Exam 2 Study Guide Drugs and Individual Behavior
Exam 2 Study Guide Drugs and Individual Behavior PSYCH 3102
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This 8 page Study Guide was uploaded by McKenna Keck on Friday October 7, 2016. The Study Guide belongs to PSYCH 3102 at University of Northern Iowa taught by Dr. Linda Walsh in Fall 2016. Since its upload, it has received 29 views. For similar materials see Drugs and Individual Behavior in Psychology at University of Northern Iowa.
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Date Created: 10/07/16
Drugs & Individual Behavior Exam 2 Study Guide Barbiturates & Benzodiazepines ● Prescription Depressants: barbiturates, benzodiazepines ● General characteristics of general CNS depressants: Additive or synergistic interactions w/ other depressants, crosstolerance & crossdependence, low doses may appear stimulating b/c of depression of inhibitions (depression of prefrontal cortex), GABA agonists, cognitive inhibition, hyperexcitability rebound afterwards, & potentially dangerous withdrawals. ○ Dosedependent depression of CNS & behavior; disinhibition: The response you get depends on the dose you take. From littlest dose to highest dose, you may experience calming, relief from stress & anxiety, disinhibition, intoxication, slowing, sedation, sleep, anesthesia, coma, death due to respiratory depression. The prefrontal cortex is acted on first, & the medulla last. ○ Primary action on GABA (how does it affect GABA?); high dose effect on glutamate: All CNS depressants are GABA agonists, increasing GABA’s effects. This causes a lot of cognitive parts of your brain to be inhibited. They also decrease the excitatory actions of glutamate. ○ Withdrawal characterized by hyperexcitability rebound: basically, you experience the opposite effects of the drug to an exaggerated degree. It’s how your body tried to compensate for the constant dose of the drug. ● Types or categories of drugs which qualify as CNS depressants: barbiturates, benzodiazepines, alcohol ● Medical use terms used to refer to depressants: Sedatives, Hypnotics (sleeping pills), Minor tranquilizers or antianxiety or anxiolytics, Anticonvulsants/antiepilepsy, Anesthetics ● NOTE: narcotic analgesics & major tranquilizers/antipsychotics are not in the pharmacological category CNS depressants, even though they have some sedating effects ● Common reasons for medical use of depressants; reasons for street/recreational use of depressants ○ Medical: Tranquilizers, Sleep Aid, Anesthetic, Muscle Relaxer, Emergency Sedation, Alcohol Detox, Antiseizure ○ Street: Intoxication ● Barbiturates (CNS Depressant) ○ Subcategories (how are barbs grouped?) & examples ■ Barbs are categorized by their length of action. ● Ultra short (minutes, because of redistribution). These are what they give you when you get your wisdom teeth out. The drug is quickly taken to other fatty parts of you body so it doesn’t affect your brain anymore. ○ Example: sodium piothental ● Short <4 hrs. These are the most abused barbs. ○ Examples: secobarbital, pentobarbital ● Intermediate 46 hrs ○ Example: amobarbital ● Long >6 hrs ○ Example: phenobarbital ○ Common effects (what might someone under the influence of barbs look like?): very similar to the effects of alcohol intoxication. You probably wouldn’t be able to tell much of a difference. ○ Adverse or less than desirable effects (why aren't barbs very desirable antianxiety or sleepinducing meds?): they aren’t selective, so you can’t take them to get just one desired effect. You’ll get them all. VERY low safety margin, really quick tolerance, there’s no antidote to overdose, interacts dangerously w/ other depressants, risk of dependence, possibly life threatening withdrawal, decreased REM sleep, memory & cognition impairment, possible birth defects (though the mother usually stays on her medication because it would be more dangerous for the baby if the mom had a seizure) ○ Risks: ■ Overdose: very low safety margin. Easy to overdose & cause lethal depression of breathing. Used frequently in suicides & lethal injections. ■ Characteristics of withdrawal: hyperexcitability rebound (the opposite of the drug’s effects). This can cause withdrawal to be very dangerous. Specific effects discussed under each drug family. ● Some wellknown "nonbarbiturate" sedativehypnotics: created because there were so many problems w/ barbs & they wanted to make something better. Several drugs were released claiming to be big improvements over the barbs (but they turned out not to be better). It just wasn’t the improvement they claimed it was. One after another have been removed from the legal market. ○ Examples: Meprobamate (Miltown), Methaqualone (Quaaludes, Sopor) ● Benzodiazepines (CNS Depressant) ○ Subcategories & examples: ■ UltraShort sodium thiopental. Lasts only minutes due to redistribution. ■ Short secobarbital, pentobarbital. <4 hours ■ Intermediate amobarbital. 46 hours ■ Long phenobarbital. >6 hours ○ Characteristic effects; action on GABA receptors: increase the calming effects of GABA (sometimes called BZRAs: benzodiazepine receptor agonists) ○ Comparison w/ barbiturates (why were benzodiazepines an improvement?): Benzos are more selective (you can take them for anxiety & not get too many of the other effects), sleep is a little more normal, withdrawal is less dangerous, there are 2 antidotes to an overdose on them, they have a much wider safety margin, & they come w/ less tolerance & dependence ○ Medical uses (today): you might take a short acting benzo if you need a sleep aid but don’t want to wake up groggy. You might take a long acting benzo to control seizures, muscle spasms, if you’re going through alcohol detox, or if you have an anxiety disorder that bothers you all the time. ○ Potential adverse effects: effect on driving (similar to driving under the influence of alcohol. It’s not safe to drive while under the influence of a benzo), effects on memory (memory & cognition are both impaired), potential idiosyncratic responses (especially in the elderly), Prenatal effects (typically in the 1st trimester), significant risk of dependence, & potentially dangerous withdrawal. All benzos are controlled substances. ■ Misuse & abuse & overprescription: from the 1960s1990s they were the most widely prescribed psychotherapeutic drug. These are controlled substances & have a risk of being abused. ■ Decreased REM sleep & morning grogginess (though not as bad as barbs) ○ Special risks in elderly: over response common (you often need a lesser dose for them), idiosyncratic responses possible, & brain damage possible in people w/ personality or impulse control disorders ○ Use in sexual assaults (Rohypnol & others): “Roofies” contain a high potency benzo not marketed in the US, but really if you’re drinking alcohol, any similar benzo would do the same thing. It impairs the consciousness & the memory of the victim. There are now some creative ways to check your drink for drugs, such as a nail polish you can dip in the drink. ● Flumazenil (Romazicon) benzodiazepine antagonist: one of the antidotes to a benzo overdose. It’s short acting, so it needs to be readministered ● Why certain benzodiazepines are selected as hypnotics: They don’t suppress REM sleep as much as barbs do, & they have a wider safety margin ● New drugs for sleep: ○ zolpidem (Ambien): Mostly hypnotic & amnesic effects w/ little antianxiety, anticonvulsant, or muscle relaxing effects. More normal sleep, less insomnia rebound. Halflife 2 hrs; shortterm use only. ○ zaleplon (Sonata): halflife > 1 hr, so can be taken in middle of night (about 4 hour effect) ● Use of benzos for anxiety: now getting replaced by antidepressants & other drugs w/ fewer risks. You might take a long acting benzo if you have an anxiety disorder that bothers you all the time. ● New drugs used for anxiety ○ buspirone (BuSpar) & its advantages & disadvantages: Selective 5HT1A agonist. It’s for antianxiety but isn’t a CNS depressant. Delayed (24 weeks) antianxiety action without sedation, incoordination, memory problems, depressant interactions, dependency (good for those w/ abuse risk or drinking problem). May not be as effective for panic disorder. Side effects: headache, dizziness, nausea Alcohol ● Types of alcohol: ○ Beverage alcohol (ethanol) ○ Rubbing alcohol (isopropyl) ■ Also in window washing fluid, antiseptics, & aftershave) ○ Methanol (common industrial/chemical form of alcohol, like in Antifreeze) ● Production of alcohol (fermentation, distillation, proof) ○ Fermentation: the action of yeast on a sugary mixture (can also come from starches when they are first turned to sugars). Yields a max of a 15% alcoholic beverage (it can’t get any higher because the alcohol eventually kills the yeast) ○ Distillation: a method to produce stronger spirits. Alcohol boils at a lower temperature than water does. If you boil it off & collect it as it evaporates, you’ll get a less diluted mixture. Distilled spirits can get up to 40%. ○ Proof: 2x the % ● Alcohol concentration of typical beverages: regular beer (5%), malt liquor (7%), table wine (12%), fortified wine (17%), brandy (40%), 80 proof spirits (40%) ● Congeners: a slew of different chemicals that are a byproduct of the way the alcoholic beverage was produced. For the most part, they’re naturally occurring, but they could be synthetic ○ Other alcohols, oils, & organic substances added or formed during the production of an alcoholic beverage ○ Congeners give these beverages their distinctive color, odor & taste ○ Congeners are 1 of the factors influencing hangover ○ Highest in congeners: bourbon, scotch, brandy, tequila, red wine, dark beers. Lowest: vodka, gin, white wine. ● Factors affecting absorption of alcohol: ethnicity, gender, stomach contents, alcohol concentration, carbonation, drug interactions ● How alcohol is metabolized: In males, about 15% of alcohol can be metabolized in stomach before it’s even absorbed; women may have half as much metabolized here. ○ There are other things besides gender that play a role, for example, ethnicity can. ○ The rest is metabolized in liver about 1 standard drink/hr by a healthy liver ■ alcohol dehydrogenase: (enzyme in liver) converts alcohol into acetaldehyde ■ Acetaldehyde: a rather nasty byproduct (toxic substance that our liver must also metabolize. Contributes to hangover symptoms) ■ aldehyde dehydrogenase: breaks down acetaldehyde into acetic acid. Acetic acid is oxidized into oxygen, carbon dioxide, & calories ● Pharmacological action of alcohol ○ CNS depressant ○ GABA facilitator ○ glutamate inhibitor ○ augments transmitters related to mood (5HT) & reward system (DA) ● BAC & how BAC relates to the behavioral & bodily effects: Blood alcohol content. The higher the blood alcohol content, the more significant the depressive effects. Our legal limit is .08. ● Behavioral/psychological effects of alcohol ( e.g. effect on inhibitions, memory, emotional control, aggressive behavior): Dilation of blood vessels in skin leading to a warm flush (but a drop in core body temp), increased urination & dehydration, gastric irritation. Enhances GABA, blocks glutamate, release of 5HT, DA, endorphin & anandamide producing rewarding/mood elevating effects. Impairs judgment & selfcontrol. Also, how we expect it to affect us plays a role in how it affects us. ● Involvement of alcohol in various crimes: Cognitive inhibition + disinhibition of behavioral/emotional control = dangerous combo. Alcohol is involved in: 50% of police arrests, 5060% of murders, 40% males committing sexual assault, 6070% males committing domestic abuse, 60% of child molestation & abuse, & 35% of suicides. ● Causes of hangover symptoms: mini withdrawal from alcohol (hyperexcitability rebound), toxic reaction to congeners, toxic reaction to alcohol & its byproduct acetaldehyde, & fatigue, hypoglycemia, loss of vitamins, etc. due to partying. ● Adverse effects of long term heavy use of alcohol: Nervous system dysfunction & brain damage affecting memory, motor function; alcoholic dementia; Fatty liver; alcoholic hepatitis; cirrhosis; Impaired reproductive functioning (alcoholic impotence, suppression of ovulation, etc.); Gastritis pancreatitis; Co Carcinogen increasing risk of oral, throat, stomach, intestinal, liver & possibly breast cancers. Increases cancer risks of smoking; Impaired immune function; Fetal Alcohol Spectrum Disorders (if pregnant) ● Adverse effects on fetus: Fetal Alcohol Spectrum Disorders ○ 2,600,000 alcoholexposed US babies/year! ○ May be subtle or severe depending on degree & timing of exposure ○ 3rd most common cause of birth defects, retardation & learning disabilities (and the most preventable) ○ Seen in 3050% babies born to alcoholic mothers, but symptoms may also be seen w/ as little as 2 drinks twice a week. ○ Binge drinking particularly damaging ○ Partial symptoms = FAE or ARND ■ Babies are usually smaller than usual (less than 5lb) ■ Smaller heads, smaller brains ■ The brains are typically very abnormally developed ■ Nervous system affected ■ Sometimes facial structure changed… still cute, but very consistent ● Characteristics of Fetal Alcohol Syndrome: Babies are usually smaller than usual (less than 5lb). Smaller heads, smaller brains. The brains are typically very abnormally developed. Nervous system affected. Sometimes facial structure changed… still cute, but very consistent. Possible mental retardation or learning disorders. ● Alcoholdrug interactions: especially dangerous with other depressants. Can be additive, but is typically synergistic & unpredictable ● Effect of alcohol overdose: Symptoms include: Stuporous or unconscious; can’t be roused; Cool or damp skin; pale or bluish skin; Shallow slow or irregular breathing <8/min; Vomiting while unconscious; & Weak rapid pulse. Can be fatal or cause brain damage ● Withdrawal syndrome: Without the depressant you are overstimulated by the “hyperexcitability rebound.” Symptoms include: Tremors; Agitation, anxiety; Insomnia (if you do sleep, vivid nightmares); Sweating, nausea, vomiting; Increased HR & BP; Delirium tremens; Seizures ○ Delirium tremens: Alcoholic hallucinosis ○ Possible lethal effects of withdrawal: Grand mal seizures in about 10%, usually 1248 hrs after last drink but may be sooner if susceptible ● Pharmacotherapies for alcohol withdrawal: ○ During Detox: Use of another depressant to gradually withdraw individual & to try to avoid seizures (gradual is easier than cold turkey) ■ Examples: Benzos like Librium, Ativan, Valium, or another anticonvulsant ○ After Detox: ■ AlcoholSensitizer Antabuse (disulfiram) (Ethanol is metabolized into acetaldehyde, but not into acetate) ■ Various anticravings Drugs ● Narcotic antagonists: Revia (naltrexone) blocks opiate receptors, so if you did drink, you wouldn’t get the pleasurable effects due to the release of endorphins both oral & extended release injection available ● Campral (acamprosate) helps restore GABA balance & blocks glutamate ● Antidepressants (most of the SSRIs) antidepressant, antianxiety effects ● Anticonvulsant mood stabilizers (topiramate, valproate, gabapentin) are looking promising Amphetamine & Cocaine ● Cocaine (source, forms, routes of administration) ○ History of cocaine use: coca leaves (from which cocaine is extracted) have been traditionally chewed for centuries in cultures like the Maya & the Inca. Still used today for religious ceremonies. It’s an ancient drug. ○ Routes of administration: oral ingestion, through mucous membranes, smoked, injected ○ Mechanism of action of cocaine: blocks reuptake of DA, 5HT, NA, & NE. Makes you feel good. ○ Effects on body: local anesthetic when applied topically, vasoconstrictor, increases heart rate & blood pressure, pupils dilate, they mimic the sympathetic nervous system, psychostimulant, blocks reuptake of DA, 5HT & NE ○ Behavioral effects: everything is “more” because of the excess DA, 5HT, NA, & NE. You have more energy. ○ Time course: shorter than amphetamines. Oral ingestion (20 minutes to take effect), through mucous membranes (35 min to take effect), injection (30 sec to take effect), inhalation (8 sec to take effect). 30 to 40 minutes altogether. ○ Risks w/ longterm or high dose use: gangrene skin, infections because of dirty needles, sensitization so you could suddenly have a really intense reaction to it, a lot of dental issues, depression, weight loss, malnutrition, bruxism, stroke, heart attack, seizures, etc. ○ Cocaine psychosis: hallucinations & paranoia you feel when you’re coming down off the drug ○ Adverse effects (both physical & psychological/behavioral): weight loss, your body is totally exhausted, nutrition issues, hallucinations, involuntary muscle contractions, paranoia, severe depression, sleep problems ○ Effects on fetus: vasoconstriction can keep the baby from getting enough blood, oxygen, & nutrients. They tend to be underdeveloped. The level of the drug is the same in the fetus as it is in the mom. The same risks apply. ● Amphetamines (source, different types, routes of administration) ○ History of amphetamine use: ■ Developed as a synthetic substitute for ephedrine (1927) for asthma ■ Was sold as OTC asthma inhaler Benzedrine ■ Pep pills used worldwide during WWII; still used by armed forces today ■ Became a prescription drug in 1965 because of growing abuse, then a “Controlled Substance” in 1971; new wave of meth popularity began in 1990s ○ Similarities to & differences from cocaine: when first administered, even experienced users would have a hard time telling a difference between them if the same doses were administered by the same route. The effects of amphetamine just last longer. You just don’t get the same degree of stimulation from amphetamines as you do from cocaine. Similar withdrawals. Similar health risks with prolonged use. ○ Mechanism of action: Amphetamines make DA & NE more available at synapses by triggering their release & decreasing reuptake. ○ Body effects: pretty much same as cocaine ○ Behavioral effects: pretty much same as cocaine ○ Risks w/ long term or high dose use: tolerance, potential dependence, heart attack, stroke, appetite suppression, motor tics, insomnia, dental issues, heart problems, etc. (same as cocaine) ○ Amphetamine psychosis: hallucinations, like amphetamine “bugs” ○ Withdrawal symptoms: serious lack of energy, depression, serious suicide risk, anhedonia, headache & stomach pain followed by hunger rebound, cravings. Not physically life threatening, but emotionally life threatening ○ Medical uses & pros & cons of such use: ■ Treatment of ADHD & its variations (including in adults) ● Pros: Allows the individual to better use their frontal lobe to control their behavior. Very effective in 7080% of users (more effective than intensive behavior therapy). Extremely welldocumented. ● Cons: Not a “cure.” Risks include: stomach ache, headache, jitters, dizziness, appetite suppression, delayed sleep onset, growth reduction, motor tics, heart attacks, stroke, & sudden death. Risk of being abused. ■ Treatment of narcolepsy, shiftwork sleep disorder, daytime sleepiness caused by sleep apnea ● Pros: Helpful in maintaining wakefulness ● Cons: Risk of being abused. Multiple health risks (see ADHD Treatment Cons) ■ Shortterm adjunct to weight loss programs ● Pros: Suppressed appetite effectively ● Cons: Weight loss not sustainable unless additional behavioral changes are made. Multiple health risks (see ADHD Treatment Cons) ○ if you died from cocaine or amphetamine abuse, what are the likely causes of death: it’s likely in an overdose that your heart would be beating so fast & working so hard, but not pumping enough blood, that it would basically fatigue & shut down. The same could happen with your lungs. Caffeine & Other Xanthines ● Use of caffeine & related substance in US & worldwide: because some countries don’t use alcohol, it’s the widest used drug ● products that contain caffeine: ○ Chocolate, coffee, NoDoz, Decaf coffee (still contains some caffeine), some allergy medications, tea, soda ● examples of other xanthines: theophylline, theobromine ● common effects of caffeine & related compounds (dose dependent) ○ 1) on the body: increased heart rate & blood pressure, release of adrenaline, increase salivation & GI secretions, bronchodilation & increased respiration, increased metabolism & increased temperature, increased urination, constricts blood brain vessels & dilates other body blood vessels ○ 2) on behavior/psychological functioning: increased wakefulness, decreased fatigue, increased attention, decreased boredom, mild mood elevation, increased motor activity, increased response to sensory stimuli, shortens reaction time, some kinds of simple repetitive tasks are improved, but fine motor control & more complex tasks might be worsened or not improved. ○ 3) on the brain (how does it work, brain chemicals affected & how, where does it exert its effects): block receptors for natural calming/sleeppromoting neurotransmitter adenosine, normally adenosine helps dilate blood vessels, slows heart, makes us sleepy, decreases body temp, constrict bronchioles, blocking adenosine causes the opposite effects ● Characteristics of caffeine absorption, distribution, metabolism & halflife: significant absorption in 1520 min, 99% in 45 min. Easily produces tolerance. Half life is 310 hours in most adults (varies a lot). Longer halflife in newborns, elderly, pregnant, & those on birth control pills or SSRIs. Shorter half life in smokers also. ● Medical uses for caffeine & related drugs & how these relate to body effects: headache relief, cardiac stimulant, respiratory stimulant, antiasthma, additive in some sedating medications, analgesia enhancer. Could lower risk of heart disease, inflammation, stroke, Type 2 diabetes, Parkinson’s, Alzheimer’s, gout, liver disease, etc. ● Positive & negative effects on performance: shortens reaction time, better performance on simple tasks, poorer performance on complex tasks ● Excessive dose effects (caffeinism): Restless, anxious, irritable, agitated, panic attack in some, insomnia, Muscle tension & tremors, Rapid, sometimes irregular heartbeat, Flushed, hot & sweaty, Sensory disturbances, Usually occurs at dose > 600 mg but depends on individual’s sensitivity, Normal dose may produce these in someone on the SSRIs mentioned earlier, Extreme overdose → seizures; symptoms of psychosis ● Possible health (including mental health) risks ( & degree to which there is evidence for those risks): Mostly you’re at risk if you have a preexisting condition. May increase blood pressure in those prone to hypertension, may aggravate ulcers or heartburn due to gastric reflux, May trigger or increase panic attacks in some, worsen generalized anxiety disorder symptoms. May cause sleep problems. ● Risks to fetus or pregnancy; effects during nursing: High doses may increase risk of miscarriage, stillbirth, or decreased growth of fetus (610 cups/day or the equivalent). Also present in breast milk. It takes much longer for caffeine to get out of a little one. ● Withdrawal symptoms: Regular use does produce moderate tolerance & dependence. Beginning about 1218 hrs after your last dose: throbbing headache, worsens with exercise, fatigue, no energy, yawning, difficulty concentrating, slowed performance, glum, irritable, mild depression. For a regular user withdrawal symptoms may last a week. **Some lines of notes copied directly from slides in order to maintain testing accuracy.**
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