Final: Schizophrenia Flashcards

1
Q

characteristics of schizophrenia

A

split mind
major disturbances in thought, emotion, movement, behavior

disordered thinking: ideas not logically related, faulty perception and attention
- perceptual distortions include hallucinations

lack of emotional expressiveness
- inappropriate or flat emotions

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2
Q

prevalence of schizophrenia

A

1% - 2.6 million adults in US
- one of top 15 leading causes of disability
affects MEN more than women
age onset: late adolescence, early adulthood (men diagnoses at earlier age than women)

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3
Q

what are some environmental risk factors

A

growining up in large cities
-air pollution - toxins
stress of the hustle and bustle
can lead to an immune rxn

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4
Q

what % of patients attempt suicide

A

20-50% (10% are successful)

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5
Q

association between immune dysfunction and schizophrenia

A

-birth season is a risk factor (late winter, early spring at inc risk, usually inc risk of getting sick then too)
-they are prone to infections
-autoimmune disorders inc risk
-proinflammatory cytokines inc and anti inflammatory cytokines reduced
antipsychotics restore levels

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6
Q

perinatal complicatons associated with inc scz rates in offspring

A

inc maternal cytokines or exposure to viral infection in 2nd trimester - inc risk of Scz in offspring
malnutrition
fetal brain injury in pregnancy/delivery caused by oxygen deprivation or drug use

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7
Q

behaviors in early infancy signal a potential risk

A

passive and apathy - no longer interested in new things
reduced responsiveness to verbal commands
difficult temperament (how well they respond to chanegs in environment)
poor sensorimotor performance

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8
Q

genetic contribution

A

varies according to hw many genes one shares with someone that has the disorder
- monozygotic twins only 50% the other will get it

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9
Q

multiple genes at different loci are effected

A

disruption of communication btw ionotropic and metabotroic families of receptors
ex: polymorphisms in DISC1gene assoiated with cognitive sypmtoms and pproper neural development

genetic vulnerability inc probability that the events during perinatal brain development will contribute to the occurence of Scz

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10
Q

2 hit model of Scz development - first hit

A

genetic vulnerability inc the probability that events during perinatal brain development will contribute to the occurrence of Scz

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11
Q

2 hit model of Scz - second hit

A

in adolescence neurodevelopmental errors and environmental events produce the diagnosable symptoms
stressors put someone over edge to develop symptoms

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12
Q

diagnosis

A

difficult
no 2 individuals show sam pattern of symptoms - no single symptom occurs in every patient
symtoms inc and dec over time
type of symptoms also change over time

symptoms often seen in other disorders

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13
Q

3 major clusters of symptoms

A

positive
negative
cognitive

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14
Q

positive symptoms

A

delusions
hallucinations
adding behavior

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15
Q

negative symptoms

A
avolition
alogia
anhedonia
blunted affect
asociality
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16
Q

cognitive/disorganized symptoms

A

disorganized behavior

disorganized speehc

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17
Q

delusions

A

+ symptoms

firmly held beliefs
contrary to reality
resistant to disconfirming evidence

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18
Q

types of delusions

A

persecutory (the CIA [lanted a listening device in my head, 65% have these)

thought insertion
thought broadcasting
outside control 
grandiose delusions
ideas of reference
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19
Q

hallucinations

A

+ symptom

sensory experiences in absence of sensory stimulation

20
Q

types of hallucinations (3)

A

auditory (74% have)
visual
hearing voices (inc activity in Brocas area in hallucinations)

21
Q

lack of interest, apathy, difficulty initiating/persisting in goal-directed behavior

A

avolition

22
Q

social withdrawal

inability to form close personal relationships

A

asociality

23
Q

inability to experience pleasure

A

anhedonia

24
Q

exhibits little or no emotion in face or voice

A

blunted/flat affect

25
Q

peculiar, rigid posture, inappropriate gestures, overt signs of tension, repetitive movement

A

motor disturbances

26
Q

reduction in speech

A

alogia

27
Q

cognitive symptoms

A

impaired working memory, executive functioning, attention

disorganized speech (incoherence - inability to organize ideas)
-loose associations (hard to stick to one topic)

disorganized behavior - silliness, agitation, unusul dress

28
Q

DSM-5 criteria for Scz

A

2 or more must be present for at least one month

hallucinations, delusions, disorganized speech, disorganized behavior, neg symptoms

29
Q

what brain region with positive symptoms

A

mesolimbic

30
Q

what brain region with affective symptoms

A

ventromedial PFC

31
Q

what brain region with aggressive symptoms

A

loss of orbitofrontal cortex

overactivity of amygdala

32
Q

what brain region with cognitive symptoms

A

dorsoloateral PFC

33
Q

what brain region with negative symptoms

A

mesocortical and Nacc

34
Q

structural abnormalities in Scz brain

A

atrophy of cerebral cortex

enlargement of ventricles

35
Q

what is the reduced brain volume due to

A

smaller neuronal cell bodies, reduced dendritic density, close packing of cells
poor connectivity btw brain regions

36
Q

where are cells dsorganized - what brain region

A

hippocampus

37
Q

loss of cortical ____

A

gray matter

38
Q

impaired integration for sensory and cognition

A

dec structural connectivity in white matter tracts btw frontal, temporal, parietal lobes

39
Q

hypofrontality hypothesis

A

dec activity in frontal lobe in Scz

Scz need to work hardr to get same executive control as healthy people

40
Q

what are the neurotransmitter systems involved in Scz

A

dopamine, glutamate, serotonin

41
Q

dopamine hypothesis

A

excess DA function results in + symptoms of Scz

hyperactivity at D2 receptors: dtrong correlation btw D2 receptor blockade and dec in Scz symptoms (inc in impulsivity, cognitive symptoms, agitation)

42
Q

what can produce psychotic reactions in healthy individuals reversable by DA antagonists

A

amphetamine

43
Q

DA imbalance hypothesis

A

neg symptoms and impaired thinking due to dec DA in mesocortical regions!

excess DA function in mesolimbic leads to + symptoms

44
Q

hypoglutamate model

A

dec glutamate activity in Scz

blocking NMDA recetors with PCP or ketamine produces psychosis similar to psychosis in Scz

45
Q

glutamate - DA interaction

A

insufficient NMDA, Glu can explain the inc in mesolimbic DA and dec in PFC activity

46
Q

hyperactivity/ imbalance of serotonin at what receptor can result in psychosis

A

5-HT2A

- always excitatory - depending on location can stimulate or inhibit glu release