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PSYC 3230 Abnormal Psychology Cyterski Exam 2 Lecture Notes UGA

by: Samantha Snyder

PSYC 3230 Abnormal Psychology Cyterski Exam 2 Lecture Notes UGA Psych 3230

Marketplace > University of Georgia > Psychlogy > Psych 3230 > PSYC 3230 Abnormal Psychology Cyterski Exam 2 Lecture Notes UGA
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This is a bundle of lecture notes that covers exam 2 material. Material that was stressed in class is highlighted in yellow and video notes are highlighted in green.
Abnormal Psychology
Trina Cyterski
Study Guide
abnormal, Psychology, trina, cyterski, uga, psych, 3230, test, review, study, guide, exam, 2
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This 12 page Study Guide was uploaded by Samantha Snyder on Saturday October 10, 2015. The Study Guide belongs to Psych 3230 at University of Georgia taught by Trina Cyterski in Fall 2016. Since its upload, it has received 43 views. For similar materials see Abnormal Psychology in Psychlogy at University of Georgia.


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Date Created: 10/10/15
Exam 2 Lecture Notes Chapters 5, 6 and 8 Lecture notes, Week 6 September 21, 2015  Stressor—stress trigger  Stress response—reaction to a stressor o Judgement of an event – not every stressor effects different people the same way o Ability to cope – people who are exposed to lots of stressors in life are more susceptible to disorders like GAD Stress, Coping, and the Anxiety Response  Arousal and fear o If a situation is especially traumatic, more vulnerable  Vulnerable o PTSD o Dissociative disorders Fight or flight response  Hypothalamus—area of the brain that sets in motion the fight or flight response  Two systems activated: o Autonomic nervous system (ANS)  Sympathetic nervous system—pupils dilate, tear glands are inhibited, dry mouth, digestion slows, heart beats faster  Parasympathetic nervous system—(calming the sympathetic system) constriction of pupils, heart slows, salivation increases o Endocrine system—glands that release hormones into your blood stream  Sympathetic Nervous System Pathway  Hypothalamic-pituitary-adrenal (HPA) Pathway (hypothalamuspituitarysecrete ACTHadrenal cortexrelease corticosteroids  Video in class: Physical Reactions to Fight-or-Flight response (“only have to know my notes for the test but the video is helpful”) o National geographic – the statue trick o Fight or Flight Response  Guy getting out of the way of an oncoming car  How, physically? Sees the car coming, processes that info, sends a message to nervous system, sends message to muscles, where there is ATP ready to go to get his body into motion  Trait Anxiety vs State anxiety – “read in book and make sure you know the difference”  Acute and Post-Traumatic Stress disorder o Became a topic of research after Vietnam – incorporated into the DSM- 3 o Acute Stress Disorder vs PTSD  Symptoms less than a month –ASD  Symptoms more than a month—PTSD  80% of cases develop into PTSD o Anybody who experiences an especially traumatic situation experience anxiety afterwards-totally normal. Not everyone will develop PTSD o MOST people don’t develop PTSD, so what is different physically/biologically/environmentally different about ppl who do?? Symptoms  Re-experiencing the event –by stimuli (Vietnamthunderstorms)  Avoidance—amnesia for parts of events, avoiding anything at all to do with event  Reduced responsiveness—reduction in positive emotions, surfacing of anxiety/panic attacks/depression  Alterations in cognitions or mood—problems concentrating, trouble sleeping, guilt for surviving  After 9/11 o 20% of survivors & rescue workers had symptoms of PTSD Triggers  Combat – 29% of Vietnam vets had ASD or PTSD  Natural and accidental disasters—more people are likely to be exposed to natural/accidental disasters than combat  Physical/sexual assault  Terrorism/torture  PTSD chart in class o Suburban police—lowest, abused children—highest  American Sniper trailer shown in class Why do People Develop PTSD?  Biological and Genetic Factors o Extreme trauma can cause physiological changes in neurotransmitters and brain areas o Norepinephrine and cortisol o Hippocampus and amygdala—fMRIs show structural and functional differences in these areas  Childhood experiences o Kids are especially susceptible to trauma—not as emotionally stable and able to handle stressors (especially younger than age 10—divorce) September 23, 2015  Review of exam Why do People Develop PTSD?  Video in class—combat vet o Vet shown pictures that remind him of combat to activate the brain circuit that controls the fear response—amygdala o Amygdala- fear center o Slower, second circuit, moves through the cortex to determine level of threat o Less activity in an area of the cortex that shuts down fear responses in the vet’s brain—slight threat sets off full-blown fear reaction o Dr in video focuses on how long people seem to dwell on the memories o Hippocampus (memory structure)—vet in video’s hippocampus is much smaller than a normal person  Childhood experiences  Social support—solid social support is considered a protective factor o Women are twice as likely to develop PTSD than men—theory is lack of social support  Personality factors o Preexisting high anxiety o Negative worldview o Resiliency or hardiness—there is research being done now to determine what makes some people more resilient than others (ideas— social support, optimism etc.) Treatment  Drug therapy  Psychological debriefing o A form of crisis intervention o Attempt to stop PTSD from developing o Idea that reliving the memories will allow a person to become habituated to the memory—“get used to the memories”  Behavioral Exposure Techniques o Typically imaginative o Insight therapy—if time allows and client is willing, gain insight to your feelings, getting a person to have insight and understand why they feel the way they do about their feelings o Controversy September 25, 2015 Dissociative Disorders  Memory loss and identity change Dissociative Amnesia  Loss of memory  Triggered by a specific upsetting event  May be o Localized—lose memory for that specific event o Selective—remember bits & pieces o Generalized—forget entire life history o Continuous—cant remember anything past a point in timepresent  Dissociative fugue  Dissociative Identity Disorder (formerly multiple personality disorder)  “subpersonalities”  Primary or host personality  Switching is usually sudden & may be dramatic  Mutually cognizant (all personalities are aware of each other)  One way amnesic How do subpersonalities differ?  Dramatically different characteristics  How common in DID? o Iatrogenic—unintentionally produced by clinicians Explanations  Psychodynamic view o Repression September 28, 2015 Explanations  Psychodynamic view o Repression—defense mechanism used to protect oneself from thoughts/memories  Behavioral view o Operant conditioning—“good test question, is this negative or positive reinforcement?” – answer is negative o Dissociating is negative reinforcement o State-dependent learning—when people can’t remember what the other personalities have done, they are extremely state-dependent learners  At first, people with DID may not be aware of their other personalities, but as time goes on, often the fact that time doesn’t add up may clue them in  Self-hypnosis—tricky treatment because people with DID are extremely suggestible, during hypnosis, clinicians can insert false memories (idea of iatrogenic disorder) How are Dissociative Amnesia and DID treated?  Complex and difficult to treat o Therapeutic alliance is critical—bonds typically form during treatment o Recovering memories is the goal o Sometimes antianxiety drugs are used o Integrating the subpersonalities  Fusion—merging all personalities into one single person  Hershel Walker Dissociative Identity Disorder video  Sybil—movie Chapter 6: Disorders of Mood  Mood disorders exist along a continuum extreme sadness ---------- extreme elation  Normal to experience varied and extreme emotions o What makes it abnormal? o Frequency extreme emotions are experienced, how often they switch between moods, how long each extreme emotion is felt Disorders of Mood  Depressive disorders (unipolar depression)—more common  Bipolar disorders  8% of adults in the US in any given year  19% lifetime prevalence  Women are twice as likely  There are environmental & social factors that affect depression rates  Recurrent—Around 40% will experience another episode later in their lives o Less likely to be recurrent if people get treated professionally Symptoms of Depression  Symptoms vary from person to person—diagnostic criteria requires a certain number of symptoms but not all to be diagnosed  Zang self-rating depression scale  6-15% of people experiencing depression-like symptoms report suicidal feelings  SOMETIMES (not recommended) people who experience bouts of depression can recover eventually on their own  Emotional symptoms—feeling “miserable, empty, humiliated”  Lack of drive, initiative, spontaneity  Less active, less productive  Hold negative views of themselves  Pessimistic  Physical symptoms Diagnosing Unipolar Depression In class I am going to focus on biological approaches----read the book though September 30, 2015  Double depression—very depressive episodes with milder depression between them  Dysthymia—moderate depression—two years or more, considered reaction to external stressor Blue Mood-----------Dysthymic Disorder--------Major Depressive Disorder Biological Factors  Key neurotransmitters: Norepinephrine and serotonin o Low activity of these neurotransmitters is one cause of depression Biological Treatments for Unipolar Depression  Antidepressant Drugs o Monoamine oxidase inhibitors (MAO inhibitors)  Inhibit production of an enzyme called MAO (MAO breaks down norepinephrine)  Leads to rise in norepinephrine  Very effective but not prescribed often—severe diet restrictions  Discovered by happenstance—tuberculosis treatment, noticed it made patients happier o Tricyclics  Block the reuptake process, thus increasing NT activity in the synapse  Proven more effective than placebo treatments by drug companies….. o Second-generation antidepressants  Structurally different than MAO inhibiters and tricyclics  More selective—Selective Serotonin Reuptake Inhibitors (SSRIs) —doesn’t block all receptor sites for serotonin, just a few types of receptor sites  Significantly less and lesser side effects  Increasing serotonin levels  Ex. Prozac (first on the market) and Zoloft  There are also Selective Norepinephrine drugs on the market  Video in class  By 1990’s, # of people seeking treatment tripled  As more people take them, side effects emerged  1 in 5 people got more anxious, 1 in 100 people went on to attempt suicide  Seroxat – put on the market and hid the fact that it raises the risk of suicidal behavior 8x o “I won’t ask you test questions about what type of drug a certain drug is”  Majority of patients do benefit from medications, but not for everyone o Alternative Treatments  Electroconvulsive Therapy (ECT)—shock treatment  Controversial but methods have improved a LOT—loss of long-term memory is a possibility but less likely  6-12 sessions, 2-4 weeks apart  Amnesia and muscle relaxers are used now  60-80% improvement rate  People don’t REALLY know how it works  Deep Brain Stimulation (TMS—Transcranial Magnetic Stimulation)  Implantation of an electrode deep in the brain circuit (Brodmann’s area 25) that is thought to be involved in depression to stimulate brain activity  Very new and experimental October 2, 2015 Psychological Models  Behavioral Model o Lewinsohn—positive rewards in life dwindle for some reason  During treatment, increase positive rewards  Cognitive Model o Learned helplessness—Belief that they no longer have control over the reinforcements of their life  Seligman’s work with laboratory dogs—discovered that when he put dogs in the lab through a procedure that was stressful l& they had no control, depression-like symptoms were induced  Cage with divider and metal grid floor that could emit an electrical current on one or both sides o Significant research support for this field o Attributions—what you credit things that happen to you to (internal, credit to yourself, “I’m not smart enough” vs internal, credit to others, “the teacher sucks”)  Internal attributions that are global and stable (typical way you attribute things) lead to greater feelings of helplessness and possibly depression o Negative thinking  Aaron Beck  People with depression typically have maladaptive attitudes  Cognitive Triad: individuals typically interpret (1) their experiences, (2) themselves, and (3) their futures, in negative waysdepression  Laughter Clubs Video: o Movement in psych field—positive psychology o Began in India o World Laughter Tour—“lead the world to health, happiness and peace through laughter” o “laughter is actually about a relationship with other people” o Laughter causes a change in brain chemistry that sends “function normally” signals to the rest of your body Bipolar Disorder  Both the lows of depression and the highs of mania o Mania—very talkative, high energy, productive, happy, feelings of creativity o Mania makes it hard to treat bc people want to get rid of depression but not mania o Full Manic Episode: full blown episode that also has psychotic symptoms—hallucinations and delusions o Hypomanic Episode: lesser than full manic episodes  Bipolar 1 Disorder o Substantial time between episodes of full depression and full mania  Bipolar 2 Disorder o Full depressive episodes and hypomanic episodes  Rapid Cycling o 4+ switching episodes within one year, additional specifier to Bipolar 1 or Bipolar 2 diagnosis  Cyclothymic Disorder o Mild depressive and mildly manic episodes  Feliziano Video o “tough time keeping it together----normally high functioning but not during this period” o Manic—“talk to people, I’m fine” o Depressive—“hermit-like, nervous, tight and compact” o “if I didn’t take my meds I wouldn’t necessarily become hypomanic, I may become depressed….and I want to avoid my depression more than I want to feel hypomanic”  Charlie Sheen interview What Causes Bipolar Disorders?  Neurotransmitters o Permissive theory  Low serotonin + low norepinephrine = depression  Low serotonin + high norepinephrine = mania  Ion activity o Remember “action potential” discussion o Ions may be improperly transported o Causes neurons to fire too easily (mania) or resist firing (depression) Treatments for Bipolar Disorders  Lithium Week 8 Lecture Notes October 5, 2015  Manic episodes are usually preceded by a major stressor—especially common is dysfunctional relationships Treatments for Bipolar Disorder  Lithium: Mood stabilizer o Helpful in majority of people—60% of patients seem to improve on lithium o Most helpful in leveling manic episodes  Combinations of drugs may be prescribed—mood stabilizers, antianxiety medication, antidepressants, antipsychotics  Psychotherapy ***Counseling and Psychiatric Services on UGA’s campus (CAPS) Chapter 8: Disorders featuring Somatic Symptoms  Very rare, not very well understood, appears VERY suddenly o May be caused by worry, stress, unconscious needs  “soma” – body  Psychological factors may contribute to somatic, or bodily, illnesses o Blindness, paralysis, loss of feeling that has no neurological basis  Freud—1900’s, “hysterical disorders”  Conversion Disorder o No apparent medical cause, or is inconsistent with known medical diseases  Conversion disorder induced paralysis does not have any evidence of muscle atrophy  Conversion disorder induced blindness—people with still react if you throw a ball near them but still truly believe they can’t see it o Glove anesthesia “whole hand is numb”  The way the nerves run, they should also not have feeling in their arm, but that isn’t the case. Clue to doctors that it is conversion disorder bc numbness in just hand is physically impossible o Attention seeking, to “get out” of something, unconsciously motivated—people don’t WANT their symptoms o Typically found in people described as anxious/very excitable/highly emotional/dramatic o Affects women more than men o La Belle indifference: when people are very casual about their symptoms, speak matter-of-factly about them  Only about 1/3 of people present la belle indifference o May go away and come back as following major life stressors o Dysfunction is selective—one symptom or the other, typically only one o Jane case study example  Several traumas in her life, beginning with rape  Speech areas in brain were fine but she couldn’t talk  Abnormalities in neural connections between speech and anxiety areas of the brain  Factitious Disorder / Munchausen Syndrome o Intentionally producing or faking symptoms to get attention  People may physically harm themselves or ingest poison in small doses  May go to great lengths to research and investigate the illness  Done in secret o Malinger: intentionally faking an illness for external personal gain (ex. insurance money, military discharge) o May suffer from depression or an extreme need for social support o Munchausen Syndrome by proxy—intentionally making another being sick for attention (children and pets, commonly)  To be seen as “ultimate caregiver” o Much more common in women o Person is viewed as intentionally lying (doesn’t truly believe daughter is sick, actually understand what she is doing but keeps doing it anyways)  Munchausen Video o Little girl and mother o 40 operations, 200+ hospitalizations o Mother accused of making her sick, father said “I truly believe my wife is the most wonderful mother” o Munchausen specialist—“most definitive way to know if it is Munchausen by proxy—does child improve when separated from her mother?”  Girl did greatly improve, mother charged with aggravated child abuse and fraud  Mother tampered with feeding tubes, machines, medical charts, induced seizures October 6, 2015 Somatic Symptom Disorder  Two patterns o Somatization Pattern (aka Briquet’s Syndrome): variety of underlying symptoms with no underlying cause o Predominant Pain Pattern: after an accident or illness that has caused genuine pain  Distinguished from Illness Disorder (anxiety with symptoms)—people with SSD aren’t afraid/anxious of their disorders  A lot more common in women than men  They love “being treated” at the doctor for their symptoms Illness Disorder  Previously known as hypochondriasis  Fear and anxiety  Don’t really have any real symptoms but are very “in tune” with their normal bodily functions o Ex. Stomach gurgles….person with Illness Disorder thinks it’s stomach cancer  Chronic anxiety about their health  Repeatedly check for signs of illness  Some sufferers recognize concerns are excessive What Causes Conversion and Somatic Symptom Disorder?  Behavioral View o May remove an individual from an unpleasant situation o May bring attention to individual from others  The Cognitive view o Emotions are being converted into physical symptoms to communicate extreme emotions Treatment  Insight therapy  Exposure therapy  Drug therapyantianxiety meds, antidepressants  Confrontation October 9, 2015 Psychophysiological disorders (psychosomatic)  Physical factors affecting medical conditions  Actual physical damage  Traditional psychophysiological disorders o Ulcers, asthma, insomnia, chronic headaches, high blood pressure, coronary heart disease What factors Contribute to psychophysiological disorders?  Biological o Defects in the autonomic nervous system  Psychological o Repressive coping styles, type A personality, feelings of hostility, time urgency  Sociocultural o Poverty o Belonging to an ethnic or cultural minority o Incidence of asthma in African Americans is much higher than in white Americans  Anxiety & Pain video: o Pain / pleasure are generated by the brain o Being anxious can make pain worse o Showing triangle, low pain showing square, high pain when shown square but given low pain, people experience more pain because of anxiety Stress  Social adjustment rating scale o Doesn’t take into consideration reaction differences  Psychoneuroimmunology o Lymphocytes Treatments  Relaxation training  Biofeedback  Meditation  Hypnosis o Video: psychologist teaching pregnant women to use hypnosis techniques on themselves during labor  Self-inoculation training


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