the goddess Poena (pain)
sensory experience secondary to tissue damage
nociception
- must have noxious stimulus
- ex. mechanical, thermal, chemical
Unpleasant sensory and emotional experience that arises from actual or potential tissue damage
pain
*ppl may experience pain BEFORE you touch them
what are the two causes of pain?
nociceptive (physical stimulus)
neuropathic (CNS damaged)
what are the two durations of pain?
- acute (know the cause and the end point)
- chronic (not sure what caused it or what will end it)
what things can cause inadequate control of acute pain
- anxiety
- inc symp output
- poor rest
- inadequate oral intake
what is the first part of the trigeminal pain pathway?
-noxious stimuli
- cell damage, chemical mediators released causing:
- -1rst order neuron impulse
- -peripheral nociceptors sensitized
where are 1rst order, second order, and third order neurons located in the trigeminal pain pathway?
1rst: periphery
2nd: spinal cord
3rd: brain
what are the types of analgesics that modulate the pain pathway and what do they do?
opioids and non-opioids:
- both act centrally and in the periphery
- interupt ascending nociceptive impulses (2nd and 3rd)
- depress impulse interpretation in CNS
what are the non-opioid analgesics?
- NSAIDS
- aspirins
- tylenol
how do NSAIDS work?
-supress arachidonic acid which supresses both COX-1 and COX-2 genes
what are the side effects of NSAIDS?
- GI toxicity
- dec renal function
- antiplatelet (like aspirin but not as intense)
- shunt activity to lipooxygenase
what is the big effect with NSAIDS and an asthema pt?
- NSAIDS shut down leukotrienes which drastically effect asthema pts
- ALWAYS ASK ASTHMATICS IF THEY TAKE IBUPROFEN!
what are the contraindications to NSAIDS?
- allergy
- pregnancy
- erosive or UC of the GI mucosa
- asthema (ask them if they can tolerate it)
- anticoagulant therapy or hemorrhagic disorders
- compromised renal fxn
what are COX-2 selective NSAIDS?
- they dont block COX-1 so they keep the good stuff
- protect normal physiologic processes
- anti-inflammatory, analgesic, antipyretic
*celecoxib is prime example
why dont we use COX-2 inhibitors exclusively?
- poor efficacy in 3rd molar model
- expensive
- only one option on market
- inc embolic phenomena
- contraindicated in sulfa allergy
how does acetominophen (tylenol) work?
- believed to be prostaglandin synthesis inhibition in the CNS
- is an analgesic and anti-pyretic (reduce fever)
- DOES NOTHING for inflammation
- none of the side effects seen with NSAIDS (COX-1) but can poison the liver (NIH is leading cause of acute liver failure)
*if cant give NSAIDS (asthematic) then give tylenol
how much acetominophen can your liver handle if you are healthy? questionable health?
healthy = 4g/d questionable = 2g/d
what are the opioid analgesics?
- oxycodone
- hydrodone
- codeine
- in that order of most potent to least
*good for pain relief but bad for dependence
what are the good effects of opioids?
- analgesia
- respiratory depression
- sedation
what are the side effects of opioids?
- euphoria
- dependence
- constipation
- dysphoria
*will not happen with our pts bc we would never prescribe for more than 3-5 days
what can you do to make opioids work better/
- the are SYNERGISTIC with tylenol
- reduces the amount of opioid required for analgesia
- acetominophen (tylenol) is the one that DICTATES dose/frequency
what must happen with oral opiates ?
synthetic oral opiates must be converted to active metabolites using cytochrome P450
*4-10% of caucasians are deficient
what is the mechanism of tramadol?
- weak binding at Mu
- inhibit incoming nociceptive impulses
