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Beschreibung
Karteikarten von Miriam Pridgen, aktualisiert more than 1 year ago
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Erstellt von Miriam Pridgen
vor mehr als 5 Jahre
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| Frage | Antworten |
| Limbic System | Group of interlinked structures involved in motivation, emotion, learning, and memory |
| Limbic System (Anatomy) | Olfactory bulb, hypothalamus, hippocampus, amygdala, and cingulate/prefrontal cortex |
| Cingulate Cortex | Pain and emotional regulation |
| Commonsense View of Emotion | Emotion causes responses People respond physiologically and behaviorally |
| James-Lange Theory | Physiological response to an event causes emotion Locked-In Syndrome is an example |
| Cannon-Bard Theory | Both physiological response and emotional response occur simultaneously but independently This enables variability between different people's emotional response |
| Schacter-Singer (two-factor) theory | Similar to Cannon-Bard theory Change in physiological response determines the quantity of an emotion, but cognitive appraisal is needed to determine the type of emotion |
| Rapid Target for Stress | Autonomic Nervous System (Sympathetic nervous activity in Alarm Reaction Stage) |
| Target of Stress Over Time | HPA Axis (produces hormones like cortisol) |
| HPA Axis | hypothalamus, pituitary gland, adrenal cortex |
| Alarm Reaction Stage | Sympathetic nervous system activity Mobilize resources for immediate recovery (short-term stress) |
| Resistance Stage | Cope with stress Autonomic functions maintained Hormones released for sustained stress (long-term) |
| Exhaustion Stage | Sympathetic nervous system starts to fail (really long-term) Body’s reserves depleted More susceptible to illness |
| Voodoo Deaths | Overwhelming emotions stop the heart Implicated by excess parasympathetic activity after sympathetic onset during overwhelming helplessness |
| Psychosomatic Illnesses | “Stress to the system” Ulcers, Heart Disease |
| Long Term HPA Effects | Heart Disease, immune system deficiency, memory loss |
| Hypothalamus Function (Aggression) | Releases Testosterone Testosterone faciliates VMH activity =Increase in aggresive behaviors |
| Stimulation of the VMH (Ventromedial Hypothalamus) | Increase in aggressive behaviors (specific behaviors depend on area stimulated) |
| Amygdala Stimulation | Aggressive, affective attacks Higher association with fear |
| Rabies | Attacks the temporal lobe (where the Amygdala is located) Leads to furious, violent behavior |
| Focal Seizure (Originating from the Amygdala) | Increase in aggressive behavior |
| Location of Amygdala | Temporal lobe |
| Temporal Lobe Epilepsy | Possible increase in aggression More generalized than focal seizure in amygdala |
| Lesion/Removal of the Amygdala | Tameness, placidity (decrease in aggression) |
| Kluver-Bucy Syndrome | Bilateral damage (lesions) to the amygdala Dramatic emotional changes, including reduction of fear and anxiety |
| Agonist | a substance that initiates a physiological response when combined with a receptor |
| Antagonist | a substance that interferes with or inhibits the physiological action of another |
| Viewing Fearful Faces = | Increased activity in the amygdala |
| Urbach-Wiethe Disease | Calcium accumulation kills cells in amygdala No experience of fear Trouble identifying or drawing fearful expressions |
| CCK (Cholecystokinin) | Main excitatory amygdala neurotransmitter |
| CCK Agonist = | increase in startle reflex |
| GABA (Gamma Amino Butyric Acid) | Main inhibitory amygdala neurotransmitter |
| GABA Antagonist | increased panic symptoms |
| Generalized Anxiety Disorder | Symptoms common, persistence abnormal ⅔ of sufferers are women (results may be skewed) Attention shifts from worry to worry (with physical symptoms) No identification for cause of worries |
| Panic Disorder | Occurs suddenly, very intense, then disappears Marked by frequent panic attacks Symptoms: racing heart, shortness of breath, dizziness, etc. Often accompanied by agoraphobia |
| Phobias | Irrational fears that disrupt “normal” functioning Can be specific or general (ex. social) Most common anxiety disorder |
| Obsessive-Compulsive Disorder | Based on repetitive thoughts (obsessions) and behaviors (compulsions) Anxiety reduction based on negative reinforcement Interferes with everyday functioning |
| Post-Traumatic Stress Disorder | Direct experience with an extremely fearful event Uncontrollable sense of fear, helplessness, and horror Must be at least 6 months since event Marked by excessive drug abuse, lashing out, hallucinations |
| Benzodiazepines | Ex. Valium, Librium, Xanax Serve as tranquilizers Amygdala and hypothalamus: anti-anxiety effects Cortex and thalamus: sleepiness and memory impairment |
| Amygdala and Hypothalamus (Benzodiazepines) | Anti-anxiety effects |
| Cortex and Thalamus (Benzodiazepines) | Sleepiness and memory impairment |
| Proband | An individual affected with a disorder who is the first subject in a study (as of a genetic character in a family lineage) |
| Proband study | studies genetics of mental illness through number of occurrences within a family tree |
| Concordance Rates | The probability that a pair of individuals will both have a certain characteristic, given that one of the pair has the characteristic; usually means the likelihood of presence of the same trait in both members of a pair of twins |
| Reuptake | The reabsorption of a secreted substance by the cell that originally produced and secreted it |
| Catecholamines | dopamine, epinephrine, and norepinephrine |
| Major Depressive Disorder | Feelings of sadness and helplessness every day for at least 2 weeks Little energy, feelings of worthlessness, contemplating suicide, trouble sleeping & concentrating 2x more women than men Can happen across lifespan Most cases are episodic |
| Major Depressive Disorder (Genetic Evidence) | Runs in families Adopted children resemble biological parents Higher risk if parents have severe, long-lasting depression before age 30 No isolated gene |
| Happy mood elicits | high activity in left prefrontal lobe |
| Depressed mood elicits | high activity in right prefrontal lobe |
| Left Hemisphere Damage | Depression |
| Right Hemisphere Damage | Mania |
| Tricyclics | 2nd course of treatment in depression Example: Tofranil Prevent reuptake of serotonin and catecholamines Increases the production of serotonin, norepinephrine, and dopamine Major side effects: Histamine receptors - drowsiness Acetylcholine receptors - dry mouth, difficulty urinating Sodium channels - heart irregularities |
| SSRIs (Selective Serotonin Reuptake Inhibitors) | First course of treatment in depression (and often anxiety) Examples: Prozac, Zoloft, Celexa, Luvox, Paxil (generics end in ‘-ine’ or ‘-pram’) Similar to tricyclics but specifically prevent serotonin reuptake Nausea, headaches, nervousness (more mild side effects) |
| MAOIs (Monoamine Oxidase Inhibitors) | Last course of treatment for depression (due to side effects) Example: Phenelzine (Nardil) Blocks the enzyme Monoamine Oxidase (MAO) MAO inactivates catecholamines and serotonin in axon terminal Avoid foods containing tyramine (cheese, raisins, liver, pickles) Consumption can lead to death (increases blood pressure) |
| Electroconvulsive Therapy (ECT) | Patients who don’t respond to drugs Electrically induces seizures, usually every other day for 2 weeks Memory problems (limited with right hemisphere shock) Downfall: huge relapse effect (50%) |
| Depressed Patients | Phase-Advanced |
| SAD Patients | Phase-delayed |
| Schizophrenia Stats | 1% of Americans exhibit over lifetime Most common in United States Equal number of men and women Average age of onset: Men = 18 to 25 years old Women = 26 to 45 years old |
| Neuroanatomical Hypothesis of Schizophrenia | Various brain regions are smaller in schizophrenics: Prefrontal cortex, hippocampus, amygdala, temporal cortex (Areas involved with emotion, coherent thought, perceptions) Ventricles are larger in schizophrenics Lower activity of regions on the left Development of larger areas (including planum temporale) on right Differences do not progress Question: if this is the case, why don’t symptoms appear earlier in life? |
| Smaller in Schizophrenics | Prefrontal cortex, hippocampus, amygdala, temporal cortex Areas involved with emotion, coherent thought, perceptions |
| Larger in Schizophrenics | Ventricles |
| Schizophrenia Lower Activity | Left regions of brain |
| Schizophrenia Larger Areas of Brain | Areas on the right (including planum temporale) |
| Dopamine Hypothesis of Schizophrenia | Excess dopamine receptor activity at synapse contributes to symptoms of schizophrenia |
| Dopamine Hypothesis of Schizophrenia (Supporting Evidence) | Antipsychotics (ex. Thorazine), and neuroleptic drugs (ex. Haloperidol, or Haldol) Certain drugs = increase in dopamine activity (cocaine, amphetamines, meth, LSD) |
| Glutamate Hypothesis of Schizophrenia | Deficient activity at glutamate synapses in the prefrontal cortex and hippocampus contribute to symptoms of schizophrenia |
| Glutamate Hypothesis of Schizophrenia (Supporting Evidence) | Antagonistic effects between glutamate and dopamine (Supported by antipsychotic drugs) PCP (phencyclidine) effects are close to schizophrenia (inhibits glutamate) Produces little effects in prepubescent monkeys, significant effects later on Produces specific and long-lasting effects (in comparison to drugs that stimulate dopamine) |
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