PSY 245 Final Exam Study Guide (LONG VERSION)
PSY 245 Final Exam Study Guide (LONG VERSION) PSY 245
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This 54 page Study Guide was uploaded by Kristi Dorsey on Thursday April 28, 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 130 views. For similar materials see Drugs and Behavior in Psychlogy at University of North Carolina - Wilmington.
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Date Created: 04/28/16
Exam Study Q’s Mentioned in Class: Drug laws, neurotransmitters and drug action, basic principles of pharmacology (tolerance and dependence), synergy (there’s synergy among opiate drugs; methadone is synergistic with heroin; synergy within depressant drugs; valium is synergistic with alcohol; there’s synergy that crosses over between opiates and depressant drugs like alcohol) 1914 Harrison Act: Banned all of the naturally occurring opiates (except for medical use) and cocaine. Looking into someone’s eyes to determine what drug they are on o Pupils normal but eyes are blood shot – cannabinoids o Pupils widely dilated – sympathomimetic drugs (ecstasy, LSD, psilocybin, cocaine, amphetamine, caffeine) o Pinpoint pupils – opiates Rebound Effect: withdrawal symptoms of drugs show effects exactly opposite the effects of taking the drug Alcohol and depressants can cause seizures which cause death Cross-Dependence (and tolerance) between all opiate drugs (but not alcohol/depressants) o Tolerance to drugs never taken that results from protracted tolerance to another drug CHAPTER 1: DRUG USE AND ABUSE 1. Define the following: a. Pharmacology; study of drug effects on living systems b. Psychopharmacology; effects of drugs (that alter the mind) on behavior c. Psychology; scientific study of behavior d. Psychoactive drug; exert direct action on brain; interfere with psych processes e. Drug abuse; drug use that causes harm to individual or others 2. Consider recent findings from the National Household Survey. What drugs are most widely used? Alcohol (1) Cigarettes (2) Marijuana (3) 3. 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. 4. Polydrug Abuse? Same person’s regular use of more than one drug. 5. What are the estimated economic costs of drug and alcohol abuse? Alcohol abuse = $235 billion; Drug abuse = $193 billion; Total = $428 billion (sources include illness, death, medical expenses, and crime). 6. DSM-IV Criteria for Substance Abuse: a. Substance dependence distinct from substance abuse; b. 3 of 7 criteria required to meet the diagnosis: Tolerance, withdrawal, taking more than intended, unable to cut down or control, excessive time spent revolved around the drug, important activities given up, & social/interpersonal problems 7. DSM-V Criteria for Substance Abuse: a. 4 additional criteria to the DSM-IV criteria b. Substance Use Disorder (pattern of substance use leading to significant impairment or distress as manifested by 2 of the following symptoms (in a 12-month period): failure to fulfill major role obligations, recurrent use in dangerous situations, social/psychological problems & cravings (Rinaldi’s definition of psychological dependence) 8. DSM-V Substance Use Disorder Continuum Criteria – mild = 2-3, moderate = 4-5, severe = 6+ 9. What is drug tolerance? Need increased amounts of substance to achieve desired effect; diminished effect with continued use of the same amount of the substance. 10. What is a withdrawal or abstinence syndrome? Definable illness that occurs with a cessation or decrease in drug use after the body has adjusted to the presence of a drug to such a degree that it cannot function without the drug. CHAPTER 2: DRUSE USE YESTERDAY AND TODAY 11. Consider the earliest forms of drug use. What were the first to be used? a. Egyptians –; alcohol viewed as a holy beverage; alcohol good candidate for the first human drug b. Greeks/Romans – Producing and consuming wine; God of wine is Bacchus/Dionysus; no chronicles of alcoholism c. Europe: alcohol used for nutrition and survival; beer preserved grain harvest; wine preserved fruit harvest d. Incas (low Andean slopes of modern day Ecuador, Peru, and Columbia) – discovered properties of coca plant (cocaine); Mama Coca (Inca Goddess of Cocaine) e. Native peoples in Central and South America in Pre-Columbian Era (Aztecs and Mayans) – hallucinogenics; mostly restricted to use by Shaman f. China and India – marijuana seen as sacred plant/part of religious ceremonies in Hinduism; not sure when psychoactive properties were discovered 12. How were drugs spread worldwide? Contact between distant cultures has often been forced by trade agreements or by wars/hostilities. 13. What were the opium wars and who won them? Conflict between Great Britain and China; Great Britain was bringing opium into China; Chinese government destroyed shipments of opium; British won the conflict. 14. Consider early drug use in America. a. Natives smoked tobacco and used a variety of psychoactive plants; Pilgrims brought alcohol b. Mid-1800s – opium sold legally at low prices; 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/over-the-counter prescription; c. 1960 – LSD used in adjunct to psychotherapy (Timothy Leary); d. Heroin synthesized in the late 1890s, available in the 1900s, and common among lowers SES; high incidence of heroin use among US soldiers in Vietnam (War); Purity of heroin < 10% in the 1980s; > 60%- 80% today 15. What was Soldier’s Disease? Widespread use of morphine in soldiers during the Civil War; first description of drug addiction. 16. What were the earliest drug laws in the U.S.? San Francisco Ordinance and The Pure Food and Drug Act. 17. San Francisco Ordinance (1875): Banned opium dens, but not smoking of opium; Large dens closed/smaller dens increased; set stage for drug regulations later on. 18. The Pure Food and Drug Act (1906): First Federal American drug law designed to control opiate addition; companies had to label amount of drug in their products; morphine, heroin, and cocaine use did not decline. 19. 1914 Harrison Act. Most important federal drug legislation in U.S. History; first federal legislation to make non- medical drug use illegal and controlled by federal law; created prescription drug use (prescribing required licensing); often called Harrison Narcotics Act; regulated opiate drugs and cocaine; introduced illegal drug use/smuggling; seen as a success because use of opiate drugs and cocaine use declined; shifted opium/morphine addiction to heroin. 20. 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; beer consumption dropped/little change in hard liquor; greatest decrease among working population; saloon so speak-easy (> women drinkers); industrial liquor produced neuropathies; decrease in cirrhosis of the liver; extensive use of Marijuana/coffee. 21. What federal drug legislation was passed following the Prohibition Era? Marijuana Tax Act of 1937 – required/authorized producers, manufacturers, and dispensers of the drug to register/pay annual licensing fee; nonmedical possession/sale of marijuana was outlawed; increased attention to nonnarcotic drug use; shift of some attention to treatment of drug use. 22. Review in detail the 1970 Controlled Substances Act. Established legal scheduled system for drug use today; drugs classified according to medical use and abuse potential. Schedule Medical Abuse Example Miscellaneous information Potential High abuse potential; no currently accepted medical use; lack of accepted safety for use of drug; Highest and harshest penalties; I No High Heroin/LSD 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?) Morphine, cocaine, High abuse potential; currently accepted medical use/ with severe PCP restriction; abuse may lead to psych/physical dependence; can be II Yes High (phencyclidine), produced by pharmacy, can be held in hospital, a physician can opium, codeine, prescribe; although schedule II drugs are highly controlled, there Ritalin, oxycodone are allowances put into place that make it possible for people who need these drugs medically to have access to them Potential for abuse less than drugs/other substances in previous III Yes Some Barbiturates, schedules; currently accepted medical use; abuse may lead to ketamine, Vicodin moderate/low physical/psych dependence; penalties for possession/sales are not felonies; prescriptions, refills, more availability Low abuse potential; currently accepted medical use; limited IV Yes Low Valium, Xanax, physical/psych dependence; prescription phoned in/multiple refills; Ambien tranquilizers, sleeping pills, Ambien are all controversial; college students have problems with drug dependence on these drugs Cough medicines Low abuse potential; currently accepted medical use; abuse may V Yes Very low (small amount of lead to limited physical/psych dependence; no prescription, show opiates), Robitussin, ID, precursors for making meth A-C In the late 1970s in NC, a decriminalization act was passed (true in many other states, but not all); In NC, if you look at our state drug VI N/A N/A Marijuana 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 23. Consider the controversy surrounding drug testing in the workplace and at home. Possible infringement on constitutional rights when administered without probable cause; is it legitimate if it doesn’t affect job performance; urinalysis/strands of hair tests are often unreliable. 24. What are “club” drugs? MDMA (ecstasy), GBH (liquid ecstasy), ketamine, Rohypnol (roofies), methamphetamine (speed/meth/crack), & lysergic acid diethylamide (LSD); Individuals add them to beverages to commit sexual assaults; stimulants, depressants, or hallucinogens; dangerous when combined with alcohol; colorless, tasteless, and odorless. 25. What was the 1986 Analogue Enforcement Act designed to prevent? Allowed for immediate classification of a synthetic drug as a controlled substance; response to increasing creation of synthetic drugs. 26. What is the Single Convention? European drug policy derived from the United Nations Single Convention on Narcotic Drugs (1961); 12 participating European countries pledged to fight drug abuse and international trafficking through national legislation. 27. 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. 28. What drugs were targeted by the Synthetic Drug Abuse Prevention Act? Synthetic Marijuana (such as Spice and K2) & synthetic stimulants (bath salts); Added synthetic compounds to Schedule I; Producers of bath salts and synthetic marijuana had avoided 1986 Analogue Enforcement Act by labeling their products “not for human consumption.” CHAPTER 3: DRUGS AND THE NERVOUS SYSTEM 29. What is a neuron? Be able to identify its parts. (1) Cell Body (2) Nucleus (3) Dendrites (4) Myelin (5) Axon (6) Axon Terminals. a. Neuron: building blocks of nervous system; communicate with one another b. Cell body (soma): includes nucleus (genetic material & processes control of metabolic activity) c. Axon: extension of cell body; conducts electrical charge (action potential) from cell body to axon terminals i. Enclosed within myelin (fatty white substance that insulates the axon) ii. Unmyelinated axons are gray d. Dendrite: extend from the cell body; branchlike; contain receptor sites (important in neural transmission) e. Axon terminals/buttons: button-like structures at end of axon branches 30. What is the Synapse? Junction between two neurons; separated by the synaptic cleft 31. What happens there? a. 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 b. Most psychoactive drugs produce their important effects by action at the synapse 32. In what sense is neural transmission an electrochemical event? Electrical along axon & chemical at synapse. 33. What is a neurotransmitter? Chemical substance stored in axon terminals that are released into the synapse when a neuron fires; “keys” 34. What is a receptor site? Large protein molecules located on the surface of a neuron; viewed as “locks” that operate before a neuron fires (to fire it must be unlocked); accomplished by neurotransmitter substances released at the terminal buttons. 35. 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. ** Receptors consist of an ion channel and a receptor site. When a 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 in 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) 36. Ionotropic Receptors? Referred to as fast receptors (process is completed in a few milliseconds). 37. Metabotropic Receptors? Slow receptors (delay changes in neuron); produce metabolic changes or activate genes (G proteins) within neurons; initiate synthesis of other chemicals (second messengers) 38. How are neurotransmitters deactivated? a. Enzyme breakdown – change structure so that it is no longer capable of occupying receptor sites (EX: some antidepressant drugs alter brain levels of the monoamines by inhibiting the activity of monoamine oxidase, the enzyme that breaks down these compounds b. Reuptake – neurotransmitters taken back up into terminal button after release; neurotransmitter is preserved, intact, and recycled (EX: cocaine) 39. 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). 40. Indirect agonist? Enhance activity of a particular neurotransmitter system without binding to the receptor (EX: cocaine does not bind to dopamine receptors but enhances dopamine transmission by blocking reuptake) 41. Antagonist? Prevents other compounds from activating the receptor; act as if they fit into the lock but jam the lock and prevent neurons from firing (EX: Naloxone reverses or blocks effects of opiates) 42. Indirect antagonist? Inhibit activity of a neurotransmitter system without binding to the receptor (EX: reserpine either blocks creation of serotonin or inhibits release of serotonin) 43. Acetylcholine? One of the first neurotransmitters discovered; sensory processing, attention, and memory; located outside of the brain (axon terminals of neurons that activate skeletal muscles); muscles contract when neurotransmitters that synapse with muscle fibers fire and release acetylcholine into the neuromuscular junction; drugs used to reduce symptoms of Alzheimer’s disease elevate levels of acetylcholine in the brain through inhibition of the enzyme acetylcholinesterase. 44. What are the three monoamines and what are their functions? a. Norepinephrine: ANS (sympathetic) activity; discovered early because it’s found outside the brain; mediates physical changes that accompany emotional arousal; regulation of hunger, alertness, and arousal b. Serotonin: found throughout the brain; regulation of sleep and mood c. Dopamine: coordinated motor movement and reward; critical chemical in producing rewarding properties of drugs; nucleus accumbens rich in dopamine 45. How do they relate to disorders like Parkinson’s disease? Characterized by progressive loss of fine motor movement, muscle rigidity, and tremors; found mostly in elderly; caused by lack of dopamine (dopamine deficiency hypothesis) 46. What is L-Dopa? Chemical precursor of dopamine used to treat Parkinson’s; effective in relieving symptoms; penetrates blood-brain barrier, reaches the brain, and is then converted to dopamine; dopaminergic neurons continue to be lost and eventually L-Dopa cannot correct the loss. 47. Schizophrenia? Major loss of contact with reality, characterized by delusions and hallucinations, social withdrawal, and distortions of emotionality; biochemical bases (dopamine and serotonin); symptoms linked to high levels of monoamine activity; trade-off between treatment of schizophrenic symptoms (too much dopamine) and developing Parkinson’s symptoms (lack of dopamine) 48. Monoamine Theory of Depression? Depression is associated with dysregulation of monoamines (norepinephrine and serotonin); originated from the finding that certain drugs that depleted monoamines seemed to produce depression; deficient serotonin activity linked to suicidal behavior a. EX: Reserpine – once used to treat high blood pressure but makes monoaminergic vesicles leaky which leads to depletion of norepinephrine, serotonin, and dopamine by an enzyme; often causes depression in people whose mood states were normal before treatment; produces Parkinson’s symptoms due to dopamine depletion (which led to L-Dopa) 49. What is the blood-brain barrier? Filters blood before it can enter the brain to protect against toxins. 50. What is neurogenesis? Birth of new neurons; may occur in the hippocampus and other areas throughout an adult brain. 51. How is it related to depression? Reduced hippocampus size linked to patients with depression; may indicate less neurogenesis; elevated serotonin levels increase neurogenesis; suggests that the increase of the birth of neurons (rather than the elevation of serotonin per se) is responsible for antidepressant action. 52. Endorphins? Neurotransmitters mimicked by opiate drugs, such as morphine and heroin. 53. What is GABA? Most abundant inhibitory neurotransmitter in the brain; opens negatively charged chloride ion channels; if a neuron has a GABAergic receptor site that is activated, a large quantity of the excitatory transmitter is required for a 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. 54. What is glutamate? Most abundant excitatory neurotransmitter; learning and memory processes; some hallucinogenic drugs (PCP and ketamine) act on glutamate receptors in some parts of the brain. 55. What drugs affect the neurotransmitter anandamide? Lipid neurotransmitters mimicked by Marijuana. 56. Central Nervous System: 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). 57. Peripheral Nervous System: all nerve tissues outside the CNS; regulates various nonconscious or automatic functions; somatic and autonomic branches. 58. What are the two branches of the Autonomic Nervous System? Sympathetic and Parasympathetic. 59. Sympathetic: activated during emotional arousal; release of epinephrine or norepinephrine from adrenal glands; “fight-or-flight,” increased heart rate, blood pressure, respiratory rates, and sweating; pupils dilate; mouth becomes dry; blood is shunted away from the internal organs and to the brain and large muscle groups. 60. Parasympathetic: balances actions of the sympathetic branch by exerting opposite effects (i.e. lowering heart rate and blood pressure). 61. What is a sympathomimetic drug? Drugs such as cocaine, amphetamines, and hallucinogens (LSD) that mimic sympathetic arousal. 62. Be able to identify functions of the following: Medulla oblongata, cerebellum, reticular activating system, thalamus, hypothalamus, mesolimbic dopaminergic pathway, hippocampus, and substantia nigra. 63. Medulla Oblongata: lowest hindbrain structure; regulation of breathing, heart rate, vomiting, swallowing, blood pressure, and digestive process; when drugs affect medulla the person is in danger due to respiratory or cardiovascular failure; when toxic chemicals reach high volume, the vomit center (located here) is triggered, which is why large quantities of alcohol often cause nausea and vomiting. 64. Cerebellum: hindbrain structure important in motor control and coordination; contains several billion neurons; largely unconscious but involves balance, coordinated movements, and speech; loss of motor control and balanced produced by drugs act here 65. Reticular Activating System: pathway running through the medulla and pons; regulates alertness and arousal; drugs that lower arousal and induce sleep (barbs and tranquilizers) thought to act here. 66. Thalamus: forebrain structure; receives/organizes sensory stimuli and sends it to relevant centers; basic biological motives, such as hunger and thirst controls body temperature, aggression, and sexual behavior; lesion in one area inhibits eating (loss results in overeating); another area seems to excite hunger (because its loss results in less eating); James Olds – the effects of electrical stimulation of a brain region generally are the opposite of lesioning or removing that region 67. Hypothalamus: regulates eating, drinking, and other basic biological drives. 68. Mesolimbic Dopaminergic Pathway: pathway that is rewarding when stimulated; discovered by James Olds; many pleasurable events result in release of dopamine in its pathway – chocolate, sex, drugs (cocaine, heroin, nicotine) 69. Hippocampus: limbic system; critical in memory storage; long-term memory intact if damaged but the ability to form new memories is impaired 70. Substantia Nigra: produces dopamine; damage produces Parkinson’s (doesn’t appear until 80% of substantia nigra is destroyed: designer drugs capable of killing neurons here; “black substance” 71. How is brain damage assessed? Consider the various ways of imaging the brain. a. Electroencephalography (EEG): measures electrical activity in the brain; direct analysis of brain tissue; reveals gross brain damage. b. Computerized Axial Tomography (CT): produces x-ray image; changed to different depths of the brain to detect abnormalities. c. Positron-emission tomography (PET): measures activity in selected brain regions by injecting weak radioisotopes into the brain; radioactive glucose, oxygen, or other neurochemicals measured; changes induced by drugs can be assessed d. Magnetic Resonance Imaging (MRI): strong magnetic field passed through head; radio waves are generated and cause molecules to emit energy of different frequencies; high-resolution 3-dimensional image of the brain e. Functional Magnetic Resonance Imaging (fMRI): measures oxygen levels in blood vessels; oxygen levels correlated with metabolism of particular brain regions; rapid imaging 72. Be able to identify the functions of the Lobes. a. Frontal Lobe: ability to plan and control impulses; control panel of our personality and our ability to communicate; Cognitive skills; emotional expression; problem solving; memory; language; judgement; sexual behavior; abnormalities may be caused by exposure to some drugs (i.e. cocaine) b. Parietal Lobe: sensory information (such as taste, temperature, and touch); humans would not be able to feel sensations of touch if damaged c. Temporal Lobe: primary auditory perception; receives sensory information such as sounds and speech from ears; key to comprehending meaningful speech d. Occipital Lobe: processes what your eyes are seeing; stimulation of the eye is perceived as a visual stimulus when the signal reaches the occipital cortex CHAPTER 4: PHARMACOLOGY 73. Define pharmacokinetics: how much drug reaches its site of action (absorption, distribution, biotransformation, and excretion) 74. Define pharmacodynamics: mechanism of drug actions; biochemical and physiological effects of drugs 75. How are drug doses determined by psychologists? Body weight; amount of drug less concentrated in a heavy person– Mg (of drug) ÷ kg (of body weight); EX: if the desired dose is 0.08 mg/kg and the person weighs 80 kg, the amount is 0.08 * 80 = 6.4 mg of the drug 76. What are the major route administrations? Consider the advantages and disadvantages of each. a. Oral (swallowing) – advantage = safest, cheapest, and most convenient; disadvantage = drug effect by stomach acid breakdown b. Subcutaneous (injecting under layers of skin) – advantage = faster absorption than subcutaneous with proper preparation of salutation at injection site with good blood flow; disadvantage = deeper penetration than subcutaneous and painful at injection site c. Intramuscular (within the muscle) – advantage = faster absorption than subcutaneous with proper preparation of salutation at injection site with good blood flow; disadvantage = deeper penetration than subcutaneous; painful at injection site; risk of infection from tissue damage d. Intravenous (into the veins) – advantages = 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; disadvantages = repeated use requires healthy vein; dose administered gradually; person’s response monitored e. Inhalation (absorbed through lung’s membrane) – advantages = absorption effective and most rapid for some drugs; disadvantage – small amount of drug absorbed in any one administration f. Intranasal (absorbed through mucous membranes – advantages = for a fat (absorbed in tissue so it can be toxic) and water soluble (can dissolve in blood/not as toxic) drug, absorption is rapid and effective; disadvantages = can cause damage when drug is irritating or disrupts flow g. Sublingual (tablet placed under tongue and dissolved in saliva) – advantage = preferable to oral administration for drugs that cause vomiting; disadvantage = unpleasant taste h. Transdermal (through the skin) – advantage = Alternative to oral route when drug causes stomach pain; absorption enhanced at sites that have greater cutaneous (affecting the skin) blood flow; mixing a drug with another substance may improve penetration of the skin; disadvantage = hard for most chemicals to penetrate the skin 77. How are drugs distribution 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 blood-brain barrier to reach the brain 78. How are drugs eliminated from the body? Enzymes in the liver; enzymes in the GI tract partially break down drugs taken orally (first-pass effect) – less drugs than administered eventually distributed to its site of action; when metabolites are active, the action ends with further metabolism of the by-products or by their direct excretion in the urine 79. Define half-life. Amount of time that passes for the amount of drug in body to be reduced by half 80. 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; positive drug test does not provide precise information about when drug was used (unless drug is detected in blood) 81. What is a dose-effect (response) curve? When the effect of drug x is at a specified dose; curve is a representation of some effect according to a dose of the drug (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 dose-effect curve). 82. What is meant by efficacy? Peak level of dose-effect curve for a given effect. 83. What is meant by potency? Minimum effect dose of a drug on a dose-effect curve; dose of a drug required to produce a given effect; the lower the dose, the more potent the drug. 84. What is an effective dose? Dose at which a given % of individuals show a particular effect of drug. 85. What is meant by ED50? Effective dose 50; the dose of a drug required to produce a given effect in 50% of individuals tested. 86. What is meant by lethal dose? Given dose at which a given % of individuals die within a specified time. 87. What is meant by LD50? Lethal dose; the dose at which 50% of animals administered a given dose of a drug died within a stated time. 88. What about LD1? This will tell you when the first mouse died; used today 89. Therapeutic Index? Measure of a drug’s safety in medical care; computed as a ratio of LD50 (dose that will kill 50% of patients who receive it) divided by ED50 (50% dose that would work). 90. Consider drug interactions? A drug interaction is when the effects of one drug are modified by presence of another (EX: sleeping pills/barbiturates & alcohol); also called potentiation. 91. What is synergism? Any enhancing drug interaction; when 2 drug are synergistic the effects of taking them together are greater than effects of taking either alone. CHAPTER 5: PSYCHOPHARMACOLOGY AND NEW DRUG DEVELOPMENT 92. 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). 93. 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. 94. Functional Tolerance. Brain and other parts of the CNS become less sensitive to drug’s effects; pharmacodynamics tolerance. 95. Acute Tolerance. Type of functional tolerance; measured within the 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 & cocaine 96. 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 short-term 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) 97. Cross-tolerance. 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 cross-tolerance to drugs used medically as anesthetics. 98. 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. 99. Reverse Tolerance. Increased sensitivity to the effects of the drug with repeated use (EX: marijuana & cocaine) 100. Cell Adaption Theory of Tolerance: Cells become adapted to presence of the drug with repeated exposure; adaption allows cells to maintain normal functioning at given drug dose; more drug required to disrupt cell functioning (and produce desired effect) 101. Downregulation: Repeated exposure to drugs may reduce the number of receptor sites on neurons that the drug activates. 102. Drug Compensatory Reactions and Learning (Tolerance): Tolerance to drugs is partially learned; compensatory reactions – when an event disrupts the body’s homeostasis the body can counteract disruption [coffee increase heart rate; simultaneously, your body works to reduce heartrate]; reactions thought to become stronger with repeated use of a given drug. 103. Classical Conditioning (Tolerance): 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; exposure to these stimuli in absence of drug may produce craving; EX: presenting syringe/tourniquet may elicit urges in IV heroin or cocaine users to consume respective drugs 104. Extinction. When people have been exposed to these stimuli many times without the drug, the effects dissipate. 105. 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 106. 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. 107. Operant Principles and Drug Dependence: Drug users derive positive or negative reinforcement from their behavior and experience little punishment for it; behavioral pharmacologists study drug access as consequences for behavior in self-administration studies. 108. Self-administration studies. testing whether research participants will self-administer a drug; important source of knowledge because they show that not all drugs have reinforcement value (LSD and Marijuana); drugs humans tend not to abuse are not self-administered by other animals; rats will usually self-administer drugs that humans like to self-administer; 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 drug-seeking behavior. 109. Drug discrimination. 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. 110. Conflict Procedures. Conflict Paradigm – concerns the effects on a behavior of a drug that has a history of both reinforcement and punishment; choose between a lever that produces a big reward (a lot of food) but then might produce also a shock vs. a choice of a very small amount of food; animal isn’t sure what to pick; different drugs will affect conflict differently; EX: rat presses lever to get food as reinforcer; after learning occurs rat is punished by pressing lever (electric shock); rat now 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. 111. Ethical issues raised in drug research with animals and humans. Nuremberg Code – 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; animals cannot give consent; unethical to have placebo control group if there is an alternative drug that has demonstrated effectiveness (many view such a design as essential to learning how drugs affect people) 112. Double-Blind: 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 113. What steps must occur before a drug receives FDA approval and goes to market? Initial synthesis and preclinical studies (1-3 years). Phase 1 clinical trial – up to 50 normal volunteers (1 year). Phase 2 clinical trial – controlled studies in 50-200 patients with a target disease (2 years). Phase 3 clinical trials – controlled and open studies of 1000 or more patients monitored for effectiveness for adverse reactions & data is used for determining doses and labeling requirements (3 years). FDA review/approval (1-2 years). Post-marketing testing (1-2 years). 114. Chemical name. Indicates drug’s structural formula and allows chemists to reproduce the drug’s structure. 115. Brand name. Commercial name given to a drug by its manufacturer; says nothing about the chemical structure. 116. Generic name. General name given to a drug that is shorter (and easier for most people to say) than chemical name. 117. 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) CHAPTER 6: COCAINE, AMPHETAIMTES, AND RELATED STIMULANTS 118. What is Erythroxylum coca? Where does it grow? Coca bush or tree whose leaves contain cocaine; first major stimulant used by humans; grown in the Andean regions of Bolivia, Ecuador, northern Argentina, and Peru. 119. Trace the early history of cocaine. How was it used by the Indian people of Peru and Bolivia? Jerome Jaffee (psychiatrist and anthropologist) observed the chewing of the coca leaf by conqueros; hold it between the cheek and gums (similar to chewing tobacco today); religious, medicinal, and work-related significance. 120. Mama Coca. Beautiful woman who was executed for adultery; divine coca plant grew from her remains; consumed only by royalty in her memory. th 121. How was cocaine introduced to Europe? Spanish Conquistadors conquered the Incas in the 16 century; they were disturbed by the religious use of coca because it was against Catholicism; they permitted/encouraged use of coca as a means of enslaving them; helped them work harder and longer, used as form of payment, & levied taxes to be paid on coca leaves; European naturalists explored Peru and experimented with coca 122. Formication Syndrome. Symptoms of itching and feeling as if insects are crawling under the skin; caused by cocaine & methamphetamine overdose. 123. Other symptoms of cocaine overdose? Paranoid delusions (similar to paranoid Schizophrenia); overdose death; dependence; Reports of violent acts committed under the influence of cocaine. 124. What are Amphetamines? Consider their history. 1914 Harrison Narcotics Act resulted in decline of cocaine use; new stimulants (amphetamines) became popular – amphetamine, dextroamphetamine, & methamphetamine; Soldier’s Disease (widespread use of morphine in soldiers during the Civil War); post WWII epidemic in Japan, Sweden, and other parts of Europe; recognized as dangerous in the US (1960s). 125. What impact has cocaine had on society in the Columbia in the past 25 years? Distribution of cocaine historically controlled by Columbian cartels; Medellin Cartel targeted government officials, judges, and court employees, with 2000+ murders in the first 6 months; Pablo Escobar [former head of Medellin Cartel] killed in gunfight with police in 1993; Cali Cartel made billions of dollars in the cocaine trade but leaders were arrested in the late 1990s; cocaine trade became less centralized and former members moved their operations to multiple sites. 126. What impact has cocaine had on society in the US in the past 25 years? Overdose deaths and other related ER visits rapidly increased in the late 1980s; organized gangs with high-tech weapons linked to shooting 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; increased risk of HIV transmission. 127. Why do people in the Andean countries of South America chew coca? Desired stimulant effects (stimulate alertness, reduce fatigue, & combat altitude sickness) 128. How did the use of cocaine change in the second epidemic of cocaine abuse? Epidemic was a movement from amphetamines to cocaine; increased availability and cheaper than before (previously, only stars and athletes could afford it); more people able to regularly use in high doses. 129. Street cocaine: produced by combining a paste made from coca leaves with a hydrochloric acid solution to form a salt; cocaine hydrochloride 130. Freebase cocaine: separate cocaine base from hydrochloride salt; produced by missing cocaine salt with baking soda and water; solution is heated, resulting in brittle sheets of cocaine; sheets are then “cracked” into small, smokeable chunks or rocks 131. What is “ice” or “speed?” Methamphetamines 132. What are issues associated with meth production? Many of the chemicals are highly flammable and the process requires ingredients be heated with a burner; risk of explosion and fire due to toxic waste; by-products can cause health hazards wherever they are dumped 133. Effects of exposure to high doses of methamphetamines. Seizures, convulsions, cardiovascular collapse, overdose (stimulant psychosis), depression (withdrawal symptom), & “meth mouth” (deteriorating and loss of teeth) 134. Brain damage and high doses of methamphetamines. 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. 135. Why are synthetic cathinones often called “bath salts” or “plant food?” Early 2000s: Applied as a means of insect control in Israel (called “plant food” because of its agricultural origins); 2009 – spread from Israel to Europe & 2010 – spread to the U.S.; called “bath salts” because it resembled products used in the bath tub 136. What are some frequently used synthetic cathinones? Mephedrone, Methylone, & MDPV (Methylenedioxypyrovalerone) 137. What law recently banned sales of the main synthetic cathinones? Synthetic cathinones moved to emergency Schedule I status in 2011; Synthetic Drug Abuse Prevention Act (2012) decreased the number of ER calls to U.S. poison centers 138. Cocaine blues: depression and lack of joy during cocaine withdrawal; long-term effects involve depletion of monoamines which is linked to clinical depression 139. Mechanism of Action for cocaine and amphetamines: stimulants initially produce activity in neural pathways sensitive to monoamine neurotransmitters; reuptake is blocked so that enzymes break down the monoamine neurotransmitters 140. Acute physiological effects of cocaine. Enhances physical strength and endurance; 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)] 141. Acute psychological effects of cocaine. Mood elevation and alertness; talkativeness and sociability; insomnia; enhances performance on some types of cognitive tasks (but with increased errors); impairs one’s ability to learn highly complex tasks. 142. State-dependent learning: Learning under the influence of a drug is best recalled when one is in the same drug- induced state; 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 143. In what ways can cocaine overdose cause death? Convulsions or seizures may result in: respiratory collapse, heart attack (due to coronary artery spasms), & stroke; Combination Effects [Alcohol + cocaine = cocathylene toxicity] [Cocaine (or amphetamine) + heroin (or opiate) = “speed ball”/overdose] [Morphine + cocaine = increased cardiovascular effects] 144. Tolerance to cocaine. Acute (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); long-term protracted (inconsistent findings); reverse tolerance/sensitization (Increase in negative effects with repeated administration; attributed to accumulation of sleep loss and reduction of caloric intake) 145. Dependence on cocaine. Withdrawal symptoms – depression, anxiety, changes in appetite, sleeping disturbances, and cravings 146. Crash phase of cocaine withdrawal. 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 ability to experience normal pleasure or anhedonia] 147. Extinction phase of cocaine withdrawal. 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) 148. Define stimulant psychosis. Delusions and hallucinations; compulsive stereotyped behavior [rocking, hair pulling, chain smoking, or fiddling]; formation (symptoms of itching and feeling as if insects are crawling under the skin]; often associated with violent behavior 149. Crack baby 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 150. Prognosis for crack babies. Difficulties may not involve permanent neurological damage induced by cocaine, but stigma may create a self-fulfilling prophecy; 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) 151. What is Attention Deficit Hyperactivity Disorder? Trouble paying attention (inattention, fidgeting, & restlessness); not necessarily hyperactive and often leads to: impaired academic performance, misbehavior at school, & conflict with peers, siblings, and parents 152. What drugs are used to treat ADHD? In 1937, physician Charles Bradley discovered that hyperactive children were calmed by a dose of amphetamine; stimulant drugs used to treat ADHD, such as – Methylphenidate (Concerta, Ritalin, & Daytrana) and amphetamines (Adderall, Vyvanse). 153. What is Khat? Plant native to East Africa (Catha edulis); most common route of administration is chewing fresh leaves; juices are swallowed; contain two stimulants – cathnie and cathinone; synthetic variations (cathinones) sold as bath salts; widely used throughout East Africa & Arabian Peninsula (5 million daily users) 154. Vitamin R: Ritalin – makes users feel energetic & enhances mood (has become a popular club/dance drug); many college students take amphetamines or methylphenidate to study; 60+% of college students with ADHD report giving/selling their meds CHAPTER 7: NICOTINE 155. What is Nicotiana tabacum? Tobacco plant where nicotine is found; provides all tobacco typically consumed in the US 156. Where did tobacco originate? Columbus found Native Americans in the New World smoking dried tobacco leaves. 157. How was tobacco introduced to Europe? Columbus/European explorers brought seeds of tobacco plant home; spread them to other parts of the world; quickly became popular among Europeans 158. What are the current smoking trends among Americans? ~ 20% of American adults smoke cigarettes today; cigarette smoking most common way to use tobacco; smoking declined in latter part of the 20th century; increase in the amount of people who quit smoking (most did so on their own) 159. What neurotransmitter is influenced by nicotine? Acetylcholine; biphasic drug – stimulates ACH receptors at low doses but its effects are more depressant in high doses 160. Describe the absorption of nicotine. Blood distributes it to a number of sites of pharmacological action; inhalation – nicotine reaches the brain from the lungs in 7 seconds and takes 3-5 minutes to reach peak levels in the brain; nicotine levels also fall rapidly; half-life is 10-20 minutes 161. Acute effects of nicotine? Increases behavioral activity, may produce tremors, stimulates vomiting center in brain stem [tolerance to this effect develops quickly], stimulates release of antidiuretic hormones from hypothalamus [increasing fluid retention], reduces muscle tone by reducing activity of efferent nerves from muscles, enhances alertness, learning, and memory, increases HR, BP, and contraction of the heart; initiates dilation of the arteries [if they are not atherosclerotic] to meet heart’s increased oxygen demand caused by nicotine 162. Nicotine and Tolerance. 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; dispositional tolerance (taking more of the drug to produce the desired effect); EX: smokers metabolize drugs more quickly than nonsmokers do 163. Nicotine and dependence. Withdrawal symptoms – cravings, irritability, anxiety, difficulty concentrating, restlessness, increased appetite, impatience, somatic complaints, insomnia; 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 164. What are the health consequences of chronic tobacco use? 440,000 people in the U.S. who smoke die prematurely every year (1200+ a day); WHO: over 5 million men and women worldwide die prematurely due to their cigarette smoking 165. Woloshin, Schwartz, & Welch 2002: the likelihood of dying from heart attack, stroke, or lung disease was significantly high in smokers as compared to nonsmokers for women and men aged 30+ 166. What aspects of smoking cause which problems? Tar [material that remains after cigarette smoke is passed through a filter; contains most of the cancer-causing substances]; Nicotine [Coronary Heart Disease and heart attacks]; Carbon monoxide [reduces amount of hemoglobin which depressives the body’s tissues of oxygen leaving the heart & brain vulnerable] 167. Passive Smoking. Third leading preventable cause of death in the U.S. behind active smoking and alcohol; Environmental Protection Agency (1993) declared secondhand smoke to be a “Group A” carcinogen [along with arsenic, asbestos, benzene, & radon]; 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; led to the banning of smoking in public places Treatments for helping People Quit Smoking 168. Behavioral Programs: goal is to teach smokers to identify situations that present a high risk for them to smoke and to use techniques to weaken the risk of smoking in these situations, and teach smokers to self-monitor their smoking behavior; ongoing contact with clinical staff in an individual group format for 2-3 months; majority of individuals who complete such programs resume smoking after 6-12 months [attributed to cravings]; overall considered an effective way to stop smoking by APA 169. Nicotine Replacement Therapies: administering nicotine to smokers as part of the effort to help them quit smoking; EX: nicotine gum, nicotine patch, nicotine nasal spray, nicotine inhalers, & nicotine lozenges; 2x larger change of quitting smoking; combining NRT’s with behavioral programs enhance the quit rates achieved by either treatment alone; little evidence for long-term negative consequences; women tended to require more intense behavioral support than men 170. Harm Reduction Programs: view behavior change that results in the reduction [or elimination] of negative consequences desirable; EX: electronic cigarette 171. Is formal treatment necessary? Although most people stop smoking without help, they tend to succeed only after multiple attempts; 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; the emphasis today is on prevention (treatment less so) 172. Omnibus Tobacco Settlement: 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; likely won due to the tobacco industry concealing early knowledge about the relationship between smoking and serious health problems 173. What is varenicline (Chantix)? Drug developed specifically for the treatment of smoking; works by competing with nicotine in binding to nicotine receptors; stimulates nicotine receptors as nicotine does so that smoking cravings are assuaged; 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 174. Describe the general history of caffeine use. Mythical origins – discovered in Arabia by a holy man; goats in a herd had been jumping around at night instead of sleeping; they had been nibbling on the beans of the coffee plant; holy man thought the beans from the same plant could help him endure long nights of prayer 175. Where does caffeine come from? Explorers found coffee in Arabia, Turkey, and Ethiopia; Methylxanthines [caffeine] found in plants 176. What are other methylxanthines and where are they found? Mythical origins of tea (2737 b.c. by Chinese Emporer Shen Nung); found kola nut in West Africa; found cacao plant [source of chocolate] in Mexico and much of Central and South America; other sources of tea discovered in parts of North and South America 177. What are the estimates of caffeine use around the world? Caffeine is the world’s most preferred drug; about 90% of the world’s population regularly consumes products that contain caffeine, with coffee, tea, and soft drinks being the most common sources; average consumption of caffeine per person worldwide is around 70 mg 178. Adenosine Hypothesis. Most accepted explanation for coffee’s acute effects; adenosine – inhibitory neurotransmitter located in the CNS & PNS; adenosine leads to behavioral sedation, regulation of oxygen delivery to cells, dilation of cerebral and coronary blood vessels, & production of asthma; caffeine and the other methylxanthines occupy adenosine receptors and then block the action of that transmitter 179. How is caffeine absorbed in the body? Readily absorbed from the gastrointestinal tract; passes through blood- brain barrier; 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 180. Tolerance to caffeine. Tolerance develops to caffeine’s effects on renal function, sleep, and physiological functions (BP and HR); little tolerance seems to develop to caffeine’s stimulant effects; one reason people are heavier or lighter caffeine users is their individual ability to tolerate caffeine 181. Dependence on caffeine. Can develop with an exposure of 300 mg of caffeine a day for only three consecutive days; symptoms range from mild to severe and begin within 12-24 hours of cessation of caffeine use; may last about a week 182. Withdrawal? Headache and fatigue (most common), depression, decreased alertness, less relaxed mood, decreased activity and energy, greater sleepiness and drowsiness, & increased irritability 183. Physiological effects of caffeine. Contraction of striated muscle (heart), relaxation of smooth muscle [especially coronary arteries, uterus, and bronchi], diuretic effects on the kidneys, stimulating effect on respiration at higher doses, elevation of basal metabolism, and various endocrine and enzymatic effects 184. Effects of caffeine on mood. Moderate doses of caffeine are reliably associated with feeling energized, creative, efficient, confident, and alert; believed that many people who are afflicted with significant depression “medicate” themselves by using caffeine products 185. Effects of caffeine on performance. Improves task performance (decreases fatigue & increases vigilance); Choice Reaction Time – impairs the decision-making part of the task but improves the motor component; enhances athletic performance including perceived exertion and endurance 186. How does caffeine interact with nicotine and alcohol? Smokers smoke fewer cigarettes after they drink coffee compared with when they have not had coffee (stronger for lighter caffeine users); excretion of caffeine from the body occurs more than 50% faster in smokers than in nonsmokers; how people react to nicotine may be associated with how they react to caffeine and alcohol 187. Describe the toxic effects of caffeine. People differ in how much caffeine they can ingest before they experience symptoms of intoxication; 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, and seeing flashes of light 188. Caffeine overdose. 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; overdose cases are rare and usually occur in people with pre-existing heart abnormalities 189. Chronic effects of caffeine. Considered a relatively safe drug; caffeine consumption should be moderated (to prevent minor symptoms that occur with high levels of use); pregnant women benefit by keeping caffeine consumption at a low to moderate level; people diagnosed with Generalized Anxiety Disorder are hypersensitive to the effects of caffeine and the drug may exacerbate anxiety symptoms 190. Therapeutic effects of the methylxanthines. Used in a variety of prescriptions and over-the-counter medications (in many remedies for headaches and colds); found in appetite-suppressant medications because of its diuretic effects; differences among xanthines and their effects are based on slight differences in their chemical structure CHAPTER 9: ALCOHOL 191. How are alcoholic beverages produced? Fermentation – creates environment for yeasts (living microorganisms); yeasts multiply rapidly by eating the sugar; sugar converted into ethanol and carbon dioxide by the yeast’s metabolic processes; carbon dioxide bubbles at the top
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