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Final Study Guide

by: Lana Rose Betts

Final Study Guide CLP4143

Lana Rose Betts
GPA 4.0

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About this Document

I spent a lot of time putting this together. It includes all of the information for Obsessive-Compulsive Disorder, Trauma, Substance Use, and Psychosis. I attended every lecture, and included mat...
Abnormal Psychology
Casey Strickland
Study Guide
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This 9 page Study Guide was uploaded by Lana Rose Betts on Friday December 4, 2015. The Study Guide belongs to CLP4143 at Florida State University taught by Casey Strickland in Fall 2015. Since its upload, it has received 139 views. For similar materials see Abnormal Psychology in Psychlogy at Florida State University.


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Date Created: 12/04/15
CLP4143 FINAL STUDY GUIDE OCD, Trauma Disorders, Substance Use, Psychotic Disorders OBSESSIVE COMPULSIVE DISORDER: ***OCD used to be categorized in the DSM as a type of anxiety disorder, because OCD & GAD are often hard to distinguish. It was until the most recent revision, DSM V, that it became its own stand-alone disorder*** Symptoms: Obsessions and/or compulsions An understanding that the behavior is unreasonable (this requirement is not necessary for kids) Distressing & time-consuming (engaging in OCD behavior for >1 hour per day) Obsessions: o Intrusive, unwanted, recurrent thoughts, images, or impulses o Cause a lot of anxiety o Attempts to ignore, suppress, or neutralize w/ a different thought or action o Ex: dirt & contamination (that dust will give me cancer); aggressive impulses (I really could punch my friend right now); unwanted , usually immoral sexual thoughts (I keep thinking about having sex with my parents); immoral behavior (smoking or drinking) o Not simply GAD. If Alicia has GAD, she may intensely worry about whether she locked her car or not, and may check it. If Alicia has OCD, she may check her car multiple times. Compulsions: o Repetitive behavior or mental acts aimed at reducing distress or preventing a dreaded event or situation o Often linked with an obsession, but there is often no causal link between the obsession and the compulsion. This is known as “magical thinking”. For example, in the clip we watched, a girl believed that if she didn’t tap everything in her house, her family would die. What OCD isn’t!!! People commonly say “you’re so OCD” when their friends like to organize. But enjoying organization does not equal OCD. Many people enjoy color-coding their M&Ms, but they do not fear a dreaded outcome if they do not. Prevalence & Course: 1-3% over life course No gender difference Onset before 30, but men tend to get it earlier than women (ex. John gets OCD at 22 while Rose gets it at 29) If someone develops OCD at a later age, they should see a neurologist; it might be a sign of another disease. Chronic ½ of sufferers are unemployed or underemployed Commonly comorbid w/ MDD, other anxiety disorders, or eating disorders Biological Theories: Genetics: OCD is substantially heritable—more than any anxiety disorder Structure: o The orbital frontal cortex is involved in higher level thinking o The basal ganglia (specifically the caudate nucleus) receives & processes the strongest thoughts & impulses—it acts as a gatekeeper o The strongest impulses are then sent to the thalamus, and then people behave in a way to ease the impulse. PET scans & fMRIs show that people with OCD have a dysfunction in this flow so that their impulses continue after their behavior. Biological Treatment:  Antidepressants that target serotonin (SSRIs) decrease OCD symptoms by 50-80% O.O Cognitive Theories:  Why can’t sufferers of OCD just “turn off” their thoughts?  People with OCD are more likely to have rigid, moralistic thinking & feelings of responsibility. o These lead to overprediction of consequences o When people have high morals, they may overreact when they have an immoral thought (remember examples of unwanted sexual behavior), and try not to think about it again. In reality, the more you try to control your thoughts, the more you are unable to. For example, if you tell someone “don’t think of a horse,” they are going to think of a horse. Behavioral Theories:  As with the all the anxiety disorders we’ve learned so far, the key is operant conditioning & negative reinforcement. Sufferers do their compulsions to decrease their distress/ease their obsession. C-B Treatment: Exposure and Response Prevention (EXRP): therapists place patients in a situation to heighten their obsession, anxiety, and prevent them from doing their compulsion (ex. have a patient with dirty hands be unable to wash their hands for a while) o 60-90% effective! O.O o 20-30 minutes—the time it takes for OCD anxiety to naturally wash out without compulsion. TRAUMA DISORDER: Traumatic Stressors: sudden/unexpected events that involve actual or threatened harm or death Features of a disorder: in order to be diagnosed with PTSD, you must exhibit these symptoms for at least 1 month:  Re-experiencing: intrusive thoughts/memories, nightmares related to the event, flashbacks, acting as if the event were occurring again (Flashbacks are more of a feeling, like feeling the weight of a rapist on top of you. Acting as if the event were happening would be like running away from a pedestrian, because you thought he was your rapist.)  Avoidance: o External: avoiding places, people, objects, & situations (ex. not driving a car because you were involved in an accident) o Internal: avoiding thoughts, memories, feelings  Change: change in belief about self & world (ex: “there’s something bad about me that caused my victimization”), persistent negative emotion, anhedonia  Excessive physiological arousal: sleep problems, irritability/anger, difficulty concentrating, hypervigilance (consistent alertness), exaggerated startle response Acute Stress Disorder: includes all of the above symptoms, but for 28 days or less. This diagnosis is helpful for people who need therapy or medication, but have not met the 1 month requirement for PTSD. Generally, however, clinicians wait before making a diagnosis, because the above symptoms are natural reactions to stressors. Prevalence & Course: 60-70% of people witness or experience traumatic events, but only 10- 12% develop PTSD. Lifetime prevalence rate of 7% Men have a higher risk of exposure to traumatic stressors, but women have a 2x risk of developing PTSD. Vulnerability: o Sociocultural: severity of the event (Did I break my ankle or both of my legs in a car crash?); duration of the event (How long did the crash occur, from impact time to arrival at the hospital?); proximity of the event (Was I in the crash? Did I drive by the crash? Did I see it on the news? Did I know a victim?); social support (Who is helping me through this?) o Psychological: belief in the “just world” hypothesis—people & fate are inherently good; preexisting distress (ex. GAD); harmful coping styles (drugs, isolation) o Biological: physiological hyperactivity, especially in the amygdala; higher hippocampus functioning (this region is involved in memory, and PTSD symptoms involve remembering the event); chronically low baseline cortisol levels (although stress is high during PTSD episodes, it is low in general situations); genetics (one study that examined Vietnam War veterans showed that if one identical twin developed PTSD, the other was more likely to also) CBT Treatment  Imaginal exposure: recount trauma in detail  In-vivo exposure: real life exposure. They do not put patients in the same traumatic event, but rather the situations they avoid. For example, a therapist might take a man to the apartment complex where he was raped.  Virtual reality: a combination of the two above, this therapy uses videogames & headsets to place the patient in the traumatic event. For example, soldiers may stand on a shakey shakey board, wear headphones that block out all other sound, and wear a headset that places them in a combat videogame.  40-60% improvement rate!!! O.O Medications: drugs do not have nearly as beneficial an effect as CBT. SSRIs have a slight but statistically significant improvement over placebos; relapse is common after patients stop taking them. Benzodiazepines do not work at all. SUBSTANCE USE Substance: any natural/synthesized product that has psychoactive effects. Demographics:  Roughly half of U.S. citizens have tried an illegal substance, men more than women.  Use is highest amongst Native Americans  Whites use drugs more than Blacks do  Those who are 26 & older use the least amount of drugs (they have more responsibilities), those who are 12-17 use more (perhaps due to peer pressure), and those who are 18-26 use the most (they are autonomous for the first time in their lives)  Impulse control isn’t fully developed until the late 20s Cohort Effects: Substance use increased in the 60s-80s, but has decreased in the 80s- 2000. Marijuana is the most common drug that people have ever tried, but alcohol is the most frequently used Intoxication v. Withdrawal: Intoxication: direct effects of substance Withdrawal: effects that occur after use is discontinued, especially when the use was heavy & frequent; these effects tend to be the opposite of intoxication o Some substances only cause effects depending on the amount you take (ex. alcohol), while others cause effects no matter how much you take (ex. ecstasy) Substance Use Disorder: Impaired control over use Social/work impairment Risky use (ex. driving while intoxicated) Tolerance or withdrawal (this symptom is not required, but is a sign of dependence) Substances:  Alcohol & Depressants (barbiturates & benzodiazepines) o Low doses of intoxication: confidence, relaxation, disinhibition. High doses: motor problems, dizziness, impaired sexual performance, depressed mood o 3 Stages of Withdrawal: 1) 2-8 hours after intoxication: hangover, tremors (“the shakes”), nausea, perspiration; 2) 1-3 days: convulsive seizures; 3) more than 3 days: delirium tremens (DTs)—hallucinations, fever, irregular heartbeat, delusions. o Less than 15% of alcoholics experience DT, & it is fatal in 10% of cases o Most common substance use disorder o Most have their first episode in their late 30s o 20% achieve long-term sobriety w/o treatment  Stimulants (cocaine, amphetamines, Adderal & Ritalin, nicotine, coffee) o Activate the CNS o Low doses: competence, energy, alertness, euphoria High doses: grandiosity, impulsiveness, compulsive behavior, agitation, panic & paranoia, cardiac failure o Withdrawal: exhaustion & depression  Hallucinogens (phenocyclodine, LSD, peyote) o Intoxication effects vary: perceptual changes, sense of clarity, euphoria, anxiety, paranoia, loss of motor control o Withdrawal: depression, lethargy  Opiates/Opioids (morphine, heroine) o Low doses: euphoria, warmth, vivid dreams, drowsiness o High doses: unconsciousness, coma, seizures, heart and lung function slows down & stops o Withdrawal: dysphoria, anxiety, agitation, aches, vomiting, diarrhea (but withdrawal is not fatal)  Cannabis o Low doses: relaxation, dizziness, grandiosity, motor impairment, lethargy, dry mouth o High doses: hallucinations, synesthesia (combining of senses— tasting color, seeing words, etc.), paranoia, depersonalization (you do not feel like yourself) o Withdrawal (only occurs with long-term users): anxiety, loss of appetite, hot flashes, sweating, nightmares Theories and Treatment: Biological: o Substance users have increased reward sensitivity. Also, there is a small amount of genetic heritability, but it is broad—if you’re at risk for one drug, then you’re at risk for other classes too. As for neurotransmitters, all types of drugs increase dopamine; cocaine, LSD, & ecstasy increase serotonin, and cocaine & amphetamines increase norepinephrine. o The mesolimbic pathway is a system of brain structures that support the transmission of dopamine (it’s the dope pathway). Drugs increase the activity in the nucleus accumbens & striatum, and decrease activity in the frontal cortex. o Aversive classical conditioning: users take medication (antabuse) that makes the substance punishing instead of rewarding. For example, alcoholics will take a medication when they drink that makes them nauseous; their bodies will then come to associate alcohol with the negative physical effects of nausea. Psychological—Cognitive: o Expectations about the effects of drugs (ex. “wine will make me more sociable”), beliefs about coping (“I cannot stop drinking”), and personality trait disinhibition (“I am not one to inhibit my thoughts and actions), cause one to begin & continue using a substance. Therapists challenge these beliefs. Psychological—Behavioral: o Social learning: substance use is modeled (“Both of my parents smoked, so I think it’s acceptable and normal”) o Enjoying the sensations leads to positive reinforcement (“That was a good trip”) o Avoiding withdrawal leads to negative reinforcement (“Last time I tried to quit drinking, I had a major headache, so I must continue drinking to avoid that pain”) o Cue Exposure & Response Prevention: the therapist exposes the patient to cues for substance use (ex. for an alcoholic, a bottle), then prevents actual substance use. Other psychotherapies: o Motivational interviewing: the therapist does not challenge the patient, but asks a series of open-ended questions. The patient explores his/herself, and makes their own decision whether or not to stop using. o Harm reduction programs: the patient keeps daily records of consumption, learns to calculate BAL (blood alcohol level), and measures the risks v. the benefits of moderate use. PSYCHOSIS Psychosis: inability to differentiate between what’s real & what’s not Psychotic Disorder: when psychosis is distressing & impairing Schizophrenia: the most common psychotic disorder  ***schizophrenia is not the same as having split personalities*** Symptoms of psychosis: Positive symptoms: unusual perceptions, thoughts, or behaviors that he/she doesn’t normally have o Delusions: ideas that an individual believes are true, but are unlikely or impossible (ex. “the nurse staff is plotting to kill me”). They are culture specific (ex. a Christian in a Christian community is more likely than a Hindu in India to have delusions that he is Jesus). Delusions are different from normal self-deception because they are bizarre, preoccupying, and resistant. o Hallucinations: unreal perceptual experiences—often bizarre, vivid, and distressing.  Auditory: can be aggressive, threatening, and/or commanding  Visual  Tactile: feeling something outside/on your body (ex. ants crawling on you)  Somatic: feeling something inside your body (ex. electric shocks in your chest) Negative Symptoms: absence of behaviors that you normally have. These are less obvious, less responsive to medication, but more impairing. o Affective flattening (monotone speech, blank face) o Alogia: less language/not talking as much o Avolition: lack of motivation/movement. This is not like anhedonia; in this case, a person may be walking down a hallway and stop halfway through. Disorganized language: o Derailment & loose associations/off track speech (ex. “I like cats and cats like to chase birds and birds are cool because they fly and airplanes also fly and I’m scare of airplanes but cats are cool.”) o Word Salad: connections of unrelated words (ex. “cats Seminoles green coffee no others fun yes running stop fear”) o Neologisms: making up words (neo=new, log=word) Disorganized behavior: o Unpredictable & untriggered (the therapist must be sure that the patient is not responding to internal stimuli—delusions or hallucinations) o Shouting, swearing, pacing, random repetitive body movements, echololia and/or echopraxia (repeating what someone has said) o Catatonic behavior: disorganized behaviors that reflect extreme lack of responsiveness  No psychomotor activity  Hold the same posture for a long period of time  Waxy flexibility: a possibly unethical act in which the doctors move the limbs of the patients to see whether they go back to their previous position Other features of psychosis/schizophrenia: o Cognitive deficits: difficulty filtering relevant info. from irrelevant info.; difficulty paying attention o Inappropriate affect: laughing at sad things, crying at happy things o Serious anhedonia Phases of Schizophrenia: 1. Prodromal: before the onset of a full episode; often display negative symptoms 2. Acute: the active phase; in order to be diagnosed, the sufferer must display negative, positive, & disorganized symptoms for at least one month 3. Residual: after the acute phase ***left untreated, schizophrenia will stay chronic & episodic. After you experience one episode, you are 80-90% likely to have another Prevalence: 1-2% lifetime prevalence in the U.S. 0.5-2% lifetime prevalence worldwide Not culture-specific Prognosis: Life expectancy is 10 years shorter than the average Increased risk for substance abuse—especially smoking Higher rates of infectious & circulatory diseases More likely to be victims of crime (ex. neglect by caretakers, assault) Gender Differences: Men are much more likely than women to suffer from schizophrenia— studies show that they may be 2-4 times more likely Men develop schizophrenia when they’re 17-21 years old; women develop it in their late twenties to early thirties Women have a better prognosis & fewer cognitive deficits Women are more likely to have positive symptoms; men are more likely to have negative symptoms Theories: Genetics: o 50% concordance rate among MZ (identical) twins, and only a 14% concordance rate among DZ (fraternal) twins o You are 50% likely to have schizophrenia if both of your parents have it. Brain structure: o Enlarged ventricles (empty space for fluid) o Reduced bra in volume—specifically in the prefrontal cortex Birth complications: o Perinatal hypoxia (oxygen deprivation while being born) Prenatal virus exposure: o If the mother gets the flu during the second trimester, the baby is more likely to develop schizophrenia. Neurotransmitters: o Dopamine is overactive in the mesolimbic pathway, but underactive in the prefrontal cortex o This is the opposite of Parkinson’s disease; in Parkinson’s, dopamine is underactive. Therefore, the drugs that treat schizophrenia give the patient side effects that resemble Parkinson’s. For example, the patient may have tardive dyskinesia: the inability to control facial expressions. Other: o If you’re at risk for schizophrenia, marijuana use as a teen can increase your risk. o Family history of epilepsy


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