pain control Flashcards

(89 cards)

1
Q

nociceptive pain

A

body pain, visceral

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2
Q

which kind of pain responds to opiates

A

nociceptive

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3
Q

neuropathic pain

A

no location, pain created by overfilling of nerve

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4
Q

nociception involves what four things

A

stimulation, transmission, perception, modulation

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5
Q

transmission has to do with

A

action potential moving from site of stimulus to dorsal horn of spinal column, then to CNS

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6
Q

a delta

A

large diameter , sparsely myelinated

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7
Q

perception of pain

A

conscious experience of pain

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8
Q

pain is relayed through

A

thalamus and higher cortical structures

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9
Q

modulation of pain

A

inhibition of impulses via the brain stem. how you deal with it. examples are endogenous opioids, serotonin, NE, GABA

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10
Q

neuropathic pain is

A

abnormal processing of sensory input

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11
Q

chronic pain

A

> 3 months or past the time of normal tissue healing

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12
Q

what are the receptors of opioids

A

delta, kappa, mu, nociceptive

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13
Q

where are opiod receptors located

A

brain, spinal cord, GI tract

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14
Q

delta

A

brain & peripheral nerves. analgesia. antidepressant. dependence

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15
Q

kappa

A

brain, spinal cord, periphery. analgesia. sedation, mitosis, dysphoria, ADH inhibition

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16
Q

primary target for opiates is

A

mu

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17
Q

MU 1

A

analgesia and dependence

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18
Q

MU 2 is most known for

A

side effects

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19
Q

MU 2 effects

A

resp depression, euphoria, reduced GI motility, dependence

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20
Q

MU 3 effects

A

unknown

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21
Q

nociceptive receptor

A

brain, spinal cord. anxiety depression, appetite, tolerance to MU agonists

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22
Q

2 ways opiates cause a reduced pain experience

A

pre-synaptic and post-synaptic

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23
Q

how do opiates cause a reduced pain experience pre-synaptic

A

opiate binds to mu receptor and reduces the release of neurotransmitters that participate in the perception of pain. by releasing calcium

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24
Q

how do opiates cause a reduced pain experience post-synaptic

A

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)

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25
methadone mech of action
NMDA receptor antagonist and MU agonist
26
how does the NMDA receptor affect opiates
may reduce opiod effectiveness
27
overstimulation of NMDA receptor by glutamate causes
neuropathic pain
28
natural opiate is
morphine
29
morphine structure
phenanthrene nucleus
30
semisynthetic morphine
dilaudid
31
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
32
peak effect of morphine
15-30min
33
how much IV morphine enters the CNS?
very little because its highly ionized
34
morphine active metabolite is
m6G
35
morphine's primary metabolite is
inactive. m3G
36
what does morphines active metabolite do
m6g causes pain modulating effects and resp depression
37
how can m6g be dangerous
chronic administration or renal failure can cause m6g to enter the CNS by mass action
38
morphine cardiac
bradycardia, reduced SNS, histamine release. vasodilation
39
morphine and histamine
release ! vasodilation, hypotension
40
morphine resp. women vs men
women have more sensitive mu effect (agonist)
41
morphine resp
decreased response to CO2, increase in resting paCO2, dispalaces CO2 curve to right
42
morphine CNS
compounded
43
caution morphine in use of what patient
head injured
44
head injured and BBB integrity?
may be compromised so increased sensitivity to opiod
45
morphine effect on eeg
resembles sleep associated change
46
morphine will make you feel ___ before ___
sleepy before pain control
47
morphine side edict in biliary tract
may cause spasm. can be misinterpreted as common bile duct stone. give glucagon
48
gu effects of morphine
urgency, difficulty voiding
49
morphine affect on neuromuscular blocking drugs
none
50
how does morphine interfere with ventilation
may cause thoracic and and muscle rigidity significant enough to interfere with adequate ventilation
51
MAO inhibitors and opiod agonists
exaggerated CNS depression and hyperpyrexia
52
dilaudid is a
semisynthetic opiod agonist
53
onset of dilaudid
15-30 min
54
peak of dilaudid
30-90 min
55
why is dilaudid a good choice for renal pt's
lacks known active metabolites
56
dilaudid has far less of a ___ release than morphine
histamine
57
all fentanyl products risk ___ buildup
renal
58
fentanyl is a
synthetic agonist of MU
59
single dose of fent has more ___ onset and ___ duration of action than morphne
rapid, shorter
60
fent has ___ passage across BBB
greater. lipophilic
61
why does fent have a shorter duration of action
redistribution to inactive tissues
62
lungs relationship to fent
inactive storage site
63
fent metabolism
hepatic. partially inactive <1%.
64
fent CV
no histamine release
65
fent CNS
modest increase in ICP
66
opiod and benzo combo
synergism with respect to hypnosis and depression of ventilation
67
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
68
fent analgesia is___ times more potent than morphine
75-125
69
fentanyl can be detected in the urine for __ hours because of its metabolite norfentanyl
72
70
transdermal fent patch peak concentration
18hours
71
sufentanil is
thinly analogue of fent
72
sufentanil potency compared to fent
5-10x
73
why is sufentanil more potent
due to the greater affinity of sufentanil for opiod receptors
74
is elimination half-time of suf affected by liver disease?
no
75
vd and elimination half time of sufentanil is __ in obese pt?
increased due to increased lipid solubility
76
suf protein binding
extensive 92.5% thus a smaller VD
77
alfetanil
analogue of fentanyl
78
alfentanil potency
1/5 to 1/10 potency of fent
79
alfentanil duration of action
1/3 of fent
80
alfentanil name of the game
rapid effect site equilibrium time
81
alfentanil gets to ___ faster than fent and su
mu receptors
82
remi MOH
selective mu agonist
83
remi similar to alafent..
rapid effect site equilibrium (works fast)
84
analgesia of remi
similar to fent
85
structure of remi
ester linkage
86
why does remi's structure matter
ester linkage is metabolized quickly by esterase's. quick onset, quick clearance, minimal accumulation.
87
high dose of remi does what to brain
decreases CMRO2 and CBF
88
remi has fastest
offset
89
clinically remi behaves like a drug with an elimination half time of
6 min or less