Substance Abuse Disorders (Psych 300) - Nov 7 PDF

Summary

These lecture notes cover various aspects of substance abuse disorders, including definitions, types, effects of various substances, historical perspectives, statistics, and complications. The document also discusses different perspectives on addiction, including biological, psychological, and socio-cultural factors. The document is geared towards an undergraduate psychology course.

Full Transcript

Addictive disorders: Nov.7 What is a substance? Any product that has a psychoactive effect. Could be natural(shrooms) or synthesized. Substance: Any product that has psychoactive effects. Damage: Changes in Perception Thoughts emotions behavi...

Addictive disorders: Nov.7 What is a substance? Any product that has a psychoactive effect. Could be natural(shrooms) or synthesized. Substance: Any product that has psychoactive effects. Damage: Changes in Perception Thoughts emotions behaviours Substance induced disorders: DSM5 1. Substance induced 2. Substance intoxication (excess substance in bloodstream) 3. Substance withdrawal (physio and psychological reaction when at once stop intake of substance dependent on) Substance use disorders: What? Recurrent use of a substance(s) that create significant problems. Cluster of symptoms to indicate the continued use. o 10 classes of drugs o Activation of brain reward system direct or indirect (drugs all have this in common) – artificial pleasure **No absolute quantity signifies addiction instead talk about level of impairment (impairment criterion) How to diagnose? In DSM5: 1. Control impairment Uses drug longer/more than intended (ex: use of opioids) Unsuccessful effort to stop or reduce use Time devoted to substance (hours spend buying the drug) Intense desire for drug 2. Social impairment Failure to fulfill major roles (working, studying…) Continue use despite damages to life and body (losing job, damaging organs) Important activities given up, birthday party…) Substance use disorder: 1. Risky use In situation where hazardous physically In situation in which worsen conditions physically and psychologically (exacerbation = making situation worse) 2. Pharmacology criteria a. Tolerance: increased/decreased dose b. Withdrawal: symptoms from stopping/reducing drug use Severity: What factors change the severity of disorder? 1. Route of administration Faster routes of administration are more addictive (sniffing or smoking) 2. Duration of effects Shorter duration of effects causes more addiction (cocaine effects leave faster) 3. Multiple substances Use of multiple substances increase serious problems Complications: What factors create more complication with addictions? Sedating drugs – depressive disorders Stimulants- psychotic disorders and anxiety disorders Health- need related diseases Aggressive behavior- addiction brings out tendencies for aggressiveness Accident-related injuries – being hit by a car, falling Suicide Fetal problems **3.8% of Canadians may have substance use disorders 3 terms: distinguish the difference 1. Use: consider impairment medically, psychologically and socially 2. Intoxication: over use of drugs where harm to body 3. Substance use disorder: recurrent use of substances despite problems it creates. Cluster of symptoms that indicate. Alcohol: Nov.14 Most frequently abused substance. 10 chemicals considered most abusive but most abused is alcohol. Historical perspective: Goes back to poliothic time Only 3 Stone Age groups survived without use of alcohol Fermented grape, honey juice (wine and beer) Ancient Greek, Egypt Long used medicinally but also in abuse Drunkenness is described to forget misery and pain Mesopotamia described ways of becoming sober Process of distillation of alcohol in Saudi Arabia for medicine and religious ceremonies 1700s became drug abuse Always tried to deal with drunkenness. 1800s-1900s perspective on alcoholism as a moral defect (not good) 1940s-60s psychodynamic model (marked by anger due to love object) 1950s disease model (may be allergic) 1960s-70s behavioural model (not a moral defect but basic learning principles that learn to drink due to modeling, positive/negative reinforcement) Contemporary models: bio, psycho, social factors why people drink and develop alcohol disorders Statistics: alcohol consumption 66% consume alcohol (11% increase over decade) More likely younger Live in cities and suburbs 9% alcohol disorder (above risking drinking) Men > Women in risking drinking (exceed low risk) Consumption patterns: 1. Age Dependent on age onset (18-24 highest consumption) People who drink younger interfere with brain wiring Into 30s drinking decreases due to physical reasons **alcoholics continue drinking disregarding age 2. Culture Asian low consumption Indigenous high consumption Religions (Islamic rule out alcohol consumption) 3. Gender Men drink more (women catching up) Clinical picture: 4 different pattern impact alcoholism and can be changed: Dependent on motivation/personality: 1. Anxiety sensitivity 2. Hopelessness 3. Impulsivity (drink impulsively without reason) 4. Sensation seeking (sensation of intoxication) Onset: 1. Early onset risk of greater abuse (age 11-12) Course: (men and women different) Men: ▪ First hospitalization occurs in 30s (brain condition) ▪ Retired men (burst of alcohol use) ▪ High remission (return to alcohol use) Women: ▪ Lower metabolism of alcohol. Why? Higher fat, lower water. ▪ Result: higher risk of damage ▪ Problem: alcoholism occurs later, mood disorders precede alcoholism. ▪ Lower remission (lower rate of return to alcohol use) Mechanism of action: How alcohol works in the body? Impact of neurotransmitter effect. GABA agonists. What? Increases GABA (normal functioning down regulated) and effects other neurotransmitters. **GABA = inhibitory system (slows down function of brain) How? o Down regulate Glutamate (ex: binge drinking, fast drinking) **glutamate = excitatory system o Low effectiveness of serotonin o Increase dopamine signalling (indirectly by influencing other neurotransmitters) Body organs: effected Liver (metabolizes) Heart (breathing) Brain Kidney Intestine Blood alcohol level: (BAL) Standard unit of ethanol = 0.5 oz Conversion: 1. Half pint of wine (5% alcohol) 2. 1 oz hard liquor 3. 5oz wine What factors effect? 1. Weight (heavier=higher toleration of alcohol) a. Less water = longer effect b. More fat = longer effect **females have higher fat, lower weight = less alcohol greater intoxication 2. Speed of drinking (quicker=more intoxicated) Effects of alcohol: **2 drinks women, 4 drinks men Complications: 1. Health related: a. Acute effects: Respiratory suppression Hemorrhagic pancreatitis Asphyxia (suffocating on own vomit) Withdrawal Alcohol withdrawal: GABA receptors desensitize (inhibitory system) Glutamate over excitation and cell death Mild = shaking Moderate (12-24 hrs) = hallucinations visual, auditory, or tactile (tangible) Severe (24-48 hrs after final drink) = heart palpitations and seizures b. Chronic effects Complications (chronic effects): 1. Gastrointestinal 2. Liver a. Fatty liver b. Hepatitis c. Cirrhosis (scar tissues) 3. Cancer (mouth and throat) 4. Chronic neurological problems a. Wernicke-korsakoff encephalopathy (most common) ▪ Due to thiamine deficiency ▪ Confusion, visual problems ▪ Confabulation (memory not working well, filling gaps) ▪ Alcohol and bad nutrition b. Alcohol induced dementia (loss of memory) c. Peripheral neuropathy (hand shaking) d. Fetal alcohol problems (damage fetus, slower development) Treatment of alcohol withdrawal: What is the first line treatment? 1. Benzodiazepines (copy function of GABA) **ethanol not effective why? Can’t iterate appropriate amount of ethanol. Other options: 1. Acamprosate (different function) GABA agonist Less addictive Control excitotoxicity when alcohol withdrawal Social complications: Accident related (43% drinking driver fatalities) Legal (50% of convictions have high alcohol use) Social (higher rate of divorce and job loss) Economic costs (BC cost of alcohol problems $2billion) Alcoholism Etiology: What are the multiple factors of alcoholism? 1. Biological 2. Psychological 3. Socio-cultural environment 1. Biological: a. Genetic factors: Family studies all support a heritability component. b. CNS circuits: Pleasure pathway: what? A circuit of dopamine receptors. Substances inhibit GABA therefore indirectly increase activity of dopamine. (Reward center) Genetic perpendcity. Alcoholics carry DRD2 gene which regulates dopamine receptors 2. Psychological influences a. Learning: behavioural perspective positive reinforcement – reward center, being together Ex: drinking with friends Negative reinforcement – reduce negative emotions (anxious, depressed) Conditioning effects – neutral stimuli paired with pleasure arousing stimuli will cause neutral stimuli cause burst of pleasure (ex. Environment of a bar burst dopamine) b. Cognitive: Expectations of what will happen when consume alcohol. Ex. Believe by consuming alcohol you are able to do things you can’t do without them Research: 1. how you expect alcohol to effect you affects your judgements. (Action towards rape, less aggressive if think drinking) c. Social modelling Drinking habits of others influence one’s (UBC pit pub) 3. Socio-cultural influences Religions bans drinking Some cultures normalize heavy drinking on certain occasions Media and ads of alcohol use reasons to promote (ex. find a mate by drinking Bailey’s) Other drugs of addiction: What are functions of Opioids? Pain management and reduction. Drugs with opioids: Opium (opus = sad) Morphine = (Morpheus = god of sleep) powerful opioid used in hospital highly addictive Withdrawal problems: ▪ Depression ▪ Heart attack ▪ Shaking of the body ▪ Nausea Codeine = 2nd most active in opioid, addictive Heroine = highly addictive, sudden rush of pleasure, fatality due to suppression of respiratory system Methadone = heroine agonist, little addictive, lower pleasure Oxycontin = believe incorrectly not addictive, many OD, many initially received prescription, very expensive therefore switched to heroine Fentanyl = illegal in Canada, highly addictive **not everyone becomes addicted to opioids Clinical picture: 1. Onset: o Prescription of pain killers (37% Canada ) o Late teens and early 20s **some hospital workers at risk of use. Why? More accessible 2. Gender o Men > Women 3. Culture o High in indigenous people. Epidemiology: How spread? 12% Canadians BC, Ontario, Alberta highest rates Most injected Recreational use for college students Mostly chronic (long term) Complications: What are problems that rise from opioids? 1. Depression/dysthymic 2. Legal crimes: stealing, forging prescriptions 3. Health: HIV/AIDS – injection drugs BC highest rate Hepatitis Skin scarring (veins destructed, inject in different areas, accidentally inject in muscle and lose muscles) Death (mostly for men use fentanyl) Why mostly men? The way men are growing up (social factors) Hallucinogens: What is its function? Chemicals that alter sensory experiences. Reactions? Initial reaction (while intoxicated) – not dangerous Ongoing reaction – sensory perception altered (flashbacks) General facts: Illegal in Canada (unless medically needed) More likely in young men Clinical trials: A. Study: **exclude ps of family history with schizophrenia or psychosis Small studies B. Psychosis: Taking hallucinogens have higher rates of psychosis diagnosis. C. Schizophrenic-spectrum disorder: Taking hallucinogens vulnerable for schizophrenic spectrum disorders within 3 years. o Alcohol vs. Cannabis Higher rate of psychotic disorder with alcohol users greater than cannabis users. Overall: ▪ Cannabis- lower vulnerability for psychosis (x1.5 chance) ▪ Hallucinogens- high vulnerability for psychosis (high risk) ▪ Alcohol – medium vulnerability for psychosis (x5 chance) Clinical implications: Believe must be legal (human freedom) Problem: high cost of health Find a hallucinogen that is safe in future (hallucinogen facilitated therapy) Cannabis: How does it function? Brain produces endocannabinoids. **endo = organic Cannabis steals the internal systems. Endocannabinoid system: Regulate many functions of the brain. Learning Memory Sleep Emotion Eating Two receptor types: 1. CB1 = control levels of other neurotransmitters. (Densely packed receptors) 2. CB2 = modulates pain and immune system. Prevalence of cannabis: Response to drug, weed, research. High in young adults Many chemical compounds in a plant (weed = 400 different chemical compounds) Type of active chemical: 1. THC – high inducing 2. CBD – anti-inflammatory Synthetic compounds: CB1 used mostly in research. Response: Varies in different people. THC: Low dose = pleasant effects Produce panic, paranoia, dizziness. Eating and smoking. Cannabis use disorder: DSM-5 Heavy use for at least one year 2 symptoms of substance use disorders (aggressiveness …) Not as addictive (dependence use) Impairment: Tolerance Withdrawal (sleep, appetite, restlessness and irritability) School/work impairment Dopamine reactivity decrease – Amotivational syndrome (not motivated to do activities) Smoking – respiratory problems MVA Schizophrenia (worst impairment) – higher vulnerability to developing by use of cannabis o Genetic history of psychosis- increase vulnerability **mechanism unclear (neurological wiring disrupted) Biological treatments: substance use disorders 1. Antagonist treatments: Naloxone: how it works? Cause opioid withdrawal by blocking the receptors. ▪ Blocks effect of Heroine ▪ Stop OD ▪ Last 30-60 min (if very addicted may need +1 dose) Naltrexone 2. Agonist treatments: Buprenorphine – partial agonist and antagonist **can be combined with naloxone 3. Acamprosate – regulate GABA Protective against alcohol withdrawal effects of alcoholism 4. Aversion treatment: (no longer used) Disulfiram for alcoholism (cause feelings of illness) Sometimes use electrical shot (cause pain) **many drop out 5. Anti-anxiety and anti-depressant drugs: If drinking due to anxiety/depression use SSRIs. Psychosocial treatments: 1. Narcanon/alcoholics anonymous: unable to use the substance allergic to alcohol religious ideas to trust higher power **high drop out 2. Residential treatment centres: Very expensive No more effective that outpatient treatment Used to detoxify use of drugs (alcohol …) Behavioural and cognitive treatments: 1. Learning principles: Self-control strategies Situation management 2. Controlled drinking: **controversial because didn’t have control group Learn to control how much drinking 3. Relapse prevention: Problem: Many can stop using drugs for some time but relapse Doesn’t prevent use permanently Behavioural addiction: Nov.21 Engaging in behavior that is harmful but continue behavior. Gambling disorder: First behavioural addiction recognized was gambling addiction. Activate same brain reward systems as pharmaceutical. Many cognitive dysfunctional beliefs Gambler’s fallacy (believe if three heads next one is ——) Hot hand fallacy (after one success will follow more success) Near wins (believe very close to a win so continue gambling) Illusions of control o Anthropomorphism = feeling of having a relationship with gambling machine Internet gaming disorder: What? Preoccupation and excessive use of internet. How? Experience a pleasure by gaming. Their tolerance increases therefore need to game more to receive the same amount of pleasure. To diagnose must have some sort of impairment. (Ex: social, job, educational) ** very common in china What is an addiction? Controversy 1. External substance Strong effect on reward/pleasure circuits Biological adjustment, tolerance and withdrawal 2. Behavioural addiction Compulsion to repeat rewarding behavior despite negative consequences Sex addiction? Hyper-sexual disorder: Recurrent sexual activity due to anger and stress. Dependent on pornography. Tolerance increases (need more stimulation to reach arousal) 1-2 hours/day Involved in compulsive masturbation, telephone sex and cybersex. Complications: STDs Relationship disruption Unwanted pregnancies How much is too much? Addiction? Not enough scientific research. (No information on genetics, developmental factors nor clinical course) But engage in pleasurable activities that can be harmful.

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