Karteikarten
Psych Natural World Final (Exam 6)
Karten in diesem Stapel (69)
- 1Limbic SystemGroup of interlinked structures involved in motivation, emotion, learning, and memory
- 2Limbic System (Anatomy)Olfactory bulb, hypothalamus, hippocampus, amygdala, and cingulate/prefrontal cortex
- 3Cingulate CortexPain and emotional regulation
- 4Commonsense View of EmotionEmotion causes responses
People respond physiologically and behaviorally - 5James-Lange TheoryPhysiological response to an event causes emotion
Locked-In Syndrome is an example - 6Cannon-Bard TheoryBoth physiological response and emotional response occur simultaneously but independently
This enables variability between different people's emotional response - 7Schacter-Singer (two-factor) theorySimilar 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 - 8Rapid Target for StressAutonomic Nervous System
(Sympathetic nervous activity in Alarm Reaction Stage) - 9Target of Stress Over TimeHPA Axis (produces hormones like cortisol)
- 10HPA Axishypothalamus, pituitary gland, adrenal cortex
- 11Alarm Reaction StageSympathetic nervous system activity
Mobilize resources for immediate recovery (short-term stress) - 12Resistance StageCope with stress
Autonomic functions maintained
Hormones released for sustained stress (long-term) - 13Exhaustion StageSympathetic nervous system starts to fail (really long-term)
Body’s reserves depleted
More susceptible to illness - 14Voodoo DeathsOverwhelming emotions stop the heart
Implicated by excess parasympathetic activity after sympathetic onset during overwhelming helplessness - 15Psychosomatic Illnesses“Stress to the system”
Ulcers, Heart Disease - 16Long Term HPA EffectsHeart Disease, immune system deficiency, memory loss
- 17Hypothalamus Function (Aggression)Releases Testosterone
Testosterone faciliates VMH activity
=Increase in aggresive behaviors - 18Stimulation of the VMH (Ventromedial Hypothalamus)Increase in aggressive behaviors
(specific behaviors depend on area stimulated) - 19Amygdala StimulationAggressive, affective attacks
Higher association with fear - 20RabiesAttacks the temporal lobe (where the Amygdala is located)
Leads to furious, violent behavior - 21Focal Seizure (Originating from the Amygdala)Increase in aggressive behavior
- 22Location of AmygdalaTemporal lobe
- 23Temporal Lobe EpilepsyPossible increase in aggression
More generalized than focal seizure in amygdala - 24Lesion/Removal of the AmygdalaTameness, placidity (decrease in aggression)
- 25Kluver-Bucy SyndromeBilateral damage (lesions) to the amygdala
Dramatic emotional changes, including reduction of fear and anxiety - 26Agonista substance that initiates a physiological response when combined with a receptor
- 27Antagonista substance that interferes with or inhibits the physiological action of another
- 28Viewing Fearful Faces =Increased activity in the amygdala
- 29Urbach-Wiethe DiseaseCalcium accumulation kills cells in amygdala
No experience of fear
Trouble identifying or drawing fearful expressions - 30CCK (Cholecystokinin)Main excitatory amygdala neurotransmitter
- 31CCK Agonist =increase in startle reflex
- 32GABA (Gamma Amino Butyric Acid)Main inhibitory amygdala neurotransmitter
- 33GABA Antagonistincreased panic symptoms
- 34Generalized Anxiety DisorderSymptoms 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 - 35Panic DisorderOccurs suddenly, very intense, then disappears
Marked by frequent panic attacks
Symptoms: racing heart, shortness of breath, dizziness, etc.
Often accompanied by agoraphobia - 36PhobiasIrrational fears that disrupt “normal” functioning
Can be specific or general (ex. social)
Most common anxiety disorder - 37Obsessive-Compulsive DisorderBased on repetitive thoughts (obsessions) and behaviors (compulsions)
Anxiety reduction based on negative reinforcement
Interferes with everyday functioning - 38Post-Traumatic Stress DisorderDirect 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 - 39BenzodiazepinesEx. Valium, Librium, Xanax
Serve as tranquilizers
Amygdala and hypothalamus: anti-anxiety effects
Cortex and thalamus: sleepiness and memory impairment - 40Amygdala and Hypothalamus (Benzodiazepines)Anti-anxiety effects
- 41Cortex and Thalamus (Benzodiazepines)Sleepiness and memory impairment
- 42ProbandAn individual affected with a disorder who is the first subject in a study (as of a genetic character in a family lineage)
- 43Proband studystudies genetics of mental illness through number of occurrences within a family tree
- 44Concordance RatesThe 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
- 45ReuptakeThe reabsorption of a secreted substance by the cell that originally produced and secreted it
- 46Catecholaminesdopamine, epinephrine, and norepinephrine
- 47Major Depressive DisorderFeelings 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 - 48Major 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 - 49Happy mood elicitshigh activity in left prefrontal lobe
- 50Depressed mood elicitshigh activity in right prefrontal lobe
- 51Left Hemisphere DamageDepression
- 52Right Hemisphere DamageMania
- 53Tricyclics2nd 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 - 54SSRIs (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) - 55MAOIs (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) - 56Electroconvulsive 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%) - 57Depressed PatientsPhase-Advanced
- 58SAD PatientsPhase-delayed
- 59Schizophrenia Stats1% 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 - 60Neuroanatomical Hypothesis of SchizophreniaVarious 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? - 61Smaller in SchizophrenicsPrefrontal cortex, hippocampus, amygdala, temporal cortex
Areas involved with emotion, coherent thought, perceptions - 62Larger in SchizophrenicsVentricles
- 63Schizophrenia Lower ActivityLeft regions of brain
- 64Schizophrenia Larger Areas of BrainAreas on the right (including planum temporale)
- 65Dopamine Hypothesis of SchizophreniaExcess dopamine receptor activity at synapse contributes to symptoms of schizophrenia
- 66Dopamine 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) - 67Glutamate Hypothesis of SchizophreniaDeficient activity at glutamate synapses in the prefrontal cortex and hippocampus contribute to symptoms of schizophrenia
- 68Glutamate 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) - 69—
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- Karteikarten am Psych Natural World Final (Exam 6), erstellt von Miriam Pridgen am 29/04/2019.
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