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Flashcards related to psychological disorders, including substance abuse, depression, and schizophrenia.
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Agonist
Drug that mimics or increases an effect.
Antagonist
Drug that blocks a neurotransmitter.
Drug’s affinity for a receptor
Measure of drug’s tendency to bind to it; ranges from strong to weak.
Efficacy
Tendency to activate the receptor.
Nucleus accumbens
Central to reinforcing experiences of all types, addictive drugs release dopamine or norepinephrine here.
Tolerance
Decrease in effect as an addiction develops.
Withdrawal
Body’s reaction to absence of the drug.
Antabuse (Disulfiram)
Results in sickness after drinking, to associate the two—learned aversion.
Acamprosate (Campral)
Medicine approved by the FDA to treat alcohol dependence; helps rebalance chemicals in the brain that may be changed by drinking too much.
Naltrexone (Narcan)
Opioid receptor antagonist that reduces alcoholism by blocking opioid receptors and prevents opioids from activating these receptors.
Naloxone and naltrexone (Narcan)
Rapidly blocks an Opioid Overdose by blocking opiate receptors, hence helps the individual to breathe.
Methadone
Safer alternative used to treat Opioid Use Disorder which activates same brain receptors and produces same effects as heroin and morphine, with reduced 'rush' and withdrawal.
Major Depressive Disorder
Absence of happiness is a more reliable symptom than increased sadness.
Selective serotonin reuptake inhibitors (SSRIs)
To elevate levels of Serotonin, these block the reuptake of the neurotransmitter serotonin.
Serotonin norepinephrine reuptake inhibitors (SNRIs)
Block reuptake of serotonin and norepinephrine, improve certain aspects of memory and have few side effects.
Norepinephrine Dopamine reuptake inhibitors (NDRIs)
Block reuptake of norepinephrine and dopamine, used to treat depression.
Monoamine oxidase inhibitors (MAOIs)
Block the enzyme monoamine oxidase that metabolizes catecholamines and serotonin into inactive forms, resulting in more transmitters available for release.
St. John’s Wort
Herb sometimes used as self treatment for depression, increases the production of a liver enzyme that decreases the effectiveness of other medications.
Brain-derived neurotrophic factor (BDNF)
Important for synaptic plasticity; people with depression have lower than average amounts which leads to a smaller hippocampus, impaired learning, and reduced production of hippocampal neurons.
Electroconvulsive Therapy (ECT)
Electrically induced seizure used for the treatment of severe depression; side effects include memory impairment, high risk of relapse without continued treatment.
Transcranial magnetic stimulation (TMS)
Procedure that uses magnetic fields to stimulate nerve cells in the brain to improve symptoms of major depression; neurons are temporarily turned off in the process.
Seasonal Affective Disorder (SAD)
Depression that regularly occurs during a particular season, such as winter.
Schizophrenia
Deteriorating ability to function in everyday life for at least six months, paired with at least two of a list of symptoms.
Positive symptoms
Behaviors that are present that should be absent; examples: hallucinations, delusions, disorganized speech, and disorganized behavior.
Negative symptoms
Absent behaviors that should be present; examples: weak emotion, blunting of affect and thought, apathy, poor socialization.
DISC1 (Disrupted In Schizophrenia 1)
Gene that controls rate of generation of new neurons; proliferation during embryonic and adult neurogenesis thought to be disrupted in Schizophrenia.
Season-of-birth effect
Tendency for people born in winter to have slightly greater probability of developing schizophrenia.
Antipsychotic/neuroleptic drugs
Category of drugs that tend to relieve schizophrenia and similar conditions; relieve the positive symptoms of most patients and inhibits dopamine at the postsynaptic D2 receptors.
Dopamine Hypothesis of schizophrenia
Schizophrenia results from excess activity at dopamine synapses in certain areas of the brain.
Substance-induced psychotic disorder
Hallucinations and delusions resulting from repeated large doses of amphetamines, methamphetamines, or cocaine; each prolongs activity at dopamine synapses.
Glutamate Hypothesis
Problem relates partially to deficient activity at glutamate synapses, especially in the prefrontal cortex.