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psych exam 4 > Chapter 8: Schizophrenia > Flashcards

Chapter 8: Schizophrenia Flashcards

1
Q

define schizoaffective disorder

A

mix of schizophrenia (delusions, hallucinations, disorganized speech, negative symptoms) with mood disorder usually major depressive or manic episode

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2
Q

what makes schizoaffective disorders differ from mood disorder with psychotic features

A

must have at least 2 weeks of hallucinations or delusions WITHOUT mood symptoms

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3
Q

schizophreniform disorder

A

meet criteria A,D,E of schizophrenia diagnosis but symptoms are only for 1-6 months
- 2/3 will later meet requirements of schizophrenia or schizoaffective disorder
- can have confusion but not blunted or flat affect

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4
Q

brief psychotic disorder

A
  • sudden onset of delusions, hallucinations, disorganized speech or behavior. lasts for 1 day - 1 month and symptoms remit
  • can occur after major stressor (accident or childbirth) while others happen with no apparent stressor
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5
Q

Delusional disorder

A

delusions lasting 1 month that pertain to real life (deceived by spouse, being followed)
- less common 0.05-0.2% prevalence
- dont have any other psychotic symptoms
- mean onset is 40 yrs old but ranges from 18-90
- men: persecutory and jealous subtype
- women: erotomanic (thinking someone is in love with you when they are not)
- best treatment: therapy + antipsychotics (50% of clients make full recovery - women better prognosis)

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6
Q

schizotypal personality disorder

A

similar eccentric behaviors like schizophrenia but more centered around personality.
- lifelong pattern of strange behavior that impacts work, social, interpersonal function
- maintain grasp of reality but behavior with very large suspicions of others and usually only have a few close friends and have odd perceptions of the world around them
- 0.6% Norwegian, 4.6% US and 0-1.9% clinical setting
- have similar but less severe problems with working memory, learning etc.

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7
Q

bio theories of Schizophrenia

A

1) genetic transmission (but cant fully explain disorder)
2) structural and functional abnormalities in specific areas of brain
3) history of birth complications or exposure to viruses
4) excess levels of dopamine (possibly serotonin, GABA, and glutamate)

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8
Q

genetic contributors to schizophrenia

A
  • definite genetic factor but also have environmental risk factors at play as well
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9
Q

family studies

A
  • as genetic similarity between family members with schizophrenia lowers their risk decreases
  • first degree relative who shares 50% of genes with has a 10% change of developing, cousins = 3%
    1% chance in general pop
  • increased risk for bipolar disorder
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10
Q

adoption studies

A

more likely to have diagnosis if biological parent had it

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11
Q

twin studies

A

heritability around 41-87%
- possible difference in rates across studies
- concordance in fraternal twin 14% and maternal 46%
- monozygotic twins that did not both have schizophrenia found differences in DNA for gene regulation of dopamine (epigenetic difference - possible environment events that changed utero brain development)

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12
Q

structural and functional brain abnormalities

A
  • researchers look at it as a neurodevelopmental disorder of the brain during utero or early life
  • Most often seen: reduction in grey matter in medial, temporal, superior temporal, and prefrontal cortexes
  • if someone in family has, more odds of other members have smaller or less active prefrontal cortex (important for language, emotional expression, planning, etc)
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13
Q

prefrontal cortex differences

A
  • this structure usually has major development between adolescence and young adulthood, which if starts dysfunction during this time makes since schizophrenia typically presents at this age
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14
Q

hippocampus

A

role: forming long-term memories
- see a difference when encoding information for storage or trying to retrieve information from memory
- differences in shape and volume of hippocamus

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15
Q

white patter

A

role: connection between ares of the brain, especially in areas of working memory
- can see changes in this structure before overt symptoms so it can be seen as early signs of the disorder
- impairs ares of the brain to work together

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16
Q

ventricles

A
  • are fluid-filled spaces in the brain
  • are enlarged which means other structures in the brain tissue have deteriorated
  • will show social, emotional, and behavioral deficits before core symptoms of schizophrenia
  • tend to have more severe symptoms and less responsive to meds
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17
Q

damage to developing brain - what causes neuroanatomical abnormalities in schizophrenia

A
  • genetic and epigenetic factors together: birth complications, TBI, viral infections, nutritional deficiencies, and cognitive stimulation deficiencies
  • birthing complications: emergency C-section, bleeding during pregnancy, preeclampsia, gestational diabetes, low birth rate
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18
Q

birthing complications

A
  • inadequate oxygen to fetus before, during, or after delivery causing damage to neuroanatomy and contributes to lower grey matter and enlargement in lateral ventricular zone
  • rodent studies found lower oxygen is associated with decreased myelination, tissue volume, and increased ventricles
  • first “hit” of prenatal complication that disrupts brain development establishes a increased vulnerability to a second “hit” that occurs later in life and onset of psychiatric symptoms occur
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19
Q

Maternal Illness and Prenantal Exposure

A

higher rates if mother was exposed to flu, rubella, toxoplasmosis, and herpes during pregnancy and delivery
- localized bacterial infection increased psychotic disorder risk 1.6x and if system wide increased 3x
- more associated with development of disorder in males than female offspring
- flu season and babies impact are born around spring which if mother contracted flu would be during vital growth periods for fetus (fall & winter)

20
Q

maternal immune response

A

MIA linked with autism and schizophrenia in offspring
- CRP is biomarker of inflammation and found at higher rates in mothers fighting an infection
- possible anti-inflammatory diet to pregnant women may reduce risk of offspring disorders
- possible impact to fetal serotonin production

21
Q

gut microbiome

A

lots of research starting on this topic

22
Q

neurotransmitters

A

the main neurotransmitters of this disorder is thought to be excess dopamine in prefrontal cortex and limbic system
- how think of role of HPA axis that can be triggered by stress and all contribute to dopamine release

23
Q

meds and their impact on neurotransmitters

A

phenothiazines and neuroleptics both block the re-uptake of dopamine

  • substances like amphetamines will increase the amount of dopamine and increase positive symptoms
  • these drugs seem to help positive symptoms but not negative symptoms so shows not just dopamine is at play
24
Q

revised dopamine theory

A
  • thought that dopamine has different types of receptors and levels in areas of the brain
    1. mesolimbic pathway: subcortical pathway and when abnormally functioning attributes to individuals finding importants in insignificant stimuli
25
2. part of revised dopamine theory
unusually low dopamine activity in prefrontal cortex (attention, motivation, and organization behavior) - thought to lead to negative symptoms (lack motivation, inability to care for oneself, restriction of affect)
26
other neurotransmitters involved in schizophrenia
serotonin help regulate dopamine neurons in mesolimbic system - new drugs made to regulate serotonin - possible GABA & Glutamate abnormal levels
27
psychosocial - social drift, trauma, and urban living
- risk factors: lack of social support, higher poverty, high crime rates, and reduced access to health care - more likely to move to ares with different deprivation in urban/rural compared to general population - younger individuals with disorder move more frequently (thought for mental health services)
28
what is the social drift theory
environmental risk factors of deprived urban areas increases risk for psychological disorder especially if genetic predisposition is present
29
trauma and social adversity
childhood risk factors for adulthood psychosis : sexual & physical abuse, emotional/psych abuse, parental death, bullying, neglect - childhood trauma more likely to experience positive schizophrenia symptoms and hallucinations - born in a urban/ large city (5x more likely) could be due to greater exposure to cannabis use, income inequality, social fragmentation, maternal complications - overcrowding in large cities and exposed to infectious agents - say these exposures can be predictive of psychotic symptoms to present 3 yrs later - if have 4+ environmental risk factors usually lower age of onset
30
stress and relapse
- immigration - more likely to relapse with stressful life events - no environmental factors that protect against disorder - having pets can change immune system and gut microbiome (having dogs while pregnant and through childhood)
31
schizophrenia and the family
- old psychodynamic theories said disorder was due to mother being overprotective and rejecting at the same time (make family feel guilt) - expressed emotion: provide care but negatively influence clinical conditions and emotions toward individual - more symptoms with family who is low warmth and high criticism
32
culture & family
- collectivist cultures: absence of positive words is more damaging than criticism (this is opposite in western cultures) - more okay with positive symptoms (hallucinations) and see them as uncontrolled as compared to negative symptoms (lack of social interest)
33
cognitive perspective
- delusions are from trying to explain strange perceptual experiences and jumping to a conclusion - hallucinations: hypersensitivity to perceptual input and to believe experiences are due to external sources - negative symptoms are from belief that social interactions will be aversive and need to withdrawal to save cognitive resources
34
cognitive treatment
- identify and cope with stressful circumstances associated with development and worsening of symptoms - helping people realize social interactions can have a positive effect - dispute delusions and hallucinations
35
biological treatment
1930s: insulin coma therapy - given massive amounts of insulin to go into coma and thought symptoms would be better when they woke up ECT: found to not be as effective, better for depression - then many were just hospitalized (were just fed and prevented from hurting themselves) - 1950s created drugs chlorpromazine now we have created drugs like neuroleptics - atypical antipsychotics are showing they can help with positive symptoms and fewer side effects
36
first generation typical antipsychotic drugs
1950s Jean Delay and Pierre Deniker found chlorpromazine part of phenothiazine and helps agitation, reduce hallucinations, - helped positive symptoms but made negative ones worse and (cognitive, affective, and motor domains) - usually have to continue use even when not having active episode if stop 78% relapse in 2 yrs and 30% within 2 yrs - try to prescribe lowest dose to help positive symptoms (maintanence dose) without additional risk for side effects
37
side affects of antipsychotics
grogginess, dry mouth, blurred vision, drooling, sexual dysfunction, visual disturbances, weight gain or loss, menstrual irregularities - can also have symptoms similar to parkinson's disease (low dopamine)
38
what is the akinesia (side effect) from antipsychotics
slowed motor activity, monotonous speech, and expressionless fact
39
akathesis
agitation that causes people to pace and unable to sit down
40
tardive dyskinesia (permanent side effect from phenothiazines)
neurological disorders that involves involuntary movement of tongue, face, mouth, jaw - 20% of long term users
41
second generation atypical antipsychotics
clozapine - binds to D4 dopamine receptor and influences serotonin - can help those who have been treatment-resistant and can lower both positive and negative symptoms - can also help dementia and those with major depressive disorder - higher nonresponse when individuals had early onset and lower symptom severity
42
possible risk factor agranulocytosis in those who take clozapine
causes deficiency of granulocytes that are produced in the bone marrow that fight infection
43
other secondary generation antipsychotics
risperidone, olanzapine etc has side effects like significant weight gain, risk of diabetes, sexual dysfunction, sedation, low blood pressure, visual problems, seizures, etc - need to start antipsychotics within 5 yrs of first acute episode
44
psychological and social treatments
use bio treatment to help positive symptoms and psych therapy to help with social skills and reduce isolation to help negative symptoms - teach them they need to continue their meds even if they feel "better" - can help find jobs etc
45
behavioral, cognitive, and social treatments
- cognitive: helping people recognize demoralizing attitudes and teach them to seek help when needed and participate in society - social learning theory: operant conditioning to teach initiating and maintaining conversations with others, asking for help, and persisting an activity - taught problem solving and group therapy to learn to interact with others - but see only little help in long run
46
Family therapy
combine basic education with family training to cope with loved one's inappropriate behaviors and disorder family taught: disorder biological causes, symptoms, medications & side effects - communication skills, encourage appropriate behavior psycho-education has helped decrease relapse by 50-60%
47
assertive community treatment programs
community based framework to improve functional deficits and reduce hospitalization through expertise of medical professionals, social workers, and psychologists 24/7 - changed from hospitalized care to community based so when they are out of hospital they have somewhere to go and continue care but programs were not funded correctly and fall on local and state governments that dont have funds - 40-60% receive little to no care in given year many can go to family but more are put in nursing homes

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