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PHAR358 > Opioid Use Disorder > Flashcards

Opioid Use Disorder Flashcards

1
Q

Differentiate opiates and opioids.

A

opiates: derived from poppy
-heroin, codeine, morphine, opium
opioids: opiates + synthetics
-Vicodin, oxycodone, fentanyl, Percocet

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2
Q

What is an opioid?

A

class of drugs (prescribed or illicit)
depressants
may be used to:
-reduce pain
-manage opioid dependance
-produce temporary euphoria

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3
Q

Differentiate the main opioid receptors.

A

mu:
-responsible for most of the opioid analgesic effect
-respiratory depression
-reduced GI motility
-sedation
-euphoria
-physical dependence
delta:
-analgesia
-euphoria
-physical dependence
kappa:
-analgesia
-sedation
-?mood
-does NOT contribute to physical dependence

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4
Q

What is opioid use disorder?

A

primary chronic disease of brain reward, motivation, memory, and related circuitry with a dysfunction in these circuits being reflected in an individual pathologically pursuing reward and/or relief of withdrawal symptoms by substance use and other behaviors

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5
Q

What can happen to people with OUD without treatment or engagement in recovery activities?

A

addiction is progressive and can result in disability and premature death

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6
Q

How was OUD previously classified?

A

formerly classified as opioid “dependence”, “addiction”, “misuse”, “abuse”
-the DSM-5 has now included all of the above scenarios in the diagnosis of OUD

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7
Q

Describe the diagnosis of OUD.

A

presence of at least 2 of these symptoms (except 10/11)
1. opioids taken in larger amounts or longer than intended
2. persistent desire/lack of success in cutting down
3. great deal of time spent to obtain opioid or recover
4. craving a strong desire to use opioid
5. recurrent opioid use resulting in failure to fulfill obligations
6. continued use despite social/personal problems
7. important activities given up because of opioid
8. recurrent opioid use in situations it is physically hazardous
9. continued use despite knowledge of problem
10. tolerance
11. withdrawal

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8
Q

What kind of disease is OUD?

A

a long-lasting chronic brain disease
is similar to other chronic diseases such as T2DM and HTN in that it cannot be cured but can be treated and managed

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9
Q

What kind of management does OUD require and why?

A

long-term chronic disease management because it is a relapsing condition

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10
Q

True or false: OUD ends when the drug is removed from the body or when acute post-drug taking illness dissipates

A

false
-it is a chronic condition

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11
Q

What is OUD associated with?

A

increased morbidity and mortality
-opioid overdose and trauma is leading cause of death
-increased rates of HIV, hepatitis, STDs

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12
Q

Describe the cycle of OUD.

A

binge/intoxication:
-individual consumes an intoxicating substance and experiences its rewarding or pleasurable effects
withdrawal/negative affect:
-individual experiences a negative emotional state in the absence of the substance
preoccupation/anticipation:
-individual seeks substance again after a period of abstinence

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13
Q

Do individuals experience the cycle of OUD the same?

A

there may be variation in how people progress through the cycle and the intensity with which they experience each of the stages
a person may go through this 3 stage cycle over the course of weeks or months or progress through it several times in a day

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14
Q

What tends to occur over time with the OUD cycle?

A

tends to intensify over time, leading to greater physical and psychological harm

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15
Q

How are the 3 stages of the OUD cycle linked?

A

the 3 stages are linked and feed on each other, but they also involve different brain regions, circuits, and NTs and result in specific kinds of changes in the brain

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16
Q

Describe the neurobiology of opioid tolerance.

A

when an opioid attaches to the mu receptor it triggers the mesolimbic reward system in the VTA
-VTA responsible for release of DA in the NAc in the basal ganglia
-release of DA in the NAc = pleasure
when taken repeatedly opioids trigger the brains reward system driving a compulsion to take the drug again and again
feedback to the prefrontal cortex to the VTA regulates the driver to obtain pleasure
over time, with repeated opioid use, this feedback pathway becomes dysregulated, impairing decision making
additionally, opioid receptors in the VTA become less sensitivity to opioid stimulation
-DA production is reduced and the experience of pleasure/opioid effect is diminished
higher and higher doses to achieve same pleasure reward

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17
Q

Describe the neurobiology of intoxication.

A

OUD results from changes in the LC
neurons in the LC produced noradrenaline and distribute it to other parts of the brain where it stimulates wakefulness, breathing, blood pressure, alertness, etc. (fight or flight)
when opioids bind to mu receptor in LC they suppress release of noradrenaline
-drowsiness, slowed respiration, low BP –> opioid intoxication

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18
Q

What is the MOA of naloxone?

A

binds the same sites as opioids in the brain (more tightly)
-displaces the opioid
-antagonist at receptor

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19
Q

What is the effect of naloxone on breathing?

A

restores breathing within 2-5 minutes when it has been dangerously slowed or stopped due to opioid use

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20
Q

What are the routes of admin for naloxone?

A

IM: can be given through clothing into muscle of upper arm/leg
IN: sprayed into nostrils ($$$)

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21
Q

What can naloxone precipitate in those with opioid dependence?

A

opioid withdrawal

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22
Q

How long do the effects of naloxone last?

A

30-90 min, so overdose may return
-especially if taking long-acting opioid
-repeated doses q2-3 mins may be required

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23
Q

What is one of the most promising and tangible pharmacist activities to decreased opioid related risks?

A

distribute naloxone
-several studies show that naloxone distribution programs decrease overdose risk
-NNT 10

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24
Q

Are take home naloxone kits covered under the Sask Formulary?

A

no
-patients must pay $40/kit or $120/nasal spray kit
-however, can refer patients to THN Site for free kit

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25
Q

What are some symptoms of opioid withdrawal?

A

sweating
mydriasis
tachycardia
vomiting
goosebumps
abdominal pain
muscle cramps
diarrhea
can range from early (hours-days) to late (days-weeks) to prolonged (weeks to 6 months)

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26
Q

What is a rating scale to assess severity of opioid withdrawal?

A

COWS

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27
Q

Is opioid withdrawal life-threatening?

A

no but super uncomfortable

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28
Q

What is the management of aches/pains/myalgias due to opioid withdrawal?

A

NSAIDs
acetaminophen

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29
Q

What is the management for bowel function due to opioid withdrawal?

A

laxatives
loperamide

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30
Q

What is the management for the physical withdrawal of opioid withdrawal?

A

clonidine

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31
Q

What is the management of sweating that has been non-responsive to clonidine during opioid withdrawal?

A

oxybutynin

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32
Q

What is the management for insomnia due to opioid withdrawal?

A

non-drug and sleep hygiene
trazodone if drug needed

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33
Q

What is the management of nausea and vomiting due to opioid withdrawal?

A

dimenhydrinate
haloperidol if refractory

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34
Q

What is the management for anxiety/irritability/rhinorrhea/cramps/insomnia caused by opioid withdrawal?

A

hydroxyzine

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35
Q

Which class of drugs should not be used for opioid withdrawal symptoms?

A

benzodiazepines
-increased risk of CNS depression/opioid toxicity

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36
Q

What are the psychosocial treatments for OUD?

A

structured counselling
motivational interviewing
case management and care coordination
psychotherapy
CBT
contingency management

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37
Q

The combination of which therapies is more effective than either alone?

A

psychosocial tx + pharm = more effective than either alone

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38
Q

What is the bottom line of OUD treatment?

A

start with the person NOT with the medications

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39
Q

What is the role of withdrawal management for OUD treatment?

A

not an effective option for OUD
-rates of dropout and relapse to opioids are high
-risk of fatal and non-fatal overdose, HIV/Hep C transmission are high

40
Q

What is the role of detox for OUD treatment?

A

important 1st point of contact and a bridge to other treatment options
however, detox alone associated with:
-increased HIV/Hep C transmission
-increased relapse
-increased morbidity and mortality

41
Q

What is an example of opioid antagonist therapy?

A

naltrexone

42
Q

What is the MOA of naltrexone?

A

opioid receptor antagonist that blocks the euphoric effects of opioids

43
Q

What are the benefits of naltrexone?

A

ease of administration
no induced tolerance during prolonged tx
no potential for dependence/misuse

44
Q

What are the risks of naltrexone?

A

increased risk of overdose for patients who stop tx and relapse to opioid use due to decreased tolerance
-mortality 3-7x higher than methadone related mortality

45
Q

What is the benefit of oral naltrexone compared to placebo?

A

limited benefit

46
Q

What is the role of naltrexone in OUD?

A

can be considered as an adjunct upon cessation of opioid use

47
Q

What is at the heart of OUD treatment?

A

OAT

48
Q

What is the 1st line treatment for OUD?

A

buprenorphine/naloxone (Suboxone)

49
Q

What is the 2nd line treatment for OUD?

A

methadone

50
Q

What is the 3rd line treatment for OUD?

A

slow-release oral morphine

51
Q

What is the analogy to compare methadone, buprenorphine, and naloxone?

A

methadone is a fast car going 100 km/h
-full agonist
buprenorphine is a slow car going 40 km/h
-partial agonist
naloxone is a dead battery
-antagonist

52
Q

Describe the formulation of Suboxone.

A

Suboxone = buprenorphine + naloxone
dose based on buprenorphine
available as SL tabs, patch (pain), buccal films (OUD), extended release injection (OUD)

53
Q

Are the different dosage forms of Suboxone bioequivalent?

A

film and tablets are not bioequivalent

54
Q

Describe the pharmacology of buprenorphine.

A

high affinity (strong binding) to mu opioid receptor
-displaces heroin or other opiates from receptors
-occupies receptor and blocks other opiate effects
-partial agonist at mu opioid receptor
-antagonist at kappa and delta opioid receptor
slow dissociation (leaving) from opioid receptor
-duration of action increases with increased dose
partial agonist –> opiate ceiling effects
-no further opioid effects above a certain dose
-safer in overdose

55
Q

Differentiate the duration of action of buprenorphine based on the different doses.

A

4 mg = 12 hours
8-12 mg = 24 hours
above 16 mg = 24-48 hours

56
Q

Why is Suboxone formulated with naloxone?

A

naloxone oral or SL is not absorbed
no effect unless injected
may negate opiates effects if injected

57
Q

What are the common adverse effects of Suboxone?

A

headache, pain, withdrawal syndrome
constipation, nausea, abdominal pain
insomnia
runny nose, sweating
others: flu-like, muscle aches, tooth disorder, dyspepsia, depression, anxiety, nervousness, somnolence, dizziness, paresthesia

58
Q

What are the drug interactions of Suboxone?

A

opioids for analgesia
-diminished effect
-may require reassessment in acute pain
alcohol, benzodiazepines
-increase risk of respiratory depression

59
Q

What are the advantages of Suboxone over methadone?

A

decreased risk of overdose
less side effects
decreased risk of diversion
less drug interactions
milder withdrawal sx when discontinued

60
Q

Where do methadone and Suboxone not show much difference?

A

decreasing illicit opioid use
treatment retention

61
Q

How should Suboxone SL be administered?

A

dissolve under tongue
may take up to 10 minutes to dissolve
avoid eating + drinking during that time
no therapeutic effect if swallowed

62
Q

What can happen to someone starting on Suboxone who has been using a full agonist opioid prior to?

A

precipitating withdrawal

62
Q

Describe the withdrawal that Suboxone can precipitate.

A

may occur 30-60 min after 1st dose
displaces full opiate agonist from opioid receptors
buprenorphine partially activates receptor compared to full agonists
-overall net decrease in receptor activation = withdrawal sx

63
Q

What are some ways to minimize the risk of precipitating withdrawal with Suboxone?

A

delay 1st dose until moderate withdrawal
-COWS scale above 12
start with low dose
communicate risk
-its likely to happen regardless of what we do
monitor patient
micro-dosing induction

64
Q

If delaying the 1st dose of Suboxone, what is the COWS score when you will start Suboxone?

A

greater than 12

65
Q

What is the con of delaying Suboxone until COWS score is > 12?

A

requires patient to be moderately uncomfortable
-may decrease patient buy in

66
Q

What is the strategy designed to mitigate the risks of delaying the 1st dose of Suboxone?

A

microdosing
-repetitive administration of very small buprenorphine doses should not precipitate opioid withdrawal
-buprenorphine will accumulate at the receptor due to long t1/2
-over time, an increasing amount of the full agonist will be replaced by buprenorphine at the receptor

67
Q

If microdosing Suboxone, what does the patient do with their original opioid?

A

stay on it at the start
-stop it on day 8 (once on bup 12 mg - nal 3 mg)

68
Q

What is the role of methadone in OUD?

A

Individuals responding poorly to bup/nal
When bup/nal not the preferred option

69
Q

What is the benefit of methadone in comparison to non-pharm treatment for OUD?

A

More effective than non-pharm for treatment retention and suppressed heroin use

70
Q

Compared to Suboxone, which patients may see better retention rates with methadone?

A

Moderate-severe OUD
Heroin addiction
Long history of OUD

71
Q

When might methadone be considered over Suboxone for OUD?

A

In certain patients who are severely unstable & who would be at great risk for harm (e.g. HCV, HIV) if lost to follow-up

72
Q

Which treatment option is safer in pregnancy for OUD?

A

Methadone
-although growing evidence that Suboxone is acceptable

73
Q

What is the onset of methadone?

A

0.5-1h

74
Q

What is the duration of action of methadone?

A

Analgesia: 4-8h
OAT: 22-48h

75
Q

What are two of the main issues with methadone?

A

Half-life: 24-36h (range 8-59)
-can accumulate
Metabolized hepatically by P450 system

76
Q

What are the adverse effects of methadone?

A

QT prolongation
Somnolence
Agitation
Mild cognitive dysfunction
Hormonal dysfunction
Weight gain
Nausea
Sweating
Constipation
Tooth decay

77
Q

What are the drug interactions of methadone?

A

numerous and clinically significant
CYP 3A4 and 2D6
Additive QT prolongation
Serotonin syndrome
Additive CNS depression

78
Q

Which doses of methadone produce more optimal outcomes?

A

Higher doses (60-120mg/day+)
Most studies suggest doses > 80 mg/day have optimal outcomes

79
Q

How soon is too soon to adjust a methadone dose?

A

No sooner than every 5 days due to long half-life

80
Q

What needs to be assessed if doses of methadone are missed?

A

Need for adjustment to avoid risk of toxicity

81
Q

What are the two different versions of methadone?

A

10 mg/ml red, cherry-flavoured oral concentrate
10 mg/ml dye-free, sugar-free, unflavoured oral concentrate
-dilute using 100 ml of Tang to discourage diversion

82
Q

What is the role of SROM?

A

in patients who 1st line and 2nd line treatment options are ineffective or contraindicated, SROM (initially prescribed as once-daily witnessed doses) can be considered

83
Q

What is the benefit of SROM in comparison to methadone?

A

SROM may provide similar benefits to methadone
-Cochrane Review: no difference in tx retention but higher ADE with SROM

84
Q

What are some differences between SROM and methadone?

A

SROM:
-shorter QTc intervals
-decreased heroin cravings
-decreased dysthymic symptoms

85
Q

In general, is there lots of evidence available for SROM?

A

less overall evidence available for SROM

86
Q

Which version of SROM is used for OUD?

A

Kadian the only studied
-24 hour release product

87
Q

What is the half-life of Kadian?

A

11-13 hours

88
Q

How long should we wait before making dosage adjustments for SROM?

A

q48h

89
Q

What should be put in place if SROM is used?

A

strict policies to reduce risk of diversion

90
Q

What are the reasons a patient with severe OUD who injects opioids may not benefit from oral OAT?

A

unable to reach therapeutic doses
cravings despite optimal OAT dosing
insufficient improvements in health, social functioning, QoL
opting not to initiate oral OAT

91
Q

What have meta-analyses found regarding the use of iOAT?

A

in individuals who are treatment refractory to methadone or prescription diacetylmorphine, administered under the supervision of a HCP in a clinic setting is beneficial in reducing in:
-illicit opioid use
-premature discontinuation of treatment
-mortality
-incarceration
-criminal activity

92
Q

What is the role of iOAT?

A

severe OUD who inject opioids who have not benefitted from previous attempts of OAT

93
Q

Which medications can be used for iOAT?

A

hydromorphone
diacetylmorphine

94
Q

How is iOAT administered?

A

patient self-administers
up to 3 visits per day

PHAR358 (20 decks)

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