The document discusses various psychoactive substances including cocaine, amphetamines, and substances used to treat attention deficit disorder. It covers the history, pharmacology, effects, risks and treatment approaches for these substances.

1. Psycho-stimulants: Cocaine, Amphetamines ADD/ADHD Weight Loss Nasal Decongestants

2. Map of Principal Coca-Growing Regions in South America

3. History

5. Coca leaves used indigenously in South America Cocaine isolated from coca in 1859 by Niemann Freud shared cocaine with his fiancee, composed a “Song of praise” to cocaine. Addicted in 1884, he named cocaine the “third scourge of humanity.” Title Page of Freud’s Tribute to the Virtues of Cocaine .

6. 1888: Asa Candler, a devout Christian, bought the rights to CocaCola, a temperance beverage It contained cocaine until 1903

8. Reasons Why You Should Use Cocarettes!! 1 st —They are not injurious. 3 rd —They are made of the finest Sun-cured Virginia Tobacco 5 th —The Coca neutralizes the depressing effects of the Nicotine in the tobacco. 6 th - Coca is the finest nerve tonic and exhilarator ever discovered 8 th – Can be freely used by persons in delicate health without injury and with positively beneficial effects

9. Cocaine Financial, psychological, & physical control over the user 2 nd most common emergency dept visit (#1 alcohol in combo with other drugs) (DAWN 2004) Street Names: snow, coke, blow, toot, white lady, crack, ready rock, rock candy

10. Cocaine preparations Coca leaves (1% cocaine) sulfuric acid Coca paste (60-80% cocaine) hydrochloric acid Cocaine HCl (80%+ cocaine, but less potent) Boil with water and either baking soda or ammonia Cocaine free base (No HCl) Crack cocaine Boil with ether

11. Enzyme metabolism of cocaine Butyrylcholinesterase (BChE) Found in plasma and in red blood cells Metabolizes cocaine, aspirin, amitriptyline; activates heroin Red blood cell activity more effective metabolizing cocaine Women have more red blood cell BChE Women are less susceptible to cocaine effects Women even more immune in luteal phase: Mucous secretion decreases absorption of snorted cocaine BChE also protects against cocaine toxicity and nerve agent toxicity

12. Administration Powder most often inhaled (snorted) Causes vasoconstriction limits amount absorbed Injected (IV) Swallowed (oral or by chewing coca leaves) Smoked Freebase More intense effect direct systemic circulation Dangerous to make & use, solvents flammable and may explode Crack Cocaine Freebase without volatile chemicals Affordable, available is smaller amounts

15. Pharmacokinetics Absorption Intranasal: 20-30%, plasma peaks in 30-60 min. Smoke: 6-32%, plasma peaks at 5 min. Intravenous: 100%, immediate, 60 sec to brain Distribution Easy access to brain Concentration in brain exceeds plasma level Crosses placental barrier freely: Crack babies

16. Pharmacokinetics Rapidly metabolized by liver Elimination t 1/2 oral, nasal, IV (50, 80, 60 minutes) User may need drug every ½ hr or less to maintain high Metabolite benzoylecgonine 48 hrs-2 weeks Metabolite cocaethylene results when cocaine and alcohol are in the body at the same time. Cocaethylene acts like cocaine, and is more toxic.

17. Dose-dependent effects Dosage/Method Outbursts Stereotypic Paranoia Insomnia Agitation Increase BP Lower appetite Improve mood Alertness Low Medium High

18. Pharmacodynamics Local anaesthetic and vasoconstrictor Blocks reuptake of monoamine NTs Blocking reuptake of DA produces stimulation and behavioral reinforcement. Ventral tegmental area (VTA) DA neurons project to medial prefrontal cortex, nucleus accumbens, amygdala, and hippocampus. Cocaine blocks DA transporter proteins.

19. Stimulants Side Effects

21. Long-term Pharmacodynamics Presynaptic DA transporter levels in nucleus accumbens and VTA rise with abstinence, then fall for several months. These phenomena produce a prolonged abstinence syndrome in the reward systems. Result? Feeling miserable and craving. Tolerance develops through decreased numbers of postsynaptic receptors.

22. Signs & Symptoms of Acute Intoxication Increased, temp. stimulation, BP, HR Euphoria, giddiness, boastfulness for 30 minutes, then 60-90 minutes of mild euphoria and anxiety Anorexia Agitation, insomnia Hallucinations Seizures, death Restlessness, anxiety persists for hours; depression rebound Nasal Passage Damage Lung damage Intense, short term high followed by dysphoria Death from overdose

23. Hazards of Use Intense psychological & physical dependence Life threatening cardiac dysrhythmias, hypertension, hemorrhagic cerebrovascular accident

25. PET images

29. High Dose Effects & Safety Risks Lethal level Chronic Users Toxic paranoid psychosis Skin Eruptions Cocaine bugs Circulatory Collapse Strokes and myocardial infarction Psychiatric disorder Psychosis, suicide, delirium

30. Reinforcement Potential of Cocaine Low doses are reinforcing Cocaine craving follows Self-administration of cocaine persists in the face of punishment Withdrawal increases craving May heighten sexual interest, but does not improve potential or performance

31. Fetal Effects Vasoconstriction of uterus and placenta Stillbirth and Preterm labor Congenital Malformations Aberrant brain and heart development Cerebral infarction & hemorrhage Sudden Infant Death Neonatal Complications Acute fetal withdrawal Neurobehavioral delays Educational difficulties, easily frustrated Difficulty dealing with stimulation Attachment disorder, AD/HD

32. Treatment Models Needs analysis Begin abstinence Diagnose co-morbid disorders Relate cocaine use to disorders Maintain abstinence while treating disorders Prevent relapse

33. Additional Treatment Models Abstinence pattern analysis Crash: 9 hours to 4 days, “out of it” Withdrawal: 1 to 10 weeks, craving and relapse Extinction: Indefinite, cued craving Pharmacotherapy Antagonize cocaine: Not yet A cocaine version of Antabuse: Not yet Treat comorbid problems: Antidepressants Reduce cocaine craving: Dopamine agonists

34. Amphetamines Therapeutic Classification Similar to natural catecholamines Epinephrine, norepinephrine, dopamine Sympathomimetic agents Three Types Amphetamine Speed, amp, jelly, rippers, uppers, Bennies Dextroamphetamine Dexies Methamphetamine Moth, crystal, meth, black beauties

35. Pharmacokinetics Administration Swallowed in pill or capsule Injected into veins- orgasmic feeling “rush” Alkalizing Urine to pH of 5 T 1/2 = 5-6 hours pH of 7 T 1/2 = 20 hours

36. Pharmacodynamics Peripheral NS effects: Sympathomimetic Constrict blood vessels: Elevate blood pressure, heart rate Irritability, nervousness, mood swings CNS effects: Psychostimulant Increases in motor activity Insomnia, Loss of appetite Hallucinations, paranoia, seizures, coma

37. Neurotransmitter Effects Increase release & block reuptake of natural catecholamines Fight or Flight Effect Dopamine and norepinephrine activation Dopamine on basal ganglia: High dose stereotype and aggression Counterintuitive calming effects in AD/HD

38. Signs and Symptoms of Intoxication Elevated HP, HR, dysrhythmias, Dilated pupils reactive to light Hyperactive tendon reflexes Shallow respiration Circulatory collapse Clear or confused sensorium Hallucinations, paranoid feelings

39. Club Drug MDMA (Ecstasy) 3,4-Methylenedioxymethamphetamine Combined w/other substances of abuse Heroin = chocolate chip cookie CI no legit use, high abuse potential Liver metabolized Ingested Onset 30-60 minutes up to 4 hours ‘Crash’ 4-12 hrs after dose Post depression can last up to 5 days

40. Symptoms of Use Hazards Muscle tension Teeth clenching Blurred vision Faintness, chills & sweating Confusion Depression Sleep disorders Anxiety, paranoia Long term memory impairment Parkinson’s Dz Eventual paralysis

41. Attention Deficit Disorder & Attention Deficit Hyperactivity Disorder

42. Sample Diagnostic Criteria Inattention Underperforming Fails to notice details Does not seem to listen/easily distracted Lacks follow through Lacks organization Avoids sustained mental effort/focus Loses things/forgetful Hyperactivity-Impulsivity Fidgets, leaves seat often Runs, climbs excessively Difficulty in quiet time Talks excessively “ on the go”, “driven by a motor”

43. Stimulant treatment of AD/HD 1.29 million children currently taking stimulants to treat AD/HD About half of cases persist into adulthood AD/HD increases antisocial personality disorder risk 10X, and perhaps in connection, quintuples incidence of drug abuse Stimulants slow growth of children, but this also rebounds with abstinence: the drug holiday See http://www.fmsnutrition.com/adhd_self_testing_or_test.htm for an AD/HD self-test. How do stimulants treat AD/HD?

44. Selected Stimulant Medications Long Acting Concerta, Metadate CD, Ritalin LA, Adderall XR, Dexedrine Spansules, Daytrana Patch Atomoxetine(Strattera) Intermediate Acting Metadate ER, Ritalin SR Short Acting Ritalin, Adderall, Dexedrine, Dextrostat

46. Anorectic Agents Oily spotting, flatus, discharge, fecal urgency, GI Orlistat (Xenical) Alli (OTC) Decrease absorption of fat Lipase Inhibitor FDA does not recommend. HTN, DM, glaucoma Ephedra, guarana, chromium picolinate Increase basal metabolic rate Herbals Nervous, HA, HR, BP, palpitations, irritable Fastin, Meridia Ionamin, Beta receptors in hypothalamus Stimulants Side Effects Agent MOA Drug Class

47. Ephedra banned but…………. Bitter orange Kola nut Green tea extract Creatine Willow bark Protein drinks Caffeine products Coffee caffeine 60-180mg/cup Coffee decaf 3-5 mg Tea 20-90 mg/cup Colas 15-30 mg Milk Chocolate 3-6 mg/ounce Dark Chocolate 5-35mg/ounce

48. Moderation Common Sense

49. Deconsal II (phenylephrine 20mg & guaifenesin 375mg)

50. Ephedrine, pseudoephedrine, and phenylephrine for nasal decongestion