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CSAM FUNDAMENTALS COURSE: STIMULANTS Lydia Vezina B.Sc. M.D. C.C.F.P. OPIOD DEPENDENCY PROGRAM RENFREW RECOVERY AND DETOX ADDICTION CENTRE (FOOTHILLS MEDICAL CENTRE) ADDICTION NETWORK HOSPITAL CONSULTANT October 23rd, 2016 Faculty/Presenter Disclosure No relevant disclosures Learning Objectives Describe popular stimulants and how they are abused. Understand the neurobiology and pharmacology of stimulants. Describe short and long-term effects of stimulant use. Understand effective treatment options for stimulant use disorders. History of Stimulants Cocaine: chewing of coca leaves prevalent in the Andean regions of South America for more than 2000 years 1860 German Graduate student Albert Niemann, isolated cocaine as the active ingredient of coca leaf Coca-Cola: introduced 1886 (containing 4.5mg of cocaine per 6 oz.) 1903 cocaine removed from Coca-Cola History of Stimulants Amphetamine: first synthesized in 1887 Methamphetamine: first synthesized in 1919 Amphetamines widely used during WWII Methamphetamine currently available with a prescription for obesity, attention deficit hyperactivity disorder, and narcolepsy ex: Desoxyn History of Stimulants Ecstasy: used unsuccessfully in psychotherapy in 1970’s, became popular in rave scene in late 1980’s, early 1990’s Crack Cocaine: 1984/1985 appears in New York, Los Angeles and Miami In late 1980’s smokable form of Crystal Meth was created in Asia and then surfaced in California in the 1990’s Epidemiology Stimulants 2013: 1% (256,000) of Canadians used a stimulant in the past 12 months, a decrease from 2012 (2%). Age groups 15 to 19: 3% (or 73,000) 20 to 24: 2% (o 45,000) 25 years and older: 1% (or 138,000) Gender No difference in prevalence between males and females: 1% or 139,000 for males and 1% or 117,000 for females. The Canadian Tobacco, Alcohol and Drugs Survey (CTADS) 2013 Epidemiology Stimulants Rates of abuse 16% of people who used stimulants (or 39,000 Canadians) reported abusing them, a decrease from the rate reported in 2012 (40%) The rate of abuse 15 to 19: 32% (20,000) 20 to 24: 40% (14,000) 25 and older was not reportable. The Canadian Tobacco, Alcohol and Drugs Survey (CTADS) 2013 Cocaine use worldwide UNODC World Drug Report 2016 Amphetamine use worldwide UNODC World Drug Report 2016 CURRENT POPULAR STIMULANTS Cocaine Natural plant alkaloid From the leaves of the coca bush (Andean regions of South America = Peru, Columbia, Bolivia) Salt form usually cocaine hydrochloride: powder Highly water soluble (easy to dissolve for injection or absorption across mucous membranes for snorting) Frequently cut with levamisole (animal dewormer) Crack Cocaine Crack Cocaine street name for freebase cocaine Cocaine hydrochloride can be converted back to the water insoluble base by heating it in an organic solvent at base pH Relatively low melting point, self administered by smoking it Absorbed into the blood stream through the lungs Can be dissolved in vinegar in order to return to form that can be injected Cocaine/Crack Cocaine Amount used usually reported in grams Piece: usually refers to crack cocaine (i.e. a 40 piece) 8 ball: refers to 3.5 grams of cocaine Speedball: refers to injection of combination of heroin and cocaine Crystal Meth Chemically similar to amphetamines White, odourless, bitter-tasting crystalline powder Route: oral, smoked, snorted, or injected Made in illegal labs by chemically altering OTC medicines (pseudoephedrine) Ecstasy • • • • • • Stimulant and hallucinogen properties First synthesized by the German pharmaceutical company Merck in 1912. Tested by the military in search for the “truth drugs” 1953 Made in illicit labs and may contain other active such as amphetamine, mephedrone, methamphetamine, ephedrine, or caffeine Some tablets sold as ecstasy do not even contain any MDMA Street names include “E” , “X”, Molly, Skittles Prescription Stimulants Methylphenidate (Ritalin, Concerta, Biphentin) Dextroamphetamine Sulphate (Dexedrine) Amphetamine and Dextroamphetamine (Adderall) Lisdexamfetamine (Vyvanse) STIMULANTS AND THE BRAIN The Reward Pathway When activated by a rewarding stimulus (e.g., food, water, sex), information travels from the VTA to the nucleus accumbens and then up to the prefrontal cortex. The Brain in Stimulant Use Disorders Cocaine: main mechanism of action is the blockage of dopamine reuptake Cocaine concentrates in the VTA, Nucleus Accumbens and the Caudate Nucleus NIDA Cocaine Blocks Reuptake of Dopamine NIDA As a Result of Cocaine’s Actions in the Nucleus Accumbens, Impulses leaving the NA activates the Reward System NIDA The Brain in Stimulant Use Disorders Methamphetamines Inhibit reuptake of synaptic dopamine AND promotes direct dopamine release Ecstasy: Acutely increases serotonin by blocking reuptake and directly releasing Chronically decreases serotonin levels by depleting serotonin stores and inhibiting the synthesis of new serotonin neurotoxicity Pharmacology of Stimulants Water soluble Onset of action depends on route of administration: rapid onset of action with injection or smoking Duration of action dependent on route of administration: oral administration produces longer duration of action Short term effects of stimulant use Stimulant Intoxication Signs or Symptoms 1. Tachycardia or bradycardia 2. Pupillary dilation 3. Elevated or lowered blood pressure 4. Perspiration or chills 5. Nausea or vomiting 6. Evidence of weight loss 7. Psychomotor agitation or retardation 8. Muscular weakness, respiratory depression, chest pain, or cardiac arrhythmias 9. Confusion, seizures, dyskinesias, dystonias, or coma DSM 5 Stimulant Intoxication Clinically significant problematic behavioural or psychological changes such as: euphoria or affective blunting changes in sociability hypervigilance interpersonal sensitivity anxiety tension or anger stereotyped behaviours impaired judgement DSM 5 Stimulant Withdrawal Dysphoric mood and two (or more) of the following physiological changes, developing within hours to several days after cessation of prolonged amphetamine-type substance, cocaine or other stimulant use 1. Fatigue 2. Vivid, unpleasant dreams 3. Insomnia or hypersomnia 4. Increased appetite 5. Psychomotor retardation, or agitation DSM 5 Acute Consequences of Stimulant Use Neuro: seizures, strokes CVS: tachycardia, arrythmia, MI, HTN Kidneys: cocaine induced rhabdomyolysis Heme: Agranulocytosis (levamisole) Repro: placenta previa ENT: nosebleeds Infectious Disease: STI’s, cellulitis, bacterial endocarditis ECSTASY: Dehydration, Hyperthermia, Hyponatremia Stimulant Induced Mental Health Disorders INTOXICATION WITHDRAWAL Psychotic Delusions Bipolar Bipolar Depression Depression Anxiety Anxiety OCD OCD Sleep Disorders Sleep Disorders Sexual Dysfunction DSM 5 Long Term effects of stimulant use Long Term Consequences of Stimulant Use Tolerance and Withdrawal Sensitization Addiction (Stimulant Use Disorder) Restlessness, anxiety, irritability, paranoia, panic attacks, mood disturbances Insomnia Sensitization Sensitization (opposite of tolerance) more you use the drugs more likely of symptoms happening such as: Seizure Psychosis (paranoia, visual, auditory, and tactile hallucinations) Stereotypical behaviors Long Term Consequences of Stimulant Use Repro: irregular menses, prematurity ENT: nasal septum perforation, loss of sense of smell, chronically runny nose Infectious Disease: Hep C, HIV Weight loss Methamphetamines (neurocognitive impairment, “meth mouth”) Psychosocial: homelessness, legal involvement, trauma Effects of Crystal Meth Permission granted by Multnomah County Sheriff’s Office TREATMENT OF STIMULANT INTOXICATION, STIMULANT WITHDRAWAL, AND STIMULANT USE DISORDER Treatment of Stimulant Intoxication Supportive Phentolamine for hypertension (no beta blockers bc unopposed alpha-adrenergic stimulation can lead to coronary vasoconstriction and ischemia) Chest pain: ECG, biomarkers, CXR, benzo and nitro Treat stimulant induced psychosis if severe Treat any infections: cellulitis, endocarditis, infectious diseases (HIV, Hep C, STI’s), abscesses, septic arthritis Treatment of Stimulant Withdrawal Supportive Suicide prevention Treatment: Medications for Cocaine Use Disorders No evidence that any of the following are helpful: Antidepressants Dopamine agonists Modafinil Cocaine vaccine Treatment of Stimulant Use Disorders SBIRT (Screening, Brief Intervention, Referral to Treatment) Stages of Change Harm Reduction (needle exchange/crack pipe programs) Motivational Enhancement Therapy Cognitive Behavioural Therapy Contingency Management Residential Treatment Self Help Support Matrix Model Treatment of Underlying Mental Health Disorders Treat any Medical Complications (HIV, HCV) Risk of Relapse Re-exposure to the Drug Exposure to stress Exposure to environmental cues Conditioned response to drug-related stimuli (e.g. craving on seeing any white powderlike substance) Cognitive Behavioural Therapy for Stimulant Use Disorders Identification of high risk situations Development of coping skills Development of new lifestyle behaviours Development of sense of self-efficacy References DSM 5 Diagnostic & Statistical Manual of Mental Disorders 5th Ed. Text Revision 2013 The ASAM Principles of Addiction Medicine Fifth Edition. Ries, Fiellin, Miller, Saitz. 2014 The Canadian Tobacco, Alcohol and Drugs Survey (CTADS) 2013 UNODC, World Drug Report 2016 (http://www.unodc.org/wdr2016/en/mapsand-graphs.html) National Institute of Drug Abuse (NIDA) www.drugabuse.gov