Sarah Akerman MD Assistant Professor of Psychiatry Director of Addiction Services Geisel School of Medicine/Dartmouth-Hitchcock Medical Center OVERVIEW OF MEDICATION ASSISTED TREATMENT
Conflicts of Interest I do not have any potential conflicts of interest to disclose.
Outline What are opioids and how do they work? Disease Model of Addiction Introduction to Medication-Assisted Treatment
Outline What are opioids and how do they work? Disease Model of Addiction Introduction to Medication-Assisted Treatment
Opioids Opiates - from P. somniferum Morphine Heroin Codeine Opioids - synthetic Oxycodone, OxyContin Methadone Buprenorphine Meperidine (Demerol)
Opioids Pharmaceuticals Swallow Chew Intranasal Intravenous Heroin Intranasal Intravenously skin popping
How do opioids work? Bind to opioid receptors in the brain, spinal cord, gastrointestinal track, other organs Opioid receptors are molecules on the surface of cells in the body (μ,δ,κ) Mu receptor (μ) most relevant to opioid abuse Reduce the perception of pain Reduce the intensity of pain signals to the brain Affect brain areas controlling emotion and reduce effects of a painful stimulus Other indications: cough, diarrhea, treatment of addiction www.the-scientist.com NIDA
Opioids Intoxication Drowsiness Confusion Decreased temperature Decreased respiration Pupils constrict Gastrointestinal movement decreases (nausea, constipation) No pain Euphoria
Why do people take drugs? Drug use starts out because it is pleasurable and/or helps avoid pain Drug use is pursued in such a way that negative consequences follow Drug use persists in the face of negative consequences and the desire to quit i.e. after it no longer makes sense
Operant Conditioning Reinforcement increases the frequency of a behavior Positive reinforcement Behavior makes a good feeling start Get high Negative reinforcement Behavior makes a bad feeling stop Avoid withdrawal, negative feelings, etc.
Not All Drug Users Become Addicted % of People Who Try a Drug and go on to Develop a Substance Use Disorder: Cocaine: 17-22% (IN) Heroin: 23% Cannabis: 9-10% Alcohol:15% Cigarettes: 32% Anthony, Warner et al. 1994
Etiology Genes - Temperament Factors - Motivation for Drug - Epigenetics - Stressful events - Trauma, maltreatment - Cumulative Stress Environment - Exposure to the drug - Adversity: - Low socioeconomic status - Unemployed - Partner/friends who use - Lack of Support
Co-Occurring Disorders PTSD Other illicit drug use Depression OUD Cigarette Smoking Personality Disorders Anxiety
DSM 5 Substance Use Disorder Maladaptive pattern of drug use for >12 months Tolerance Withdrawal More use than intended (loss of control) Unsuccessful efforts to quit Significant time spent in procurement, use, recovery Activities (occupational, social etc.) given up Continued use in the face of adverse health effects Recurrent interpersonal problems from use Use under dangerous conditions Craving Failure to live up to obligations
DSM 5 Substance Use Disorder 2-3- Mild 4-5- Moderate 6- Severe Physiological dependence is neither necessary nor sufficient to diagnosis an addiction
Outline What are opioids and how do they work? Disease Model of Addiction Introduction to Medication-Assisted Treatment
Brain Centers Involved in Addiction INHIBITORY CONTROL PFC ACG OFC MOTIVATION/ DRIVE SCC NAcc Amyg MEMORY/ LEARNING Hipp VTA LC REWARD WITHDRAWAL After Nora Volkow, Director NIDA, 2004 Locus Ceruleus added, after Koob
Disease Model of Addiction All addictive substances act on specific areas of the brain Prolonged use pervasive change in brain function Changes persist after drug use stops The addicted brain is different from the non-addicted brain: Brain metabolic activity Receptor availability Gene expression Responsiveness to environmental cues
Disease Model of Addiction Identifiable symptoms A predictable course Treatment that is as successful as that of many chronic diseases (e.g. diabetes, hypertension, asthma)
Relapse
Outline What are opioids and how do they work? Disease Model of Addiction Introduction to Medication-Assisted Treatment
Plasma Concentration Opioid Agonist Treatment Heroin /short acting MAT medication Euphoria/High Feeling Normal Craving/Withdrawal Time
Methadone Dispensed at Opioid Treatment Programs Staffing and practices directed by Federal law (42 CFR Part 8); Schedule II Can use it in taper and maintenance Compared to psychosocial interventions alone Increased treatment retention Decreased opioid use Better enables participation in a comprehensive treatment program
Methadone Works on the same receptor (mu opioid receptors) as heroin and other abused opioids Binds to receptor and activates it Increasing doses produces increasing effects until a maximum effect is achieved (receptor fully activated) Prevents withdrawal, diminishes drug craving Long half life Stops negative reinforcement Tolerance attenuates the effects of heroin and other opioids Prevents positive reinforcement naabt.org
Buprenorphine (Subutex) and Buprenorphine/Naloxone (Suboxone) Available as office based treatment with qualified providers, Schedule III Can be used in taper or maintenance treatment Compared to psychosocial interventions alone: Improves treatment retention Reduces opioid use Better enables participation in a comprehensive treatment program
Buprenorphine (Subutex) and Buprenorphine/Naloxone (Suboxone) Works on the same receptor (mu opioid receptors) as heroin and other abused opioids Partial agonist - binds to the receptor and activate the receptor partially Increasing the dose does not lead to as great an effect as does increasing the dose of a full agonist- less of a maximal effect is achieved Binds with high affinity Prevents positive reinforcement Long half life (20-44 hours) Prevents negative reinforcement
Buprenorphine (Subutex) and Buprenorphine/Naloxone (Suboxone) Pros Ceiling effect imparts safety Less respiratory depression compared to full agonists Less risk of overdose than full agonists Blocks effects of other opioids Flexibility of office based treatment Cons Potential for abuse, diversion Risk of complications during induction
Naloxone/Naltrexone (Vivitrol) Works on the same receptor (mu opioid receptors) as heroin and other abused opioids Antagonist Binds to the receptor, but doesn t activate the receptor Blocks the receptor from being bound by a full agonist or partial agonist Like putting gum in a lock harmreduction.org
Opioid Use Disorder Treatment Outcomes Without opioid agonist therapy (methadone/buprenorphine) 90-95% relapse within months Sub-groups with better outcomes (short term use, no IV use, good social support) With opioid agonist therapy 66% treatment retention at one year 50% of those in treatment with some drug use Decreased mortality, criminal involvement & healthcare emergencies Increased employment CEPAC 2014, Cochrane 2014
Remaining in treatment (nr) Buprenorphine Maintenance/Detoxification: Retention 20 15 10 5 0 Detox/placebo Buprenorphine 0 50 100 150 200 250 300 350 Treatment duration (days) (Kakko et al., 2003)
Length of Treatment? Guidance from SAMHSA TIP 43 is at least 2 years Stability in multiple domains of life Social Occupational Family Consider chronic disease model Consider Naltrexone/Vivitrol after taper
THANK YOU sarah.c.akerman@dartmouth.edu