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PSY 245 Exam 2 Study Guide

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by: Kristi Dorsey

PSY 245 Exam 2 Study Guide PSY 245

Kristi Dorsey
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Hey Guys! Here is my completed study guide for exam 2. It is 31 pages, color coded, and includes information from the text, as well as class notes. Hope this helps! :) ~ Kristi
Drugs and Behavior
Mark Galizio
Study Guide
PSY 245, Drugs and Behavior, Mark Galizio, uncw, Psychology
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This 31 page Study Guide was uploaded by Kristi Dorsey on Friday March 18, 2016. The Study Guide belongs to PSY 245 at University of North Carolina - Wilmington taught by Mark Galizio in Spring 2016. Since its upload, it has received 312 views. For similar materials see Drugs and Behavior in Psychlogy at University of North Carolina - Wilmington.

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Date Created: 03/18/16
Study Questions Unit II CHAPTER 6: COCAINE, AMPHETAMINES, AND RELATED STIMULANTS 1. What is Erythroxylum coca? Where does it grow? a. Coca bush/tree b. Leaves contain cocaine c. First major stimulant used by humans d. Grown in Andean regions of Bolivia, Ecuador, northern Argentina, and Peru 2. Trace the early history of cocaine. How was it used by the Indian people of Peru and Bolivia? a. Jerome Jaffee; psychiatrist & anthropologist b. Observed chewing of coca leaf by conqueros c. Hold it between cheek and gum (like chewing tobacco today) d. Religious Significance, medicinal significance, & work-related significance  Mama Coca: beautiful woman executed for adultery  Divine coca plant grew from her remains  Consumed only by royalty in her memory 3. How was cocaine introduced to Europe? a. Spanish Conquistadors in the 16 century  Disturbed by the religious use of coca (against Catholicism)  Conquered Incas and permitted/encouraged use of coca as a means of enslaving them 1. Helped them work harder and longer, used as form of payment, & levied taxes to be paid on coca leaves b. European naturalists explored Peru and experimented with coca 4. What is formication syndrome? a. Symptoms of itching b. Feeling as if insects were crawling under skin c. Caused by cocaine & methamphetamine overdose 5. What are the other symptoms of cocaine overdose? a. Paranoid delusions (similar to paranoid schizophrenia) b. Overdose death c. Dependence d. Reports of violent acts committed under the influence of cocaine 6. What are amphetamines? Consider their history. a. 1914 Harrison Narcotics Act resulted in decline cocaine use b. New stimulants (amphetamines) became popular  Amphetamine  Dextroamphetamine  Methamphetamine c. Soldier’s disease (widespread use of morphine in soldiers during the Civil War) d. Post WWII epidemic in Japan, Sweden, & other parts of Europe e. 1960s – Recognized as dangerous in the U.S. 7. What impact has cocaine had on society in the USA and Columbia in the past 25 years? a. Late 1980s: overdose deaths & other related ER visits rapidly increase b. Distribution of cocaine historically controlled by Columbia cartels  Medellin Cartel (1989) – targeted government officials, judges, & court employees; 2000+ murders in the first 6 months 1. Pablo Escobar: formed head of Medellin Cartel; killed in gunfight with police in 1993 2. Decline led to Cali Cartel  Cali Cartel (1990s) – made billions of dollars in the cocaine trade 1. Late 1990s: almost all leaders arrest, cocaine trade became less centralized, & former members moved their operations to multiple sites c. United States: organized gangs with high-tech weapons control the black market; linked to shootings and urban violence  Black market developed due to cravings and dependence  Crack houses created (place where crack is sold and smoked)  Addicts turn to prostitution  > risk of HIV transmission 8. Why do people in the Andean countries of South America chew coca? a. Chewing of coca and drinking tea brewed from coca leaves b. Desired stimulant effects (stimulate alertness, reduce fatigue, & combat altitude sickness) c. Lost religious significance 9. How did the use of cocaine change in the second epidemic of cocaine abuse? a. Movement from amphetamines to cocaine b. Increased availability & cheaper (previously, only stars and athletes could afford it) c. More people able to regularly use in high doses 10. What is crack? Compare it to other forms of cocaine in terms of risk of overdose and dependence. a. Street cocaine: produced by combining a paste made from coca leaves with a hydrochloric acid solution to form a salt (cocaine hydrochloride) b. Freebase: separate cocaine base from hydrochloride salt  Mix street cocaine with ether (highly flammable substance)  Can be produced more simply and safely by dissolving the cocaine salt in an alkaline solution (such as baking soda)  When the water in the solution is boiled off, what remains is a hard, rocklike substance called crack c. Crack/free-base cocaine (1986): produced by mixing cocaine salt with baking soda & water  Solution is heated, resulting in brittle sheets of cocaine  Sheets then “cracked” into small, smokeable chunks or rocks 11. What is “ice” or “speed”? Methamphetamine 12. What are issues associated with meth production? a. Many of the chemicals are highly flammable and the process requires ingredients be heated with a burner b. Risk of explosion and fire due to toxic waste c. By-products can cause health hazards wherever they are dumped 13. Consider the studies linking methamphetamine use to brain damage and other health issues. a. Exposure to very high doses poses a risk of: seizures, convulsions, cardiovascular collapse, overdose (stimulant psychosis), depression (withdrawal symptom), & “meth mouth” (deteriorating and loss of teeth) b. New animal and human research suggests that meth may produce long-lasting damage to the brain  PET scan to study chronic meth users  Damage in dopaminergic pathways  Long-lasting motor and memory impairments  Higher rates of Parkinson’s disease  Some studies have shown improvement in brain & cognitive function after extended periods of abstinence from meth 14. In what parts of the US is meth use posing the biggest problems? a. California & Mexico (organized criminal groups for meth trafficking) b. Midwest (early 2000s) c. 2005: spread to east coast 15. Why are synthetic cathinones often called "bath salts" or "plant food"? a. Early 2000s: Applied as a means of insect control in Israel (called “plant food” because of its agricultural origins) b. 2009: spread from Israel to Europe & 2010: spread to the U.S. c. Called “bath salts” because it resembled products used in the bath tub 16. What are some frequently used synthetic cathinones? a. Mephedrone b. Methylone c. MDPV (Methylenedioxypyrovalerone) 17. What law recently banned sales of the main synthetic cathinones? a. Synthetic Drug Abuse Prevention Act (2012) b. Banned sales of the 3 main synthetic cathinones c. 2011: moved synthetic cathinones to emergency Schedule I status d. Impact: number of ER calls to U.S. poison centers dropped 18. What is the neurochemical mechanism for the actions of cocaine and amphetamines? How has this been related to the cocaine withdrawal syndrome? What are the causes of cocaine blues? a. Cocaine blues: depression and lack of joy during cocaine withdrawal b. Neural Process:  Stimulants initially produce activity in neural pathways sensitive to monoamine transmitters  Reuptake is blocked so that enzymes break down the neurotransmitters  Long-term effects involve depletion of monoamines (linked to clinical depression) 19. What are the acute physiological effects of cocaine? a. Enhances physical strength and endurance b. Sympathomimetic: stimulates or mimics activity in the sympathetic branch of the ANS (emotional arousal, increased … heart rate, blood pressure, respiratory rate, sweating, blood flow to large muscle groups & brain, body temperature; decreased … blood flow to internal organs and extremities, hunger; pupils dilated) 20. What are the acute psychological effects of cocaine? a. Mood elevation & alertness Talkativeness & sociability b. Insomnia c. Enhances performance on some types of cognitive tasks (but with increased errors) d. Impairs one’s ability to learn highly complex tasks 21. What is state-dependent learning? a. Learning under the influence of a drug is best recalled when one is in the same drug-induced state b. Suggests that people will have problems learning information when under the influence of a drug because the ability to retrieve the information will not be as good when sober 22. In what ways can cocaine overdose cause death? a. Convulsions or seizures may result in: respiratory collapse, heart attack (due to coronary artery spasms), & stroke b. Combination Effects  Alcohol + cocaine = cocathylene toxicity  Cocaine (or amphetamine) + heroin (or opiate) = “speed ball”/overdose  Morphine + cocaine = increased cardiovascular effects 23. What are the chronic effects of stimulant abuse? Tolerance & dependence 24. What about tolerance to cocaine? a. Acute Tolerance: Effects obtained from the first administration of the drug are not produced by a second administration shortly afterward, unless a higher dose is used; dissipates rapidly (within 24 hours)  EX: On a given day, the effects of the first cocaine injection were not matched by subsequent injections, but strong effects could still be obtained the next day b. Long-Term Protracted Tolerance: inconsistent findings c. Reverse Tolerance (Sensitization): tolerance to positive subjective effects of meth use  Increase in negative effects with repeated administration  Attributed to accumulation of sleep loss and reduction of caloric intake 25. Dependence (Psychological)? a. Withdrawal Symptoms: depression, anxiety, changes in appetite, sleeping disturbances, &cravings b. Crash Phase: several days of intense craving and exhaustion alternating with agitation and depression  In meth withdrawal, users may show greatly increased sleep time and food intake  For several weeks, addicts continue to feel intense cravings, moderate to severe depression, and an inability to experience normal pleasure (anhedonia) c. Extinction Phase: improvement gradually occurs but intermittent cravings continue for months or years; Cravings seem to be caused by exposure to particular cues in the environment that were associated with cocaine use in the past and continue to “trigger” craving until the craving response is extinguished to those cues (through Classical Conditioning) 26. Define stimulant psychosis. a. Delusions & hallucinations b. Compulsive stereotyped behavior (rocking, hair pulling, chain smoking, or fiddling) c. Formication (symptoms of itching & feeling as if insects are crawling under he skin) d. Often associated with violent behavior 27. What is a crack baby? What is the prognosis for these children? a. Symptoms: lower both weights and lengths, > likely to die during infancy, permanent neurological damage, learning disabilities, abnormal arousal patterns, & IQ scores well below national average b. Prognoses  Difficulties may not involve permanent neurological damage induced by cocaine, but stigma may create a self-fulfilling prophesy  Some studies have reported long-term learning and behavior problems but lack appropriate comparison/control groups  Difficult to separate effects of prenatal cocaine exposure from other problems children face after birth (maternal neglect or impoverished family/social environment) 28. What is Attention Deficit Hyperactivity Disorder? a. Trouble paying attention (inattention, fidgeting, & restlessness) b. Not necessarily hyperactive and often leads to: impaired academic performance, misbehavior at school, & conflict with peers, siblings, and parents 29. What drugs are used to treat ADHD and what are the issues involved? a. Stimulant drugs: in 1937, physician Charles Bradley discovered that hyperactive children were calmed by a dose of amphetamine  Methylphenidate (Concerta, Ritalin, & Daytrana)  Amphetamines (Adderall, Vyvanse) 30. What is Khat? a. Plant native to East Africa (Catha edulis) b. Most common route of administration is chewing fresh leaves  Juices are swallowed  Contain two stimulants – cathnie and cathinone c. Synthetic variations (cathinones) sold as bath salts d. Widely used throughout East Africa & Arabian Peninsula (5 million daily users) 31. Vitamin R? a. Ritalin – makes users feel energetic & enhances mood (has become a popular club/dance drug) b. Many college students take amphetamines or methylphenidate to study c. 60+% of college students with ADHD report giving/selling their meds CHAPTER 7: NICOTINE 1. What is Nicotiana tabacum? a. Tobacco plant where nicotine is found b. Provides all tobacco typically consumed in the US 2. Where did tobacco originate? a. Columbus found Native Americans in the New World smoking dried tobacco leaves 3. How was tobacco introduced to Europe? a. Columbus/European explorers brought seeds of tobacco plant home b. Spread them to other parts of the world c. Quickly became popular among Europeans 4. What are the current smoking trends among Americans? a. ~ 20% of American adults smoke cigarettes today b. Cigarette smoking most common way to use tobacco c. Smoking declined in latter part of the 20 century d. Increase in the amount of people who quit smoking; most did so on their own 5. How do factors such as ethnicity, education, and employment affect smoking trend outcomes? a. Ethnicity: whites have highest rate of smoking among those 12-17 and 18-25 & blacks have a higher rate of smoking among those 26+ b. Education: highest rates of use among 18-25 year olds  Full time college students – 23.8% reported full time use  Not full time college students – 39.2% reported full time use  Hookah (water pipe): used by 15-20% of college students (smoke inhaled first passes through water & smoke contains nicotine, tar, & carbon monoxide) c. Employment: smoking prevalence > for unemployed individuals 6. What neurotransmitter is influenced by nicotine? Acetylcholine a. Raises dopamine levels in the mesocorticolimbic system b. Biphasic drug: stimulates ACH receptors at low doses but its effects are more depressant in high doses 7. Describe the Absorption of nicotine. a. Most readily absorbed through lungs b. Absorption depends on: site of absorption, how nicotine was delivered, & length of contact of the nicotine-containing substance with the absorption site 8. Describe the Distribution of nicotine. a. Blood distributes it to a number of sites of pharmacological action b. Inhalation: nicotine reaches the brain from the lungs in 7 seconds and takes 3-5 minutes to reach peak levels in the brain c. Nicotine levels also fall rapidly; half-life is 10-20 minutes 9. What are the acute effects of nicotine? 10. Consider the issues of tolerance with regard to nicotine. a. Person’s first attempt at smoking usually results in palpitations, dizziness, sweating, nausea, or vomiting (acute signs of nicotine poisoning)  Signs of tolerance to these autonomic effects of nicotine are evident even within the time of smoking the first cigarettes b. Dispositional tolerance (taking more of the drug to produce the desired effect)  EX: smokers metabolize drugs more quickly than nonsmokers do 11. Consider the issue of dependence on nicotine. a. Withdrawal symptoms: cravings, irritability, anxiety, difficulty concentrating, restlessness, increased appetite, impatience, somatic complaints, insomnia b. Physical Dependence  Rapid rise and fall of nicotine blood levels creates the demand for many nicotine reinforcements  Each inhalation results in a drug reinforcement that must be replaced quickly because of a rapid fall in the blood level of nicotine  Social and environmental associations with nicotine use strengthen psychological dependence 12. What are the health consequences of chronic tobacco use? a. 440,000 people in the U.S. who smoke die prematurely every year (1200+ a day) b. WHO: over 5 million men and women worldwide die prematurely due to their cigarette smoking 13. Consider the data of Woloshin, Schwartz & Welch (2002) on death rates among smokers and non-smokers. a. Compared rates of death from different diseases among adults 20 years of age and older who currently smoke or who never smoked b. Computed changes of dying in the following 10 years for a given medical problem for different age groups c. For women and men age 30+, the likelihood of dying from heart attack, stroke, or lung cancer was significantly higher in smokers as compared to nonsmokers d. Smokers and nonsmokers did not differ in projected death rates from diseases like colon or prostate cancer, and they did not differ in rates of death by accidents 14. What aspects of smoking cause which problems? a. Tar: material that remains after cigarette smoke is passed through a filter; contains most of the cancer- causing substances b. Nicotine: Coronary Heart Disease & heart attacks c. Carbon monoxide: reduces amount of hemoglobin, which deprives the body’s tissues of oxygen (leaves the heart & brain vulnerable) 15. What about passive smoking? a. Third leading preventable cause of death in the U.S. (behind active smoking and alcohol) b. Environmental Protection Agency (1993) declared secondhand smoke to be a “Group A” carcinogen [along with arsenic, asbestos, benzene, & radon] c. A study published in 2011 provided the estimate that, in 2004 passive smoking killed about 600,000 people around the world – 379,000 from heart disease, 165,000 due to lower respiratory infections, 36,900 from asthma, and 21,400 from lung cancer d. Led to the banning of smoking in public places 16. What types of treatments are available for helping people quit smoking and what kinds of results occur? Behavioral programs, Nicotine replacement therapies, & Harm Reduction Approaches Behavioral Programs  Goal: Teach smokers to identify situations that present a high risk for them to smoke and…. o Apply techniques to weaken the habit components of high risk situations o Teach smokers competing (with smoking) coping responses in high-risk situations o Teach smokers to self-monitor their smoking behavior  Ongoing contact with clinical staff in an individual group format for a period of 2-3 months  Overall considered an effective way to stop smoking by APA o Majority of individuals who complete such programs resume smoking after 6 months to a year o Attributed to cravings the smokers experience when they abstain from smoking Nicotine Replacement Therapies  Administering nicotine to smokers as part of the effort to help them start smoking  EX: nicotine gum, nicotine patch, nicotine nasal spray, nicotine inhalers, & nicotine lozenges  Overall Effectiveness o 2x larger chance of quitting smoking o Combining NRTs with behavioral programs enhance the quit rates achieved by either type of treatment alone o Little evidence for long-term negative consequences o Craving reduced to a limited degree o For men, NRTs with “low-intensity” behavioral support were effective in reducing or stopping smoking throughout the follow-up period (12 months) o Longer-term effectiveness of NRT for women tended to require more intensive behavioral support Harm Reduction Programs  View behavior change that results in the reduction, if not the elimination, of negative consequences associated with behaviors such as smoking desirable  EX: Electronic Cigarette 17. Is formal treatment necessary? a. Although most people stop smoking without help, they tend to succeed only after multiple attempts b. If smoking treatments increase the rate of smoking cessation compared to what people do on their own, then they would be more than worth their cost c. The emphasis today is on prevention (treatment less so) 18. What is the Omnibus Tobacco Settlement? a. The attorney generals of 46 states and five territories signed an agreement with tobacco companies worth $206 billion to settle Medicaid lawsuits to cover the costs in Medicaid payments for smoking-related illnesses b. Likely won due to the tobacco industry concealing early knowledge about the relationship between smoking and serious health problems 19. What is varenicline (Chantix)? a. Drug developed specifically for the treatment of smoking b. Works by competing with nicotine in binding to nicotine receptors c. Stimulates nicotine receptors as nicotine does so that smoking cravings are assuaged d. If smokers smoke while on varenicline, they feel reduced nicotine effects compared to when not on the medication so that smoking is less reinforcing CHAPTER 8: CAFFEINE 1. Describe the general history of caffeine use. Where does caffeine come from? a. Explorers found coffee in Arabia, Turkey, and Ethiopia b. Methylxanthines (caffeine) found in plants c. Mythical origin of coffee i. Discovered in Arabia by a holy man ii. Goats in a herd had been jumping around at night instead of sleeping iii. They had been nibbling on the beans of the coffee plant iv. Holy man thought the beans from the same plant could help him endure long nights of prayer 2. What are the other methylxanthines and where are they found? a. Mythical Origin of Tea (China) i. 2737 b.c. by Chinese Emperor Shen Nung ii. Produced first pot of tea (leaves from a nearby bush fell into pot while boiling water) b. Found kola nut in West Africa c. Found cacao plant (source of chocolate) in Mexico and much of Central and South America d. Other sources of tea discovered in parts of North and South America 3. Consider Table 8-1. 4. What are the estimates of caffeine use around the world (Table 8-2)? a. Caffeine is the world’s most preferred drug b. About 90% of the world’s population regularly consumes products that contain caffeine, with coffee, tea, and soft drinks being the most common sources c. Average consumption of caffeine per person worldwide is around 70 mg per day d. U.S. – 170 mg per day; mostly from coffee; largest consumer of cocoa e. World’s top per capita rates of caffeine consumption are the Scandinavian countries (Finland, Sweden, Denmark, and Norway) along with the Netherlands; 414 mg per person per day via coffee f. U.K. and neighbors – tea dominant source of caffeine g. Denmark – 21 mg caffeine consumption via chocolate per day 5. What is the adenosine hypothesis? a. Most accepted explanation for caffeine’s acute effects b. Adenosine: chemical the body produces/inhibitory neurotransmitter c. Receptors located in the CNS & PNS d. Leads to: behavioral sedation, regulation of oxygen delivery to cells, dilation of cerebral and coronary blood vessels, & production of asthma e. Caffeine and the other methylxanthines occupy adenosine receptors and then block the action of that transmitter 6. How is caffeine absorbed in the body? a. Readily absorbed from the gastrointestinal tract b. Quickly reaches the brain because it passes through blood-brain barrier c. Equally distributed in total body water; after consumption, concentration of caffeine is similar throughout the body NOTE***  Caffeine can induce tolerance without dependence  Rarely produces dependence without tolerance 7. What about tolerance? a. Develops to caffeine’s effects on: renal function, sleep, & physiological functions (blood pressure and heart rate) b. Little tolerance seems to develop to caffeine’s stimulant effects c. One reason people are heavier or lighter caffeine users is their individual ability to tolerate caffeine 8. Dependence? a. Can develop with an exposure of 300 mg of caffeine a day for only three consecutive days b. Symptoms range from mild to severe and begin within 12-24 hours of cessation of caffeine use; may last about a week 9. Withdrawal? a. Headache & Fatigue (most common) b. Depression c. Decreased alertness d. Less relaxed mood e. Decreased activity and energy f. Greater sleepiness and drowsiness g. Increased irritability 10. What are the physiological effects of caffeine? a. Contraction of striated muscle (heart) b. Relaxation of smooth muscle, especially: coronary arteries, uterus, bronchi c. Diuretic effects on the kidneys d. Stimulating effect on respiration at higher doses e. Elevation of basal metabolism f. Various endocrine and enzymatic effects 11. What are the effects of caffeine on mood? a. Moderate doses of caffeine are reliably associated with feeling energized, creative, efficient, confident, and alert b. Believed that many people who are afflicted with significant depression “medicate” themselves by using caffeine products 12. Effects on Performance? a. Improves task performance (decreases fatigue & increases vigilance b. Choice Reaction Time: impairs the decision-making part of the task but improves the motor component c. Enhances athletic performance including perceived exertion and endurance 13. How does caffeine interact with nicotine and alcohol? a. Smokers smoke fewer cigarettes after they drink coffee compared with when they have not had coffee (stronger for lighter caffeine users) b. Another effect of nicotine is in the excretion of caffeine from the body, which occurs more than 50% faster in smokers than in nonsmokers c. How people react to nicotine may be associated with how they react to caffeine and alcohol 14. Describe the toxic effects of caffeine. a. People differ in how much caffeine they can ingest before they experience symptoms of intoxication b. 600 mg of caffeine a day greatly increases the chance of developing toxic symptoms over time  Muscle twitching  Rambling flow of thought and speech  Cardiac arrhythmia  Period of inexhaustibility  Psychomotor agitation  Ringing in the ears  Seeing flashes of light 15. Can you overdose on caffeine? a. Lethal dose of caffeine taken orally  10 grams for adults = 75 cups of coffee, 125 cups of tea, 200 colas, or 100 noDoz tablets  100 mg/kg for children b. Reports due caffeine overdose are rare 16. What about chronic effects of caffeine? a. Considered a relatively safe drug b. Caffeine consumption should be moderated (to prevent minor symptoms that occur with high levels of use) c. Pregnant women benefit by keeping caffeine consumption at a low to moderate level d. People diagnosed with Generalized Anxiety Disorder are hypersensitive to the effects of caffeine and the drug may exacerbate anxiety symptoms 17. What are the therapeutic effects of the methylxanthines? a. Used in a variety of prescriptions and over-the-counter medications (in many remedies for headaches and colds) b. Found in appetite-suppressant medications because of its diuretic effects c. Differences among xanthines and their effects are based on slight differences in their chemical structure CHAPTER 9: ALCOHOL 1. How are alcoholic beverages produced? Fermentation a. Creates environment for yeasts (living microorganisms) b. Yeasts multiply rapidly by eating the sugar c. Sugar converted into ethanol and carbon dioxide by the yeast’s metabolic processes d. Carbon dioxide bubbles at the top of the mixture, leaving ethanol (10-15%) 2. What is beer made from? Grains 3. What is wine made from? Grape Juice 4. What about distilled beverages such as whiskey, rum and vodka? Distillation a. Heating a fermented mixture b. Alcohol has lower boiling point than water, so the steam emitted through boiling as a greater alcohol content than the original fermented mixture c. Vapor condensed through cooling d. Resulting liquid has a greater alcohol content than the original fermented mixture e. Repeating this cycle increases alcohol content of a beverage 5. How do these vary in alcohol content? a. Varying the substances that form the base of the beverage and varying the alcohol concentration produce different alcoholic beverages b. Alcohol % denoted by volume (EX: 16 oz of a beverage that is 50% ethanol contains 8 oz of alcohol) 6. What is “proof”? a. Alcohol content of distilled beverages b. Equal to twice the % of alcohol by volume c. EX: 86 proof = 43% alcohol 7. Consider the history of alcohol use. a. Non-distilled alcoholic beverages: made inadvertently by natural fermentation  First wines made from fruit juice  First beer produced in Egypt between 6000 b.c. & 5000 b.c. (blending water & malt to yield a refined liquid) b. Distilled spirits produced in China around 1000 b.c. c. Alcoholic beverages have played a role in important social occasions, such as births, religious ceremonies, marriages, and funerals d. Colonial America  Tavern: center of town politics, business, trade, and pleasure  Drank beer, wine, cider, and distilled spirits in considerable quantities (by 1830, almost 5 alcoholic beverages a day for each adult) th e. 19 Century U.S.: Saloon was the focal scapegoat of the temperance movement and was blamed for social ills such as thievery, gambling, prostitution, and political corruption; led to Prohibition (repealed in 1933) 8. What are the current trends of alcohol consumption in the U.S? 9. What about heavy alcohol consumption? a. Associated with negative consequences b. Defined as volume consumed on one drinking occasion, even if these occasions do not occur with great frequency is important c. Men reported a rate of heavy drinking almost 3x higher than women reported d. Over 12% of 18-25 year olds reported heavy drinking  Men (16.4%) & women (7.9%)  White reported a higher rate (15.6%) than did either blacks (4.8%) or Hispanics (9.8%) 10. What about binge drinking? a. Defined as consuming at least five (for men) or four (for women) drinks on at least one occasion in the last two weeks b. Associated with accidental death, injury, assault, unwanted and unprotected sex, drunk driving, vandalism, suicide, & academic problems c. Students who drink the most are first-year students, whites, members of fraternities and sororities, and athletes d. Research has shown that significant percentages of people who do have alcohol problems as adults drank heavily in college, but most people who drink heavily in college do not have later alcohol problems 11. What receptors mediate alcohol’s actions? a. Alcohol acts on GABA-benzodiazepine receptors b. Enhances serotoninergic and dopaminergic activity c. Pinpointing a site of action or a single mechanism of alcohol effects is difficult because the drug affects cell membranes, all neurochemical systems, and all endocrine systems 12. What are some factors influencing alcohol absorption? a. Factors that alter the rate of alcohol’s passage from the stomach to the intestines (food & milk slow absorption) b. Rate at which an alcoholic beverage is consumed (faster drinking = faster absorption; higher concentration absorbed more quickly; carbonated absorbed more quickly) c. Pylorospasm: the shutting of the pylorus valve that occurs in some people when they drink very large quantities of alcohol  Prevents whatever is in the stomach from passing to the intestines  Large amounts of alcohol may remain in the stomach unabsorbed  Natural defense against an individual becoming a heavy drinker 13. What is a "standard drink" and how much alcohol is in one? a. The alcohol equivalent in a drink of beer, wine, or distilled spirits (5 ounces of alcohol) b. 12 ounces of beer c. 4 ounces of table wine d. 1 ounce of 90 to 100 proof whiskey 14. Be able to compute your BAC after various levels of alcohol consumption. a. Three ways to measure BAC 1) Metabolize about 1 drink every 2 hours – if you have a standard drink at the end of a shot, your BAC will approach 0 about 2 hours later 2) BAC drops about .01% every 40 minutes 3) BAC = # of standard drinks * 0.25% (rate at which your blood alcohol level is rising) minus the # of hours drinking * 0.015% (rate at which alcohol is being metabolized) 15. How is alcohol metabolized and what factors affect the rate of metabolization? a. >90% of alcohol absorbed is broken down in the liver b. Broken down to acetaldehyde by the enzyme alcohol dehydrogenase c. Broken down to carbon dioxide and water d. Release of energy (calories) e. Carbon dioxide excreted from the lungs f. Water excreted in urine g. Alcohol that is not metabolized is excreted in pure form through the kidneys and the lungs 16. Characterize the development of tolerance to alcohol. What types of tolerance develop? Dispositional, functional, acute, protracted, and cross-tolerance Dispositional  Increase in metabolic rate of drug  Drinker must consume greater quantities of alcohol to maintain a certain BAC  Can be reversed with a period of abstinence from alcohol Functional  Brain and other parts of CNS become less sensitive to drug’s effect  Greater influence than dispositional tolerance in altering how alcohol affects a person with repeated use Acute  Course of action of a single dose or few doses  The effects of alcohol at a given BAC are greater when the BAC curve is rising than on the descending limb of the curve  EX: At a BAC of 0.10% as it is ascending, an individual may show considerably impaired performance on tasks related to driving o If the BAC peaks at, say, 0.15% and then hits 0.10% as it is falling, however, an individual’s performance on those same driving-related tasks would be improved, although still probably far from its level with no alcohol in the blood Protracted  Requires an individual to drink greater amounts of alcohol to achieve an effect once achieved with less alcohol  Person becomes more susceptible to serious health and other consequences of heavy alcohol consumption o EX: drinking large quantities of alcohol still results in a high BAC o With higher BAC’s the body is more vulnerable to alcohol’s toxic effects Cross-tolerance  Alcohol & other CNS depressant drugs  Taking one drug can suppress withdrawal symptoms of the other o EX: alcohol & benzodiazepine drugs such as Valium show cross-dependence 17. Characterize the symptoms of the alcohol withdrawal syndrome (delirium tremens). 18. What are the physiological effects of alcohol? a. As BAC increase, acute effects increase in number and intensity b. Inhibits the secretion of antidiuretic hormone, which causes increased urination (happens when BAC is rising but not when it is falling) c. Long-term increased body fat and weight gain when alcohol is used in addition to normal food intake d. Peripheral dilator (causes skin to feel warm and turn red) e. Increased gastric secretion that stimulates the appetite  Alcohol at high doses harms the stomach mucosa and causes gastric distress f. Vomiting may occur at BACs > 0.15% g. When BAC increases rapidly there is a release of corticosteroids, part of the body’s general reaction to stress (stressor = alcohol, which is toxic) 19. Characterize the effects of alcohol on sleep. a. REM Sleep: rapid eye movements; stage of sleep cycle when most dreaming occurs b. Alcohol suppresses REM sleep  At a low dose, REM is suppressed only in the first half of the night; REM time rebounds & increases in the second half  At larger doses, REM is suppressed throughout the night 20. Characterize the effects of alcohol on memory. What is a blackout? a. Short-term memory: memory for recent events b. Long-term memory: memory for remote events; info enters long-term memory through short-term memory c. Blackout: failure to recall events that occurred while drinking even though there is no loss of consciousness  Thought to result from a failure in the transfer of information in STM to LTM  Animal studies suggest that the mechanism for this effect is alcohol’s interference with receptors in the brain that enhance connections among neurons and are fundamental to learning and memory d. Grayout: can partially recall events that occurred in full 21. What is a hangover? a. Appear 4-12 hours after reaching the peak BAC b. Symptoms: headache, dizziness, nausea, vomiting, increased heart rate, fatigue, thirst 22. What are the sensorimotor effects of alcohol? a. Deterioration of psychomotor task performance b. Impairs performance on divided-attention tasks c. Complex reaction time may be impaired in regards to speed and accuracy d. Significantly impairs STM e. Vision decreases in acuity f. Taste and smell not as sensitive g. Body sway impaired by 40% h. Pain sensitivity decreases i. Abnormality in motor functions (standing & walking) 23. What is the relationship between alcohol and automobile accidents? a. Motor vehicle crashes are the most common non-natural cause of death in the United States b. They are the leading cause of death overall of people aged 1 to 24 c. Young drivers are disproportionately more likely to be involved in alcohol-related accidents d. Young people seem to be at higher risk for motor vehicle accidents across the range of BACs e. Statistics not conclusive because we only have correlational studies f. At a BAC of 0.02% to 0.03% a crash is 1.4 times as likely as it is at a BAC of 0% g. At a BAC of 0.05% to 0.09%, it is 11.1 times as likely h. At a BAC of 0.10% to 0.14%, it is 48 times as likely i. At BACs of 0.15% and higher, it is 380 times as likely 24. What is the relationship between alcohol and aggression? a. Aggression: behavior intended to harm a person who would prefer not to receive such treatment b. Anger and fatigue common when BAC is rising c. > 0.10% BAC = may change abruptly from friendly to hostile d. When people commit violent crimes, they tend to be under the influence of alcohol (especially among men 18-30 years old) e. Domestic violence issues - alcohol has been estimated to be involved (offender or victim) in 25% to 50% of spousal abuse incidents f. Major cause of aggression at sporting events g. The misconduct and violence against property and people that some fraternities are known for seem to be highly correlated with alcohol h. Not proven that alcohol causes aggression because studies have been correlational 25. What is the balanced placebo design? a. Four groups:  Told they are receiving a drug & actually receive the drug  Told they are receiving the drug, but receiving a placebo  Told they are not receiving the drug & actually receive the drug  Told they are not receiving the drug, but receiving a placebo 26. How does alcohol affect sexual responding? a. Men  BACs of 0.05% to 0.10%, alcohol pharmacologically retards sexual arousal  When the BAC climbs to more than 0.10%, erection and ejaculatory competence are inhibited or eliminated b. Women  Women’s sexual response deceases with increasing alcohol dose  Unlike men, women continue to perceive increased sexual arousal and sexual pleasure even as the physiological indexes of their response and arousal are declining 27. Consider the effects of alcohol across various doses (Table 9.5). 28. What are the effects of alcohol use? Consider the issues of: Brain damage (Wernicke-Korsakoff’s syndrome), liver damage, sexual dysfunction, & FAS. Brain Damage (Wernicke-Korsakoff’s syndrome)  Results from the combination of extreme nutritional deficiency (vitamin B1 or thiamine) and chronic heavy drinking  Symptoms: confusion, loss of memory, staggering gait, and inability to focus on the eye o In the absence of permanent brain damage, it is reversible by giving the patient vitamin B1 o Serious impairments in STM and learning Liver damage (fatty liver, alcohol hepatitis, & cirrhosis)  Fatty Liver: characterized by fat accumulating in the liver; reversible with abstinence  Alcohol Hepatitis: inflammation and death of liver cells; reversible with abstinence and medical treatment; can cause death if were and without treatment; can be caused by means other than heavy drinking  Cirrhosis: inflammatory disease of the liver involving cell death and the formation of scar tissue o 8th leading cause of death by disease in the U.S. (~25,000 each year) o Only 10-20% of people with alcohol dependence develop cirrhosis o Not reversible; death occurs because liver fails to metabolize various toxins with accumulate in the body o Only 50% of people are alive 5 years after receiving the diagnosis Sexual dysfunction  Men o Gynecomastia: formation of breasts in men (shift in balance due to damage to the liver from alcohol and resorption of estrogen in the blood) o Loss in sexual desire & drop in sexual performance o Hypogonadism & sterility: reduction or absence of hormone secretion or other physiological activity of the gonads (testes or ovaries)  Women o Dysfunction of the ovaries o Disruption of the luteal phase of fertilization o Amenorrhea (cessation of menstrual period) Fetal Alcohol Syndrome  Falls into class of alcohol teratology (defined in biology as the study of monsters or deformities)  Symptoms: small eyes, small eye openings, drooping eyelids, underdeveloped mid face, skin folds across the inner corners of the eyes, underdevelopment of the depression above the upper lip, small head circumference, abnormal creases in the hand palm, abnormalities in the joints, cardiac defects, benign tumors consisting of dilated blood vessels, and minor ear abnormalities  Occurs in 0.2 to 1.5 of every 1,000 live births  Much higher among Native American and African American mothers of low SES  10 year follow up: low-normal to severely retarded intellectual functioning, physical deformities similar to those originally reported, & development of additional physical problems  No “safe” level of alcohol use during pregnancy has been determined 29. What about the consequence of moderate (1-3 drinks a day) drinking? a. Drinking can be healthful: Association between moderate alcohol use and cardiovascular health  Alcohol consumption increases the production of HDLs (high-density lipoproteins) which take damaging cholesterol away from artery walls b. French Paradox  Co-occurrence of a diet high in saturated fats and a low incidence of coronary heart disease  French consume the equivalent of one to two 4-ounce glasses of wine a day 30. Consider the theories of the etiology of alcoholism (biological, psychological & sociological). Biological Approaches  Physiological or structural anomaly causes the individuals to develop alcohol use disorder  Most prevalent position among U.S. treatment providers is that alcohol use disorder is a physical disease  Genetic factors may account for up to half of the variance in the etiology of alcohol dependence Psychological Approaches  Centered on identifying the alcoholic personality (psychological trait or set of traits that predispose someone to having alcohol dependence  Personality dimensions of neuroticism – emotionality, extraversion-sociability, and impulsivity-disinhibition predispose people to alcohol dependence Sociological Approaches  Proposed in repose to failure to discover the unique alcoholic personality  Findings of cross-cultural differences in drinking patterns  Demographic factors correlated with drinking patterns and problems Biopsychosocial Approaches: Alcohol, as well as drug use disorder, is caused and maintained by a combination of biological, psychological, and sociological factors 31. Is alcoholism a disease? a. Disease: clearly identified physical process that is pathological b. Once a disease is contracted, the afflicted individual has no control, or is not responsible, for the disease running its course c. The dominant position among U.S. treatment professionals, as well as Alcoholics Anonymous, is that alcohol use disorder is a disease 32. How is tolerance to alcohol related to ethnicity (note the Asian flushing response)? a. Cultural factors: in Japan and throughout Asia, moderate alcohol is valued and excessive drinking is not; alcohol linked to social and religious rituals; customs tend to discourage alcohol abuse b. Biological Factors: Asian Flushing Reponses  Occurs only in Asians  Physical reaction that occurs with drinking alcohol  Consists of cutaneous flushing, heart palpitations, tachycardia, perspiration, and headache CHAPTER 13: PSYCHOTHERAPEUTIC MEDICATIONS Intro**  Psychotherapeutic/psychotropic medication: exerting a special or unique action on psychological functioning  Four major classes: antipsychotics, antidepressants, antianxiety agents, and anti-manic/mood stabilizing drugs  Psychopharmacology: coined by David Macht, an American pharmacists, in 1920 1. How was mental illness treated prior to the advent of chlorpromazine? a. Pre-Chlorpromazine Era had little understanding of mental illness b. Many of the treatments were cruel (bloodletting, hot irons, flogging, revolving chairs, starvation, & sneezing powder) c. Emil Kraepelin, Phillippe Pinel, & J.E. Esquirol: believed that a scientific understanding and categorizing of mental illness were prerequisites to the identification of effective treatments 2. How did chlorpromazine (Thorazine) change our approach? a. Initially used at the Val-de-Grace military hospital in Paris  Agitated psychotic patients appeared calm following administration  Patients’ thoughts appeared to become less chaotic and the patients were less excitable  Patients did not exhibit any loss of consciousness, but rather a disinterested and detached demeanor b. Word of the successful use of chlorpromazine spread rapidly and was adopted throughout Europe and then the U.S. and the rest of the world c. Since 1955, the number of hospitalized psychiatric patients in the United States has decreased significantly d. In 1955, the figure was 600,000, and today, there are fewer than 150,000 hospitalized psychiatric patients, despite an increase in the general population 3. Consider the antipsychotic (American term) or neuroleptic (European term) drugs. What is the disorder they are designed to treat? a. Major approach to drug treatment of Schizophrenia b. Symptoms most likely to respond to antipsychotic medications are agitation, mania, hallucinations, delusions, fury, and accelerated and disorganized thinking processes (positive symptoms) 4. What are some of the major antipsychotic drugs? a. Thorazine (chlorpromazine) – launched a revolution that changed mental health across the world; became treatment of choice for Schizophrenia by the mid-1950s b. Mellaril (thioridazine) c. Haldol (haloperidol) 5. What is the mechanism of action for antipsychotic drugs? Dopamine hypothesis a. Psychosis is induced by increased levels of dopaminergic activity b. Most antipsychotic drugs block postsynaptic dopamine receptors c. Postsynaptic receptor blockade in the limbic system is thought to reduce the schizophrenic symptoms 6. What side effects are associated with them? a. Acute side effects: motor disturbances (block postsynaptic receptors in the basal ganglia)  Parkinsonian symptoms: tremor, blank rigidity, gait and posture changes, and excessive salivation  Dyskinesia: disordered movements  Akinesia: slowness of movement and underactivity b. Long-term effects (>2 years of use): tardive dyskinesia  Characterized by involuntary movements of the mouth and tongue, trunk, and extremities  Occurs among up to one-third of treated patients  Most of the symptoms are permanent  Incidence rates increase with age and with years of use of antipsychotic medications  Effects seen more among women than men 7. What about newer antipsychotics such as risperidone (Risperdal), olanzapine (Zyprexa), quetiapine (Seroquel) etc.? a. Called Atypical or Second-Generation Antipsychotics b. Focus is to develop neuroleptics that provide symptoms relief through a different mechanism & avoid or minimize side effects (especially tardive dyskinesia) of current antipsychotic medications c. Zyprexa: helps patients controls symptoms for a longer period of time, but has a higher risk of diabetes d. Risperidone/Risperdal: increased risk of diabetes e. Risperidone, quetiapine, olanzapine, and clozapine: increased risk of sudden death from cardiac arrhythmias and other cardiac causes f. Abilify: seeks to stabilize the dopamine system 8. Why are they becoming so popular? They show more positive outcomes and fewer/less severe negative side effects 9. What is depression? Differentiate between endogenous and exogenous depression. a. Most common psych disorders in the U.S. b. Vary in severity, duration, and frequency of occurrence c. Most common symptoms characterized as a depressive syndrome – dysphoric mood, loss of interest, disturbances in appetite and weight, sleep disturbance, fatigue, withdrawal, thoughts of suicide, and difficulties in concentration d. Endogenous: symptoms tend to be chronic and associated with genetic constitutional factors e. Exogenous: symptoms are thought to be in response to some situation or event 10. Consider theories of the etiology of depression. a. Postulated Biochemical Hypothesis: It is believed that depression results from a deficiency in biogenic amines, specifically catecholamine and serotonin, which act as CNS neurotransmitters b. Catecholamine Hypothesis: Depression results from a deficiency in catecholamines (particularly norepinephrine) at varied neuron receptor sites in the brain c. Serotonin Hypothesis: Depression is the result of a deficiency of serotonin in the brain stem; people who are depressed have reduced levels of serotonin and chemicals involved in its metabolism in their cerebrospinal fluid 11. What are the types of drugs used in the treatment of depression and how they are thought to work? In particular, be able to differentiate the MAOI's, the tricyclics, and the SSRI's. What are the side effects of antidepressants? MAOIs: Monoamine Oxidase Inhibitors  Used in treatment of tuberculosis in the 1950s  Used less frequently than cyclic antidepressants  Consistent with the Catecholamine Hypothesis o Enzyme monoamine oxidase metabolizes norepinephrine and serotonin o Inhibit this degradation process and enhance the availability of the transmitter within the neuron  Common Side Effects: drowsiness, dry mouth, dizziness, weight gain, insomnia, constipation, and fatigue, low blood pressure when changing position, and impaired sexual functioning  Requires dietary restrictions: avoiding substances that contain tyramine (most cheeses and some alcoholic beverages)  Overdose is not common Tricyclics  Refers to a specific group of antidepressants  Three-ring chemical structure nucleus  Investigated as antipsychotics in the 1950s  Antidepressant effects SSRIs (cyclic antidepressants)  Often treat symptoms of depression more effectively than the tricyclics and are associated with fewer side effects for many users  Most common – fluvoxamine (Luvox), paroxetine (Paxil), fluoxetine (Prozac), and sertraline (Zoloft)  Consistent with the Catecholamine hypothesis: produce immediate elevation in serotonin/norepinephrine  Absorbed readily through the gastrointestinal tract  Metabolism occurs primarily in the liver & excreted through urine  Common side effects: drowsiness, dry mouth, constipation, difficulty urinating, blurred vision, dizziness, decreased libido, weight gain, and tachycardia  Withdrawal symptoms: nausea, headache, insomnia, flu-like symptoms  Associated with a greater risk of bone breaks and an increased rate of bone loss at the hip (older women)  Overdose: coma, respiratory difficulties, and a variety of cardiac problems 12. Prozac and related SSRI's are today's most popular antidepressants. Why? a. Cyclics markedly alleviate depressive symptoms b. MAOIs, when compared directly with cyclics, tend to be less effective c. Led to a tendency for cyclics and the newer medications to be the treatment of choice for most depression d. MAOIs used when these do not produce desired results 13. Are there special issues for children? a. Effective in children and adolescents b. Possibility of suicide among young children (under 18)  Suicidal ideation and suicide attempts more common during first few weeks of SSRI treatment than in general population  2007, Bridge et al.: suggests suicide rates higher in untreated depression 14. Consider the effects of depressant drugs. What is meant by the terms anxiolytic; Sedative-hypnotic? General anesthetic? a. Anxiolytic: anxiety-reducing b. Sedative-hypnotic: the calming and sleep-inducing effects of some drugs c. General anesthetic: the reduction of pain by rendering the subject unconscious 15. What is nitrous oxide? How did it contribute to the discovery of anesthesia? a. 1776: discovered inhalation of nitrous oxide produced a short period of intoxication similar to drunkenness b. 1845, Hartford Connecticut: Horace Wells (dentist) – experimented with nitrous oxide and discovered that teeth could be pulled without pain c. 1846: Morton believed ether might make a better anesthetic i. Ether: highly flammable liquid that vaporizes at room temperature; when the fumes are inhaled, they produce intoxication ii. Gave the first public demonstration of surgical anesthesia 16. What are barbiturates? Consider their history and development. a. History  The first barbiturate was developed in 1862 in the Bayer laboratories in Munich, Germany  Barbiturate compounds are synthesized using, among other things, chemicals found in urine, and some say Bayer gave the drugs their name to honor a woman named Barbara who provided the urine samples (Barbara’s urates?)  Others claim the name was to honor St. Barbara, and there are other stories as well b. Class of depressant drugs (~50 out of 2000 available in the U.S.) c. Effects are similar, but differ in potency and duration of action d. Thought to act by influence inhibitory neurotransmission e. Current Uses  Short-acting barbs produce anesthesia  Emergency treatment of convulsions and prevention of seizures in people with certain types of epilepsy 17. Consider the physiological and psychological effects of barbs. a. Physiological Effects  Produce a drunken euphoric state in moderate doses (loss of coordination, staggering gait, & slurred speech)  Respiratory depression (responsible for most overdose deaths)  Depression of heart rate, blood pressure, & gastrointestinal activity b. Psychological Effects  Loss of emotional control  Behavior disinhibition c. Tolerance develops fairly rapidly to many effects d. Barbiturate withdrawal symptoms: shakes, perspiration, confusion, delirium tremons (convulsions and seizures more likely to occur) 18. What is rebound insomnia? After chronic use of barbs, abstinence produces insomnia even in someone who was untroubled with insomnia previously 19. REM rebound? a. Barbiturates reduce the amount of time spent in the REM stage of sleep b. Experience REM rebound when subjects try to sleep without a pill after taking it for several nights c. Spend more time than normal in REM (vivid dreams and nightmares with nocturnal awakening) 20. What are the other adverse effects associated with barbiturates? a. Barbs are somewhat more sedating and more likely to be abused than alcohol, although the effects are virtually the same b. Accidental overdose: lethal dose of many barbiturates if fairly low compared to the effective dose in inducing sleep i. Particularly when taken in combination with alcohol or other depressant drugs ii. Barbs have been a lethal drug in many suicides (i.e. Marilyn Monroe) 21. What is methaqualone? Compare it with barbiturates. a. Important candidate as an alternative to barbiturates b. Marketed under Quaalude and Sopor in 1965 c. Became evident that it was toxic at high doses, especially when taken in combination with alcohol d. Dependence develops rapidly, with abstinence symptoms similar to those produced by alcohol and barbs e. Has become a Schedule I drug (street use in 1970s under belief that it would enhance sexual performance) f. Replaced by benzodiazepines 22. What are benzodiazepines? Most widely prescribed anxiolytic drugs a. Animal tests showed sedative, anticonvulsant, and muscle-relaxant effects similar to those of barbs b. Additional feature is that they produced a “taming” effect in monkeys c. Showed low toxicity – the lethal dose is high/difficult to attain d. The first of the benzodiazepines, chlordiazepoxide (Librium), was first marketed in 1960  Closely followed by the introduction of its more potent cousin, diazepam (Valium) in 1963  These two drugs quickly came to dominate the market as treatments for anxiety and insomnia 23. Consider their mechanism of action. a. Common mechanism of action for all depressant drugs is GABA (brain’s most abundant inhibitory neurotransmitter) b. GABA/benzodiazepine receptor complex c. Benzos act by enhancing neural inhibition in the GABA system 24. How are benzodiazepines used in psychotherapy? a. Longer-acting benzos (i.e. Valium) are considered most useful for anxiety b. Short- and intermediate-duration benzos are more useful for treating insomnia when it is desirable to have the drug effects wear off by morning 25. Why are benzos preferred to other depressants? a. Effe


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