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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
Mu1 specific effects (7)
supra spinal and spinal analgesia* bradycardia euphoria low abuse potential miosis hypothermia urinary retention
26
Mu2 specific effects (5)
analgesic* (spinal only) bradycardia* resp depression* constipation* physical dependence*
27
Mu3 specific effects
immune suppression
28
ventilatory effects of opioids
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
29
pupillary effects of opioids
edinger westphal nucleus stimulation --PNS stimulation of ciliary ganglion oculomotor nerve (CN3)- pupil constriction tolerance does not develop to miosis
30
n/v and opioids
CTZ stimulation (in area postrema of medulla) possible interaction with vestibular apparatus
31
SSEP and opioids
minimal effects on evoked potentials
32
BP and opioids (is baroreceptor reflex affected)
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
33
myocardial function and opioids
myocardial contractility not affected (myocardial depression can occur if combined with N2O)
34
biliary pressure and opioids
contraction of sphincter of oddi--> increased biliary pressure reversed by naloxone or glucagon meperidine causes lowest increase
35
gastric emptying and opioids
prolonged
36
peristalsis and opioids
slowed (constipation)
37
urinary retention and opioids
detrusor relaxation (contraction needed to pass urine into urethra) urinary sphincter contraction
38
immunologic response and opioids (3)
histamine release (morphine, meperidine, codeine) inhibition of cellular and humoral immune function suppression of NK cell function
39
thermoregulation and opioids
resets hypothalamic temperature set point (decrease in core body temp)
40
in women, morphine is associated with a (4)
greater analgesic potency slower onset of action longer DOA lower postop opioid consumption
41
give examples of semi synthetic morphine derivatives (4)
hydromorpone, heroine, naloxone, naltrexone,
42
give an example of semi synthetic thebaine derivative
oxycodone
43
give an example of synthetic piperdine
meperidine
44
give an example of synthetic drug class we use every day
phenylpiperdines
45
give an example of synthetic diphenylpropylamines
methadone
46
relative potency to 10mg of morphine: meperidine
.1 (100mg is equivalent dose)
47
relative potency to 10mg of morphine: hydromophone
7x, (1.4mg is equivalent dose)
48
relative potency to 10mg of morphine: alfentanil
10x (1000mcg is equivalent dose(
49
relative potency to 10mg of morphine: remifentanil
100x more potent (100mcg is equivalent dose)
50
relative potency to 10mg of morphine: fentanyl
100x more potent (100mcg is equivalent dose)
51
relative potency to 10mg of morphine: sufentanil
1000x more potent (10mcg is equivalent dose)
52
what are tolerance and physical dependence likely attributed to
receptor sensitization and increased synthesis of cAMP
53
s/sx of withdrawal
diaphoresis, insomnia, restlessness (early) n/v, abdominal cramping (late)
54
except for fentanyl, all opioids are metabolized how
hepatic transformation
55
morphine is conjugated into
morphine 3 glucuronide (inactive) and morphine 6 glucoronide (active)
56
morphine 6 glucoronide is a concern in which patient population
renal failure patients- cannot excrete without HD
57
metabolism of meperidine
demethylated in the liver to normeperidine byCYP450
58
caution with meperidine
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
how is remifentanil metabolized
hydrolyzed in the plasma by erythrocyte and tissue esterases (NOT pseudocholinesterase) -metabolized this way because of an ester linkage
60
how to dose remi, solubility
acts like a hydrophillic drug with low Vd but is very lipophilic. dose on lean body weight
61
which drug is associated with anticholinergic side effects
meperidine (structurally related to atropine)
62
MOA of meperidine
synthetic phenylpiperdine opioid that stimulates Mu and Kappa receptors
63
SE of meperidine metabolite normeperidine (3)
causes myoclonus, reduces seizure threshold, increases CNS excitability
64
co administration of meperidine with what is contraindicated
its a weak serotonin reuptake inhibitor, do not administer with MAOI's for risk of serotonin syndrome
65
s/sx serotonin syndrome (5) (also compare and contrast with MH and neuroleptic malignant syndrome)
hyperthermia, mental status changes, hyperreflexia, seizures, death
66
does meperidine cause histamine release from mast cells
yes
67
alfentanil pKa % non ionized (at physiologic pH) % protein binding Vd (mL/kg)
pKa: 6.5 % non ionized (at physiologic pH): 89 % protein binding: 92 Vd (mL/kg): 0.6
68
remifentanil pKa % non ionized (at physiologic pH) % protein binding Vd (mL/kg)
pKa: 7.2 % non ionized (at physiologic pH): 58 % protein binding: 93 Vd (mL/kg): 0.39
69
morphine pKa % non ionized (at physiologic pH) % protein binding Vd (mL/kg)
pKa: 7.9 % non ionized (at physiologic pH): 23 % protein binding: 35 Vd (mL/kg): 2.8
70
sufentanil pKa % non ionized (at physiologic pH) % protein binding Vd (mL/kg)
pKa 8 % non ionized (at physiologic pH) 20 % protein binding 93 Vd (mL/kg) 2
71
fentanyl pKa % non ionized (at physiologic pH) % protein binding Vd (mL/kg)
pKa 8.4 % non ionized (at physiologic pH) 8.5 % protein binding 84 Vd (mL/kg) 4
72
meperidine pKa % non ionized (at physiologic pH) % protein binding Vd (mL/kg)
pKa: 8.5 % non ionized (at physiologic pH) 7 % protein binding 70 Vd (mL/kg) 2.6
73
alfentanil effect site equillibration
~1.4m (fent and sufent are 6.8 and 6.2m)
74
metabolism of alfentanil
n dealkylation and o demethylation by CYP3A4 -because of its lower extraction ratio, it is more susceptible to alterations in CYP3A4 function
75
can you give alfentanil to renal patients
yes
76
what can you not co administer with alfentanil
erythromycin, inhibits alfents metabolism and prolongs resp depression
77
name each drug on this chart
78
postoperative hyperalgesia can be prevented with
ketamine or magnesium sulfate
79
methadone MOA
Mu agonist NMDA antagonist inhibits reuptake of monoamines in synaptic cleft
80
bioavailability of PO methadone half life metabolism
bioavailability 80% half life 3-6h metabolism CYP450
81
what can methadone do to EKG
can increase QT interval -inhibits delayed rectifier potassium ion channel -can lead to torsades
82
Oliceridine MOA and indication for use
IV opioid analgesic (Mu)- indicated for adults for pain when other opioid analgesics have not worked
83
Oliceridine dosing (bolus and PCA) cumulative daily dose limit
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
Oliceridine dosage adjustment for renal patients?
no
85
contraindications to oliceridine (4)
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
best tx for opioid induced skeletal muscle rigidity and receptor believed to be the cause
paralysis and intubation Mu receptor is cause
87
complications of skeletal muscle rigidity
88
ID drug categories outlined on this chart
89
common characteristics of partial agonists
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
buprenorphine MOA analgesia compared to morphine reversed by naloxone key features
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
nalbuphine MOA analgesia compared to morphine reversed by naloxone key features
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
butorphanol MOA analgesia compared to morphine reversed by naloxone key features
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
naloxone dose DOA metabolism
1-4mcg/kg (better to give 20-40mcg at a time) DOA 45m metabolism: liver (significant first pass metabolism)
94
how to cause less n/v with naloxone
slow titration over 2-3m
95
methylnaltrexone "difference"
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
nalmefene dose, difference, use
0.1-0.5mcg/kg -profile similar to naloxone but much longer DOA (10h) -can be used to maintain recovering opioid abusers
97
naltrexone difference, uses
-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
incidence of resp depression with PCA is not higher at baseline but is higher with these risk factors
basal infusion rate other sedatives administered old age pulmonary disease OSA
99
3 patient populations that benefit from methadone therapy
chronic opioid abuse chronic pain syndrome cancer pain
100
name 4 disadvantages of using partial agonist opioids
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
partial agonist that can be administered via intranasal route
butorphanol
102
partial agonist that can be administered via transdermal route
buprenorphine
103
2 partial agonists that provide better analgesia than morphine
buprenorphine, butorphanol

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