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CSAM FUNDAMENTALS COURSE: STIMULANTS

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 23 rd , 2016. No relevant disclosures. Faculty/Presenter Disclosure.

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CSAM FUNDAMENTALS COURSE: STIMULANTS

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  1. 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

  2. No relevant disclosures Faculty/Presenter Disclosure

  3. 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. Learning Objectives

  4. 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

  5. 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

  6. 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 History of Stimulants

  7. 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. Epidemiology Stimulants The Canadian Tobacco, Alcohol and Drugs Survey (CTADS) 2013

  8. 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. Epidemiology Stimulants The Canadian Tobacco, Alcohol and Drugs Survey (CTADS) 2013

  9. Cocaine use worldwide UNODC World Drug Report 2016

  10. Amphetamine use worldwide UNODC World Drug Report 2016

  11. CURRENT POPULAR STIMULANTS

  12. 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) Cocaine

  13. 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 Crack Cocaine

  14. 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 Cocaine/Crack Cocaine

  15. 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) Crystal Meth

  16. 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 Ecstasy

  17. Methylphenidate (Ritalin, Concerta, Biphentin) Dextroamphetamine Sulphate (Dexedrine) Amphetamine and Dextroamphetamine (Adderall) Lisdexamfetamine (Vyvanse) Prescription Stimulants

  18. STIMULANTS AND THE BRAIN

  19. 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.

  20. Cocaine: main mechanism of action is the blockage of dopamine reuptake The Brain in Stimulant Use Disorders

  21. Cocaine concentrates in the VTA, Nucleus Accumbens and the Caudate Nucleus NIDA

  22. Cocaine Blocks Reuptake of Dopamine NIDA

  23. As a Result of Cocaine’s Actions in the Nucleus Accumbens, Impulses leaving the NA activates the Reward System NIDA

  24. 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 The Brain in Stimulant Use Disorders

  25. 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 Pharmacology of Stimulants

  26. Short term effects of stimulant use

  27. 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 Stimulant Intoxication DSM 5

  28. 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 Stimulant Intoxication DSM 5

  29. 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 Stimulant Withdrawal DSM 5

  30. 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 Acute Consequences of Stimulant Use

  31. Stimulant Induced Mental Health Disorders DSM 5

  32. Long Term effects of stimulant use

  33. Tolerance and Withdrawal Sensitization Addiction (Stimulant Use Disorder) Restlessness, anxiety, irritability, paranoia, panic attacks, mood disturbances Insomnia Long Term Consequences of Stimulant Use

  34. 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 Sensitization

  35. 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 Long Term Consequences of Stimulant Use

  36. Effects of Crystal Meth Permission granted by Multnomah County Sheriff’s Office

  37. TREATMENT OF STIMULANT INTOXICATION, STIMULANT WITHDRAWAL, AND STIMULANT USE DISORDER

  38. 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 Intoxication

  39. Supportive Suicide prevention Treatment of Stimulant Withdrawal

  40. No evidence that any of the following are helpful: • Antidepressants • Dopamine agonists • Modafinil • Cocaine vaccine Treatment: Medications for Cocaine Use Disorders

  41. 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) Treatment of Stimulant Use Disorders

  42. 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) Risk of Relapse

  43. Identification of high risk situations Development of coping skills Development of new lifestyle behaviours Development of sense of self-efficacy Cognitive Behavioural Therapy for Stimulant Use Disorders

  44. 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/maps-and-graphs.html) National Institute of Drug Abuse (NIDA) www.drugabuse.gov References

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