Psychopathology Flashcards

1
Q

Mental illnesses and psychological disorders

A

MDD, BPD, schizophrenia etc

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2
Q

Neurological disorders

A

Don’t need a cognitive component

e.g. chronic numbness, MS

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3
Q

Brain dysfunctions

A

Brain damage that leads to symptoms

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4
Q

should psych disorders, neurological disorders, and brain dysfunctions be considered separately?**

A

No, they all have a biological basis and some interconnectedness

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5
Q

principles of psych disorders

A
  • developmental in nature
  • represent multiple disorders categorized together by symptoms
  • biological predisposition interacts with environment (diathesis stress model)
  • represent extreme ends of normal spectrum of NS functioning, not fundamentally different
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6
Q

PDs relation to crime

A

not any more likely to commit crimes, more likely to be a victim of crime

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7
Q

psychosis is not…

A

Dissociative identity disorder

psychopathy

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8
Q

what type of assessment is psychopathy?

A

forensic, not psychological

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9
Q

types of symptoms related to schizophrenia

A

positive
negative
cognitive
mood

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10
Q

positive symptoms (schiz)

A

hallucinations (auditory), delusions, and disorganized thought/speech/behaviour
similar symptoms associated with drug use (hallucinations are more likely somatosensory)

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11
Q

negative symptoms (schiz)

A

decrease in emotional range, poverty of speech, difficulty manifesting motivation

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12
Q

what symptoms do schizophrenic drugs usually target?

A

positive symptoms

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13
Q

cognitive symptoms (schiz)

A

deficit in working memory, attention, executive functioning

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14
Q

mood symptoms

A

extremely sad or cheerful when they shouldn’t be. general mood disorder component

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15
Q

schizoaffective disorder

A

aspects of schizophrenia and MDD

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16
Q

prevalence/onset of schizophrenia

A

0.5-1.5%, slightly more in men

teens to early 30s, can see atypical behaviour in childhood processes

17
Q

risks with schizophrenia

A

unemployment, poverty, homelessness (1:2 ratio)

18
Q

Causes of schizophrenia

A

big role of genetics

marijuana as big of a risk factor as urbanicity or maternal prenatal infection

19
Q

brain changes in schizophrenia (structural)

A

reduced grey matter, reduces as time passes. results in large ventricles
abnormal connectivity of white matter, disorganized
hippocampus; atypical layering structure and neuronal shape
PFC: fewer dendritic spines and GABAergic interneurons

20
Q

brain changes in schizophrenia (functional)

A

hypoactive frontal and temporal lobes (executive functioning and theory of mind)
dysfunctional dopamine neurotransmission

21
Q

brain difference in schizophrenia show us the illness is most likely….

A

neurodevelopmental

22
Q

pharmacological treatments (schiz)

A

antipsychotic drugs for positive symptoms

no successful treatment of negative symptoms because a psychostimulant would increase positive symptoms

23
Q

dopamine theory of schizophrenia

A

schizophrenia is caused by too much activity at the receptors for the NT dopamine

24
Q

findings that support dopamine theory (schiz)

A
  • brains with Parkinson’s disease have dopamine depletions in the substantia nigra, antipsychotic drugs produce symptoms similar to Parkinson’s
  • drugs that increase dopamine levels produce symptoms of schizophrenia
  • efficient antipsychotic drugs correlates with degree to which it blocks activity at dopamine receptors
  • individuals with schizophrenia have hypersensitive dopamine release
25
Q

what was the study showing that people with schizophrenia have hypersensitive dopamine release

A

administered amphetamine to 15 control and 15 experimental people and measured dopamine receptor availability before and after administration
there was decreased receptor availability in exp. group

26
Q

problems with dopamine theory**

A
  • newer antipsychotic drugs were just as good as traditional antipsychotics (both D2 antagonists)
  • it takes 2-3 weeks for drugs to work yet their effect on dopamine receptor activity is immediate (downstream instead?)
  • no improvements after first antipsychotic given
27
Q

glutamate hypofunction theory

A

Dysfunction in glutamate NMDA receptors on GABAergic interneurons leads to decreased GABA especially in the PFC
lost inhibition meant for synchrony and organized thought

28
Q

support for glutamate theory

A
  • brains show fewer glutamate receptors
  • glutamate antagonists (PCP, ketamine) can mimic symptoms and cog problems of schizophrenia
  • NMDAR co-agonists provide small improvements
  • activating cannabis receptor has inhibitory effects that cause CB1-NMDA receptors to internalize**
  • chronic NMDAR antagonism changes dopamine transmission
29
Q

problems with glutamate theory

A
  • positive symptoms don’t respond to glutamatergic medication
  • previous support has confounds such as studies not only targeting NMDA receptors, but others simultaneously
30
Q

support for schizophrenia being an autoimmune disorder

A

bone marrow transplants between individuals with and without schizophrenia seemed to “transfer” the schizophrenic symptoms
autoimmune disorders are more prevalent in schizophrenia therefore hypothesize bone marrow transplants restores microglia functions
Auto immune disorders also target NMDA receptors

31
Q

“success” of psychopaths

A

how well psychopaths go about society without being noticed