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pharm1 S.Horvath > pain control > Flashcards

pain control Flashcards

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
Q

methadone mech of action

A

NMDA receptor antagonist and MU agonist

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26
Q

how does the NMDA receptor affect opiates

A

may reduce opiod effectiveness

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27
Q

overstimulation of NMDA receptor by glutamate causes

A

neuropathic pain

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28
Q

natural opiate is

A

morphine

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29
Q

morphine structure

A

phenanthrene nucleus

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30
Q

semisynthetic morphine

A

dilaudid

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31
Q

opioids must exist in the ___ state in order to form a strong bond at the opiod receptor

A

ionized. but doesn’t need to be super lipophillic

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32
Q

peak effect of morphine

A

15-30min

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33
Q

how much IV morphine enters the CNS?

A

very little because its highly ionized

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34
Q

morphine active metabolite is

A

m6G

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35
Q

morphine’s primary metabolite is

A

inactive. m3G

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36
Q

what does morphines active metabolite do

A

m6g causes pain modulating effects and resp depression

37
Q

how can m6g be dangerous

A

chronic administration or renal failure can cause m6g to enter the CNS by mass action

38
Q

morphine cardiac

A

bradycardia, reduced SNS, histamine release. vasodilation

39
Q

morphine and histamine

A

release ! vasodilation, hypotension

40
Q

morphine resp. women vs men

A

women have more sensitive mu effect (agonist)

41
Q

morphine resp

A

decreased response to CO2, increase in resting paCO2, dispalaces CO2 curve to right

42
Q

morphine CNS

A

compounded

43
Q

caution morphine in use of what patient

A

head injured

44
Q

head injured and BBB integrity?

A

may be compromised so increased sensitivity to opiod

45
Q

morphine effect on eeg

A

resembles sleep associated change

46
Q

morphine will make you feel ___ before ___

A

sleepy before pain control

47
Q

morphine side edict in biliary tract

A

may cause spasm. can be misinterpreted as common bile duct stone. give glucagon

48
Q

gu effects of morphine

A

urgency, difficulty voiding

49
Q

morphine affect on neuromuscular blocking drugs

A

none

50
Q

how does morphine interfere with ventilation

A

may cause thoracic and and muscle rigidity significant enough to interfere with adequate ventilation

51
Q

MAO inhibitors and opiod agonists

A

exaggerated CNS depression and hyperpyrexia

52
Q

dilaudid is a

A

semisynthetic opiod agonist

53
Q

onset of dilaudid

A

15-30 min

54
Q

peak of dilaudid

A

30-90 min

55
Q

why is dilaudid a good choice for renal pt’s

A

lacks known active metabolites

56
Q

dilaudid has far less of a ___ release than morphine

A

histamine

57
Q

all fentanyl products risk ___ buildup

A

renal

58
Q

fentanyl is a

A

synthetic agonist of MU

59
Q

single dose of fent has more ___ onset and ___ duration of action than morphne

A

rapid, shorter

60
Q

fent has ___ passage across BBB

A

greater. lipophilic

61
Q

why does fent have a shorter duration of action

A

redistribution to inactive tissues

62
Q

lungs relationship to fent

A

inactive storage site

63
Q

fent metabolism

A

hepatic. partially inactive <1%.

64
Q

fent CV

A

no histamine release

65
Q

fent CNS

A

modest increase in ICP

66
Q

opiod and benzo combo

A

synergism with respect to hypnosis and depression of ventilation

67
Q

opioids r/t cardiopulmonary bypass

A

all opioids demonstrate a decrease in plasma concentration with initiation of cardiopulmonary bypass. more significant with fent because it adheres to the circuit

68
Q

fent analgesia is___ times more potent than morphine

A

75-125

69
Q

fentanyl can be detected in the urine for __ hours because of its metabolite norfentanyl

A

72

70
Q

transdermal fent patch peak concentration

A

18hours

71
Q

sufentanil is

A

thinly analogue of fent

72
Q

sufentanil potency compared to fent

A

5-10x

73
Q

why is sufentanil more potent

A

due to the greater affinity of sufentanil for opiod receptors

74
Q

is elimination half-time of suf affected by liver disease?

A

no

75
Q

vd and elimination half time of sufentanil is __ in obese pt?

A

increased due to increased lipid solubility

76
Q

suf protein binding

A

extensive 92.5% thus a smaller VD

77
Q

alfetanil

A

analogue of fentanyl

78
Q

alfentanil potency

A

1/5 to 1/10 potency of fent

79
Q

alfentanil duration of action

A

1/3 of fent

80
Q

alfentanil name of the game

A

rapid effect site equilibrium time

81
Q

alfentanil gets to ___ faster than fent and su

A

mu receptors

82
Q

remi MOH

A

selective mu agonist

83
Q

remi similar to alafent..

A

rapid effect site equilibrium (works fast)

84
Q

analgesia of remi

A

similar to fent

85
Q

structure of remi

A

ester linkage

86
Q

why does remi’s structure matter

A

ester linkage is metabolized quickly by esterase’s. quick onset, quick clearance, minimal accumulation.

87
Q

high dose of remi does what to brain

A

decreases CMRO2 and CBF

88
Q

remi has fastest

A

offset

89
Q

clinically remi behaves like a drug with an elimination half time of

A

6 min or less

pharm1 S.Horvath (18 decks)

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