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opioid and non opioid analgesics Flashcards

1
Q

4 steps for pain

A

transduction
transmission
modulation
perceptioin

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2
Q

transduction

A

injured tissues release a variety of chemicals that cause proimflammatory compounds. This is transduced into an AP via either A delta fibers (fast pain, sharp, well localized) or C fibers (slow pain, dull and poorly localized)

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3
Q

drugs that target transduction (5)

A

NSAIDS
LA’s
steroids
antihistamines
opioids

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4
Q

transmission

A

the pain signal is relayed through 3 neuron afferent pain pathway along spinothalamic tract

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5
Q

review of spinothalamic tract

A

first order neuron: periphery to dorsal horn (cell body in dorsal root ganglion)
second order neuron: dorsal horn to thalamus (cell body in dorsal horn)
third order neuron: thalamus to cerebral cortex (cell body in thalamus)
(can synapse at dorsal horn or go up/down tract of lesseiuer? and synapse somewhere else)

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6
Q

drugs that target transmission

A

LA’s

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7
Q

modulation and where it most frequently takes place

A

pain signal is modified (inhibited or augmented) as it advances to the cerebral cortex.
-takes place mostly in dorsal horn of SC

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8
Q

most important site of pain modulation

A

substantia gelatinosa in dorsal horn (rexed lamina 2 and 3)

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9
Q

descending inhibitory pain pathway begins in the ____________________ and __________________. it projects to the ____________________-

A

descending inhibitory pain pathway begins in the periaqueductal grey and rostroventral medulla. it projects to the substantia gelatinosa

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10
Q

pain is inhibited (modulated/augmented) when

A

spinal neurons release GABA and glycine (inhibitory neurotransmitters)
descending pain pathway release NE, serotonin, endorphins

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11
Q

modification: pain is augmented by (increase or decrease)

A

central sensitization
wind up

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12
Q

drugs that target modulation (5)

A

neuraxial opioids
NMDA antagonists
alpha 2 agonists
AchE inhibitors (apparently Ach helps with analgesia)
SSRI’s, SNRI’s

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13
Q

perception

A

describes processing of pain signals in cerebral cortex and limbic system

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14
Q

drugs that target perception (3)

A

GA
opioids
alpha 2 agonists

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15
Q

MOA of opioid receptors in order (6)

A
  1. opioid binds to receptor
  2. GPCR is activated
  3. adenylate cyclase is inhibited
  4. less cAMP is produced
  5. Ca2+ conductance is decreased
  6. K conductance is decreased
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16
Q

where are opioid receptors located in the brain? (3)

A

periaqueductal grey, locus coreuleus, rostral ventral medulla

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17
Q

where are opioid receptors located in SC?

A

primary afferent neurons in the dorsal horn and interneurons

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18
Q

where are opioid receptors located in periphery?

A

sensory neurons and immune cells

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19
Q

endogenous ligands of Mu

A

endorphins (beta endorphin, endo morphin)

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20
Q

endogenous ligands of delta

A

enkephalins (leu and met enkephalin)

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21
Q

endogenous ligands of kappa

A

dynorphins (A B and neo dynorphin)

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22
Q

physiologic functions of Mu (13)

A

supra spinal and spinal analgesia
resp depression
bradycardia
sedation
euphoria
prolactin release
mild hypothermia
mitosis
urinary retention
n/v
increased biliary pressure
peristalsis
pruritis

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23
Q

physiologic functions of delta (4)

A

supra spinal and spinal analgesia
respiratory depression
urinary retention
pruritis

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24
Q

physiologic functions of kappa (9)

A

supra spinal and spinal analgesia
plausible resp depression????
sedation
dysphoria
hallucinations
delirium
miosis
diuresis
anti shivering effect

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25
Q

Mu1 specific effects (7)

A

supra spinal and spinal analgesia*
bradycardia
euphoria
low abuse potential
miosis
hypothermia
urinary retention

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26
Q

Mu2 specific effects (5)

A

analgesic* (spinal only)
bradycardia*
resp depression*
constipation*
physical dependence*

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27
Q

Mu3 specific effects

A

immune suppression

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28
Q

ventilatory effects of opioids

A

shifts CO2 response curve to right and reduces ventilatory response to CO2
decrease RR and increase Vt
increased PaCO2 increases ICP if ventilation is not maintained

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29
Q

pupillary effects of opioids

A

edinger westphal nucleus stimulation –PNS stimulation of ciliary ganglion oculomotor nerve (CN3)- pupil constriction
tolerance does not develop to miosis

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30
Q

n/v and opioids

A

CTZ stimulation (in area postrema of medulla)
possible interaction with vestibular apparatus

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31
Q

SSEP and opioids

A

minimal effects on evoked potentials

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32
Q

BP and opioids
(is baroreceptor reflex affected)

A

minimal effects on BP in healthy patients
deceased BP with morphine and meperidine is likely the results of histamine
dose dependent vasodialtion
baroreceptor reflex not affected

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33
Q

myocardial function and opioids

A

myocardial contractility not affected (myocardial depression can occur if combined with N2O)

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34
Q

biliary pressure and opioids

A

contraction of sphincter of oddi–> increased biliary pressure
reversed by naloxone or glucagon
meperidine causes lowest increase

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35
Q

gastric emptying and opioids

A

prolonged

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36
Q

peristalsis and opioids

A

slowed (constipation)

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37
Q

urinary retention and opioids

A

detrusor relaxation (contraction needed to pass urine into urethra)
urinary sphincter contraction

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38
Q

immunologic response and opioids (3)

A

histamine release (morphine, meperidine, codeine)
inhibition of cellular and humoral immune function
suppression of NK cell function

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39
Q

thermoregulation and opioids

A

resets hypothalamic temperature set point (decrease in core body temp)

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40
Q

in women, morphine is associated with a (4)

A

greater analgesic potency
slower onset of action
longer DOA
lower postop opioid consumption

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41
Q

give examples of semi synthetic morphine derivatives (4)

A

hydromorpone, heroine, naloxone, naltrexone,

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42
Q

give an example of semi synthetic thebaine derivative

A

oxycodone

43
Q

give an example of synthetic piperdine

A

meperidine

44
Q

give an example of synthetic drug class we use every day

A

phenylpiperdines

45
Q

give an example of synthetic diphenylpropylamines

A

methadone

46
Q

relative potency to 10mg of morphine: meperidine

A

.1 (100mg is equivalent dose)

47
Q

relative potency to 10mg of morphine: hydromophone

A

7x, (1.4mg is equivalent dose)

48
Q

relative potency to 10mg of morphine: alfentanil

A

10x (1000mcg is equivalent dose(

49
Q

relative potency to 10mg of morphine: remifentanil

A

100x more potent (100mcg is equivalent dose)

50
Q

relative potency to 10mg of morphine: fentanyl

A

100x more potent (100mcg is equivalent dose)

51
Q

relative potency to 10mg of morphine: sufentanil

A

1000x more potent (10mcg is equivalent dose)

52
Q

what are tolerance and physical dependence likely attributed to

A

receptor sensitization and increased synthesis of cAMP

53
Q

s/sx of withdrawal

A

diaphoresis, insomnia, restlessness (early)
n/v, abdominal cramping (late)

54
Q

except for fentanyl, all opioids are metabolized how

A

hepatic transformation

55
Q

morphine is conjugated into

A

morphine 3 glucuronide (inactive) and morphine 6 glucoronide (active)

56
Q

morphine 6 glucoronide is a concern in which patient population

A

renal failure patients- cannot excrete without HD

57
Q

metabolism of meperidine

A

demethylated in the liver to normeperidine byCYP450

58
Q

caution with meperidine

A

reduces seizure threshold and increases CNS excitability (myoclonus and seizures are 2 significant side effects of meperidine active metabolite)
should be avoided in patients on HD and used with caution in the elderly

59
Q

how is remifentanil metabolized

A

hydrolyzed in the plasma by erythrocyte and tissue esterases (NOT pseudocholinesterase)
-metabolized this way because of an ester linkage

60
Q

how to dose remi, solubility

A

acts like a hydrophillic drug with low Vd but is very lipophilic. dose on lean body weight

61
Q

which drug is associated with anticholinergic side effects

A

meperidine (structurally related to atropine)

62
Q

MOA of meperidine

A

synthetic phenylpiperdine opioid that stimulates Mu and Kappa receptors

63
Q

SE of meperidine metabolite normeperidine (3)

A

causes myoclonus, reduces seizure threshold, increases CNS excitability

64
Q

co administration of meperidine with what is contraindicated

A

its a weak serotonin reuptake inhibitor, do not administer with MAOI’s for risk of serotonin syndrome

65
Q

s/sx serotonin syndrome (5)
(also compare and contrast with MH and neuroleptic malignant syndrome)

A

hyperthermia, mental status changes, hyperreflexia, seizures, death

66
Q

does meperidine cause histamine release from mast cells

A

yes

67
Q

alfentanil
pKa
% non ionized (at physiologic pH)
% protein binding
Vd (mL/kg)

A

pKa: 6.5
% non ionized (at physiologic pH): 89
% protein binding: 92
Vd (mL/kg): 0.6

68
Q

remifentanil
pKa
% non ionized (at physiologic pH)
% protein binding
Vd (mL/kg)

A

pKa: 7.2
% non ionized (at physiologic pH): 58
% protein binding: 93
Vd (mL/kg): 0.39

69
Q

morphine
pKa
% non ionized (at physiologic pH)
% protein binding
Vd (mL/kg)

A

pKa: 7.9
% non ionized (at physiologic pH): 23
% protein binding: 35
Vd (mL/kg): 2.8

70
Q

sufentanil
pKa
% non ionized (at physiologic pH)
% protein binding
Vd (mL/kg)

A

pKa 8
% non ionized (at physiologic pH) 20
% protein binding 93
Vd (mL/kg) 2

71
Q

fentanyl
pKa
% non ionized (at physiologic pH)
% protein binding
Vd (mL/kg)

A

pKa 8.4
% non ionized (at physiologic pH) 8.5
% protein binding 84
Vd (mL/kg) 4

72
Q

meperidine
pKa
% non ionized (at physiologic pH)
% protein binding
Vd (mL/kg)

A

pKa: 8.5
% non ionized (at physiologic pH) 7
% protein binding 70
Vd (mL/kg) 2.6

73
Q

alfentanil effect site equillibration

A

~1.4m (fent and sufent are 6.8 and 6.2m)

74
Q

metabolism of alfentanil

A

n dealkylation and o demethylation by CYP3A4
-because of its lower extraction ratio, it is more susceptible to alterations in CYP3A4 function

75
Q

can you give alfentanil to renal patients

A

yes

76
Q

what can you not co administer with alfentanil

A

erythromycin, inhibits alfents metabolism and prolongs resp depression

77
Q

name each drug on this chart

A
78
Q

postoperative hyperalgesia can be prevented with

A

ketamine or magnesium sulfate

79
Q

methadone MOA

A

Mu agonist
NMDA antagonist
inhibits reuptake of monoamines in synaptic cleft

80
Q

bioavailability of PO methadone
half life
metabolism

A

bioavailability 80%
half life 3-6h
metabolism CYP450

81
Q

what can methadone do to EKG

A

can increase QT interval
-inhibits delayed rectifier potassium ion channel
-can lead to torsades

82
Q

Oliceridine MOA and indication for use

A

IV opioid analgesic (Mu)- indicated for adults for pain when other opioid analgesics have not worked

83
Q

Oliceridine dosing (bolus and PCA)
cumulative daily dose limit

A

bolus
-loading dose IV 1-2mg
-supplemental IV doses 1-3mg every 1-3h PRN

PCA
-leading dose 1.5mg
-demand dose .35-.5
-lockout 6 minutes

cumulative daily dose limit 27mg

84
Q

Oliceridine dosage adjustment for renal patients?

A

no

85
Q

contraindications to oliceridine (4)

A

can cause mild QT prolongation
risk of HoTN (d/t vasodilation) is increased with GA
increased risk of seizures in patient with seizure DO
patients on serotenergic drugs can be at greater risk of serotonin syndrome

86
Q

best tx for opioid induced skeletal muscle rigidity and receptor believed to be the cause

A

paralysis and intubation
Mu receptor is cause

87
Q

complications of skeletal muscle rigidity

A
88
Q

ID drug categories outlined on this chart

A
89
Q

common characteristics of partial agonists

A

produce analgesia with a reduced risk of resp depression
ceiling effect beyond which additional analgesia is not possible
reduce efficacy of previously administered opioids
can cause acute opioid withdrawal in the opioid dependent patient
can cause dysphoric reactions
carry low risk of dependence
are used in patients who cannot tolerate full opioid agonist

90
Q

buprenorphine
MOA
analgesia compared to morphine
reversed by naloxone
key features

A

MOA: mu agonist (partial)
analgesia compared to morphine: greater
reversed by naloxone: difficult due to high affinity for mu receptor
key features: long duration (8h), avail via transdermal route

91
Q

nalbuphine
MOA
analgesia compared to morphine
reversed by naloxone
key features

A

MOA: kappa agonist, mu antagonist
analgesia compared to morphine: similar
reversed by naloxone: yes
key features: does not increase BP, PAP, HR, RAP. useful with hx of heart disease

92
Q

butorphanol
MOA
analgesia compared to morphine
reversed by naloxone
key features

A

MOA: kappa agonist, mu antagonist (weak)
analgesia compared to morphine: greater
reversed by naloxone: yes
key features: useful for postop shivering, avail via intranasal route

93
Q

naloxone dose
DOA
metabolism

A

1-4mcg/kg (better to give 20-40mcg at a time)
DOA 45m
metabolism: liver (significant first pass metabolism)

94
Q

how to cause less n/v with naloxone

A

slow titration over 2-3m

95
Q

methylnaltrexone “difference”

A

has a quarternary amine group that prohibits passage across BBB
-since it does not enter the brain, it does not reverse respiratory depression
-useful for mitigating peripheral effects of opioids such as opioid induced bowel dysfunction

96
Q

nalmefene dose, difference, use

A

0.1-0.5mcg/kg
-profile similar to naloxone but much longer DOA (10h)
-can be used to maintain recovering opioid abusers

97
Q

naltrexone difference, uses

A

-unlike naltrexone, does not undergo significant first pass metabolism
-can be given PO, has DOA up to 24h
-ER may be used for ETOH withdrawal tx
-can be used to maintain recovering opioid abusers

98
Q

incidence of resp depression with PCA is not higher at baseline but is higher with these risk factors

A

basal infusion rate
other sedatives administered
old age
pulmonary disease
OSA

99
Q

3 patient populations that benefit from methadone therapy

A

chronic opioid abuse
chronic pain syndrome
cancer pain

100
Q

name 4 disadvantages of using partial agonist opioids

A
  1. reduces efficacy of previously administered opioids
  2. can cause acute opioid withdrawal in opioid dependent patient
  3. can cause dysphoric reactions
  4. has ceiling effect beyond which additional analgesia is not possible
101
Q

partial agonist that can be administered via intranasal route

A

butorphanol

102
Q

partial agonist that can be administered via transdermal route

A

buprenorphine

103
Q

2 partial agonists that provide better analgesia than morphine

A

buprenorphine, butorphanol

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