Pain & Opioids Flashcards
(47 cards)
acute pain that is not treated promptly and properly transitions into ____ that causes _____
persistent pain; irreversible changes to nervous system
eudynia
symptomatic or normal pain
maldynia
pathophysiologic disease of the nervous system, “abnormal” pain
3 dimensions of pain
1) sensory-discriminative (sensation, location, quality)
2) motivational-effective (unpleasantness)
3) cognitive-evaluative (past experiences modify other 2 dimensions; negative or positively affect outcome and pain experience; based on patient beliefs, cultural background, past experience)
opioids affect which dimension of pain
motivational-effective
Which cells initiates the motor, sensory, and ANS responses of pain? which is inhibitory?
T cell; SG neuron
which NT release allows pain transmission?
Substance P (blocked by intrathecal opioids) and glutamate
opioid receptors on ____ are probably on Substance P terminals and block it’s release
substantia gelatinosa
non-opioid inhibitory NT
Endorphins (are excitatory for the descending p/ways that inhibit pain)
Serotonin (inhib in brain)
Norepi (RAS & hypothalamus)
glycine (inhibs at spinal chord by increasing Cl-)
GABA (cerebral cortex, basal ganglia, cerebellum, SC (increases cl- and hyperpolarizes)
Glutamate
excitatory NT in hippocampus, outer layer of cerebral cortex, and substantia gelatinosa (learning & memory recall, central pain transduction, excitotoxic neuronal injury)
-there are also inotropic glutamate receptors (ligand-gated channel opens, influx of cation (na+) and depolarization
opioids
- have receptor agonist activity with morphine-like effects at mu receptors throughout body, but also at kappa and delta receptors
- mu receptors produce analgesic and SE
- inhib NT, block Ca influx and increase K efflux
analgesia
absence of pain without loss of consciousness
Which endogenous opioids affect mu receptors
endomorphins and endorphins
Which endogenous opioids affect delta receptors
endorphins and enkephalins
Which endogenous opioids affect kappa receptors
dynorphins
mu receptors
brain: sedation, analgesia, physical dependence
spinal cord (SG): resp depression, miosis
peripheral sensory neurons: euphoria
GI tract: reduced GI motility, vasodilation
kappa receptors
brain: analgesia, anticonvulsant effects, delirium
SC: diuresis
Peripheral: dysphoria, miosis, sedation, reduces shivering
delta
location: brain
action: analgesia, antidepressent effects, convulsant, dependence
generalized opioid SE
sedation & resp depression, N/V, CV effects (vasodilation d/t histamine release), euphoria (esp meperidine), antitussive, miosis, pruritis, biliary spasm, myoclonus/seizures with high dosage, chest wall rigidity
morphine
-classic mu receptor agonist
-influences the motivational-effective aspect of pain
-analgesia in the brain mu-1 and spinal mu-2
-only 23% unionized and able to cross BBB
-lipid solubility low (1.4) slow onset
1/2 life 2-3 hours
DOA 4-6
morphine SE
- resp depression (shift to right of the CO2 response curve)
- vent response to hypoxia decreased
- N/V
- large doses or rapid admin cause skeletal muscle rigidity (eliminated with GABA agonists and paralytics)
- miosis
- pruritis (not histamine related, but rx with antihistamines)
- hyperalgesia with prolonged use
- decreased cough reflex
- decreased GI motility
- increased biliary pressure by increasing phasic wave frequency of the sphincter of oddi
- release of histamine
- reduces centrally mediated SNS –> vasodilation
morphine metabolism
70% metabolized in liver via glucuronidation (liver disease has minimal effect, but reduced liver blood flow reduces clearance [very old and young])
excretion of metabolites by kidney (renal disease affects)
-m3 glucuronide (75-85%) inactive metabolite, no analgesia
-m6 (5-10%) active, 10x more potent than morphine
codeine
3-methyl-morphine
- 10% converted to morphine which causes analgesia
- less 1st pass metabolism when taken orally
hydromorphone
5x more potent than morphine
onset : 5 min, peaks 10-20 min
1-2 mg dilaudid = 10-20 mg morphine