Management of Acute Postoperative Pain Flashcards
according to International Association for
the Study of Pain, what is the definition of pain?
unpleasant sensory and emotional experience that arises from actual or potential tissue damage
types of causality of pain
- nociceptive
2. neuropathic
what type of pain do we normally tx in dentistry?
acute nociceptive pain
inadequate management of acute pain may cause what?
- anxiety
- increased sympathetic output
- poor rest
- inadequate oral intake
noxious stimulus causes cell damage and what to release?
chemical mediators
what happens when chemical mediators are released after a noxious stimulus?
- 1st order neuron impulse
2. peripheral nociceptors sensitized
what modulates the trigeminothalamic tract pathway?
opioids and non-opioids
how does analgesics modulate the trigeminothalamic tract pathway?
- by interrupting ascending nociceptive impulses
2. depressing impulse interpretation in CNS
what does NSAIDs block?
cyclooxygenases which activates prostaglandins that cause pain, inflammation and fever
common side effect of traditional NSAIDs
- stomach pain
2. heartburn
serious side effect of traditional NSAIDs
- GI toxicity
2. decreased renal fxn
why is traditional NSAIDs a relative contraindication for asthmatic patients?
shunt activity to lipoxygenase
if asthmatic pt takes ibuprofen, cyclooxygenase is inhibited –> activity has to go somewhere so goes towards lipoxygenase pathway –> a lot of leukotrienes are created which induces broncospasm and asthmatic rxns
absolute contraindications to NSAIDs
- allergy
- pregnancy
- erosive or ulcerative conditions of the GI mucosa
relative contraindications to NSAIDs
- asthma
- anticogulant therapy or hemorrhagic disorders
- compromised renal fxn
example of COX-2 selective NSAID
celecoxib (celebrex)
effect of celecoxib (celebrex)
- anti-inflammatory
- analgesic
- anti-pyretic
T/F: celecoxib (celebrex) protects normal physiologic processes
true
COX-2 activates what?
- prostaglandins
2. prostacyclin
effect of prostaglandins when activated by COX-2
- pain, inflammation, fever
2. renal fxn
effect of prostacyclins when activated by COX-2
- platelet inhibition
2. vasodilation
effect of prostaglandins when activated by COX-1
- gastric mucosal barrier
2. renal fxn
effect of thromboxane A2 when activated by COX-1
- platelet aggregation
2. vasoconstriction
why don’t we use COX-2 inhibitors exclusively to manage acute postoperative pain?
- poor efficacy in 3rd molar model
- expensive since it’s the only one option on the market
- increased embolic phenomena
when is COX-2 inhibitors contraindicated?
pts with sulfa allergy
mechanism of action of acetaminophen
believed to be prostaglandin synthesis inhibition in CNS
what are the effects of acetaminophen?
- analgesic
2. anti-pyretic
T/F: acetaminophen has anti-inflammatory effects
FALSE
which organ conjugates acetaminophen into non-toxic metabolites?
liver
what dosage can the liver no longer conjugate acetaminophen into non-toxic metabolites?
200-250 mg/kg/24 hr
what cyctochrome breaks down acetaminophen?
P450
what is the toxic acetaminophen metabolite?
NAPQI (N-acetyl-p-benzo-quinone imine)
what is the recommended daily maximum of acetaminophen by the FDA? by McNeil Consumer Healthcare (ppl that make Tylenol)?
FDA - 4000 mg/day
McNeil Consumer Healthcare - 3000 mg/day