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110 Cards in this Set
- Front
- Back
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overview, neurobiology of addiction |
-genetic vulnerability leads to a unique response to exposure to a drug -individual engages in repeated exposure due to positive reinforcement and activation of reward centers - these repeated exposures lead to change in the brain which leads to change in response to drug( tolerance) -the person changes his/her methods of use to counteract tolerance -the brain needs the drug, and stopping use immediately causes a dramatic change again called withdrawal - the person takes the drug to counter withdrawal effects |
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neural reward circuitry |
centers around connections between ventral tegmental area to basal system such as amygdala, nucleus accumbens, olfactory tubercle and frontal cortex |
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reinforcement |
theoretical construct by which a stimulus increases the probability of a response -contributes to initial short term effects of drug and potential for long term cravings |
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neuroadaption |
the process by which initial drug affects are either attenuated or enhanced by repeated exposure -has the potential for permanence - contributes to initial short term effects of drug and potential for long term cravings -neuroadaptive changes that occur with chronic drug use lead to changes in reinforcing effects which then impact addictive behavior |
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drugs as reinforcers |
both positive and negative reinforcers, important in maintaining drug use following the development of addiction positive-motivated because of positive state, primarily operate in establishing addictive behavior negative- motivated because of removal of negative symptoms (withdrawal) |
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behavioral models of reinforcement |
intracranial electrical self-stimulation intravenous drug self-stimulation place conditioning drug discrimination |
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sensitization |
increased response to a drug after repeated administration of the drug wanting vs liking |
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counteradaption |
processes initiated to counter the acute effects of a drug such as tolerance and withdrawal |
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theories of addiction |
abberant learning theory frontostriatal dysfunction hedonic-allostasis theory of addiction incentive-sensitization theory genetics psychomotor stimulant theory |
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abberant learning theory |
theme is that heightened responsiveness to drug cues is insensitive to punishment, leading to continued drug use even when it has adverse consequences repeated exposure to addictive drugs heightens pavlovian and instrumental responsiveness to drug associated cues through neurons that respond to non drug associated cues ***through ventral striatum, dorsal striatum or both |
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fronto striatal dysfunction |
top down deficits in cognitive control, leading to loss of impulse control, impaired decision making processes, exaggerated responses to drug associated cues and compulsive drug use
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compulsive drug use |
is due to drug induced changes in cortical and limbic circuits, leading to exagerated responses to drugs and drug associated cues and impaired inhibitory control |
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hedonic allostasis theory |
based on opponent process theory of motivation initial drug use is based on drugs rewarding effects, additional drug use leads to decrease in rewarding effects and recruitment of stress related symptoms
hedonic allostatic state-chronic change in normal reward setpoint
causes loss in control over drug use through cortico-striatal-thalamic circuits involved in compulsive behavior |
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incentive sensitization theory |
addictive drugs increase mesocorticolimbic dopamine NTs the dopaminergic system increases salience drugs cause this system to become hypersensitive to drugs and drug cues |
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psychological theories |
psychoanalytic psychodynamic behavioral cognitive cognitive behavioral |
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psychoanalytic |
freudian beliefs ego, id, superego , inner conflicts arise because all of these three are fighting ---if this is unresolved, that is what leads to a mental disorder ----concept of anxiety ----ego defense mechanisms help to deal with moral anxiety making the unconscious conscious |
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symptom |
defined by freud as the ability for a repressed idea or memory to come to consciousness |
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id |
drives desires, wants |
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ego |
combination between id and superego reality |
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superego |
morals |
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pyschoanalytic theory and substance abuse |
conceptualized as a symptom response to underlying conflicts emphasis placed on origins and maintanence of behavior developmental history plays an important role in relationships --understanding does not necessarily lead to cure |
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psychoanalytic theorists |
wurmser-drive theory khantzian-self psychology theory krystal object relations theory mcdougall-psychosomatic theory |
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wurmser |
substance abuse results from harsh superegos which threaten to overwhelm the person so the person is fleeing from these *affects ---emphasis on early trauma as an origin |
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trauma and wurmser |
exposure to violence, sexual seduction and abandonment results in hostility to authority and self-doubt and guilt -drugs help to disable this internal authority, are a way to avoid the feelings of pain, anxiety --drugs neutralize feelings of doubt and anxiety and limit superego function --focus of treatment is the analysis of the superego ---problem is when there is too much superego --therapist should offer strong emotional presence
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khantzian |
founder of self medication theory of addiction challenged the theory that people who use drugs are weak willed ppl who abuse drugs suffer more strongly that people who dont --theory is to turn uncontrolled passive suffering into controlled active suffering --*** I can do life while addicted --deficits and not conflicts underlie substance abuse ---there are holes in the organization of the self ---reflects how a person chooses which drug they use, opiates are used for anti-aggressive effect |
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krystal |
2 theories- object relations and alexithymia
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object relations |
krystal -drug experience is symbolically a primary maternal object and satisfies needs associated with the mother -related to persons developmental experience -drug abuse is acting out based upon infantile fantasies -disturbance in object relations as at the base of substance abuse |
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alexithymia |
lack of insight into cognitive aspect of feelings |
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mcdougall |
views substance abuse as similar to psychosomatic disorders -externalizing and physicalizing psychic disturbances -avoidance of emotions that would be experienced as painful if internalized ---thereby avoiding the awareness of their existence |
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critiques of psychoanalytic theory |
little empirical evidence conclusions result from case studies restrospective little evidence of treatment effectiveness the field recognizes these limitations |
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behavioral theory |
experience modifies behavior major theories: classical conditioning instrumental/operant conditioning observational learning |
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classical conditioning |
pavlov environmental cues elicit cravings to use substance users condition environmental stimuli to rituals and paraphanelia and drug use to settings, people and ritual |
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instrumental/operant |
drugs serve as positive and negative reinforcers **thorndike and skinner |
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observational learning |
learning through observation alone without an UCS or reinforcer drug treatment involves observations of skilled others **bandura |
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cognitive behavioral theory-bandura |
**bandura was one of first placed emphasis on cognitive aspects of learning learned by internal reinforcement- regulation of behavior by internal symbolic processes cognitive abilities allow us to solve problems internally, do not need external reinforcement ***social learning theory |
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social learning theory |
CBT bandura cognitive processes mediate learning processes human behavior develops by conditioning and modeling, which produce behaviors but also influence patterns of thought which then also shape behavior **reciprocal determinism- people influence and are influence by their environments ***self- efficacy- a persons expectations that he or she will be able to perform a coping response in a given situation, coupled with the expectation that this response will be reinforced **VIEWS SUBSTANCE ABUSE AS A FAILURE OF COPING |
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ellis and CBT |
rational emotive therapy -role of cognition in development of emotional disturbance - in abusers, irrational beliefs are coupled with low frustration tolerance (i cant stand it itis) -ABC model (a-activating events, b-beliefs, interpreations, c-consequence) |
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beck and CBT |
cognitive theory -focus more exclusive to cognitive processes, less learning -SCHEMA- an underlying representation of knowledge that guides the current processing of info and leads to distortions in attention, memory and comprehension, people develop difference schemas based on experiences, abilities, temperaments -psychopathlogy reflects maladaptive schemas which leads to disortions in thinking CORE BELIEFS- inventory of irrational reasoning -in abusers, core beliefs are coupled with automatic thoughts which activate cravings |
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automatic thought vs core belief |
core belief- i am a failure automatic thought- i am going to screw this up |
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CBT as related to substance abuse |
-human behavior is largely learned rather than being determined by genetic factors -same learning process can be used to change them -behavior is determined by contextual and environmental factors **practicing new behaviors in the context in which they are performed is important for behavioral change -adequate treatment thorough CB analysis |
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the biopsychosocial model |
bio- genetics, epigenetics, neurobiology psycho-thoughts behaviors emotions coping social-peers culture society and environment --not a theory but model for understanding --influence of any given factor may vary with individuals --important in both conceptualization and treatment of substance related disorders |
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synaptic connections between neurons |
if one is effected, then the rest can be affected too |
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blood brain barrier |
a semi permeable barrier between the blood and brain produced by the cells in the walls of the capillaries -all drugs must cross blood brain barrier in order to have an effect |
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voltage gated ion channel |
opens or closes according to the value of the membrane potential |
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all or none law |
once an action potential is triggered, it is propagated without to the end of the fiber |
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ligand |
a chemical that binds with the binding site of the receptor |
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release zone |
region on interior of presynaptic membrane of a synapse to which synaptic vesicles attach and release their NTs in to the synaptic cleft |
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neurotransmitter dependent ion channel |
ion channel that opens when a molecule of a NT binds with a postsynaptic receptor |
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ionotropic receptor |
receptor that contains a binding site for a NT and ion channel that opens when the NT attaches to it directly coupled with ion channels |
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metabotropic receptor |
receptor that contains the site for an NT which then activates an enzyme which opens ion channel elsewhere |
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g protein |
part of metabotropic receptor, conveys messages when ligand binds and activates the receptor |
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second messenger |
chemical produced when protein activates an enzyme; carries a signal that results in the opening of the ion channel or causes other events to occur in the cell |
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reuptake |
when NTs reenter through membrane back into terminal button |
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enzyme deactivation |
destruction of NT by an enzyme after its release ex. destruction of acetylcholine by acetylcholinesterase |
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neural integration |
the process by which inhibitory and excitatory potentials summate and and control the rate of firing of neuron |
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autoreceptor |
receptor molecule located on a neuron that responds to the NT released by that neuron |
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EPSP |
depolarize cell caused by release of NT by terminal button |
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IPSP |
hyperpolarize cells caused by release of NT by terminal button |
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acetylcholine |
memory, sensory reception, behavioral arousal, attention, energy conservation, mood, REM |
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catecholamines |
dopamine and norepinephrine, mood, emotion, motor behavior |
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3 dopamine pathways |
mesolimbin mesocorticostriatal
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serotonin |
mood, sleep, sex, regulation of body temp |
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glutamate |
major excitatory NT |
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GABA |
major inhibitory NT |
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peptide NT |
endorphins, enkephalins |
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monoamine |
include indolamines such as serotonin and catecholamines such as dopamine, norepinephrine, and epinephrine |
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nigrostriatal system |
dopamine pathway originates from substantia nigra and ends in neostriatum (putamen and caudate nucleus) |
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mesolimbic |
dopamine pathway originating from ventral tegmental area and ending in nucleus accumbens, amygdala and hippocampus |
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mesocortical |
dopamine pathway originating in vental tegmental area and terminating in prefrontal cortex |
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direct agonist |
binds directly and activates receptor exactly like NT |
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direct antagonist |
receptor blocker |
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noncompetitive binding |
does not interfere with binding of principal ligand |
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indirect antagonist |
does not interfere with binding site for the ligand but binds to a sight on receptor and interferes with action of receptor |
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the drug experience |
often affected by persons age, characteristics, setting or context tolerance may eventually develop if drug use is stopped, withdrawal may result |
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pharmacology |
two branches -pharmacokinetics -pharmacodynamics
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pharmicokinetics |
- deals with absorption, distribution, biotransformation and excretion of drugs |
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drug dose |
computed according to the recipient's body weight mg/kg is standard |
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pharmacokinetic components |
routes of administration absorption and distribution binding inactivation/transformation/metabolism excretion/elimination |
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routes of administration |
determines how quickly and how completely drug is absorbed into blood influences physiological and subjective effects for the user -oral -intravenous -subcutaneous -transdermal -inhalation -rectal -intranasal -intramuscular -sublingual-under tongue |
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drug absorption |
passage of a drug into the bloodstream the rate and extent to which a drug leaves its site of administration -affects bioavailability, the portion of the original drug that reaches its site of action -bioavailability determines its effect on the body -drugs that are more soluble in lipids are absorbed much more quickly, those that are able to cross the ***BLOOD BRAIN BARRIER |
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drug distribution |
affected by diffusability of tissues and membranes: significant membranes are cell membrane, placental membrane, blood brain barrier, stomach and intestinal lining also affected by solubility and selective binding |
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binding |
once in plasma, some drug molecules move to the tissue to bind to active target sites or receptors while in blood, drug may also bind to plasma proteins -or may be stored temporarily in bone or fat where it will be inactive, this creates a slow unbinding |
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depot binding |
drug binding to plasma proteins |
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inactivation/metabolism |
occurs primarily bc of metabolic processes of liver -metabolites may be pharmacologically active and may contribute to drug side effects ***the amount of drug in body at any one time is dependent on the balance between absorption and metabolism --inactivation influences both the intensity and duration of drug effects |
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excretion |
occurs through direct excretion of the drug from the body, or through metabolism and excretion of by products -may be eliminated through urine, feces, breast milk, liver bile --half- life- the time it takes to reduce the amount of the drug by half rate of metabolism *zero order kinetics-independent of concentration ex. alcohol *first order kinetics- dependent on concentration |
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pharmacodynamics |
involved with how biochemical and physiological effects and their mechanisms of action effects of drug on receptors **experience of person on drug is dependent on receptors |
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pharmacodynamic factors |
receptors dose/effect response curve drug interactions drug tolerance and withdrawal what happens when multiple drugs are taken? |
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receptors |
drugs affect by binding to receptors need to know where these receptors are located and which ones are acted on -protein molecules located on the surface or within cells - they are the initial site of action for biologically active agents such as hormones and drugs and nts -most drugs do not pass directly through the membrane to affect intracellular processes |
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ligand |
molecule that binds to a receptor with some **selectivity |
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partial agonist |
not full effect of agonist but has some effect more than antagonist want dopamine levels to rise a little so that you get some high but not the full effect |
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inverse agonist |
initiate biological action but it is an action that is opposite to that produced by an agonist decreasing through active means of doing so, decrease some side effects |
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receptor modification |
brain is trying to restore balance can be modified in number and sensitivity -up regulation-increasing the number -down regulation- decreasing the number these changes can be permanent or reverisble |
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receptor subtypes |
within receptor category, have diff specialized receptors -some drugs may bind with greater affinity to one receptor subtype which creates a highly selective effect -this specificity impacts the drug experience ex. can be used to treat depression broadly or can block specific subtypes ex. if treating anxiety, target GABAa receptor specifically |
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dose effect /response curve |
graphic representation of relationship between drug dose and size of an effect |
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prototype dose effect curve |
has an sigmoidal (S) shape larger effect as the dose increases but graph plateaus for the highest doses |
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slope of curve |
reflects how much the drug dose changes before the effect gets larger |
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efficacy |
most intense or peak level of a drug effect |
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potency |
minimum effective dose of a drug , amount of drug necessary to produce a specific effect |
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effective dose |
the dose at which a particular percentage of individuals show a particular effect of a drug ex. ED 50, 50% of individuals have this effect at this dose |
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lethal/ toxic dose |
dose at which a given percentage of individuals die or experience a toxic effect (LD 50)- 50% of people who take this dose will die |
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therapeutic index |
goal is to find a drug that alleviates symptoms but also is effective with minimal side effects and low risk for lethal effects |
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four analgesic curve |
most potent drug shows shift to the left, more of a response at a lower dose |
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biphasic action |
upside down u heart rate is affected by marijuana and alcohol response increases with increasing amounts of drug but then levels off and decreases but when at the same level, may feel different |
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drug interactions |
multiple drugs may interact and influence the drug experience -diminishing or enhancing -drug antagonism- reduced effect of drug when another drug is present -drug potentiation or synergism-enhancement of the effects of a drug when another is present -----synergism(additive) vs. potentiation |
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drug withdrawal |
physiological and psychological reaction to the cessation of drug use --results from acute(in the moment) and chronic use ( abuse) --withdrawal may be related to the central or peripheral effects of a drug --withdrawal may indicate compensatory changes at the receptor level ---intensity of withdrawal is related to amount, duration and frequency of drug use psychological dependence-cant go to party without pregame physiological dependence- physically need it |
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drug tolerance |
diminished response to a drug after repeated exposure increased dosages must be used to induce the same biological effect cross tolerance-tolerance to one drug can diminish effectiveness of a second drug types: acute, metabolic, behavioral --reversible when drug stops --depends on dose and frequency of drug use ---may occur rapidly, over long periods of chronic use or never --may experience in difference degrees and to difference effects ---may reflect changes on receptor level |
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acute tolerance |
develops during a single administration alcohol user has diff effects when blood level is rising then when it is going down and is at the sam point |
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metabolic/ dispositional tolerance |
repeated use of a drug reduces amount of drug available at the target tissue ex. when drugs increase their own rate of metabolism by inducing liver microsomal enzymes |
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pharmacodynamic tolerance |
changes in nerve cell function compensate for continued presence of drug ex. receptor down or up regulation |
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behavioral tolerance |
context specific tolerance --tolerance is not apparent or reduced in a novel environment ex. some types of learning (classical and operant conditioning); withdrawal syndrome |
