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| any substance that alters the physiology of the body that is intended to be consumed for the purpose of treatment or to get high |
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| The Food, Drug, and Cosmetic Act employs |
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| preclinical animal testing and preclinical trials |
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| The DEA and HHS have the power to... |
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| add, remove or change the schedule of drugs and substances of the drug scheduling list |
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High potential for abuse Medical use is accepted but limited with severe restrictions Prolonged use increases the propensity for dependence |
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High potential for abuse Not used in the medical profession for treatment of any physical or psychological ailment Drug safety is of high concern |
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Potential for abuse is less than those drugs listed in Schedule 1 and 2 Medical use is accepted, normally without restrictions Prolonged use modestly increases the propensity for dependence |
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formal chemical jargon; molecular structure 7 – chloro-1, 3, -dihydro-1-methyl-5-phenyl-2H-1, 4-benzodiazepin-2-one |
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| propriety name (patented name) |
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| Drug scheduling is based on |
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| Abuse liability, use in medical practice, risk for dependence |
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| the concentration (m/v) or quantity of a particular drug |
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| the maximum effect that a drug will produce |
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| refers to the affinity for the drug at the receptor |
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a value indicating drug safety
ED50 – median effective dose LD50 – median lethal dose |
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| – the blood concentration level of a drug that is above the level of the therapeutic level but below the toxic level |
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| demonstrates the relationship between the drug and response |
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| The range of time that the drug has a therapeutic effect |
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| the desired drug effect or response for a specific situation |
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| a drug that shifts the DRC of another drug to the right; blocks the effects of the neurotransmitter |
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| a drug that mimics the action of another drug; mimics the effect of the neurotransmitter |
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| when the action of one drug does not have an effect yet it increases the effect of another in adjunctive therapy |
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| when two drugs mutually increase both of the desired effects |
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| the study of how drugs move into, get around in and are eliminated from the body |
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| The rate at which an administered drug is absorbed into the circulatory system |
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| stomach --> small intestines --> capillaries --> circulatory system |
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| What is the site of action (SOA) for drugs of abuse |
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| The process by which drugs are transported throughout the body to get to the site of action |
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| How does protein binding inhibit drug distribution |
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| When drug binds to protein, it is too big to pass through bilayer. We must wait until they break apart so the drug can pass through the bilayer |
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| capillaries, glial cells, and extra membrane |
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| How do drugs get through the BBB |
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| Drugs heighten stress level on brain causing a breakdown of the BBB letting drugs in |
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| The biotransformation and restructuring of molecules (i.e. drugs) |
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| Enzyme induction is present when... |
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| the baseline level of a particular enzyme is increased after repeated activation |
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| The suppression of an enzyme system as a result of two drugs competing for the same enzyme |
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| determining the rate at which a drug is eliminated from the body |
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| the amount of time it takes for the body to remove 50% of the drug |
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| excretion of a drug once peak levels have been reached |
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| The nervous system is made up of the CNS and PNS. What two components make up the CNS? |
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| What two components make up the PNS? |
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| Somatic NS (voluntary control of muscles) and Autonomic NS (involuntary) |
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| What two components make up the Autonomic NS? |
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| Sympathetic NS (Fight) and Parasympathetic NS (Flight) |
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| area of the brain responsible for gauging stimuli valence, controlling emotions based on sensory stimuli, and motivate (or drive) the organism to repeat actions that produced pleasure |
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| The frontal lobe controls... |
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| motor function, problem solving, memory, judgement, impulse control, social/sexual behavior |
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| The parietal lobe controls... |
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| The temporal lobe controls... |
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| Language, emotion, memory |
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| The occipital lobe controls... |
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| receives, analyzes and transmits information |
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| provide metabolic and structural functions |
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| intercellular communication via chemical messengers; dependent on four main ions: Sodium, potassium, calcium, chlorine |
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| refer to stimulation of a cell, release of a chemical messenger |
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| increasing positivity of the membrane (potassium out) |
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| increasing negativity of the membrane (sodium in) |
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| resting state of a neuron |
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| the chemical messengers, conveying information from one neuron to another; they bind to receptors of the postsynaptic cell exciting (activating) or inhibiting (stopping) the postsynaptic neuron |
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| drugs that mimic the effect of the NT |
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| drugs that block the effect of the NT |
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| Drugs exert their effects on the brain by... |
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| Occupying receptors (agonist/antagonist), decreasing enzyme activity, altering enzyme reuptake, interfering with ion channels, increasing or decreasing secretion of NT from presynaptic nerve |
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| A maladaptive pattern of substance use, leading to clinically significant impairment or distress |
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| The defining characteristics of drug addiction are... |
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| Impaired control over the use of a drug and the drug use has harmful consequences |
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| Addiction as a physical/psychological dependence |
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Assumption: The drug is a necessity to maintain functioning of physical body and the brain
Caveat: Relapse manifests after long periods of sobriety |
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| Addiction as a method of self-medication |
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Assumption: The drug is consumed to provide relief of unpleasant symptoms
Caveat: Anxious subjects do not consistently choose diazepam over a placebo |
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| Expectancy Theory of Addiction |
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Assumption: Past experience with a drug or the knowledge of taking a drug (even if a placebo is given) sets a drug expectation influencing drug effects
Caveat: Despite negative consequences associated with alcohol abuse and addiction, leading to aversive expectancies, persistent use presents |
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| Limitations to proposed theories |
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1. Self reported so they are biased 2. Limited control over variables 3. Addiction can be explained as circular (addiction results in physical dependence where the person must take drugs in order to keep a normal functioning body and are driven by withdrawals) |
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| the study of how stimuli influence behavior; human behavior is shaped by the environment |
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| Positive Reinforcement Model |
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| drugs are self-administered because they act as positive reinforcers; it is the reinforcement that conditions, shapes or molds self-administration |
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| the event in which a previously neutral stimulus elicits a conditioned response |
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| Conditioned Place Preference (CPP) |
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| a Pavlovian model of drug addiction, highlighting the importance of environmental stimuli in drug addiction |
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| the training of voluntary behavior to acquire a specific response |
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| a model of drug reinstatement; aimed at elucidating the mechanisms associated with drug-seeking and drug-taking behavior |
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| the increase in the motivational “incentive” properties of a drug and associated drug-associated stimuli. A model of drug addiction, specifically focusing on mechanisms driving relapse. |
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| the increase in drug-taking behavior to eliminate a negative, aversive state. Concentrated on negative reinforcement. A conditioning model of drug addiction, elucidating the influence of aversive states in the reinstatement of drug addiction. |
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