Exam 1 Study Guide; PSY 245; UNCW; Galizio
Exam 1 Study Guide; PSY 245; UNCW; Galizio PSY 245
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This 25 page Study Guide was uploaded by Kristi Dorsey on Thursday February 4, 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 400 views. For similar materials see Drugs and Behavior in Psychlogy at University of North Carolina - Wilmington.
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Chapter 1: 1. Define the following: Pharmacology; study of drug effects on living systems Psychopharmacology; effects of drugs (that alter the mind) on behavior Psychology; scientific study of behavior Psychoactive drug; exert direct action on brain; interfere with psych processes Drug abuse; drug use that causes harm to individual or others 2. How are drugs classified? Origin Therapeutic use Site of drug action Chemical structure Mechanism of action Street name 3. What are pharmacological factors that help us understand drug experience? Chemical properties Drug dosage Route of drug administration 4. What are nonpharmacological factors that help us to understand the drug experience? Characteristics of drug user Genetic makeup Gender Age Drug tolerance Personality Psychological set Placebo Setting 5. Consider recent findings from the National Household Survey. What drugs are most widely used? Alcohol (1), cigarettes (2), marijuana (3) 6. What subgroup differences are apparent? Men 1.75x as likely as women to report illicit drug use in the past month Men 20% more likely than women to report any alcohol use Whites showed highest rate of alcohol use in last month followed by Hispanics and Blacks Blacks showed highest use prevalence of illicit drugs followed by whites and Hispanics 7. What issues might affect accuracy of drug surveys? Sample might not reflect population’s characteristics People may not admit to using illegal drugs Memory limits regardless of intention to tell the truth 8. What is polydrug abuse? Same person’s regular use of more than one drug Important because effects that drug combinations have on the body 9. What are the estimated economic costs of drug and alcohol abuse? Alcohol abuse = $235 billion Estimated cost of drug abuse = $193 billion Total = $428 billion (sources include illness, death, med expenses, and crime) 10. What changed in the move from DSMIV to V? How does Rinaldi define psychological dependence? DSMIV: substance dependence distinct from substance abuse; 3 of 7 criteria o Tolerance o Withdrawal o Taking more than intended o Unable to cut down or control o Excessive time spend revolved around the drug o Important activities given up o Social/interpersonal problems DSMV; 4 additional criteria to DSMIV; substance use disorder (pattern of substance use leading to significant impairment or distress as manifested by 2 of the following symptoms in a 12month period): o Failure to fulfill major role obligations o Recurrent use in dangerous situations o Social/psychological problems o Cravings (Rinaldi) DSMV Substance Use Disorder Symptoms Continuum Criteria o Mild; 23 o Moderate; 45 o Severe; 6+ 11. What is drug tolerance? Need increased amounts of substance to achieve desired effect Diminished effect with continued use of same amount of substance 12. What is a withdrawal or abstinence syndrome? Decrease in drug use after body has adjusted so that it cannot function without the drug Syndrome (symptoms that occur together) 13. What are some issues relating to drug information available on the internet? Use a search engine (e.g., Google) to find some drugrelated web sites. Try to evaluate these sites using the criteria specified in Table 15. Accuracy of web documents Authority of web documents Objectivity of web documents Currency of web documents Coverage of web documents __________________________________________________________________________________________________ Chapter 2 1. Consider the earliest forms of drug use. What drugs were the first to be used? Egyptians Old World; wine and beer Egyptian alphabet (cuneiform) deciphered; recipe discovered in one of the tombs (brewing beer); doesn’t taste good, highly alcoholic, produce intoxication Alcohol viewed as holy beverage Alcohol good candidate for first human drug Used opium to relieve pain Greeks/Romans Producing and consuming wine Bacchus/Dionysus (God of Wine) No chronicles of alcoholism Europe Fertile Crescent Greece, Egypt, and Italy Alcohol important food substance Beer used to preserve grain harvest Wine preserved fruit harvest Alcohol used for nutrition and survival Hallucinogenics The Incas in the low Andean slopes of modern day Ecuador, Peru, and Columbia discovered properties of coca plants and chewed coca leaf (1000 years ago) Cocaine; comes from the coca tree Mama Coca (Inca Goddess) was the goddess of cocaine/important deity in Inca Pantheon Hallucinogenic drugs (vivid and dramatic visual hallucinations) native to Central and South America were discovered by Native peoples in the PreColumbian Era Mayan and Aztecs believed spirits (Gods) spoke to them Mostly restricted to use by Shaman Artifacts depicted Mushroom worship in Guatemala/Mayan peoples (3000 years ago); cultivated psilocybin (chemical in mushrooms)/used as entry to gods Marijuana China and India 10,000 years ago Not sure when psychoactive properties discovered Seen as sacred plant/part of religious ceremonies; Hinduism 2. How were drugs spread worldwide? Contact between distant cultures has often been forced by trade agreements or by wars/hostilities Crusades exposed Europeans to opium and hashish South America brought cocaine to Europe Central America brought hallucinogens to Europe North America brought tobacco to Europe Ethiopia brought coffee bean to Europe Europe spread coffee bean to South America Europe brought distilled alcohol and cannabis to Chile 3. What were the opium wars and who won them? Conflict between China and Great Britain British bringing opium to China Chinese government destroyed shipments of opium being brought from British/Americans British won the conflict 4. Consider early drug use in America. Native smoked tobacco and had variety of psychoactive plants Pilgrims brought alcohol Mid1800s; opium sold legally at low prices Some opium poppies grown in U.S. Morphine commonly used (especially before and after Civil War); “dope fiend’s paradise” Opium, morphine, and cocaine thought to cure illness Laudanum used to calm babies(1 grain of opium to 25 drops of alcohol) Most narcotics legal; overthecounter or prescription Opium and morphine “God’s medicine” Late 1800s/early 1900s cocaine used for weight control Amphetamines used to treat depression (1930s); became widely available in 60’s/70’s Tranquilizers/solvent inhaling (1950s); among most prescribed psychiatric drugs 1960s; LSD used in adjunct to psychotherapy Timothy Leary (Harvard psychologist) found mindaltering advantages of LSD (1960s) Heroin synthesized in late 1890s; available in early 1900s; common among lower SES/higher SES high incidence of heroin among US soldiers in Vietnam (War); soldiers who returned did not continue use Purity of heroin < 10% in 1980s; > 60%80% today 5. What was soldier’s disease? First description of drug addiction Widespread use of morphine in soldiers during Civil War Facilitated by hypodermic needle (late 1840’s) Pain reduced in solders for first time; after wounds healed soldiers still demanded morphine Morphine named after Morpheus (god of sleep/dreams) 6. What were the earliest drugs laws in the U.S.? Consider the San Francisco ordinance AND Opium dens banned, but not smoking of opium Conviction for operating or frequenting an opium den carried a fine of $50 to $500 and/or a jail sentence of 10 days to 6 months Large opium dens closed/smaller dens increased Set stage for drug regulation later on 7. The Pure Food and Drug Act First federal American drug law Designed to control opiate addiction Companies had to label amount of drug in their products Morphine, heroin, and cocaine use did not decline Also mandated accurate labeling of alcohol, marijuana, and cocaine 8. What was the significance of the 1914 Harrison Act? Most important drug legislation in U.S. history First federal legislation to make nonmedical drug use illegal/controlled by federal law Created prescription drug use (prescribing required licensing +) Really a tax act Often called Harrison Narcotics Act Regulated opiate drugs and cocaine Introduced illegal drug use/smuggling Seen as a success; use of opiate drugs and cocaine use declined Has shifted opium/morphine addiction to heroin; easier to obtain on black market Addiction treatment centers opened in larger cities for a short time 9. What were the effects of alcohol Prohibition in the twenties? First women’s rights movement (Cary Nation & Women’s Temperance Union) Growth in organized crime and government corruption Millions became criminals Bee consumption dropped; little change in hard liquor Greatest decrease among working population Saloon to Speakeasy (> women drinkers) Industrial liquor produced neuropathies Decrease in cirrhosis of liver/hospitalization Extensive use of marijuana/coffee 10. What federal drug legislation was passed following the Prohibition Era? Marijuana Tax Act of 1937 3 class of drugs to be illegal in U.S. Provided independent status for narcotic control agents Federal Bureau of Narcotics spearheaded by Harry J. Anslinger Required/authorized producers, manufacturers, & dispensers of drug to register/pay annual licensing fee Nonmedical possession/sale of marijuana outlawed Increased attention to nonnarcotic drug use Shift of some attention to treatment of drug use 11. Review in detail the 1970 Controlled Substances Act. Developed from 1965 act Established legal scheduled system for drug use today Drugs classified according to medial use and abuse potential Schedule Medical Abuse Potential Example Miscellaneous information High abuse potential; no currently accepted medical I No High Heroin/LSD use; lack of accepted safety for use of drug; Highest and harshest penalties; possession is a felony; pharmaceutical firms can’t create drugs without permit; hospitals can’t keep Schedule I drugs except for researchers; protocol has to be reviewed by the DEA; only viable for research purposes; controversy over heroin (should it be a schedule II drug?) High abuse potential; currently accepted medical II Yes High Morphine, use/currently accepted medical use with severe cocaine, PCP restriction; abuse may lead to psych/physical (phencyclidine), dependence; can be produced by pharmacy, can be opium, codeine, held in hospital, a physician can prescribe; although Ritalin, schedule II drugs are highly controlled, there are oxycodone allowances put into place that make it possible for people who need these drugs medically to have access to them III Yes Some Barbiturates, Potential for abuse less than drugs/other substances ketamine, in previous schedules; currently accepted medical Vicodin use; abuse may lead to moderate/low physical/psych dependence; penalties for possession/sales are not felonies; prescriptions, refills, more availability Low abuse potential; currently accepted medical IV Yes Low Valium, Xanax, use; limited physical/psych dependence; prescription Ambien phoned in/multiple refills; tranquilizers, sleeping pills, Ambien are all controversial; college students have problems with drug dependence on these drugs Cough Low abuse potential; currently accepted medical V Yes Very low medicines use; abuse may lead to limited physical/psych (small amount dependence; no prescription, show ID, precursors of opiates), for making meth Robitussin, AC In the late 1970s in NC, thousands of young people were being charged with felonies for possession of VI N/A N/A Marijuana marijuana; in NC, a decriminalization act was passed (true in many other states, but not all); In NC, if you look at our state drug Schedule, the 6th schedule is marijuana only; state law that allows NC to treat marijuana possession as a misdemeanor, rather than a felony, in contradiction to federal law 12. Consider the controversy surrounding drug testing in workplace and at home. Possible infringement on constitutional rights when administered without probable cause Is drug testing in workplace legitimate if use doesn’t affect job performance? Urinalysis/strands of hair tests often unreliable 13. What are “club” drugs? Originally used to describe drugs used by young adults at “raves” and “trances (dance parties/clubs/bars) More linked to nonrave social contacts and polysubstance abuse Can cause serious health problems/death Stimulants, depressants, or hallucinogens Dangerous when combined with alcohol Colorless, tasteless, and odorless Individuals add them to beverage to commit sexual assaults MDMA (ecstasy), GBH (liquid ecstasy), ketamine, Rohypnol (roofies), methamphetamine (speed/meth/crack), & lysergic acid diethylamide (LSD) 14. What was the 1986 Analogue Enforcement Act Designed to prevent? Response to increasing creation of synthetic drugs Enforcement officials went through timeconsuming process to document/certify synthetic drug as controlled substance Allowed for immediate classification of a synthetic drug as a controlled substance 15. What is the Single Convention? European drug policy derived from United Nations Single Convention on Narcotic Drugs (1961) 12 participating European countries pledged to fight drug abuse and international trafficking through national legislation Single Convention document amended to encourage efforts to prevent substance abuse and to provide treatment services for abusers (1972) 16. What is the significance of the 2009 Family Smoking Prevention and Tobacco Control Act? Authorized FDA to regulate manufacture, marketing, and sale of tobacco products Does not provide authority to impose ban on tobacco products Focus on deterring young people from smoking 17. What drugs were targeted by the Synthetic Drug Abuse Prevention Act? Synthetic marijuana (such as Spice and k2) and synthetic stimulants (bath salts) Added synthetic compounds to Schedule I Produces of bath salts and synthetic marijuana had avoided 1986 Analogue Enforcement Act by labeling their products “not for human consumption” __________________________________________________________________________________________________ Chapter 3 1. What is a neuron? Be able to identify its parts. Neuron; nerve cells; building blocks of nervous system; communicate with one another Cell body (soma); includes nucleus (genetic material & processes control of metabolic activity) Axon; extension of cell body; conducts electrical charge (action potential) from cell body to axon terminals; enclosed within myelin (fatty white substance that insulates axon); similar to insulation for a wire; unmyelinated axons are gray Dendrite; extend from cell body; branchlike; contain receptor sites (important in neural transmission) Axon terminals/buttons; buttonlike structure at end of axon branches; most do not come into direct contact with dendrites of neighboring neurons (Spark vs. Soup theorists) 2. What is the Synapse? What happens there? Junction between 2 neurons; separated by gap (synaptic cleft) When an action potential reaches the axon terminal, chemical substances stored in terminal buttons are released into the synapse and these chemical substances (neurotransmitters) trigger activity in the adjacent neuron Most psychoactive drugs produce their important effects by action at the synapse (where chemical transmission takes place) 3. In what sense is neural transmission an electrochemical event? Electrical along axon Chemical at synapse 4. What is a neurotransmitter? Chemical substance stored in axon terminals that are released into the synapse when a neuron fires Influence activity in postsynaptic neurons Viewed as keys 5. What is a receptor site? Large protein molecules located on surface of neuron Viewed as locks that operate before neuron fires (to fire it must be unlocked) Accomplished by neurotransmitter substances released at terminal buttons 6. Be able to trace the processes involved in neurotransmission. Neurotransmitters and receptors have an affinity for one another (neurotransmitter attracted to receptor site) When a neurotransmitter key occupies a receptor lock it becomes attached (bonding) When neurotransmitter bonds to receptor changes occur in neuron that may make neuron more or less likely to fire 2 mechanisms for these changes are ionotropic and metabotropic 7. Ionotropic receptors? Situated in neuron membrane Consists of an ion channel and receptor site When neurotransmitter binds to the receptor site it causes the channel to open and allows charged particles to enter or leave the cell If the receptor opens a channel that allows more positively charged ions into the neuron it will be more likely to fire If enough of these channels are opened the neuron will generate an action potential (excitatory) Ion channels that result in more negative ions make it less likely to fire (inhibitory) Ionotropic receptors referred to as fast receptors; process completed in a few milliseconds 8. Metabotropic Receptors? Slow receptors (delay changes in neuron) Release or activate G proteins o May act like ionotropic receptors and open ion channels in the neuron o Initiate synthesis of other chemicals (referred to as second messengers) o Produce metabolic changes or activate genes within neuron Some metabotropic receptors increase likelihood of neural firing (excitatory) and others decrease firing (inhibitory) 9. How are neurotransmitters deactivated? 1. Enzyme breakdown (change structure so that it is no longer capable of occupying receptor sites) o Drug can alter neural transmission by affecting enzyme activity o EX: some antidepressant drugs alter brain levels of the neurotransmitters norepinephrine, dopamine, and serotonin by inhibiting the activity of monoamine oxidase, the enzyme that breaks down these compounds 2. Reuptake (neurotransmitters taken back up into terminal button after release) o Neurotransmitter is preserved, intact, and recycled o Some drugs (EX: cocaine) exert some of their action by blocking reuptake 10. What are major ways that drugs affect neural transmission? Synthesis (drugs increase or decrease creation of neurotransmitters) Transport (drug may interfere with transport of molecules to axon terminals) Storage (interfere with storage of neurotransmitters in vesicles of axon terminal) Release (cause axon terminals to release molecules into synapse prematurely) Degradation (drug may influence breakdown by enzymes) Reuptake (drug may block reuptake of neurotransmitters in axon terminals) Receptor activation (drug may activate receptor site by mimicking neurotransmitter) Receptor blocking (drug may cause receptor to become inactive by blocking it) 11. What is an agonist? Similar to a duplicate key that fits into an open lock Drugs affect receptor by mimicking activity of natural neurotransmitters EX: heroin mimics endorphins 12. What is an indirect agonist? Enhance activity of a particular neurotransmitter system without binding to receptor EX: cocaine does not bind to dopamine receptors but enhances dopamine transmission by blocking reuptake 13. What is an antagonist? Act as if they fit into the lock but jam the lock and prevent neuron from firing Blocks normal synaptic transmission; prevents other compounds from activating the receptor EX: naloxone antagonist to opiate drug receptors (heroin); if administered to patient who has taken lethal dose the patient will survive; ]reverses or blocks effects of opiates 14. What is an indirect antagonist? Inhibit activity of a neurotransmitter system without binding to receptor EX: reserpine either blocks creation of serotonin or inhibits release of serotonin 15. What is acetylcholine and what does it do? One of the first neurotransmitters found Located outside the brain (axon terminals of neurons that activate skeletal muscles) Neuromuscular junction; site where nerve muscles meet Muscles contract when neurotransmitters that synapse with muscle fibers fire and release acetylcholine into neuromuscular junction Important in sensory processing, attention, and memory Drugs used to reduce symptoms of Alzheimer’s disease elevate levels of acetylcholine in the brain through inhibition of enzyme acetylcholinesterase Botulinum blocks release of acetylcholine at neuromuscular junction resulting in muscle paralysis or death by asphyxiation; carefully prepared form is now Botox 16. What are the three monoamine neurotransmitters and what are their functions? 1. Norepinephrine/nonadrenaline o ANS (sympathetic) activity o Discovered early because found outside the brain o Mediates physical changes that accompany emotional arousal o Regulation of hunger, alertness, and arousal 2. Serotonin o Regulation of sleep and mood o Found throughout brain 3. Dopamine o Coordinated motor movement and reward o Critical chemical in producing rewarding properties of drugs o Nucleus accumbens rich in dopamine 17. How do they relate to disorders like Parkinson’s disease? Progressive loss of fine motor movements Muscle rigidity Tremors Mostly found in elderly Caused by lack of dopamine (dopamine deficiency hypothesis) 18. What is LDopa? Chemical precursor of dopamine Used in treatment of Parkinson’s Effective in relieving symptoms LDopa penetrates bloodbrain barrier, reaches the brain, and is converted to dopamine Dopaminergic neurons continue to be lost and eventually LDopa cannot correct the loss 19. Schizophrenia? Major loss of contact with reality Delusions and hallucinations Social withdrawal Distortions of emotionality Biochemical basis (dopamine and serotonin) Stimulant drugs (cocaine and amphetamines) increase monoamine activity Symptoms linked to high levels of monoamine activity Low to moderate doses enhance mood; overdoses lead to paranoid delusions & loss of reality When drugs wear off and monoamine activity returns to normal symptoms dissipate Tradeoff between treatment of schizophrenic symptoms (too much dopamine) and developing Parkinson’s symptoms (lack of dopamine) 20. Depression? Monoamine theory of depression associated with dysregulation of monoamines (norepinephrine/serotonin) Originated with finding that certain drugs that depleted monoamines seemed to produce depression Deficient serotonin activity linked to suicidal behavior Drugs useful in treatment of depression (Prozac) influence either norepinephrine, serotonin transmission, or both EX: reserpine (once used to treat high blood pressure); makes monoaminergic vesicles leaky; depletion of norepinephrine, serotonin, and dopamine by enzyme; often causes depression in people whose mood states were normal before treatment; produces Parkinson’s symptoms due to dopamine depletion (which led to LDopa) 21. What is the bloodbrain barrier? Filers blood before it can enter the brain to protect against toxins 22. What is neurogenesis and how is it related to depression? Birth of new neurons Neurogenesis may occur in hippocampus and other areas throughout an adult brain Reduced hippocampus size linked to patients with depression May indicate less neurogenesis Elevated serotonin levels increase neurogenesis Antidepressants increase serotonin levels rapidly; takes several weeks for depression to lift Suggests that increase birth of neurons (rather than elevation of serotonin per se) responsible for antidepressant action 23. What are the endorphins? Neurotransmitters mimicked by opiate drugs such as morphine and heroin Effects of opiate drugs mediated through endorphinergic activity 23. What is GABA? Most abundant inhibitory neurotransmitter in the brain Opens negatively charged chloride ion channels If neuron has a GABAergic receptor site that is activated, a large quantity of the excitatory transmitter is required for neuron to fire A number of drugs are now thought to act on the GABA system; classic depressant drugs: barbiturates, tranquilizers such as Valium (diazepam) and Xanax (alprazolam), and alcohol 24. Glumate? Excitatory amino acid neurotransmitter Most abundant of excitatory neurotransmitters Learning and memory processes Some hallucinogenic drugs (PCP and ketamine) act on glutamate receptors in some parts of the brain 25. What drugs affect the neurotransmitter anandamide? Lipid neurotransmitters mimicked by marijuana 26. Contrast Central Nervous System and Peripheral Nervous System. CNS; brain and spinal cord; includes nerves (bundles of axons) that send input from senses to the brain (sensory nerves) and nerves that send output from brain to muscles (motor nerves) PNS; all nerve tissues outside CNS; regulates various nonconscious or automatic functions; somatic and autonomic branches 27. What are the two branches of the Autonomic Nervous System? Sympathetic o Activated during emotional arousal o Release of epinephrine or norepinephrine from adrenal glands o Fightorflight o Heart rate, blood pressure, respiratory, and sweating rates increase o Pupils dilate o Mouth becomes dry o Blood is shunted away from the internal organs and to the brain and large muscle groups. Parasympathetic o Responsible for lowering heart rate and blood pressure o Balances action of the sympathetic branch by exerting opposite effects 28. What is sympathomimetic drug? Some psychoactive drugs mimic sympathetic arousal Drugs such as cocaine, amphetamines, and hallucinogens (LSD) that produce the physiological effects of sympathetic activity 29. Be able to identify functions of the following: Medulla oblongata o Lowest hindbrain structure o Regulation of breathing, heart rate, vomiting, swallowing, blood pressure, and digestive processes o When drugs affect medulla the person is in danger due to respiratory or cardiovascular failure o When toxic chemicals reach high volume, the vomit center is triggered; why large quantities of alcohol often cause nausea and vomiting Cerebellum o Hindbrain structure o Important in motor control and coordination o Contains several billion neurons o Largely unconscious but involves balance, coordinated movements, and speech o Loss of motor control and balance produced by drugs act on cerebellum Reticular Activating System o Pathway running through medulla and pons o Regulates alertness and arousal o Drugs that lower arousal and induce sleep (barbiturates and tranquilizers) thought to act on this region Thalamus o Forebrain structure o Receives/organizes sensory stimuli and sends it to relevant centers o Hunger, thirst, and basic biological motives o Control of body temperature, aggression, and sexual behavior o Lesion in one area inhibits eating (loss results in overeating) o Other seems to excite hunger (because its loss results in less eating) o The effects of electrical stimulation of a brain region generally are the opposite of the effects of lesioning or removing that region (James Olds) Hypothalamus o Regulates eating, drinking, and other basic biological drives Mesolimbic dopaminergic pathway o Pathway that is rewarding when stimulated o Discovered by James Olds o Many pleasurable events result in release of dopamine in its pathway; chocolate, sex, drugs (cocaine, heroin, nicotine) Hippocampus o Limbic system o Critical in memory storage o If damaged longterm memories are intact but difficulty forming new memories Substantia Nigra o “Black substance” o Produces dopamine o Damage produces Parkinson’s (doesn’t appear until 80% of substantia nigra is destroyed) o Designer drugs appear to be capable of killing neurons here 30. Be able to identify the functions of the Lobes. 1. Frontal o Ability to plan and control impulses; cognitive skills; emotional expression; problem solving; memory; language; judgement; sexual behavior o Control panel of our personality and our ability to communicate o Abnormalities may be caused by exposure to some drugs (cocaine) 2. Parietal o Where information such as taste, temperature, and touch are processed o Humans would not be able to feel sensations of touch if damaged 3. Temporal o Primary auditory perception o Hearing/selective listening o Receives sensory info such as sounds and speech from ears o Key to comprehending meaningful speech 4. Occipital o Visual projection area o Processes what your eyes are seeing o Fast to process rapid information o Stimulation of eye is perceived as a visual stimulus when the signal reaches the occipital cortex 31. How is brain damaged assessed? Consider the various ways of imaging the brain. 1. Electroencephalography (EEG) o Measure electrical activity in brain o Direct analysis of brain tissue o Reveal gross brain damage 2. Computerized axial tomography (CT) o Produces xray image o Changed to different depths of brain to detect abnormalities 3. Positronemission tomography (PET) o Measure activity in selected brain regions o Inject weak radioisotopes into brain o Radioactive glucose, oxygen, or radioactive neurochemicals measured o Changes induced by drugs can be assessed 4. Magnetic resonance imaging (MRI) o Strong magnetic field passed through head o Radio waves generated and cause molecules to emit energy of different frequencies o Highresolution 3dimensional image of brain 5. Functional magnetic resonance imaging (fMRI) o Rapid imaging o Measure oxygen levels in blood vessels o Oxygen levels correlated with metabolism of particular brain region __________________________________________________________________________________________________ Chapter 4 1. Define pharmacokinetics. Absorption, distribution, biotransformation, and excretion of drugs Essential for determining how much drug reaches its site of action 2. Define pharmacodynamics. Biochemical and physiological effects of drugs Mechanisms of drug action 3. What are the steps of the drug experience? 1. Drug of specified chemical structure present 2. Quantity of drug measured 3. Quantity of drug administered 4. Drug absorbed into blood; distributed to site of action 5. Pharmacological effects produced 6. Pharmacological effects may be modified depending on person’s characteristics 7. Setting or context may be used to modify pharmacological effects 4. How are drug doses determined by psychologists? Body weight Amount of drug less concentrated in body of heavier person Mg (of drug) ÷ kg (of body weight) Ex: if the desired dose is 0.08 mg/kg and the person weights 80 kg, the amount is 0.08 * 80 = 6.4 mg of the drug 5. What are the major routes of administration? Consider the advantages and disadvantages of each. Oral (swallowing) o Advantage; safest, cheapest, & most convenient o Disadvantage; food in stomach may diminish amount of drug absorbed; reduced drug effect by stomach acid breakdown Subcutaneous (injecting drugs under layers of skin) o Advantage; easiest injection route; absorption rates faster than oral o Disadvantage; should not be used when drug irritates body tissue or when large volumes of solution must be taken Intramuscular (within the muscle) o Advantage; faster absorption that subcutaneous with proper preparation of solution at injection site with good blood flow o Disadvantage; deeper penetration than subcutaneous; painful at injection site; risk of infection from tissue damage Intravenous (into the veins) o Advantage; potential for large quantity of drug to reach site of action; doses adjusted according to person’s response to drug effects; better for irritating drugs because blood vessel walls are insensitive; blood dilutes the drug o Disadvantage; repeated use requires healthy vein; dose administered gradually; person’s response monitored Inhalation (absorbed through lung’s membrane) o Advantage; absorption effective and most rapid for some drugs o Disadvantage; small amount of drug absorbed in any one administration Intranasal (absorbed through mucous membranes) o Advantage; for a fat and water soluble drug absorption is rapid and effective o Disadvantage; can cause damage when drug is irritating or disrupts flow Sublingual (tablet placed under tongue and dissolved in saliva) o Advantage; preferable to oral administration for drugs that cause vomiting o Disadvantage; unpleasant taste Transdermal (through the skin) o Advantage; Alternative to oral route when drug causes stomach pain; absorption enhanced at sites that have greater cutaneous blood flow; mixing a drug with another substance may improve penetration of the skin o Disadvantage; hard for most chemicals to penetrate the skin 6. How are drugs absorbed? Define bioavailability Bioavailability; portion of original drug dose that reaches site of action or fluid in body that gives it access to site of action Absorption (of drug into bloodstream); rate and extent to which a drug leaves its site of administration Drugs soluble in lipids (fat) more readily absorbed; EX: alcohol Drugs taken in water solution absorbed more rapidly because they are dissolved more readily at site of absorption In solid form drug’s solubility depends on conditions at site of absorption; EX: aspirin insoluble in stomach acid More blood flow speeds absorption Drugs absorbed more rapidly from larger surface areas 7. How are drugs distributed to sites of action? Regions of body that get the most blood get the most drug (heart, brain, kidney, liver, etc.) Parts of body that receive less blood flow (muscle & fat) take longer to receive drug Substances must cross bloodbrain barrier to reach the brain 8. What factors influence this? Blood flow Diffusiblity; more diffusible tissues receive the drug more rapidly Fat solubility; drugs that are more soluble in lipids penetrate body membranes and reach sites of action more easily less lipidsoluble drugs Whether it selectively binds to elements of the body; the more tightly bound a drug the slower its distribution to sites of action Drugs with affinity for fatty tissue are slowly released so psychoactive effects are insignificant o EX: marijuana; distribution throughout the body is uneven because of selective binding and effects are weak; dose does not immediately reach action site 9. How are drugs eliminated from the body? Enzymes in the liver Enzymes in GI tract partially break down drugs taken orally (firstpass effect); less drugs than administered eventually distributed to its site of action When metabolites are active, the action ends with further metabolism of the byproducts or by their direct excretion in the urine 10. Define halflife. Amount of time that passes for the amount of drug in body to be reduced by half 11. How long after use can drugs be detected in urine? The range of elimination times pertains to elimination of the drug itself (shorter time) and to elimination of the drug’s metabolites (longer time) from the body o At some point the testing method is not sensitive enough to pick up the metabolite(s); point depends on metabolite and testing method Positive drug test does not provide precise information about when drug was used (unless drug is detected in blood) Alcohol has no range because its metabolites are used too efficiently in the body to be measured reliably An acute dose of marijuana can be detected for up to 8 days In chronic users the drug can be detected for a month+ after last dose 12. What is a doseeffect (response) curve? What the effect of drug x is at a specified dose Curve is a representation of some effect according to a dose of the drug. o EX: people may drink different doses of alcohol; asked to report degree of relaxation at given point; if average reports of relaxation for each person were plotted, we would have a doseeffect curve Increasing a dose beyond a given level does not increase the drug’s effects o EX: alcohol and reaction time; 2 beers in 1 hour (little effect) four beers in 1 hour (person’s response slower) 9+ beers in 1 hour (hard to stay conscious; measured reaction time would yield little info o 13. What is meant by efficacy? Peak level of doseeffect curve for a given effect 14. Potency? Minimum effective dose of a drug on doseeffect curve; line extends from point of efficacy down to horizontal axis 15. What is an ED50? Effective dose; dose at which a given % of individuals show a particular effect of drug ED50; standard term that pharmacologists use for sedation; 50% of people who receive that amount of drug will experience sedation 16. An LD50? Lethal dose; given dose at which a given 5 of individuals die within a specified time LD50; dose at which 50% of animals administered a given dose of a drug died within a stated time 17. A therapeutic index? Measure of a drug’s safety in medical care Computed as ratio of LD50 ÷ ED50 ED is alleviation of symptoms of disease or injury The higher the index, the more useful the drug in medical treatment Steeper doseeffect curves have smaller indexes 18. Consider drug interactions. What is synergism? How else can drugs interact? Drug interaction; when the effects of one drug are modified by presence of another Also called potentiation Synergism; any enhancing drug interaction; when 2 drug are synergistic the effects of taking them together are greater than effects of taking either alone Antagonism; reduced effect of drug when another drug is present __________________________________________________________________________________________________ Chapter 5 1. What are some characteristics of the user that contribute to the nature of drug effects? Inherited differences in reactions to drugs Initial sensitivity; effect of drug on firsttime user (determined genetically) Gender; specified dose of drug will have greater effects on women than men (women have > % of body fat & < % of body water) Weight; heavier people have more blood/fluids, so for a given quantity of drug they would have a smaller concentration of it than lighter people would Age; children and elderly more sensitive The more sensation seeking a person is, the more the person tends to use alcohol and drugs Addictive personality; hypothesis of personality structure common to all people with substance use disorders (little evidence for this) Drug expectancy; person’s anticipation of what he/she will experience upon taking the drug Setting (important with alcohol, marijuana, and hallucinogens) 2. What is a placebo? Chemically inactive substance 3. What are placebo effects? Strong belief that a drug will produce a certain effect may be enough to produce the effect even though person has injected a chemically inactive substance (placebo) 4. Dispositional Tolerance? Metabolic tolerance Increase in metabolic rate of drug Users must consume greater quantities to maintain a certain level of it in their body 5. Functional Tolerance? Pharmacodynamics tolerance Brain and others parts of CNS become less sensitive to drug’s effects 6. Acute Tolerance? Type of functional tolerance Sometimes called tachyphylaxis Measured within course of action of a single dose or few doses With some drugs, at any point when the blood level is rising to peak, users may experience greater drug effects than at the same point when the blood level is falling EX: alcohol and cocaine 7. Protracted tolerance? Type of functional tolerance Occurs over course of 2+ drug administrations Individual consumes greater amounts of a drug to achieve an effect that was once achieved at a lesser dose EX: alcohol and shortterm memory (people who drink may show impairment in memory today after drinking 6 cans of beer, when they formerly showed the same degree of impairment after drinking only 3 beers) 8. What is crosstolerance? Tolerance to drugs never taken that results from protracted tolerance to another drug EX: Anesthetic drugs are used in surgery because of their depressant effects, so people who use drugs like alcohol or the barbiturates show crosstolerance to drugs used medically as anesthetics. 9. Behavioral tolerance? Learned tolerance Adjustment to behavior through experience in using a drug to compensate for its intoxicating effects EX: individuals who have had considerable experience with the effects of alcohol on motor coordination may learn to compensate for their intoxication by walking slowly or with a lower center of gravity to keep from falling even if they are drunk 10. Reverse tolerance? Increased sensitivity to effects of drug with repeated use EX: marijuana and cocaine 11. Consider the various explanations of tolerance. 1. Cell Adaption Theory o Homeostasis hypothesis o Cells become adapted to presence of the drug with repeated exposure o Adaption allows cells to maintain normal functioning at given drug dose o More drug required to disrupt cell functioning (and produce desired effect) o Partially dispositional tolerance but protracted functional tolerance more important o Downregulation; repeated exposure to drugs may reduce # of receptor sites on neurons that the drug activates 2. Drug Compensatory Reactions and Learning o Tolerance to drugs is partially learned o Compensatory reaction; when an event disrupts body’s homeostasis the body can counteract the disruption (coffee increase heart rate; simultaneously, your body works to reduce heartrate) o Reactions thought to become stronger with repeated use of a given drug Classical conditioning Cues associated with use are conditioned stimuli that become associated with drug actions and compensatory reactions The higher the number of pairings, the larger the compensatory reaction and the smaller the observed drug effect. EX: presenting syringe/tourniquet may elicit urges in IV heroin or cocaine users to consume respective drugs Exposure to these stimuli in absence of drug may produce craving Extinction; when people have been exposed to these stimuli many times without drug, the effects dissipate 12. What is a reinforcer? Consequence of a behavior that increases its future likelihood EX: if studying for an exam produces an A then studying is more likely to occur before the next exam 13. A punisher? Consequence of behavior that decreases it future likelihood EX: we touch a hot stove only once because of the consequence (pain) transmitted to our fingertips 14. How are these operant principles used to help understand drug dependence? Drug users derive + or – reinforcement from their behavior and experience little punishment for it Behavioral pharmacologists study drug access as consequences for behavior in selfadministration studies 15. How and why are animals used in drug research? Consider particularly the selfadministration AND Selfadministration studies; testing whether research participants will selfadminister a drug Important source of knowledge because they show that not all drugs have reinforcement value Drugs humans tend not to abuse are not selfadministered by other animals Reinforcers are more effective when they are presented immediately following a behavior Rats will continue to press a lever to receive a drug Humans and animals prefer the drug experience under certain conditions Abused drugs are positive reinforcers that maintain drugseeking behavior 16. Drug discrimination, AND Provides a way of asking nonhuman subjects about subjective effects of drugs Animals can discriminate between drug and nondrug states Allowed pharmacologists to classify experimental drugs according to subjective effects before administered to people 17. Conflict procedures. Conflict paradigm; concerns the effects on a behavior of a drug that has a history of both reinforcement and punishment EX: rat presses lever to get food as reinforcer; after learning occurs rat is punished by pressing lever (electric shock); rat has learning history of reinforcement and punishment for the same behavior; typically suppresses behavior in question Conflict paradigm sensitive to antianxiety drugs (benzodiazepines) Anticonflict effects in animals have been found for a range of drugs that have been shown to have the effect of reducing the perception of anxiety in humans 18. What ethical issues are raised in drug research with animals and humans? Nuremberg Code o Subjects must agree to participate in the study and must give their consent without coercion after being told all the risks or potential problems related to the research o Animals cannot give consent Unethical to have placebo control group if there is an alternative drug that has demonstrated effectiveness o Many view such a design as essential to learning how drugs affect people 19. What is a doubleblind? Drug study in which neither the experimenter nor subjects knows whether the drug or placebo is administered to any subject Prevents biases from experimenters and subjects 20. What steps must occur before a drug receives FDA approval and goes to market? 1. Initial synthesis and preclinical studies (13 years) 2. Please 1 clinical trial; up to 50 normal volunteers (1 year) 3. Phase 2 clinical trial; controlled studies in patients with a target disease; 50200 patients (2 years) 4. Phase 3 clinical trials; controlled and open studies of 1,000 or more patients monitored for effectiveness and for adverse reactions; data used for determining doses and labeling requirements (3 years) 5. FDA review/approval (12 years) 6. Postmarketing testing (12 years) 21. What is a chemical name? Indicates drug’s structural formula and allows chemists to reproduce the drug’s structure 22. Brand name? Commercial name given to a drug by its manufacturer Says nothing about chemical structure 23. Generic name? General name given to a drug that is shorter (and easier for most people to say) than chemical name 24. Why do consumers seem to prefer generic versions of prescription drugs? Drug company is granted right to market the drug for 20 years (patent) Afterwards, generic drug companies can sell their versions of the same compound as long as they use the generic rather than the brand name Not chemical copies but considered equivalent by FDA Sold at lower price (~ 50% lower)
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