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13. Substance Use + Addictions > OAT Prescribing Course > Flashcards

OAT Prescribing Course Flashcards

1
Q

how is opioid use disorder best conceptualized

A

as a CHRONIC relapsing illness which, although associated with elevated rates of morbidity and mortality, has the potential to be in SUSTAINED long term REMISSION with appropriate treatment

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2
Q

what is the prevalence of opioid use disorder in the USA

A

affects 2.1% of americans

canadian estimates not available

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3
Q

define addiction

A

a PRIMARY, CHRONIC illness of REWARD, MOTIVATION, MEMORY and related circuitry in the brain

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4
Q

what stage of substance use disorder is the word “addiction” used to describe

A

the most severe, chronic stage of a SUD

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5
Q

DSM V definition of opioid use disorder

A

recurrent use of opioids causing clinically and functionally significant impairment

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6
Q

how many criteria are there in the DSM V to diagnose opioid use disorder

A

11

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7
Q

how is severity determined for opioid use disorder

A

it is established by the number of criteria met

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8
Q

define mild OUD

A

2-3 criteria are met

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9
Q

define moderate OUD

A

4-5 criteria are met

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10
Q

define severe OUD

A

6+ criteria are met

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11
Q

what are the specifiers for OUD

A
  1. in early remission
  2. in sustained remission
  3. on maintenance therapy
  4. in a controlled environment
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12
Q

define “in early remission” for OUD

A

after full criteria for OUD were previously met, NONE of the criteria for OUD have been met for at least THREE MONTHS but for less that 12 months

(with the exception of criterion A4–> “Craving, or a strong desire or urge to use opioids”, which may continue to be met)

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13
Q

define “in sustained remission” for OUD

A

after full criteria for OUD were previously met, NONE of the criteria for OUD have been met any ANY TIME during a period of TWELVE MONTH or longer

(with the exception of criterion A4–> “Craving” which may continue to be met)

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14
Q

when do you use the specifier “on maintenance therapy” for OUD

A

it is an additional specifier

it is used if the individual is taking a prescribed agonist medication such as methadone or suboxone and NONE of the criteria for OUD have been met for that class of medication (except tolerance to, or withdrawal from, the agonist)

also applies to those on partial agonists, agonost/antagonist, or full antagonist like oral naltrexone or depot naltrexone

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15
Q

when do you use the specifier “in a controlled environment”

A

it is an additional specifier

used if the individual is in an environment where access to opioids is restricted

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16
Q

how many diagnostic categories (of individual criteria) are there for OUD in the DSM

A

4

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17
Q

list the diagnostic categories (made up of individual criteria) in the DSM for OUD

A
  1. impaired control
  2. social impairment
  3. risky use
  4. pharmacological properties
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18
Q

list the criteria in the “impaired control” category of criteria for OUD in the DSM (4)

A
  1. opioids are used in larger amounts or for longer than intended
  2. there have been unsuccessful efforts or desire to cut back or control opioid use
  3. an excessive amount of time is spent obtaining, using or recovering from opioids
  4. there is craving to use opioids
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19
Q

list the criteria in the “social impairment” category of criteria for OUD in the DSM (3)

A
  1. failure to fulfill major role obligations at work, school or home as a result of recurrent opioid use
  2. persistent or recurrent social or interpersonal problems that are exacerbated by opioids or continued use of opioids despite these problems
  3. a person has reduced or given up important social, occupational ore recreational activities because of opioid use
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20
Q

list the criteria in the “risky use” category of criteria for OUD in the DSM (2)

A
  1. opioids used in physically hazardous situations
  2. there is continued opioid use despite knowledge of persistent physical or psychological problems likely caused by opioid use
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21
Q

list the criteria in the “pharmacological properties” category of criteria for OUD in the DSM (2)

A
  1. tolerance is demonstrated by increased amounts of opioids needed to achieve desired effect–> diminished effects with continued use of the same amount
  2. withdrawal as demonstrated by symptoms of opioid withdrawal syndromes –> opioids taken to relieve or avoid withdrawal
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22
Q

how can the symptoms of addiction be explained

A

by the underlying neurocircuitry changes to the brain related to opioid use

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23
Q

opioids activate reward regions in what part of the brain? what does this result in?

A

opioids activate reward regions in the LIMBIC SYSTEM

causes sharp INCREASE in release of DOPAMINE

triggers CONDITIONED CUES in response to opioids

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24
Q

what are conditioned cues?

A

cues in the environment that lead humans to seek out important, life sustaining things–> food, water, shelter, relationships

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25
Q

what happens to a persons conditioned cues with repeated opioid use over time

A

the drive to use opioids becomes as strong or stronger than the drive for natural re-enforcers and results in compulsive drug seeking behaviours

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26
Q

how does ongoing opioid use effect the functioning of the reward circuits of the limbic system

A

ongoing opioid use causes DESENSITIZATION of reward circuits

RESETS the dopamine reward system (i.e to feel happiness, reward, you need more dopamine than your body can provide)

causes ANHEDONIA and DYSPHORIA in withdrawal states

–> over time, the neurocircuitry pathways that enforce drug use are strengthened and pathways in the brain that cultivate self control related processes and the ability to inhibit impulses are diminished

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27
Q

how does chronic opioid use affect executive functioning

A

becomes impaired, contributing to relapses into drug use

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28
Q

list the three parts of the cycle of addiction

A
  1. intoxication
  2. withdrawal
  3. preoccupation
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29
Q

what is the effect of the INTOXICATION phase of the addiction cycle?

A

drug induced activation of Brain Reward Pathway–> enhanced by conditioned cues

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30
Q

what brain regions are affected in the INTOXICATION phase of the addiction cycle?

A

ventral tegmentum

nucleus accumbens

dorsal striatum

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31
Q

what is the effect of the WITHDRAWAL phase of the addiction cycle?

A

negative mood

enhanced sensitivity to stress

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32
Q

what brain regions are affected in the WITHDRAWAL phase of the addiction cycle?

A

amygdala

basal nucleus of stria terminalis

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33
Q

what are the effects of the PREOCCUPATION phase of the addiction cycle

A

craving

impaired decision making, inhibitory control and self regulation

relapse

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34
Q

what brain regions are affected in the the PREOCCUPATION phase of the addiction cycle

A

pre frontal cortex

anterior cingulate cortex

hippocampus

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35
Q

what proteins begin to be transcribed more in the brain during OUD? what does this cause?

A

corticotropin releasing factor and dynorphin

causes negative effect on persons mood and function due to disrupting dopamine, glutamate and stress control systems of the brain

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36
Q

list factors that increase vulnerability to addiction

A

family history of substance use disorder/addiction

trauma

early exposure to drug use such as during childhood or adolescence

exposure to high risk environments (drug accessibility, permissive normative attitudes to drug use, social stress + poor supports)

psychiatric disorders (anxiety, PTSD, depression, ADHD etc)

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37
Q

list examples of evidence based harm reduction that should be offered to everyone

A
  1. education involving safer use of sterile syringes/needles and other applicable substance use equipment
  2. access to sterile syringes and other supplies
  3. access to supervised injection sites
  4. take home naloxone kits
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38
Q

describes the three categories along the continuum of care for OUD, from low treatment intensity to high treatment intensity

A

low treatment intensity–> withdrawal management

then agonist therapies

then high treatment intensity–> specialist led alternative approaches to OUD treamtent

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39
Q

when should you consider moving someone up the treatment continuum to higher intensity treatment

A

if opioid use continues despite treatment

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40
Q

list treatments that focus on withdrawal management

A

tapered methadone, buprenorphone or alpha-2 adrenergic agonists

+/- psychosocial tx
+/- residential tx
+/- oral naltrexone

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41
Q

list the treatments among the agonist therapies for OUD

A

buprenorphine/naloxone (preferred)

methadone

+/- psychosocial tx
+/- residential tx

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42
Q

list the specialist led alternative approaches for OUD

A

slow release oral morphine

+/- psychosocial tx
+/- residential tx

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43
Q

is withdrawal management alone recommended for management of OUD? why or why not?

A

no–> it is generally ineffective if done alone without transition to OAT or continuation of addiction care

can lead to high rates of relapse which in turn icnreases risk of HIV and hep C transmission, morbidity and mortality (i.e overdose)

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44
Q

what is the role of withdrawal management

A

often is first point of engagement in clinical care and can serve important role as bridge to treatment

*not recommended unless a strategy is in place for referral to ongoing addiction treatment (i.e intensive outpatient, residential, or access to long term OAT)

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45
Q

how do you response to someone asking for withdrawal management only

A

provide them with clear, concise discussion about known risk to personal and public safety and engage in discussion about safer treatment options

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46
Q

what are the relapse rates for withdrawal management alone (with methadone taper off opioids)

A

53-66.7% at 1 month

60-90% at 6 months post methadone taper

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47
Q

how do HIV rates compare between those undergoing withdrawal management and those receiving no treatment

A

higher amongst those receiving withdrawal management alone

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48
Q

in what treatment measures has OAT been shown to be superior to withdrawal management alone

A

retention in treatment

sustained abstinence from opioid use

reduced risk of morbidity and mortality

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49
Q

what is first line OAT according to the BC guidelines

A

suboxone

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50
Q

what patient specific factors should guide treatment of choice of OAT

A

initial presentation

comorbidities (liver disease, prolonged Qtc)

drug-drug interactions

treatment preference

response to treatment

prescriber experience

appropriate education and training

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51
Q

why is suboxone preferred as first line OAT

A

superior safety profile

can take it at home which is easier

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52
Q

when might methadone be preferred over suboxone

A

when suboxone not preferred i.e challenging induction

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53
Q

in women with OUD in residential treatment settings, what % have trauma

A

90%

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54
Q

define trauma according to the provincial OAT course

A

an experience that overwhelms an individuals ability to COPE

(both internal and external resources are inadequate to cope w the external threat)

life events that are OUT OF ONES CONTROL with potentially devastating emotional, physical and behavioural consequences

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55
Q

what are the four types of trauma listed in the provincial OAT course

A
  1. single incident trauma
  2. complex, repetitive trauma
  3. developmental trauma
  4. historical trauma
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56
Q

define single incident trauma

A

an unexpected and overwhelming event

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57
Q

define complex, repetitive trauma

A

ongoing abuse, domestic violence, war

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58
Q

define developmental trauma

A

occurs during infancy, childhood or adolescence

includes physical, emotional, sexual abuse or beglect

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59
Q

define historical trauma

A

massive GROUP trauma causing emotional wounding over the lifespan and across GENERATIONS i.e genocide, colonialism, slavery, war

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60
Q

list psychological effects of trauma

A

anxiety, terror, shock

shame, guilt, helplessness, powerlessness

emotional numbness

disconnection

impaired memory

intrusive memories

flashbacks

nightmares

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61
Q

list developmental effects of trauma

A

impaired attachment to caregivers

poor impulse control

impaired ability to form intimate relationships

cognitive impairments and attention deficits

*especially damaging if abuse is ongoing or perpetrator is a trusted person

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62
Q

what is the relationship between adverse childhood experiences and likelihood of developing a SUD

A

the higher number of ACEs, the more at risk an individual is of developing SUD

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63
Q

list physiological effects of trauma

A

hyperarousal–> anxious, jumpy, easily startled, sleep disturbance

hypervigilance–> external focus of attention

dissociation–> precludes need to develop other affect regulating skills

chronic pain syndromes

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64
Q

list behavioural effects of trauma

A

can develop behavioural adaptations–> maladaptive coping–> patients may engage in these behaviours in order to try and SOOTHE themselves when they are feeling overwhelmed
i.e:

self harm–> reduces tension, downgrades high levels of arousal, increases adrenaline/endorphins

disordered eating

substance use (“chemical coping”)

avoidance of triggers (via isolating, social impairment)

risky behaviours

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65
Q

list interpersonal effects of trauma

A

patients may have confusion about identity and agency–> can have poor internal sense of self

have lack of trust that can result in–> frequent conflicts, misinterpretation of others motives, difficulty establishing/maintaining relationships

poor boundaries–> unrealistic expectations of health care provider, overly familiar

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66
Q

how to respond to the interpersonal challenges related to trauma?

A

with compassionate and consistent boundaries

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67
Q

list spiritual effects of trauma

A

loss of meaning/faith

loss of connection

shame, guilt, self blame, self hate

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68
Q

what is the % risk of addiction with the use of opioids

A
  1. 5% risk of addiction
    * canadian guidelines recommend avoiding use of opioids for those with hx SUD or dx mental illness and recommends against use of opioids for those with current substance use concerns
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69
Q

what are the C’s of addiction

A

Craving

Compulsive use

loss of Control

Consequences

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70
Q

list the elements of an opiate use history

A
  1. type of opioid
  2. quantity used
  3. frequency of use
  4. age of initiation
  5. route of administration
  6. overdose history
  7. tolerance and withdrawal
  8. time of last use
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71
Q

how much is a “point”

A

a point = 0.1 g

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72
Q

what two other substances should be asked about in hx as they significantly increase risk of opioid overdose and death

A

alcohol and benzos

–> benzos seem to be higher risk than alcohol for overdose when combined with opioids

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73
Q

what other types of behaviours should be asked about in a SUD ax

A

other compulsive behaivours–> gambling, compulsive sex, eating disorders, spending, shoplifting

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74
Q

what medication is contraindicated in those on OAT or using illicit opioids

A

naltrexone

it is an opioid antagonist

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75
Q

which med has the best safety profile of all the OAT options

A

suboxone

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76
Q

list specific purposes for urine drug testing in OAT management

A
  1. confirming illicit opioid use during baseline assessment
  2. supporting decision making regarding take home doses
  3. confirming that a medication is being taken
  4. screening for ongoing non prescribed or illicit opioid use–> may indicate patient is udner treated or needs more support
  5. detecting presence of other substances, including substances the patient may need to be unaware they have ingested
  6. evaluating treatment response and outcomes
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77
Q

what types of information do UDS not provide

A

do not provide accurate info on:

  • time of last substance use
  • quantity of substance use
  • frequency of substance use
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78
Q

when should you provide UDS testing

A

prior to OAT initiation

during treatment initiation, stabilization, and maintenance

as part of assessment for changes to treatment plan

generally: at baseline, and when patient displays change in clinical status

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79
Q

how often should you do UDS during OAT induction and stabilization phase

A

monthly or more or less frequently

when clinically indicated

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80
Q

how many random UDS should you do per year when someone has takehome doses of OAT (maintenance phase)

A

at least 2-4 if on suboxone

at least 6-8 if on methadone or kadian

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81
Q

for how many days is the longest the following substance can be detected in urine:

alcohol

A

about 1 day

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82
Q

for how many days is the longest the following substance can be detected in urine:

amphetamines

A

about 5 days

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83
Q

for how many days is the longest the following substance can be detected in urine:

benzodiazepines

A

short acting–> 2 days

intermediate acting–> 5 days

long acting (regular use)–> 28+ days

84
Q

for how many days is the longest the following substance can be detected in urine:

cocaine

A

1 day

cocaine metabolite benzoylecgonine can be up to 5 days

85
Q

for how many days is the longest the following substance can be detected in urine:

buprenorphine

A

7 days

86
Q

for how many days is the longest the following substance can be detected in urine:

fentanyl

A

short term use–> 3-4 days

long term use–> 28 days

87
Q

for how many days is the longest the following substance can be detected in urine:

hydromorphone

A

3 days

88
Q

for how many days is the longest the following substance can be detected in urine:

morphine or codeine

A

5 days

89
Q

for how many days is the longest the following substance can be detected in urine:

methadone

A

3 days

90
Q

for how many days is the longest the following substance can be detected in urine:

THC

A

single use–> 3 days

chronic use–> 28+ days

91
Q

is passive inhalation of cannabis likely to cause a positive urine test?

A

no

92
Q

does cocaine cross react with other substances

A

no not really

93
Q

what class of drug has the highest rate of false positive results on UDS

A

amphetamines

94
Q

what are some things that can lead to a false positive amphetamine UDS

A 
abilify
wellbutrin
chlorpromazine
ephedrine
fluoxetine
labetolol
venlafaxine
methylphenidate
ranitidine
trazodone
95
Q

what are possible explanations if UDS is positive for hydromorphone

A
  1. patient is taking prescribes or illicit HM
  2. patient is taking high doses of morphine i.e prescribe slow release morphine as OAT (because shows up at HM positive on UDS)
    * differentiate by calling the lab and asking for relative amounts–> if HM low relative to morphine, suggests it is a breakdown of morphine and not separately ingested. If HM high relative to morphine, then likely HM ingested separately
96
Q

why can fentanyl be detected for so long after chronic use

A

because so lipophilic

97
Q

define harm reduction

A

policies and programs which attempt primarily to reduce the adverse health, social and economic consequences of mood altering substances to individuals who use drugs, their families and communities, WITHOUT requiring decrease in drug use

  • pragmatic* response that focuses on keeping people safe and minimizing death, disease and injury
  • value neutral and humanistic*
98
Q

how does harm reduction save lives and improve quality of life

A

by allowing people who use drugs to remain integrated into society

99
Q

what is naloxone

A

medication that quickly reverses the effects of an overdose from opioids by binding to opioid receptors and displacing the opioid

100
Q

how long does naloxone effect last

A

reverses effect of overdose for 30-90 MINUTES

101
Q

signs of opioid overdose

A

unconsciousness

respiratory depression

bradycardia

muscle rigidity (from fentanyl)

small pupils

cyanosis

102
Q

list three evidenced based options for smoking cessation

A

varenicline

buproprion

NRT

103
Q

what is varenicline

A

nicotine receptor partial AGONIST

*most effective based on 2016 lancet RCT

104
Q

what receptor does methadone act on

how does it act on this receptor

A

the mu-opioid receptor

it is a FULL mu-opioid receptor AGONIST

105
Q

how does methadone act on the patient

A

prevents opioid withdrawal

reduces opioid cravings

mitigates the euphoric effects of non medicinal uses of opioids such as heroin

106
Q

what can make methadone risky as a medication

A

LONG duration of action

NARROW therapeutic index

107
Q

is methadone a synthetic opioid

A

yes

108
Q

other than the mu-opioid receptor, what other receptors does methadone have affinity for

A

NMDA glutamate receptor–> ANTAGONIST

109
Q

how quickly is tolerance to methadone lost

A

within a FEW DAYS of methadone cessation (i.e 3 days)

110
Q

what are the risks of the loss of tolerance to methadone

A

overdose–> occurs if blood level exceeds developed tolerance

111
Q

what is another use of methadone

A

as an ANALGESIC (is an effective analgesic)

112
Q

what is the oral bioavailability of methadone

A

80-95%

113
Q

what is the time to peak plasma concentration and peak clinical effect for methadone

A

3 hours (range of 2-6 hours)

114
Q

how many drug half lives does it take to achieve steady state concentration

A

5

115
Q

what is methadone’s plasma half life

A

RANGES from 6-90 hours–> average of 24 hours

116
Q

approx how many days does it take to achieve steady state of methadone after a dose change

A

about 5 days (if assume average of 24 hour plasma half life)

117
Q

how is methadone metabolized

A

primarily a function of liver enzyme activity –>

cytochrome P450!!

118
Q

does compromised renal function preclude the use of methadone

A

no–> and dose does not need to be adjusted for those on dialysis

119
Q

is methadone safe for rapid titration to therapeutic dose

A

NO

not safe for this because of long and variable half life

120
Q

how do the makers of methadone prevent it from being injected

A

methadone contains SUCROSE to prevent it being injected

121
Q

does methadone require DWI

A

yes–> until ongoing clinical and social stability is demonstrated

*there were high death rates from methadone before DWI instated

122
Q

list some side effects of methadone

A

risk of dental caries due to the sucrose

sedation

weight gain

erectile dysfunction

cognitive blunting

123
Q

how does methadone affect QTc

A

prolonges it

124
Q

can you prescribe naltrexone with methadone

A

no–> because naltrexone blocks the pharmacologic action of methadone and can lead to precipitated withdrawal

125
Q

what medication should you consider for AUD in someone on methadone for OAT

A

acamprosate

126
Q

which CYP enzyme metabolizes methadone

A

CYP3A4

127
Q

list three medications that are CYP34A inducers

A

carbamazepine

phenytoin

rifampicin/rifampin

*may lead to undertreatment of OUD with methadone–> may require dose adjustment

128
Q

list three types of medication that are CYP34A inhibitors

A

azole antifungals

macrolide antibiotics

protease inhibitors

cannabidiol

citalopram/escitalopram

*may require dose adjustment

129
Q

what should you consider if patient on methadone and an SSRI/SNRI/MAOI

A

risk of serotonin syndrome–> monitor patient

130
Q

what antidepressant/anxiolytic is a strong CYP34A inhibitor

A

citalopram and escitalopram

131
Q

what common drinks are moderate CYP34A inhibitors

A

caffeine

grapefruit juice

132
Q

what antipsychotic is a moderate CYP34A inhibitor

A

haloperidol

133
Q

how often should you see patients when initiating methadone

A

at least WEEKLY

*in person clinical assessment always required before adjusting dose

134
Q

what is the starting dose of methadone in the outpatient setting

A

30mg daily or lower

135
Q

how do you increase methadone

A

start at 30mg or lower

increase by 10 mg every 5 days (or no more than 10%… so 5-10 mg at a time)

136
Q

how do you know youve reached the therapeutic dose of methadone

A

until illicit opioids have no positive reward effect (i.e no euphoria)

withdrawal symptoms are controlled for more than 24 hours

craving for opioids are reduced or eliminated without causing excessive sedation or other intolerable side effects

137
Q

recommended starting dose of methadone in the following patient:

no tolerance/opioid naive (i.e just out of withdrawal management)

A

5-10mg daily

138
Q

recommended starting dose of methadone in the following patient:

unknown tolerance (also those who use etoh, benzos)

A

10-20 mg daily

139
Q

recommended starting dose of methadone in the following patient:

known tolerance (i.e those actively using opioids)

A

20-30mg daily

140
Q

what are the two methadone formulation options

A

methadose (pink, cherry flavored)

metadol-D (unflavored, no color; requires diluent)

(there is also a sugar free methadone option)

141
Q

are methadose and metadol-D interchangeable

A

yes

142
Q

what is the usual effective dose of methadone

A

60-120mg daily –> higher doses may be required

143
Q

methadone is implicated in what % of prescription-opioid related deaths in BC

A

25%

144
Q

what receptor do benzos act on

A

GABA-A

–> causes relaxation of smooth muscle cells in the upper airway + sedation + anxiolysis

145
Q

benzodiazapines are implicated in what % of methadone related deaths

A

75%

146
Q

why do benzos increase the risk of overdose from methadone

A

increased upper airway obstruction leading to respiratory depression

interaction with CYP 450 enzymes affecting methadones metabolism

increased incidence of feeling “high” on methadone if benzos combined–> unsafe practices

147
Q

what receptor does alcohol act on

A

GABA-A–> resp depression

148
Q

what is the prevalence of HCV in those with OUD

A

64-100%

149
Q

how to adjust dose if 3-4 missed days of methadone

A

if dose was 30-60mg–> restart at 30mg

if dose was above 60mg–> restart at 50% of previous dose

150
Q

how to adjust dose if 5+ missed days of methadone

A

restart at 5-30mg daily depending on tolerance

151
Q

how often should you see someone who is on a stable methadone dose

A

at least monthly

152
Q

how long should someone be on a stable dose of methadone before considering carries (at minimum)

A

4 weeks

153
Q

what is the ratio of buprenorphine to naloxone in suboxone

A

4: 1

i. e a 2mg tab has 2mg buprenorphine and 0.5mg naloxone

154
Q

what is the admin route of suboxone

A

sublingual

155
Q

why is the naloxone component included in suboxone

A

only to prevent diversion and injection use

the naloxone is not bioavailable when taken as prescribed SL–> it is available when injected

156
Q

is buprenorphine a synthetic opioid

A

yes

157
Q

what receptor does buprenorphine act on, and how does it act on that receptor

A

PARTIAL mu-opioid agonist

very high affinity for the receptor

it will displace full opioid agonists like heroin from the receptor

158
Q

what is the effect of buprenorphine

A

alleviates opioid withdrawal and reduces cravings

159
Q

why is there a better safety profile with buprenorphine than with the full receptor agonists

A

because there is a “ceiling effect” in terms of respiratory depression with the patrial opioid receptor agonists

leads to less overdose risk

160
Q

time to onset of action with buprenorphine

A

30-60 minutes

161
Q

time to peak action of buprenorphine

A

1-4 hours

162
Q

length of peak effect of buprenorphine

A

1-2 hours

163
Q

half life of buprenorphine

A

24-60 hours –> average 32 hours

164
Q

what determines the duration of action of buprenorphine

A

it is dose dependent

low doses (2-4mg) last 4-12 hours

moderate doses (4-8 mg)–> last approx 24 hours

higher doses (above 8 mg)–> last 36-72 horus

165
Q

how is buprenorphine metabolized

A

in the liver by the CYP P450 3A4 enzyme

mostly eliminated in feces, some in urine

166
Q

sublinguial bioavailablility of buprenorphine

A

good

167
Q

oral bioavailability of buprenorphine

A

low (due to first pass metabolism)

*this is why it must be taken as SL and not just orally swallowed)

168
Q

common side effects of buprenorphine

A 
headache
pain
nausea
vomiting
hyperhidrosis
constipation
vasodilation
169
Q

can you prescribe buprenorphine with naltrexone

A

no because naltrexone counteracts buprenorphine

170
Q

do you worry as much about drug-drug interactions/CYP 3A4 interactions with buprenorphine as you do with methadone

A

no you dont

these interactions tend to be less clinically relevant with buprenorphine compared to methadone and the dose rarely needs to be adjusted

171
Q

what are the types of buprenorphine induction

A

microdosing induction and traditional induction

172
Q

what is microdosing induction of buprenorphine

A

the dose is slowly up titrated using micro doses of buprenorphine while the patient CONTINUES prescribed or illicit opioid use

once therapeutic dose reached, other opioids can be abruptly stopped

173
Q

what is traditional induction of buprenorphine

A

requires a period of abstinence from opioids before induction is initiated to ensure withdrawal is not precipitated

*risk of precipitated withdrawal may be higher than with microdosing inductions

174
Q

how many days does it take to reach therapeutic dose with micro inductions of buprenorphine

A

5-10 days

175
Q

can buprenorphine tablets be cut

A

yes–> i.e if an 8mg tablet is dispensed, it can be cut smaller so it dissolves dfaster

176
Q

how does micro induction of buprenorphine reduce the risk of precipitated withdrawal

A

it allows the buprenorphine to slowly accumulate at the mu-opioid receptors over time —>
gradually displaces other opioids

177
Q

in what size tablets does buprenorphine come in

A

2mg or 8mg

can be cut or combined

178
Q

how long do you usually have to wait since last illicit opioid use to start buprenorphine

A

about 12-24 hours

more than 12 hours for heroin, oxy, HM

more than 24 for oral morphine, fentanyl

24-72 hours for methadone

179
Q

what COWS score is recommended before taking first dose of buprenorphine to avoid precipitated withdrawal

A

COWS above 12

180
Q

signs and symptoms of opioid withdrawal

A 
"something coming out of every part of your body"
ie
lacrimation
salivation
rhinorrhea
diaphoresis
vomiting
diarrhea
PLUS
piloerection
temperature dysregulation
hyperreflexia
agitation
anxiety
insomnia
myalgias
nausea
yawning
tachycardia
elevated BP
elevated RR
181
Q

how do you evaluate someone for buprenorphine induction who hasn’t used opioids in a few days (i.e coming from jail)

A

start with a 2mg test dose of buprenorphine (their COWS may never get above 12 if they havent used in a few days)

182
Q

what is the usual starting dose of buprenorphine

A

2mg

183
Q

in which patients might you start with a dose of 8mg of buprenorphine

A

in those in severe withdrawal with COWS above 24 and whose last documented used of illicit opioids is more than 48 hours ago

184
Q

how quickly does precipitated withdrawal usually present

A

within about 30 min of the first dose of buprenorphine

185
Q

what is the maximum total dose of buprenorphine that can be administered on day 1

A

16mg

186
Q

what is the maximum total daily dosing of buprenorphine generalyl

A

24mg

187
Q

what medications can be used to help manage symptoms of withdrawal

A 
clonidine
acetaminophen
ibuprofen
dimenhydrinate
loperamide
188
Q

what are the three options for managing precipitated withdrawal from induction of buprenorphine

A

continue induction

delay induction

stop induction

189
Q

what scale do you use for home buprenorphine inductions

A

the SOWS scale (subjective)

190
Q

what score do you need on SOWS before taking buprenorphine in a home induction

A

17

191
Q

what is the target total daily dose for suboxone

A

16-24mg daily

192
Q

list side effects of methadone

A 
sedation
euphoria
bradycardia
hypotension
constipation
diaphoresis
low testosterone
xerostomia
pruritis
weight gain
peripheral edema
dyspepsia
dysphoria
cognitive impairment
sleep disturbance
193
Q

which of the side effects of methadone typically are the first to resolve

A

sedation and euphoria

tend to resolve over the course of a few weeks

194
Q

of all the side effect of methadone, which may persist beyond the first few weeks

A

constipation and diaphoresis

195
Q

how many doses of suboxone can someone miss before you have to make dose adjustments

A

5 or less

196
Q

for those that miss five or less doses of suboxone, how do you adjust the dose

A

you dont–dose stays the same and you just restart at the previous dose

197
Q

what do you do if someone has missed 6 or more doses of suboxone

A

if they’re on 2mg–> stay the same

if they’re on 6mg-8–> restart at 4mg

if they’re on more than 8 mg, and its been 6-7 days–> restart at 8mg

if they’re on more than 8mg and its been more than 7 days–> restart at 4 mg

198
Q

list the benefits of take home OAT dosing

A

improved motivation to participate in OAT

improved treatment retention

increased patient autonomy and flexibility

decreased treatment burden

decreased costs related to daily witnessed ingestion

199
Q

what criteria should be met before considering take home dosing for methadone?

A
  1. appropriate UDS for minimum 12 weeks (no evidence of cocaine, amphetamine, illicit opioid use)
  2. social, cognitive and emotional stability
  3. ability to safely store meds at home (i.e secure, locked cabinet)
200
Q

how often are doses witnessed per week in most take home dosing regimens for methadone

A

2x / week

201
Q

how should you taper OAT if someone wants to come off

A

outpatient tapering regimen of 5-10% of the dose every 2-4 weeks over the course of 52+ weeks

202
Q

what % of tapers from methadone are unsuccessful

A

87%

203
Q

why would you consider switching from methadone to suboxone

A

compared to methadone, suboxone has a:

reduced risk of overdose

reduced risk of respiratory depression

lower risk of cardiac arrhythmias

204
Q

what is one of the challenges of switching from methadone to suboxone?

A

patient needs to be in withdrawal to avoid precipitated withdrawal, and methadone has a ++ long half life

205
Q

what are the two recommended options for switching from methadone to suboxone

A

microdosing subxone or bridge with SROM

*no longer recommend taper and stop methadone before starting suboxone

206
Q

why might you consider transitioning to SROM as a bridge between methadone and suboxone

A

because SROM has a shorter and more predictable half life than methadone which makes the switch easier

207
Q

what ratio should you use transitioning from methadone to SROM (if SROM is the final target med)

A

1:4 or 1:6

13. Substance Use + Addictions (13 decks)

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