pain control Flashcards
nociceptive pain
body pain, visceral
which kind of pain responds to opiates
nociceptive
neuropathic pain
no location, pain created by overfilling of nerve
nociception involves what four things
stimulation, transmission, perception, modulation
transmission has to do with
action potential moving from site of stimulus to dorsal horn of spinal column, then to CNS
a delta
large diameter , sparsely myelinated
perception of pain
conscious experience of pain
pain is relayed through
thalamus and higher cortical structures
modulation of pain
inhibition of impulses via the brain stem. how you deal with it. examples are endogenous opioids, serotonin, NE, GABA
neuropathic pain is
abnormal processing of sensory input
chronic pain
> 3 months or past the time of normal tissue healing
what are the receptors of opioids
delta, kappa, mu, nociceptive
where are opiod receptors located
brain, spinal cord, GI tract
delta
brain & peripheral nerves. analgesia. antidepressant. dependence
kappa
brain, spinal cord, periphery. analgesia. sedation, mitosis, dysphoria, ADH inhibition
primary target for opiates is
mu
MU 1
analgesia and dependence
MU 2 is most known for
side effects
MU 2 effects
resp depression, euphoria, reduced GI motility, dependence
MU 3 effects
unknown
nociceptive receptor
brain, spinal cord. anxiety depression, appetite, tolerance to MU agonists
2 ways opiates cause a reduced pain experience
pre-synaptic and post-synaptic
how do opiates cause a reduced pain experience pre-synaptic
opiate binds to mu receptor and reduces the release of neurotransmitters that participate in the perception of pain. by releasing calcium
how do opiates cause a reduced pain experience post-synaptic
opiate increases the effux of K so action potential is pushed into hyper polarization and it will take a greater signal to kickstart a pain impulse(changes electric field)
methadone mech of action
NMDA receptor antagonist and MU agonist
how does the NMDA receptor affect opiates
may reduce opiod effectiveness
overstimulation of NMDA receptor by glutamate causes
neuropathic pain
natural opiate is
morphine
morphine structure
phenanthrene nucleus
semisynthetic morphine
dilaudid
opioids must exist in the ___ state in order to form a strong bond at the opiod receptor
ionized. but doesn’t need to be super lipophillic
peak effect of morphine
15-30min
how much IV morphine enters the CNS?
very little because its highly ionized
morphine active metabolite is
m6G
morphine’s primary metabolite is
inactive. m3G
what does morphines active metabolite do
m6g causes pain modulating effects and resp depression
how can m6g be dangerous
chronic administration or renal failure can cause m6g to enter the CNS by mass action
morphine cardiac
bradycardia, reduced SNS, histamine release. vasodilation
morphine and histamine
release ! vasodilation, hypotension
morphine resp. women vs men
women have more sensitive mu effect (agonist)
morphine resp
decreased response to CO2, increase in resting paCO2, dispalaces CO2 curve to right
morphine CNS
compounded
caution morphine in use of what patient
head injured
head injured and BBB integrity?
may be compromised so increased sensitivity to opiod
morphine effect on eeg
resembles sleep associated change
morphine will make you feel ___ before ___
sleepy before pain control
morphine side edict in biliary tract
may cause spasm. can be misinterpreted as common bile duct stone. give glucagon
gu effects of morphine
urgency, difficulty voiding
morphine affect on neuromuscular blocking drugs
none
how does morphine interfere with ventilation
may cause thoracic and and muscle rigidity significant enough to interfere with adequate ventilation
MAO inhibitors and opiod agonists
exaggerated CNS depression and hyperpyrexia
dilaudid is a
semisynthetic opiod agonist
onset of dilaudid
15-30 min
peak of dilaudid
30-90 min
why is dilaudid a good choice for renal pt’s
lacks known active metabolites
dilaudid has far less of a ___ release than morphine
histamine
all fentanyl products risk ___ buildup
renal
fentanyl is a
synthetic agonist of MU
single dose of fent has more ___ onset and ___ duration of action than morphne
rapid, shorter
fent has ___ passage across BBB
greater. lipophilic
why does fent have a shorter duration of action
redistribution to inactive tissues
lungs relationship to fent
inactive storage site
fent metabolism
hepatic. partially inactive <1%.
fent CV
no histamine release
fent CNS
modest increase in ICP
opiod and benzo combo
synergism with respect to hypnosis and depression of ventilation
opioids r/t cardiopulmonary bypass
all opioids demonstrate a decrease in plasma concentration with initiation of cardiopulmonary bypass. more significant with fent because it adheres to the circuit
fent analgesia is___ times more potent than morphine
75-125
fentanyl can be detected in the urine for __ hours because of its metabolite norfentanyl
72
transdermal fent patch peak concentration
18hours
sufentanil is
thinly analogue of fent
sufentanil potency compared to fent
5-10x
why is sufentanil more potent
due to the greater affinity of sufentanil for opiod receptors
is elimination half-time of suf affected by liver disease?
no
vd and elimination half time of sufentanil is __ in obese pt?
increased due to increased lipid solubility
suf protein binding
extensive 92.5% thus a smaller VD
alfetanil
analogue of fentanyl
alfentanil potency
1/5 to 1/10 potency of fent
alfentanil duration of action
1/3 of fent
alfentanil name of the game
rapid effect site equilibrium time
alfentanil gets to ___ faster than fent and su
mu receptors
remi MOH
selective mu agonist
remi similar to alafent..
rapid effect site equilibrium (works fast)
analgesia of remi
similar to fent
structure of remi
ester linkage
why does remi’s structure matter
ester linkage is metabolized quickly by esterase’s. quick onset, quick clearance, minimal accumulation.
high dose of remi does what to brain
decreases CMRO2 and CBF
remi has fastest
offset
clinically remi behaves like a drug with an elimination half time of
6 min or less
