OAT Prescribing Course Flashcards
how is opioid use disorder best conceptualized
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
what is the prevalence of opioid use disorder in the USA
affects 2.1% of americans
canadian estimates not available
define addiction
a PRIMARY, CHRONIC illness of REWARD, MOTIVATION, MEMORY and related circuitry in the brain
what stage of substance use disorder is the word “addiction” used to describe
the most severe, chronic stage of a SUD
DSM V definition of opioid use disorder
recurrent use of opioids causing clinically and functionally significant impairment
how many criteria are there in the DSM V to diagnose opioid use disorder
11
how is severity determined for opioid use disorder
it is established by the number of criteria met
define mild OUD
2-3 criteria are met
define moderate OUD
4-5 criteria are met
define severe OUD
6+ criteria are met
what are the specifiers for OUD
- in early remission
- in sustained remission
- on maintenance therapy
- in a controlled environment
define “in early remission” for OUD
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)
define “in sustained remission” for OUD
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)
when do you use the specifier “on maintenance therapy” for OUD
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
when do you use the specifier “in a controlled environment”
it is an additional specifier
used if the individual is in an environment where access to opioids is restricted
how many diagnostic categories (of individual criteria) are there for OUD in the DSM
4
list the diagnostic categories (made up of individual criteria) in the DSM for OUD
- impaired control
- social impairment
- risky use
- pharmacological properties
list the criteria in the “impaired control” category of criteria for OUD in the DSM (4)
- opioids are used in larger amounts or for longer than intended
- there have been unsuccessful efforts or desire to cut back or control opioid use
- an excessive amount of time is spent obtaining, using or recovering from opioids
- there is craving to use opioids
list the criteria in the “social impairment” category of criteria for OUD in the DSM (3)
- failure to fulfill major role obligations at work, school or home as a result of recurrent opioid use
- persistent or recurrent social or interpersonal problems that are exacerbated by opioids or continued use of opioids despite these problems
- a person has reduced or given up important social, occupational ore recreational activities because of opioid use
list the criteria in the “risky use” category of criteria for OUD in the DSM (2)
- opioids used in physically hazardous situations
- there is continued opioid use despite knowledge of persistent physical or psychological problems likely caused by opioid use
list the criteria in the “pharmacological properties” category of criteria for OUD in the DSM (2)
- tolerance is demonstrated by increased amounts of opioids needed to achieve desired effect–> diminished effects with continued use of the same amount
- withdrawal as demonstrated by symptoms of opioid withdrawal syndromes –> opioids taken to relieve or avoid withdrawal
how can the symptoms of addiction be explained
by the underlying neurocircuitry changes to the brain related to opioid use
opioids activate reward regions in what part of the brain? what does this result in?
opioids activate reward regions in the LIMBIC SYSTEM
causes sharp INCREASE in release of DOPAMINE
triggers CONDITIONED CUES in response to opioids
what are conditioned cues?
cues in the environment that lead humans to seek out important, life sustaining things–> food, water, shelter, relationships
what happens to a persons conditioned cues with repeated opioid use over time
the drive to use opioids becomes as strong or stronger than the drive for natural re-enforcers and results in compulsive drug seeking behaviours
how does ongoing opioid use effect the functioning of the reward circuits of the limbic system
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
how does chronic opioid use affect executive functioning
becomes impaired, contributing to relapses into drug use
list the three parts of the cycle of addiction
- intoxication
- withdrawal
- preoccupation
what is the effect of the INTOXICATION phase of the addiction cycle?
drug induced activation of Brain Reward Pathway–> enhanced by conditioned cues
what brain regions are affected in the INTOXICATION phase of the addiction cycle?
ventral tegmentum
nucleus accumbens
dorsal striatum
what is the effect of the WITHDRAWAL phase of the addiction cycle?
negative mood
enhanced sensitivity to stress
what brain regions are affected in the WITHDRAWAL phase of the addiction cycle?
amygdala
basal nucleus of stria terminalis
what are the effects of the PREOCCUPATION phase of the addiction cycle
craving
impaired decision making, inhibitory control and self regulation
relapse
what brain regions are affected in the the PREOCCUPATION phase of the addiction cycle
pre frontal cortex
anterior cingulate cortex
hippocampus
what proteins begin to be transcribed more in the brain during OUD? what does this cause?
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
list factors that increase vulnerability to addiction
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)
list examples of evidence based harm reduction that should be offered to everyone
- education involving safer use of sterile syringes/needles and other applicable substance use equipment
- access to sterile syringes and other supplies
- access to supervised injection sites
- take home naloxone kits
describes the three categories along the continuum of care for OUD, from low treatment intensity to high treatment intensity
low treatment intensity–> withdrawal management
then agonist therapies
then high treatment intensity–> specialist led alternative approaches to OUD treamtent
when should you consider moving someone up the treatment continuum to higher intensity treatment
if opioid use continues despite treatment
list treatments that focus on withdrawal management
tapered methadone, buprenorphone or alpha-2 adrenergic agonists
+/- psychosocial tx
+/- residential tx
+/- oral naltrexone
list the treatments among the agonist therapies for OUD
buprenorphine/naloxone (preferred)
methadone
+/- psychosocial tx
+/- residential tx
list the specialist led alternative approaches for OUD
slow release oral morphine
+/- psychosocial tx
+/- residential tx
is withdrawal management alone recommended for management of OUD? why or why not?
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)
what is the role of withdrawal management
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)
how do you response to someone asking for withdrawal management only
provide them with clear, concise discussion about known risk to personal and public safety and engage in discussion about safer treatment options
what are the relapse rates for withdrawal management alone (with methadone taper off opioids)
53-66.7% at 1 month
60-90% at 6 months post methadone taper
how do HIV rates compare between those undergoing withdrawal management and those receiving no treatment
higher amongst those receiving withdrawal management alone
in what treatment measures has OAT been shown to be superior to withdrawal management alone
retention in treatment
sustained abstinence from opioid use
reduced risk of morbidity and mortality
what is first line OAT according to the BC guidelines
suboxone
what patient specific factors should guide treatment of choice of OAT
initial presentation
comorbidities (liver disease, prolonged Qtc)
drug-drug interactions
treatment preference
response to treatment
prescriber experience
appropriate education and training
why is suboxone preferred as first line OAT
superior safety profile
can take it at home which is easier
when might methadone be preferred over suboxone
when suboxone not preferred i.e challenging induction
in women with OUD in residential treatment settings, what % have trauma
90%
define trauma according to the provincial OAT course
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
what are the four types of trauma listed in the provincial OAT course
- single incident trauma
- complex, repetitive trauma
- developmental trauma
- historical trauma
define single incident trauma
an unexpected and overwhelming event
define complex, repetitive trauma
ongoing abuse, domestic violence, war
define developmental trauma
occurs during infancy, childhood or adolescence
includes physical, emotional, sexual abuse or beglect
define historical trauma
massive GROUP trauma causing emotional wounding over the lifespan and across GENERATIONS i.e genocide, colonialism, slavery, war
list psychological effects of trauma
anxiety, terror, shock
shame, guilt, helplessness, powerlessness
emotional numbness
disconnection
impaired memory
intrusive memories
flashbacks
nightmares
list developmental effects of trauma
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
what is the relationship between adverse childhood experiences and likelihood of developing a SUD
the higher number of ACEs, the more at risk an individual is of developing SUD
list physiological effects of trauma
hyperarousal–> anxious, jumpy, easily startled, sleep disturbance
hypervigilance–> external focus of attention
dissociation–> precludes need to develop other affect regulating skills
chronic pain syndromes
list behavioural effects of trauma
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
list interpersonal effects of trauma
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
how to respond to the interpersonal challenges related to trauma?
with compassionate and consistent boundaries
list spiritual effects of trauma
loss of meaning/faith
loss of connection
shame, guilt, self blame, self hate
what is the % risk of addiction with the use of opioids
- 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
what are the C’s of addiction
Craving
Compulsive use
loss of Control
Consequences
list the elements of an opiate use history
- type of opioid
- quantity used
- frequency of use
- age of initiation
- route of administration
- overdose history
- tolerance and withdrawal
- time of last use
how much is a “point”
a point = 0.1 g
what two other substances should be asked about in hx as they significantly increase risk of opioid overdose and death
alcohol and benzos
–> benzos seem to be higher risk than alcohol for overdose when combined with opioids
what other types of behaviours should be asked about in a SUD ax
other compulsive behaivours–> gambling, compulsive sex, eating disorders, spending, shoplifting
what medication is contraindicated in those on OAT or using illicit opioids
naltrexone
it is an opioid antagonist
which med has the best safety profile of all the OAT options
suboxone
list specific purposes for urine drug testing in OAT management
- confirming illicit opioid use during baseline assessment
- supporting decision making regarding take home doses
- confirming that a medication is being taken
- screening for ongoing non prescribed or illicit opioid use–> may indicate patient is udner treated or needs more support
- detecting presence of other substances, including substances the patient may need to be unaware they have ingested
- evaluating treatment response and outcomes
what types of information do UDS not provide
do not provide accurate info on:
- time of last substance use
- quantity of substance use
- frequency of substance use
when should you provide UDS testing
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
how often should you do UDS during OAT induction and stabilization phase
monthly or more or less frequently
when clinically indicated
how many random UDS should you do per year when someone has takehome doses of OAT (maintenance phase)
at least 2-4 if on suboxone
at least 6-8 if on methadone or kadian
for how many days is the longest the following substance can be detected in urine:
alcohol
about 1 day
for how many days is the longest the following substance can be detected in urine:
amphetamines
about 5 days
for how many days is the longest the following substance can be detected in urine:
benzodiazepines
short acting–> 2 days
intermediate acting–> 5 days
long acting (regular use)–> 28+ days
for how many days is the longest the following substance can be detected in urine:
cocaine
1 day
cocaine metabolite benzoylecgonine can be up to 5 days
for how many days is the longest the following substance can be detected in urine:
buprenorphine
7 days
for how many days is the longest the following substance can be detected in urine:
fentanyl
short term use–> 3-4 days
long term use–> 28 days
for how many days is the longest the following substance can be detected in urine:
hydromorphone
3 days
for how many days is the longest the following substance can be detected in urine:
morphine or codeine
5 days
for how many days is the longest the following substance can be detected in urine:
methadone
3 days
for how many days is the longest the following substance can be detected in urine:
THC
single use–> 3 days
chronic use–> 28+ days
is passive inhalation of cannabis likely to cause a positive urine test?
no
does cocaine cross react with other substances
no not really
what class of drug has the highest rate of false positive results on UDS
amphetamines
what are some things that can lead to a false positive amphetamine UDS
abilify wellbutrin chlorpromazine ephedrine fluoxetine labetolol venlafaxine methylphenidate ranitidine trazodone
what are possible explanations if UDS is positive for hydromorphone
- patient is taking prescribes or illicit HM
- 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
why can fentanyl be detected for so long after chronic use
because so lipophilic
define harm reduction
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*
how does harm reduction save lives and improve quality of life
by allowing people who use drugs to remain integrated into society
what is naloxone
medication that quickly reverses the effects of an overdose from opioids by binding to opioid receptors and displacing the opioid
how long does naloxone effect last
reverses effect of overdose for 30-90 MINUTES
signs of opioid overdose
unconsciousness
respiratory depression
bradycardia
muscle rigidity (from fentanyl)
small pupils
cyanosis
list three evidenced based options for smoking cessation
varenicline
buproprion
NRT
what is varenicline
nicotine receptor partial AGONIST
*most effective based on 2016 lancet RCT
what receptor does methadone act on
how does it act on this receptor
the mu-opioid receptor
it is a FULL mu-opioid receptor AGONIST
how does methadone act on the patient
prevents opioid withdrawal
reduces opioid cravings
mitigates the euphoric effects of non medicinal uses of opioids such as heroin
what can make methadone risky as a medication
LONG duration of action
NARROW therapeutic index
is methadone a synthetic opioid
yes
other than the mu-opioid receptor, what other receptors does methadone have affinity for
NMDA glutamate receptor–> ANTAGONIST
how quickly is tolerance to methadone lost
within a FEW DAYS of methadone cessation (i.e 3 days)
what are the risks of the loss of tolerance to methadone
overdose–> occurs if blood level exceeds developed tolerance
what is another use of methadone
as an ANALGESIC (is an effective analgesic)
what is the oral bioavailability of methadone
80-95%
what is the time to peak plasma concentration and peak clinical effect for methadone
3 hours (range of 2-6 hours)
how many drug half lives does it take to achieve steady state concentration
5
what is methadone’s plasma half life
RANGES from 6-90 hours–> average of 24 hours
approx how many days does it take to achieve steady state of methadone after a dose change
about 5 days (if assume average of 24 hour plasma half life)
how is methadone metabolized
primarily a function of liver enzyme activity –>
cytochrome P450!!
does compromised renal function preclude the use of methadone
no–> and dose does not need to be adjusted for those on dialysis
is methadone safe for rapid titration to therapeutic dose
NO
not safe for this because of long and variable half life
how do the makers of methadone prevent it from being injected
methadone contains SUCROSE to prevent it being injected
does methadone require DWI
yes–> until ongoing clinical and social stability is demonstrated
*there were high death rates from methadone before DWI instated
list some side effects of methadone
risk of dental caries due to the sucrose
sedation
weight gain
erectile dysfunction
cognitive blunting
how does methadone affect QTc
prolonges it
can you prescribe naltrexone with methadone
no–> because naltrexone blocks the pharmacologic action of methadone and can lead to precipitated withdrawal
what medication should you consider for AUD in someone on methadone for OAT
acamprosate
which CYP enzyme metabolizes methadone
CYP3A4
list three medications that are CYP34A inducers
carbamazepine
phenytoin
rifampicin/rifampin
*may lead to undertreatment of OUD with methadone–> may require dose adjustment
list three types of medication that are CYP34A inhibitors
azole antifungals
macrolide antibiotics
protease inhibitors
cannabidiol
citalopram/escitalopram
*may require dose adjustment
what should you consider if patient on methadone and an SSRI/SNRI/MAOI
risk of serotonin syndrome–> monitor patient
what antidepressant/anxiolytic is a strong CYP34A inhibitor
citalopram and escitalopram
what common drinks are moderate CYP34A inhibitors
caffeine
grapefruit juice
what antipsychotic is a moderate CYP34A inhibitor
haloperidol
how often should you see patients when initiating methadone
at least WEEKLY
*in person clinical assessment always required before adjusting dose
what is the starting dose of methadone in the outpatient setting
30mg daily or lower
how do you increase methadone
start at 30mg or lower
increase by 10 mg every 5 days (or no more than 10%… so 5-10 mg at a time)
how do you know youve reached the therapeutic dose of methadone
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
recommended starting dose of methadone in the following patient:
no tolerance/opioid naive (i.e just out of withdrawal management)
5-10mg daily
recommended starting dose of methadone in the following patient:
unknown tolerance (also those who use etoh, benzos)
10-20 mg daily
recommended starting dose of methadone in the following patient:
known tolerance (i.e those actively using opioids)
20-30mg daily
what are the two methadone formulation options
methadose (pink, cherry flavored)
metadol-D (unflavored, no color; requires diluent)
(there is also a sugar free methadone option)
are methadose and metadol-D interchangeable
yes
what is the usual effective dose of methadone
60-120mg daily –> higher doses may be required
methadone is implicated in what % of prescription-opioid related deaths in BC
25%
what receptor do benzos act on
GABA-A
–> causes relaxation of smooth muscle cells in the upper airway + sedation + anxiolysis
benzodiazapines are implicated in what % of methadone related deaths
75%
why do benzos increase the risk of overdose from methadone
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
what receptor does alcohol act on
GABA-A–> resp depression
what is the prevalence of HCV in those with OUD
64-100%
how to adjust dose if 3-4 missed days of methadone
if dose was 30-60mg–> restart at 30mg
if dose was above 60mg–> restart at 50% of previous dose
how to adjust dose if 5+ missed days of methadone
restart at 5-30mg daily depending on tolerance
how often should you see someone who is on a stable methadone dose
at least monthly
how long should someone be on a stable dose of methadone before considering carries (at minimum)
4 weeks
what is the ratio of buprenorphine to naloxone in suboxone
4: 1
i. e a 2mg tab has 2mg buprenorphine and 0.5mg naloxone
what is the admin route of suboxone
sublingual
why is the naloxone component included in suboxone
only to prevent diversion and injection use
the naloxone is not bioavailable when taken as prescribed SL–> it is available when injected
is buprenorphine a synthetic opioid
yes
what receptor does buprenorphine act on, and how does it act on that receptor
PARTIAL mu-opioid agonist
very high affinity for the receptor
it will displace full opioid agonists like heroin from the receptor
what is the effect of buprenorphine
alleviates opioid withdrawal and reduces cravings
why is there a better safety profile with buprenorphine than with the full receptor agonists
because there is a “ceiling effect” in terms of respiratory depression with the patrial opioid receptor agonists
leads to less overdose risk
time to onset of action with buprenorphine
30-60 minutes
time to peak action of buprenorphine
1-4 hours
length of peak effect of buprenorphine
1-2 hours
half life of buprenorphine
24-60 hours –> average 32 hours
what determines the duration of action of buprenorphine
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
how is buprenorphine metabolized
in the liver by the CYP P450 3A4 enzyme
mostly eliminated in feces, some in urine
sublinguial bioavailablility of buprenorphine
good
oral bioavailability of buprenorphine
low (due to first pass metabolism)
*this is why it must be taken as SL and not just orally swallowed)
common side effects of buprenorphine
headache pain nausea vomiting hyperhidrosis constipation vasodilation
can you prescribe buprenorphine with naltrexone
no because naltrexone counteracts buprenorphine
do you worry as much about drug-drug interactions/CYP 3A4 interactions with buprenorphine as you do with methadone
no you dont
these interactions tend to be less clinically relevant with buprenorphine compared to methadone and the dose rarely needs to be adjusted
what are the types of buprenorphine induction
microdosing induction and traditional induction
what is microdosing induction of buprenorphine
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
what is traditional induction of buprenorphine
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
how many days does it take to reach therapeutic dose with micro inductions of buprenorphine
5-10 days
can buprenorphine tablets be cut
yes–> i.e if an 8mg tablet is dispensed, it can be cut smaller so it dissolves dfaster
how does micro induction of buprenorphine reduce the risk of precipitated withdrawal
it allows the buprenorphine to slowly accumulate at the mu-opioid receptors over time —>
gradually displaces other opioids
in what size tablets does buprenorphine come in
2mg or 8mg
can be cut or combined
how long do you usually have to wait since last illicit opioid use to start buprenorphine
about 12-24 hours
more than 12 hours for heroin, oxy, HM
more than 24 for oral morphine, fentanyl
24-72 hours for methadone
what COWS score is recommended before taking first dose of buprenorphine to avoid precipitated withdrawal
COWS above 12
signs and symptoms of opioid withdrawal
"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
how do you evaluate someone for buprenorphine induction who hasn’t used opioids in a few days (i.e coming from jail)
start with a 2mg test dose of buprenorphine (their COWS may never get above 12 if they havent used in a few days)
what is the usual starting dose of buprenorphine
2mg
in which patients might you start with a dose of 8mg of buprenorphine
in those in severe withdrawal with COWS above 24 and whose last documented used of illicit opioids is more than 48 hours ago
how quickly does precipitated withdrawal usually present
within about 30 min of the first dose of buprenorphine
what is the maximum total dose of buprenorphine that can be administered on day 1
16mg
what is the maximum total daily dosing of buprenorphine generalyl
24mg
what medications can be used to help manage symptoms of withdrawal
clonidine acetaminophen ibuprofen dimenhydrinate loperamide
what are the three options for managing precipitated withdrawal from induction of buprenorphine
continue induction
delay induction
stop induction
what scale do you use for home buprenorphine inductions
the SOWS scale (subjective)
what score do you need on SOWS before taking buprenorphine in a home induction
17
what is the target total daily dose for suboxone
16-24mg daily
list side effects of methadone
sedation euphoria bradycardia hypotension constipation diaphoresis low testosterone xerostomia pruritis weight gain peripheral edema dyspepsia dysphoria cognitive impairment sleep disturbance
which of the side effects of methadone typically are the first to resolve
sedation and euphoria
tend to resolve over the course of a few weeks
of all the side effect of methadone, which may persist beyond the first few weeks
constipation and diaphoresis
how many doses of suboxone can someone miss before you have to make dose adjustments
5 or less
for those that miss five or less doses of suboxone, how do you adjust the dose
you dont–dose stays the same and you just restart at the previous dose
what do you do if someone has missed 6 or more doses of suboxone
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
list the benefits of take home OAT dosing
improved motivation to participate in OAT
improved treatment retention
increased patient autonomy and flexibility
decreased treatment burden
decreased costs related to daily witnessed ingestion
what criteria should be met before considering take home dosing for methadone?
- appropriate UDS for minimum 12 weeks (no evidence of cocaine, amphetamine, illicit opioid use)
- social, cognitive and emotional stability
- ability to safely store meds at home (i.e secure, locked cabinet)
how often are doses witnessed per week in most take home dosing regimens for methadone
2x / week
how should you taper OAT if someone wants to come off
outpatient tapering regimen of 5-10% of the dose every 2-4 weeks over the course of 52+ weeks
what % of tapers from methadone are unsuccessful
87%
why would you consider switching from methadone to suboxone
compared to methadone, suboxone has a:
reduced risk of overdose
reduced risk of respiratory depression
lower risk of cardiac arrhythmias
what is one of the challenges of switching from methadone to suboxone?
patient needs to be in withdrawal to avoid precipitated withdrawal, and methadone has a ++ long half life
what are the two recommended options for switching from methadone to suboxone
microdosing subxone or bridge with SROM
*no longer recommend taper and stop methadone before starting suboxone
why might you consider transitioning to SROM as a bridge between methadone and suboxone
because SROM has a shorter and more predictable half life than methadone which makes the switch easier
what ratio should you use transitioning from methadone to SROM (if SROM is the final target med)
1:4 or 1:6
