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Abnormal Psychology > Unit 2 > Flashcards

Unit 2 Flashcards

Chapters 5-7 and 9-10

1
Q

stress

A

a perception that environmental demands overwhelm one’s personal resources available to deal with them

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2
Q

how to respond constructively to stress:

A
  • changing perceptions
  • reducing, reframing, or renegotiation demands
  • increasing personal resources to meet demands
  • deploying personal resources more effectively
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3
Q

characteristics of stressful events

A
  • uncontrollable
  • unpredictable
  • change/challenge capabilities or self concepts
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4
Q

the body’s response to stress

A
  • must turn on, then turn off the stress response
  • active sympathetic nervous system, then activate the parasympathetic nervous system to restore homeostasis
  • problems if homeostatic balance is not properly restored or stress response stays active long term
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4
Q

Hans Seyle General Adaptation Syndrome

A
  • series of physiological changes in response to stressful events
  • alarm stage: initial symptoms the body experiences when under stress (fight-or-flight)
  • resistance stage: body enters recovery phase but is still on high alert for a period of time
  • exhaustion stage: result of prolonged or chronic stress; signs included fatigue, burnout, depression, anxiety, decreased stress tolerance
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5
Q

gender differences with stress

A
  • “authoritarian control” originally identified, male subjects used (fight-or-flight)
  • “tend and befriend” response often characteristic of females; theory that humans rely on taking care of young ones and connecting with others during stressful situations
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6
Q

hypothalamic-pituitary-adrenal pathway

A

hypothalamus –> pituitary gland –> secretion of ACTH –> adrenal cortex –> corticosteroids

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7
Q

what happens in the brain in the face of stress?

A
  • sensory input (see, hear, etc)
  • amygdala: threat detected
  • activated hypothalamus
  • initiates the “fight-or-flight” response
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8
Q

sympathetic nervous system pathway response to stress

A
  • nerve fibers of the autonomic nervous system that quicken the heartbeat and produce other changes experienced as arousal
  • nerves can stimulate the body directly or indirectly, by stimulating the adrenal glands to release epinephrine and norepinephrine
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9
Q

emotional brain response to stress

A
  • sensory information goes to the thalamus
  • immediate response initiated via the fast path (thalamus to amygdala to response)
  • longer pathway activates follow-up response (thalamus to visual cortex to amygdala to response)
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9
Q

DSM-5 criteria for diagnosing PTSD

A
  • post traumatic stress is a normal reaction to an abnormal event
  • the person has been exposed to a traumatic event in which they experienced, witnessed, or were confronted with an event involving actual or threatened death or serious injury, or a threat to the physical integrity of oneself or others
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10
Q

symptom categories of PTSD

A
  • re-experiencing the trauma
  • avoidance of things relating to the trauma
  • reduced responsiveness (detached, dissociation, derealization)
  • increased arousal, negative emotions, and reactivity
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11
Q

prevalence of PTSD

A
  • 61% or men and 51% of women experience at least one traumatic event in their lifetime
  • about 4% of the population, aged 18-54 will experience symptoms of PTSD in a given year (5.2 million people)
  • lifetime rates: 10% for women and 5% for men
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12
Q

history of PTSD

A
  • Da Costa’s Syndrome/Soldier’s Heart
  • Combat Fatigue/War Neuroses
  • Myers’ ‘Shell Shock’
  • Freud’s Hysteria
  • Rape trauma syndrome
  • Battered woman syndrome
  • DSM-III Ptsd
  • acute stress disorder: symptoms begin soon and last less than a month
  • PTSD: onset and duration of symptoms variable
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13
Q

additional problems of PTSD

A
  • attention and memory issues
  • functional impairment (occupational conflicts, aggression, divorce, legal altercations, difficulties parenting)
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14
Q

course of PTSD

A
  • onset: within 3 months or not until years later
  • duration: varies, some people recover within 6 months while others suffer much longer
  • pattern: periods of acute symptoms followed by remissions, some experience severe and unremitting symptoms, variable
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14
Q

associated comorbid disorders with PTSD

A
  • major depressive episodes
  • alcohol/drug abuse/addiction/dependence
  • simple and social phobias (more in women)
  • conduct disorders (more in men)
  • in children: anxiety disorders and acting-out
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15
Q

PTSD symptoms in children

A
  • generalized fears
  • sleep disturbances
  • posttraumatic play and reenactment
  • lose an acquired developmental skill
  • omen formation
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16
Q

post-trauma variables for PTSD

A
  • rate of physical recovery
  • social support
  • involvement in work and social activities
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16
Q

pre-trauma variables for PTSD

A
  • poor coping skills
  • pre-existing mental-health problems
  • poor social support
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17
Q

trauma-related variables for PTSD

A
  • amount of physical injury
  • potential life-threat
  • loss of significant others
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18
Q

treatment for PTSD

A
  • varies depending on type of trauma
  • general clinical goals: end lingering stress reactions, gain perspective on painful experiences, and return to constructive living
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19
Q

process goals for PTSD treatment

A
  • exposing the client to what they fear in order to extinguish that fear
  • challenging distorted cognitions
  • helping reduce stress in daily lives
  • improving coping capacity
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19
Q

biological and genetics variables for PTSD

A
  • abnormal levels of cortisol and norepinephrine
  • system remains unstable, triggering symptoms, possible brain damage
  • vulnerability may be passed on genetically
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20
Q

basic recommendations for PTSD treatment

A
  • immediate aftermath: reestablish routines, find support network, avoid major life decisions
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21
Q

drug therapy for PTSD

A

antianxiety and antidepressant medications

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22
Q

behavioral exposure techniques for PTSD

A
  • prolonged exposure using in vivo exposure or imaginal exposure
  • reduce specific symptoms, increase overall adjustment
  • flooding and relaxation training
  • eye movement desensitization and reprocessing (EMDR)
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23
Q

insight therapy for PTSD

A
  • client centered type of talk therapy that can help you better understand yourself better
  • bring out deep-seating feelings, create acceptance, lessen guilt
  • often use family or group therapy formats; “rap groups”
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24
Q

cognitive processing therapy for PTSD

A

guides the individual to identify ways that the trauma has impacted different areas of their life and to identify and change ways of thinking that are disrupting daily functioning

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25
Q

additional treatment options for PTSD

A
  • psychological debriefing
  • psychosocial rehabilitation
  • inpatient treatment
  • hypnosis
  • marital and family therapy
  • creative therapies
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26
Q

dissociation

A
  • an involuntary disruption of the normal integration of consciousness, memory, identity, or perception
  • aspects of an individual’s identity, memories, and consciousness become split off from one another
  • Freudian idea is that by “walling off” traume as not part of the self, dissociations serve as a protective function
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27
Q

dissociative identity disorder

A

there are separate, multiple personalities in the same individual

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28
Q

symptoms of dissociative amnesia

A
  • loss of memory due to psychological rather than physiological causes
  • the memory loss is usually confined to personal information only
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28
Q

dissociative amniesia

A

the person loses memory of important personal facts, including personal identity, for no apparent organic cause

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29
Q

symptoms of dissociative fugue

A

person suddenly moves away from home assumes an entirely new identity, with no memory of previous identity

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30
Q

etiology of dissociative amnesia

A
  • typically occurs following traumatic events
  • may involve motivated forgetting of events, to poor storage of information during events due to overarousal, or to avoidance of emotions experience during an event
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31
Q

treatment of dissociative amnesia

A

help the individual remember traumatic events and accept them

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32
Q

dissociative fugue

A
  • the person moves away and assumes a new identity, with amnesia for the previous identity
  • DSM 5 not defines dissociative fugue as a subcategory of dissociative amnesia
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33
Q

etiology of dissociative fugue

A

fugue states usually occur in response to some stressor, but because they are extremely rare, little is known

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34
Q

treatment of dissociative fugue

A

psychotherapy to help the person identify the stressors leading to the fugue state and learn better coping skills

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35
Q

depersonalization-derealization disorder

A
  • frequent episodes where individual feels detached from his or her mental state or body, or from the outside world
  • individuals may show inhibitory responses to negative emotional information
  • lower activity in sensory areas and less cortical thickness found in those with depersonalization disorder
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36
Q

treatment for depersonalization disorder

A

general principles are to help the person regain their memory, help the person find out what stress precipitated the disorder and work through it, and improve coping skills with training

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37
Q

symptoms of dissociative identity disorder (multiple personality disorder)

A
  • presence of two or more separate personalities or identities in the same individual
  • these personalities may have different ways of speaking and relating to others and may even have different ages, genders, and physiological responses
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38
Q

etiology of identity disorder

A
  • alters may be created by people under conditions of extreme stress, often child abuse
  • self-hypnosis may be involved
  • some evidence it runs in families
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39
Q

treatment for identity disorder

A
  • long-term psychotherapy and use of hypnosis to discover functions of the personalities and to assist in “integration”
  • antidepressants and antianxiety drugs may be used
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40
Q

differences in alters (identity disorder)

A
  • identifying features (age, gender)
  • abilities and preferences (vision, personality, musical ability)
  • physiological responses (allergies, brain imaging)
  • “host”, “precursor”, other functional types
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41
Q

what causes are proposed for dissociative and identity disorders?

A
  • almost all patients have histories of severe child abuse
  • most are also highly suggestible
  • DID is believed to represent a mechanism to escape from impact of trauma
  • closely related to PTSD
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42
Q

psychodynamic approach to dissociative and identity disorders

A
  • massive repression
  • self-hypnosis: hypnotic amnesia of trauma
  • treatment: focus is on reintegration of identities, hypnotic techniques used
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43
Q

cognitive-behavioral approach to dissociative and identity disorders

A
  • state dependent learning, based on level of arousal
  • extremes of normal memory functions
  • treatment: identify and neutralize the cues/triggers that provoke memories of trauma and dissociation, apply cognitive therapy techniques
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44
Q

mood disorder

A

involves persistent feelings of sadness or periods of feeling overly happy or fluctuations from extreme sadness to extreme happieness

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45
Q

unipolar depression

A

experiencing only depression

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46
Q

bipolar disorder (main depression)

A

cycle between period of depression periods of mania

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47
Q

diagnostic note to causes of bipolar depression

A
  • reactive (exogenous) depression is response to external stressors
  • endogenous depression arises dependent of external stressors
  • hard to distinguish, important to include both internal and external assessments in diagnosis
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48
Q

symptoms of depression

A
  • emotional: sadness, anhedonia
  • physiological/behavioral: sleep disturbances, psychomotor retardation, fatigue and loss of energy, catatonia
  • cognitive: poor concentration, difficulty making decisions, feelings of being worthless/hopeless, delusions and hallucinations with depressing themes, suicidal thoughts
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49
Q

how common is depression?

A
  • 17% of americans experience an acute episode at some point in their life
  • 6% experience chronic depression
  • highest levels of depression are aged 15-21
  • lowest levels of depression are aged 55-70
  • women are about twice as likely as men top experience symptoms
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50
Q

persistent depressive disorder (chronic)

A

with major depressive episodes and dysthymic syndrome, 3 or more symptoms including depressed mood, lasting at least two years

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51
Q

major depressive disorder

A

5 or more symptoms including sadness or loss of interest, lasting at least two weeks

52
Q

symptoms of mania

A
  • emotional: elation, irritability, and agitation
  • physiological: more talkative than usual, decreased need for sleep, increase of activity towards achieving goals, impulsive behaviors
  • cognitive: inflated self-esteem, grandiosity, hallucinations, racing thoughts, distractibility
53
Q

how common is bipolar disorder?

A
  • about 1/100 will experience at least one episode of bipolar disorder in their life
  • mostly develops in late adolescence or early adulthood
  • men and women seem to be equally likely to develop the disorder
54
Q

bipolar I disorder

A

elevated mood for at least a week, plus 3 other symptoms, depressive episodes can be mild or infrequent

55
Q

bipolar II disorder

A

milder episodes of mania (hypomania), fit criteria for major depression

56
Q

Sam Goldstein approach to mood disorders

A
  • increased default mode network activity and stronger connectivity between nodes of default mode network (long range connectivity)
  • stronger connectivity within each node of the default mode network (short range connectivity)
  • central executive network has less of an ability to downregulae deafult mode network
57
Q

role of genetics in mood disorders

A
  • family studies, probands
  • twin studies: 72% concordance for identical twins, 14% concordance for fraternal twins
  • adoption studies
  • molecular biology: serotonin transporter gene abnormality
  • evidence for interaction of genetic and environmental-stress effects
58
Q

neurotransmitter dysregulation in mood disorders

A
  • serotonin levels low
  • more complex than simple levels, serotonin may act as neuromodulator
  • norepinephrine and perhaps dopamine also implicated
  • may be problems within rather than between neurons
59
Q

biological treatments for mood disorders

A
  • drug treatment: tricyclic antidepressants, monoamine oxidase inhibitors, SSRIs, lithium
  • anticonvulsants: electroconvulsive therapy
  • antipsychotics
  • calcium channel blockers
  • repetitive magnetic stimulation
  • vagus nerve stimulation
  • light therapy
60
Q

endocrine system involvement in mood disorders

A
  • chronic hyperactivity of stress hormones (cortisol)
  • abnormalities in melatonin released in SAD
  • possible dysfunction in immune system responses
61
Q

brain abnormalities in mood disorders

A
  • reduced metabolic activity in left prefrontal cortex, but not right side
  • possible over- and under-activity in different emotion centers
  • brain circuit responsible for unipolar depression emerging (prefrontal cortex, hippocampus, amygdala, cingulate cortex)
62
Q

behavioral theories of mood disorders

A
  • reduced positive reinforcers: life stress creates a reduction in positive reinforcers leading to withdrawal
  • learned hopelessness
63
Q

psychodynamic theories of mood disorders

A
  • depression develops when a person perceives he or she has been abandoned or has failed
  • Freud’s theory of Introjected hostility
  • therapeutic technique: transference
64
Q

behavioral therapy treatments for mood disorders

A
  • functional analysis
  • change aspect of environment
  • teach skills to change person’s negative circumstances
  • teach mood-management skills
65
Q

cognitive behavior therapy treatment for mood disorders

A
  • change negative patterns of thinking
  • teach skills so no longer have deficits in reinforcers
66
Q

interpersonal theory treatments for mood disorders

A
  • concerned with people’s close relationships and roles in relationships (contingencies of self-worth)
  • grief and loss, interpersonal role disputes, role transitions, interpersonal skill deficits
67
Q

suicide

A
  • the purposeful taking of one’s own life
  • must distinguish between suicide, suicide attempts, and suicide ideation
  • subintentional death: indirect, covert, partial, or unconscious
68
Q

DSM diagnosis of suicide

A
  • suicide is not officially classified as a mental disorder in DSM-5
  • suicide behavior disorder has been proposed for possible inclusion in the next revision
  • NSSI (non-suicidal self-injury) also proposed for possible inclusion
69
Q

studying suicide

A
  • retrospective analysis: piecing together available evidence
  • study survivors of suicide attempts
  • pros and cons of both methods
70
Q

facts and demographics of suicide

A
  • one of the leading causes of death in the world
  • approximately 1 million people die by suicide each year, including more than 48,000 in the US
  • around 25 million people throughout the world, 1.4 in the US, make nonfatal attempts or gestures to kill themselves
70
Q

suicide rates vary by…

A
  • country
  • gender
  • marital status
  • race and ethnicity
  • social environment
  • religious devoutness (not exclusively affiliation)
  • underreporting may exist
71
Q

impact of gender on suicide rates

A
  • women are 3 times more likely than men to attempt suicide
  • men are four or five times more likely to take their own lives
72
Q

impact of ethnic/cultural group on suicide rates

A
  • european american men make up 72% of all suicides
  • native americans’ rate doubles national average
  • black and hispanic fewer suicides, but youth do make attempts, and rates are rising
  • cultural and religious norms very important, countries differ
73
Q

Shneidman’s approach to suicide

A
  • people have different motivations
  • death seekers: clearly and explicitly seek to end their life
  • death initiators: believe they’re hastening inevitable death
  • death ignorers: intend to end their life, as distinct from ending their existence
  • death darers: ambivalent about dying, take risks that defy death, increasing their likelihood of dying
74
Q

bio-psycho-social approach to suicide

A
  • genetics: disordered genes increase risk for suicide
  • neurotransmitters: deficiencies in serotonin lead to impulsive, violent, and suicidal behavior
  • impulsivity: may have biological basis, inadequate coping skills and low threshold for frustration
  • psychological disorders: depression, bipolar, substance use, personality dissociative identity disorders, and schizophrenia
75
Q

cognitive theories of suicide

A
  • hopelessness
  • dichotomous thinking
  • narrowing of perspective
76
Q

psychodynamic view of suicide

A
  • depression and anger at others that is directed toward self
  • introjecting lost peron (Freud, Abraham): anger over a lost loved one turns to self-hatred and then depression
  • later suicidal behaviors related to childhood losses or parental rejection (Freud)
  • death instincts/Thanatos (Freud)
  • research does not establish suicidal people are dominated by intense anger
77
Q

Durkheim’s sociocultural view on suicide

A
  • suicide probability is determined by attachment to social groups such as family, religious institutions, and community
  • suicide categoies
  • egoistic: isolated, alienated; non religious people
  • altruistic: social well-integrated peopl
  • anomic: inhabitants of personally unstable social environment and structures
78
Q

what sets the stage for suicide?

A
  • biological vulnerability
  • environmental stress
  • emotional pain
  • impaired cognition
  • inadequate coping
  • inadequate support
79
Q

what is the impact of suicide on other people?

A
  • suicide “contagion”: group member commits suicide, other members at increased risk; media reports of suicide; may be modeling, increased acceptability, or the impact of traumatic event on already vulnerable people
  • many emotions: shock, horrow, guilt, anger, loss, depression
80
Q

eating disorders

A
  • often start with body dissatisfaction
  • mostly drive by extreme fear and apprehension about gaining weight
  • develop into severe disruptions in eating behavior
  • fit in diathesis-stress analysis
  • strong sociocultural origins
81
Q

gender differences in eating disorders

A
  • females overestimate their weights, males underestimate theirs
  • females see their ideal weight as being lower than what they judge as attractive in females, which is lower in weight than what males would say would be attractive
  • males see their ideal weight, the weight they would be most attractive, and their current weight as being almost identical, and all three are higher than what females say would be most attractive
82
Q

anorexia nervosa overview

A
  • hallmark: excessive/extreme weight loss
  • defines as 15% below expected weight
  • intense fear of obesity
  • relentless pursuit of thinness, fear of eating
  • often begins with dieting
83
Q

DSM-5 criteria for anorexia nervosa

A
  • refusal to maintain body weight at or above a minimally normal weight for age and height
  • intense fear of gaining weight or becoming fat, despite being underweight
  • distortions in the perception of one’s body weight or shape, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of current low body weight
  • women: amenorrhea, the absence of at least three consecutive menstrual cycles
84
Q

subtypes of anorexia nervosa

A
  • restricting: limit caloric intake via diet and fasting
  • binge-eating-purging
  • anorexia “trumps” bulimia in diagnosis
85
Q

associated features of anorexia nervosa

A
  • marked disturbance in body image
  • high comorbidity with other psychological disorders
  • weight loss methods have life threatening consequences
86
Q

facts and stats on anorexia nervosa

A
  • majority are female and white
  • from middle-to-upper middle class families
  • usually develops around age 13 or early adolescence
  • more chronic and resistant to treatment than bulimia
  • westernized cultures primarily
87
Q

bulimia nervosa overview

A
  • hallmark: binge eating, eating is perceived as uncontrollable
  • compensatory behaviors: purging, excessive exercise, fasting
88
Q

DSM-5 criteria for bulimia nervosa

A
  • recurrent episodes of binge eating
  • eating in discrete period of time an amount of food that is definitely larger than most people would eat during similar period of time
  • a sense of lack of control over eating during the episode
  • recurrent inappropriate behaviors to prevent weight gain such as self-induced vomiting or misuse of laxatives
  • binge eating and inappropriate purging behaviors both occur, on average, at least twice a week for 3 months
  • self evaluation is unduly influenced by body shape and weight
89
Q

subtypes of bulimia nervosa

A
  • purging: most common, vomiting, use of laxative
  • nonpurging: about 1/3 of bulimics, excessive exercise, fasting
90
Q

associated medical features of bulimia nervosa

A
  • generally within 10% of normal weight
  • purging can result in severe medical problems
  • erosion of dental enamel, electrolyte imbalance
  • kidney failure, cardiac arrhythmia, seizures, intestinal problems, permanent colon damage
91
Q

associated psychological features of bulimia nervosa

A
  • generally overly concerned with body shape
  • fear gaining weight
  • high comorbidity: anxiety, mood, and substance abuse
92
Q

facts and stats of bulimia nervosa

A
  • majority are female
  • onset around 16-19 years of age
  • lifetime prevalences is about 1.1% for females and 0.1% for males
  • 6-8% of college women suffer
  • tends to be chronic if left untreated
93
Q

binge eating disorder overview

A
  • engage in food binges without compensatory behaviors
  • differences from anorexia and bulimia
94
Q

DSM criteria for binge eating disorder

A

requires 3 of the 5
- eat much more rapidly than normal
- eating until feeling uncomfortably full
- eating large amounts of food when not hungry
- eating alone and being embarrassed by how much one is eating
- feeling disgusted, guilty, or depressed after eating

95
Q

associated features of binge eating disorder

A
  • often obese
  • often older than bulimics and anorexics
  • more psychopathology vs non-binging obese people
  • concerned about shape and weight
96
Q

individual risk factors for developing EDs

A
  • perfectionistic
  • low self-esteem
  • dichotomous (all-or-none) thinking
  • mood disorders (depression)
  • anxiety disorders (OCD)
  • personality disorders
97
Q

family influences on developing EDs

A
  • family as carrier of sociocultural pressures
  • family dynamics may include little affection, a lot of conflict, overly critical, negative interactions, over controlling, enmeshed boundaries, no expression of emotions
98
Q

biological influences on developing EDs

A
  • genetics (probably contributing to temperament)
  • serotonin
  • physical or sexual abuse
99
Q

treatment for eating disorders

A
  • multifaceted approach
  • medical care
  • medication
  • psychotherapy
  • nutritional counseling
100
Q

treatment for anorexia nervosa

A
  • hospitalization and refeeding
  • behavior therapy: make rewards contingent upon eating, teach relaxation techniques
  • techniques help the patient accept and value his or her emotions
  • psychotherapy: address eating disorder behaviors and psychological/emotional issues
101
Q

treatment for bulimia nervosa

A
  • cognitive behavioral therapy: teach client to recognize cognitions and to confront the maladaptive cognitions
  • interpersonal therapy: help identify interpersonal problems associated with bulimic behaviors
  • supportive-expressive therapy: provide support and encouragement for client’s expression of feelings about problems
  • tricyclic antidepressant and selective serotonin reuptake inhibitors
  • help to reduce impulsive eating and negative emotions
102
Q

drug

A

any substance other than food affecting our bodies or minds, including alcohol, tobacco, and caffeine

103
Q

substance intoxication

A
  • cluster of changes in behavior, emotion, or thought caused by substances
  • temporary, reversible, drug-specific syndrome due to recent ingestion of drug
  • clinically maladaptive behavioral or psychological changes on the CNS
104
Q

substance use disorder

A

individual displays maladaptive patterns and reactions caused by repeated substance use, leading to significant impairment or stress

105
Q

clinical diagnosis of substance use disorder

A

at least two of the following symptoms in a year
- use resulting in failure to fulfill major role in obligations at work, school, or home
- use when it is physically hazardous
- persistent social problems caused or exacerbated by the effects of the substance
- taking larger amounts of for longer period than intended
- unsuccessful attempts to cut down or control
- continued use despite persistent problems
- much time spent obtaining, using, and recovering
- important social, occupational, recreational activities given up or reduced
- craving, tolerance, withdrawal

106
Q

brain involvement in substance use disorders

A
  • different parts of the brain are involved in a variety of functions
  • substances can affect different parts, and hence different functions of the brain
  • “psychoactive” or “psychotropic” substances affect how we experience the world and ourselves, that is, they have psychological effects
107
Q

brain’s reward pathway

A
  • reward: basic mechanism for learning and for the preservation of life
  • formed by projections of the midbrain dopamine neurons of the ventral tegmental area (VTA) to the striatum, prefrontal cortex, amygdala, hippocampus, and other structures of the limbic system
108
Q

tolerance

A

biological need for greater amounts to get the same effects

109
Q

withdrawal

A

aversive symptoms when the substance use is discontinued

110
Q

dependence

A

need of a substance to feel normal

111
Q

addiction

A
  • life revolves around substance
  • pleasure pathway: start with just trying the substance, and gradually get more and more reliant on it, resulting in addiction
112
Q

depressants

A
  • “downers”
  • slows the activity of the central nervous system
  • reduce tension and inhibitions
  • may affect judgement, motor activity, and concentration
  • includes: alcohol, opioids, benzodiazepines (minor sedatives), barbiturates (sleep), inhalants (glue)
112
Q

alcohol

A
  • short term: block messages between neurons
  • increase levels of GABA, major inhibitory neurotransmitter
  • only psychoactive drug with calories
  • carbonation increases absorption rate
  • effects subside only after alcohol is metabolized by the liver (you can’t increase the speed of this process)
113
Q

acute effects of alcohol use

A
  • behavioral disinhibition
  • impaired motor coordination
  • gross personality changes, sedation (or agitation)
  • memory lapse (blackout)
114
Q

chronic effects of alcohol use

A
  • depression
  • anxiety
  • sexual dysfunction
  • ulcer
  • pancreatitis
  • cardiomyopathy
  • liver cirrhosis
  • cancer risk
  • immune system problems
  • memory impairments (Korsakoff’s syndrome)
115
Q

fetal alcohol syndrome

A
  • short in length for height
  • head circumference below the 3rd percentile
  • facial and joint abnormalities
  • mental retardation
116
Q

opioid facts and stats

A
  • affects 2.6 million people in the US in a given year
  • 80% are addicted to pain relievers, 20% are addicted to heroin
  • mortality rate is 63% higher than in a non-addicted person when untreated
117
Q

opioid dangers

A
  • overdose
  • ignorance of tolerance
  • getting impure drugs
  • infection from dirty needles and other equipment
118
Q

stimulants

A
  • “uppers”
  • speed up messages travelling between the brain and body
  • includes: cocaine, amphetamines, nicotine, caffeine
119
Q

effects of high doses of cocaine

A
  • intoxication
  • cocaine-induced psychotic disorder
  • depression-like letdown (crashing)
120
Q

physical dangers of cocaine use

A
  • overdose (greatest risk)
  • excessive doses can depress the brain’s respiratory function and stop breathing
  • heart failure
  • increased likelihood of miscarriage and of having children with abnormalities
121
Q

effects of amphetamines

A
  • restlessness and insomnia
  • poor appetite
  • tremor
  • palpitations, cardiac arrhythmia
  • growth suppression can be side effect of Ritalin
  • prolonged used can result in psychotic state that resembles paranoid schizophrenia
122
Q

methamphetamine

A
  • neurotoxic: decreased levels of dopamine
  • symptoms resembling Parkinson’s
  • increased respiration and insomnia
  • hyperthermia
  • irritability, confusion, anxiety
  • tremors and convulsions
  • paranoia and aggressiveness
123
Q

hallucinogens and phencyclidine (PCP, angel dust

A
  • produce powerful changes primarily in sensory perception (trips)
  • natural hallucinogens: mescaline and psilocybin
  • lysergic acid diethylamide (LSD)
124
Q

MDA (ecstasy)

A
  • related to methamphetamine
  • affects dopamine levels in the brain, can cause symptoms of Parkinson’s
  • affects serotonin levels
125
Q

biological theories of substance use disorder

A
  • genetic vulnerability to dependence
  • reward sensitivity, both physiological and experienced
  • physical dependence: how tolerance develops, can only function normally with the substance
  • withdrawal, usually the opposite of intoxication symptoms
126
Q

psychological theories of substance use disorder

A
  • reinforcement theory
  • modeling theory
  • expectations that alcohol will help with coping
  • personality: behavior under-control
127
Q

sociocultural approaches to substance use disorder

A
  • stress, especially severe chronic stress
  • environment that models and supports substance use
128
Q

treatment for substance use disorders

A
  • detoxification, usually under medical care
  • relapse, prevention, both physical and psychological
  • address psychological problems with various forms of psychotherapy
  • ongoing support
129
Q

treatment approaches for substance use disorders

A
  • medication: to manage withdrawal (includes antianxiety and antidepressant drugs), antagonists
  • methadone maintenance programs
  • behavioral and cognitive treatment
  • relapse prevention programs
  • twelve step programs (AA)
  • prevention programs, including harm reduction models
130
Q

gambling disorder

A
  • defined by the addictive nature of behavior
  • genetic predisposition
  • heightened dopamine activity and dysfunction when gambling
  • impulsive, novelty-seeking personality style
  • repeated and cognitive mistakes
131
Q

treatment of gambling disorder

A
  • cognitive-behavioral approaches: relapse prevention training
  • biological approaches: opioid antagonists
  • self-help programs: gamblers anonymous
132
Q

prevalence of gambling disorder

A
  • 3-10% of teenagers and college students
133
Q

internet gaming disorder

A
  • people increasingly turn to the internet for activities that used to take place in the real world, giving rise to an uncontrollable need to be online
  • internet addiction
  • specific symptoms of this pattern parallel those found in substance use disorder or gambling disorders, extending from the loss of outside interests to possible withdrawal reactions when internet is not possible

Abnormal Psychology (3 decks)

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