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Abnormal > Exam 3: Schizophrenia > Flashcards

Exam 3: Schizophrenia Flashcards

1
Q

Prevalence

A

1%, m=f

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2
Q

Psychotic Disorder

A

thinking an emotions are so impaired that there is a loss of contact with reality; for example, not being able to tell if a sound is real or a hallucination

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3
Q

Delusions

A

fixed beliefs that are not shared by others and cannot be changed

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4
Q

Hallucinations

A

major distortions in perception; can occur with any sense, but auditiory is most common

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5
Q

Loose Association

A

common thinking disturbance in schizophrenia, characterized by rapid shifts from one topic of conversation to another;

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6
Q

Positive Symptoms

A

things that aren’t there in normal/baseline behavior: delusions, hallucinatons, disorganized thought/speech (loose association), abnormal motor behavior (no reaction to events, rigid posture, unpredictable aggression); often fluctuate

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7
Q

Negative Symptoms

A

emotional lack of expression, lack of motivation, apathy; tend to be more stable

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8
Q

Schizophrenic Spectrum: Schizophrenia

A

signs of disturbance for 6 mo+, 2 groups of symptoms for 1 mo+

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9
Q

Schizophrenic Spectrum: Schizophreniform

A

signs of disturbance from 1-6 mo+

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10
Q

Schizophrenic Spectrum: Brief Psychotic Disorder

A

sudden onset, <1 month, no negative symptoms

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11
Q

DSM Criteria

A

2 or more symptoms for at least 1 month (one must be from the first three): delusions, hallucinatons, disorganized speech, grossly disorganized or catatonic behavior, negative symptoms; requires an mpairment in major area of functioning, and symptoms have been present for at least 6 months

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12
Q

Negative symptom: alogia

A

person says very little when they talk, when they do speak, it has little content

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13
Q

Negative symptom: avolition

A

lack of motivation/interest

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14
Q

Negative symptom: anhedonia

A

lack of pleasure

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15
Q

Negative symptom: flat affect

A

lack of expression of emotion

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16
Q

Negative symptom: psychomotor

A

awkward movements, odd gestures, rigidity, over excitement

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17
Q

Type I Schizophrenia

A

positive symptoms; overattention

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18
Q

Type II Schizophrenia

A

negative symptoms; underattention

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19
Q

Prodromal Phase

A

precedes active phase; categorized by deterioration in functioning and change in personality; onset is difficult to date accurately, and length of phase varies

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20
Q

Active Phase

A

positive symptoms are frequent; onset could be a stressor

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21
Q

Residual Phase

A

symptoms similar to prodromal phase; positive symptoms can be present, but are often milder; negative symptoms are often still present

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22
Q

Higher rates of schizophrenia are seen in…

A

low socioeconomic urban areas

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23
Q

Social Drift Hypothesis

A

(Explains low SES) reduced ability to work due to schizophrenia leads to a drift into poverty

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24
Q

Environmental Hypothesis

A

(Explains low SES) higher levels of stress contribute to people who are genetically predisposed

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25
Q

Comorbidity

A

Anxiety Disorders (PTSD 29%, Panic 15% OCD 23%), Depression (50%), Substance Abuse (50-60%), higher rate of suicide

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26
Q

Marijuana

A

worsens positive symptoms

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27
Q

Nicotine

A

90% of people with schizophrenia smoke; form of self-medication; nicotine affects dopamine, which improves some cognitive function, specifically attention and spatial working memory

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28
Q

Life expectancy

A

much shorter than general population, potentially due to poor environments and health problems

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29
Q

Aggression and violence

A

majority are not more violent than average; more common in younger males, people with higher impulsivity, and a history of violence; violence could potentially be attributed to substance abuse; violence is typically directed at family members; more likely to be victims, not aggressors

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30
Q

Age of Onset

A

later adolescence/early adulthood; males 21-23, females 27-28; rare in childhood and after 45

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31
Q

Gender patterns

A

females respond better to meds, spend less time in hospitals, and have better social interactions

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32
Q

Prognosis Patterns: most likely to succeed

A

females with acute onset, better premorbid functioning, supportive family environment, available programs, and no substance abuse

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33
Q

Prognosis “Rule of Thirds”

A

1/3 improve significantly, 1/3 stay the same (episodic relapses, lapse in functioning), 1/3 are severely and chronically disabled

34
Q

Historical Perspective: Bleuler

A

Schizophrenia term (1908): splits between associations in thoughts and emotions

35
Q

Historical Perspective: Freud

A

thought it involved some sort of regression, but did not treat any patients

36
Q

Historical Perspective: Fromm-Reichman

A

Schizophrenogenic Mother (1948): a cold, domineering mother that is simultaneously overprotective can cause schizophrenia; appears to be self-sacificing, but uses child to satisfy own needs

37
Q

Historical Perspective: Bateson

A

Double-Bind Family Communication (1956): people who are important to you who send conflicting verbal and nonverbal messages in situations that are inescapable can cause relapse; children cannot avoid displeasing their parents because nothing they do is right

38
Q

Historical Perspective: RD Laing

A

Radical Psychiatry (50-60’s): schizophrenia isn’t a disease, it’s a “sane way of dealing with an insane world;” someone with a difficult life needs to do this to give their life meaning

39
Q

Behavioral View

A

operant conditioning and reinvordement: people who are not reinforced for their attention to social cues will stop attending to them; causes more bizarre responses which are given attention

40
Q

Revealed Differences Approach

A

family is given an issue to discuss that they previously disagreed on and told to reach agreement; 3 patterns emerge: 1) more conflict 2) more communication difficulties 3) more critical, yet over-involved

41
Q

Expressed Emotion (EE)

A

combination of criticism and emotional over-involvement; relapse rates are higher with higher EE (stressor, not causal)

42
Q

Cognitive View

A

cognitive deficits: attention (selective and sustained), verbal learning, memory, executive function, spatial working memory, processing speed (frontal lobe)

43
Q

Biological View

A

genetic predisposition; negative symptoms may have higher heritability; fathers over 50 when child is born have higher risk; MZ: 50% DZ: 17%; offspring of MZ’s have higher risk, whether it was the twin with schizophrenia or not; adopted children still higher with biological parent

44
Q

Smooth Pursuit Eye Movement

A

majority have irregular pursuit/more extraneous eye movements, relatives have worse scored than control groups

45
Q

Sensory Gating

A

ability to filter out auditory signals is worsened

46
Q

Diathesis-Stress Model

A

includes both environmental and biological factors, interactive model; biological vulnerability and environmental factors (prenatal or postnatal stressors) interact lead to disease; typically high rate of exposure to abuse

47
Q

Dopamine Theory

A

Indirect evidence of increased dopamine: drugs can create Parkinsonian side effects, and bind to the same receptors as DA; amphetamine psychosis looks a lot like schizophrenia

48
Q

Revised Dopamine Hypothesis

A

excess of DA receptors, or oversensitized DA receptors; backed by brain scans, brain autopsies, and animal studies

49
Q

Problems with Dopamine Hypothesis

A

Timing: drugs can block receptors within hours, but symtpoms are not affected for weeks
Drugs affect positive symptoms, but not negative ones

50
Q

Mesolimbic Pathway

A

ventral tegmental area (midbrain) to limbic system (amygdala): leads to positive symptoms and excess dopamine activity

51
Q

Mesocortical Pathway

A

ventral tegmental area to frontal lobe, specifically prefrontal cortex: affects negative symptoms; underactive dopamine neurons in profrontal cortex fail to inhibit DA neurons in the limbic system

52
Q

Serotonin

A

newer drugs affect this, often a moderating neurotransmitter, can regulate dopamine neurons in the mesolimbic pathway

53
Q

Glutamate

A

also plays a moderating role, low levels of glutamate affects levels of DA

54
Q

GABA

A

may contribute

55
Q

Neuroimaging/Brain Structure

A

reduction in frontal lobe function, less connectivity between frontal and parietal lobes; enlarged ventricles (more cerebrospinal fluid) = less brain tissue (affects 1/3); less gray matter in frontal and temporal lobes, fewer dendrites, no reduction of neurons (may be more densely packed); causes unknown

56
Q

Childhood indicators

A

subtle differences in childhood behavior and cognition; more involuntary movements than average

57
Q

Why adolescents?

A

maturation of prefrontal cortex, more DA activity in the brain, new synapses formes, excessive pruning (getting rid of synapses we do not need)

58
Q

Prenatal and Birth Risk Factors

A

poor nutrition, vitamin D deficiency, maternal infection, birth complications (reduced oxygen)

59
Q

First Generation Antipsychotics: Major Tranquilizers

A

Phenothiazines: (Thorazine) block DA receptors (D2), work better at controlling positive symptoms
Haldol is a similar drug

60
Q

Adverse Affects of 1st Generation Drugs

A

sedation, low blood pressure, constipation, urinary problems, dry mouth, blurred vision

61
Q

Extrapyramidal Side Effects of 1st Generation Drugs

A

Parkinsonian symptoms (muscle tremors, muscular rigidity, lack of facial expression)
dystonia (involuntary muscle contractions)
akathesia (restlessness)
occur within days of starting medication
Tardive Dyskinesia: 1+ year after starting meds, involuntary, tic-like contractions, doesn’t always disappear; 10-20% develop this, high risk: high dose, long term, type II, 55+, female, mood disorder
2 types: Breakthrough (usually not reversible)
Withdrawal (less likely to be permanent)

62
Q

Second Generation Atypical Antipsychotics: Clorazil

A

Affects D4 and serotonin receptors, few extra-pyramidal symptoms, helped negative symptoms
Adverse effects: weight gain, sedation, increased risk of diabetes, low blood pressure, seizures
Agranulocytosis: drop in white blood cells; affects young, f>m)

63
Q

Second Generation Atypical Antipsychotics: Resperidone

A

Affects serotonin more than others, weaker blocker of DNA, less adverse effects but affects acne, bone density, and sexual function

64
Q

Second Generation Atypical Antipsychotics: General

A

affects fewer D2 receptors, more D1, D4, and serotonin

65
Q

Effectiveness: 1st gen vs. 2nd gen

A

2009 meta-analysis: only 4 2nd gen drugs proved to be more effective, Clozapine was #1

66
Q

Adverse Effects: 1st gen vs. 2nd gen

A

extra-pyramidal effects occur mostly in high-potency 1st gen drugs (Haldol and Risperidone)

67
Q

Short term vs. long term

A

Short term: most people on meds do better than those who aren’t
Long term: those on meds do worse than those who aren’t
Need to consider length of use and patient characteristics

68
Q

Social Skills Training

A

problem solving, group work, geeral social skills, interacting with others, using schedules, applying for jobs, etc.; especially used for negative symptoms

69
Q

Family Therapy

A

reduces hospitalization; teaches family about the disease and medication, increases problem solving and communication, teaches family not to blame the patient, helps both family and patient; can be used with individual therapy

70
Q

Supportive Counseling

A

supports and coaches the client

71
Q

Cognitive/Behavioral Therapy

A

reduces hospitalization by 50%; helps with interpretation of symptoms and coping with them
Acceptance & Commitment: rather than trying to stop abnormal cognitions, patient accepts them and tries to learn from them
Cognitive Enhancement Training: addesses attention and memory problems with practice

72
Q

Living situations

A

many are placed in homes with untrained supervisors, or are barely supervised at all

73
Q

Hospitalization in the Past

A

prior to 1950’s, there were no treatments so patients were just put in hospitals

74
Q

Milieu Therapy

A

humanistic; people will do better if they are treated with respect and given responsibilities

75
Q

Token Economy

A

still used today; based on operant conditioning; people work on behaviors like self-care or social skills and get tokens for good behavior that they can spend on objects or priviledges; needs to be individualized to work well

76
Q

Hospitals Today

A

mostly short-term hospitalization for people in acute phase in danger of hurting themselves or others; purpose is to stabilize them and work out medications

77
Q

Community Mental Health Act

A

1963: goal of getting people out of hospitals and provide a network of services to them; created community mental health centers; only partial short-term hospitalization with day treatments, sheltered workshops, job training and halfway houses; works well when all services are available and coordinated; more treatment in rural areas

78
Q

How has community treatment failed?

A

40-60% a year do not recieve treatment, shortage of beds for people who do need hospitals, shortage of community mental health centers, shortage of day programs, residences, and sheltered workshops

79
Q

Community Mental Health Act Funding

A

most money goes to medications, SSI Disability income, patients with less severe illnesses

80
Q

Why has community treatment failed?

A

funding is not going to schizophrenia, therapists prefer to work with milder illnesses because they are easier to treat and more likely to improve, constrained by zoning laws, or people want the services, but not near their homes

81
Q

Homelessness and Prisons

A

1/3 of homeless people have mental illnesses, more than 1/2 of inmates have mental illnesses; substance abuse is an issue

82
Q

Social Policy

A

it is expensive to keep people in jail, and people in prisons/hospitals cannot work

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