Opioid Analgesics and Non Opioids Flashcards
2 types of pain
- duration: acute (sudden) or chronic (3+ months)
- origin
- somatic: skin, bone, soft tissues - burning, throbbing, localized
- visceral: abd/thorasic - dull, aching, hard to locate (loss of consciousness, N/V)
- neuropathic: nerves - shooting, stabbing
Categories for pain management (3)
- opiates: morphine (pain 7-10)
- non-opiates: acetaminiphen, salicylates (ASA), NSAIDs (pain 1-3)
- adjuvant (in addition to others): benzodiazepines, TCA, corticosteroids; treating anxiety, hypnotic, anti-nausea to help comfort
pathway to pain receptors
- injury to cell produces aracadonic acid - cyclooxygenase - prostaglandin release (pain response - vasodilation, increased vascular perm, edema)
- injury to cell also produced bradykinin (pain receptors)
ADE opiates
- serious: decrease respiration (if RR
route of administration: opiates
PO, IM, IV(can titrate), patch, PCA
common clinical uses: opiates
- relief of moderate to severe pain
- acute pulmonary edema
- severe non productive cough (codeine)
infrequent uses: opiates
- invasive diagnostic tests
- pre-op sedation
- labor and delivery
use opiates cautiously when…
- respiratory depression (CNS depressant)
- chronic lung disease (CNS depressant)
- kidney/liver disease (met/exc)
- increased ICP (watch consciousness)
opiate antagonists
- will counteract opiate/block receptors, NOT stimulants
- naloxone (narcan)
- works for 2 hours, fast acting, may need repeat dose
opiate abuse/withdrawal
- tx with methadone (still addictive, but can fx)
- tolerance and cross tolerance fast
- babies can die from withdrawal
non-opiates (examples/fx)
ASA, acetaminophe, NSAIDs
- work to block cyclooxygenase 1 and 2
pathway for non-opiates
stimuli to cell -> arachidonic acid -> non-opioid will stop process to cox1 and 2
cyclooxygenase 1
(physiologic/protective prostaglandins)
- GI: protects stomach
- renal: maintain blood flow
- regulates smooth muscle (vessels, lungs)
- regulates blood clotting (keeps regular)
cyclooxygenase 2
(pathologic prostaglandins - ADE)
- inflammation (vasodilatation, increased perm)
- edema
- leukocytosis (increase WBC to injury)
- cytokine release (play part in pain)
ASA - Acetylsalicyclic Acid: therapeutic effects
(aspirin)
- mild analgesic: pain 1-3
- anti-inflammatory
- antipyrectic: effects hypothalamus - sweat
- anti thrombotic: bind irreversibly to inhibit platelet aggregation “slippery”