Schizophrenia Flashcards

1
Q

What is psychosis?

A

This is the hallmark of schizophrenia

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2
Q

What is schizophrenia?

A

Disorder characterized by major disturbances in
thought, emotion, & behaviour

Disordered thinking

Ideas not logically related

Faulty perception & attention

Flat or inappropriate affect

Highly unusual motor activity

(a disorder characterized by thoughts, behaviorus, emotions, there are a lot of disordered thoughts and the perception and attention is different. Think about this in terms of what kind of info you are taking in. If you are looking to your environment to see whats real and not real you aren’t really dealing with the same world. Flat affect, unusual motor activity. Not just i’m different from someone else but I’m different from me before)

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3
Q

What are the hallmark symptoms of schizophrenia?

A

you have to have at least 2 of these and so the dots reflect when you will have schizophrenia.

  • delusions
  • disorganized speech and or behaviour
  • hallucinations
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4
Q

What are the positive symptoms of schizophrenia?

A

Excess or distortion in
typical range of
behaviour & perception

Delusions:
* Erroneous beliefs
* Highly unusual thought content
* Firmly held belief despite evidence

Hallucinations:
* Sensory experience
(any sensory modality)

  • Seems real despite no external stimulus

the thought content of delusions have to be highly unusallly. Not shared by others Hullicinations are oftne sensory experiences and they seem very real despite the actual outside stimulus not being there.

part of what we do in treatment is reality testing and it takes a lot to ebe considerate of what the other people around you are saying.

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5
Q

What are the negative symptoms of schizophrenia?

A
  • Deficit of typically
    present behaviours

we generally see positive and negative symptoms. Positive means more added on, negative means taking things away. Positive is voices, flat emotions is negative. You usually get more negative symptoms the older you get and the further along you get in the disorder.

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6
Q

What are examples of Positive Symptoms?

A

Delusions
* Thought insertion
* Broadcast thoughts
* Thought withdrawal
* Made feelings

(there are different kinds of delusions. One is though insertions. AKA someone put a thought in your head. Broadcast ing is someone can read your thoughts, thought withdrawal is someone took your thought and deleted it Made feelings is someone put ian emotion in you but it isn’t related to you.)

Hallucinations
* Voices talking about
person (if they think the voices are different from each other thats a good indication that you are going down this path. )
* Unusual images
* Sensations of thing

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7
Q

What are examples of negative symptoms?

A
  • behavioural deficits (anything that is a belief is a delusion and if you also see it, the seeing of it would be a hallucination.)

a lot of reduced expressive behaviour

Reduced expressive behaviour:
* Alogia (minimal speech) (more flat affect)
* Flat affect

Reduced Motivation/pleasure:
* Avolition (minimal goal-directed activity)
* Anhedonia
* Asociality (a hedonist is someone who gets into the pleasure of things and anhedonia is the opposite of pleasure, no pleasure.)

(reduced motivation or pleasure so ess goal directed activity. Anadonia, lack of sociality )

for negative symptoms you have a much poorer prognosis.

*Poorer prognosis

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8
Q

Explain disorganization in schizophrenia?

A

Speech:
Content – grammatically correct form, but does not make sense

  • Ex. Loose associations
    If I went to the store to kick a pot, I should twirl up the sky.
    Form – grammatically incorrect
  • Ex. Clang associations, “word salad”
    I went to the store, door, floor, find a puppy poor.
    Flying about three bananas out cat.

Behaviour
Catatonia
* Unusual complex movements
* Waxy flexibility (immobile posture)
Inappropriate affect

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9
Q

What are positive symptoms of schizophrenia?

A

Positive symptoms
* Delusions (grandiose?
persecutory?)
* Ideas of reference
* Disorganized thinking

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10
Q

What are negative symptoms of schizophrenia?

A

Negative symptoms
* Blunted affect
* Asociality
* Anhedonia

the longer you have schizophrenia the more flat affect you will tend to have.

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11
Q

What are the 3 phases of schizophrenia?

A
  • Prodromal
  • Obvious deterioration in role functioning
  • Personality change (e.g., schizotypal PD)
  • active
  • Psychosis
  • residual
  • Improvement in positive symptoms
  • Continued negative symptoms

the cycle aspect is just between active and risidual phase.

there are 3 phases: prodromal something in your personality is shifting, you are no longer able to function in your role as ya student etc. you are not able to continue to do things as you did before.

you are going to have an active phase and you are going to get out of that phase but the disorder continues. Medication is often used t put off another active phase. In the risidual phase, we often don’t see a change in negative symptoms.

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12
Q

What is the epidemiology of schizophrenia?

A

Lifetime risk 1% (1% for the regular population cross cultural)

Risk factors
* Father over 50 (if you are concieved when your dad is over 50)

  • Parents in dry cleaning business
  • Severity: males > females
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13
Q

What is the age of onset of schizophrenia?

A

Most common: ages 18-30

menopause can make you more likely to develop schizophrenia.

not a whole lot of people pre puberty and a lot ar 21

estrogen is a protective factor.

LOOK AT GRAPH

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14
Q

What is the life expectancy of schizophrenia?

A
  • shorter (life expectancy is much shorter. Folks start living outside of protective social circles. A disproportionate amount of folks who are unhoused and using a lot of substances. )
  • increased risk for suicide
    20-40% attempt suicide
    10% complete suicide
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15
Q

What is the prevalence of Schizophrenia in terms of SES?

A

is it you are from a lower SES you develop it or you develop it and then become low SES.

highest annual prevalence at lower class and it goes down as SES goes up.

causal direction?

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16
Q

What are the factors affecting the course of schizophrenia?

A

Gender

Stress/Family environment
Expressed Emotion (this is for relapse, not onset. )

Age of onset

Premorbid
functioning

(if your functionign is super high, the course is going to be more severe, if its lower, you will have less to work with )

Cognitive ability
(lower cognitive ability to start with less functioning. Cognitive flexibility.)

Access to treatment

First 3-5 years is key

(this is key but it is not quickly diagnosed)

(Emotional overinvolvement criticism and hostility.)

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17
Q

What is the prognosis of schizophrenia?

A
  • males
  • birth complications
  • severe hallucinations & delusions
  • delay in treatment
    (1st episode)
    (acute issues)

delay in treatment in the first episode or delay in treating acute issues.

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18
Q

What is the biological etiology of schizophrenia?

A

Most important in etiology

~ 80% of risk

(genes are the most important piece of etiology)

Environment affects expression of symptoms

  • Inherit a tendency for schizophrenia
  • Not specific forms of schizophrenia

(typically the environmenttal affect is how it is expressed. You are basically inheriting a tendency for schizophrenia but not schizophrenia.)

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19
Q

What is the risk of schizophrenia based on genetic relatedness?

20
Q

What are the genetic markers for schizophrenia?

A

smooth-pursuit eye movement

(tracking deficits)
(people with SCZ and relatives)

really squiggly lines

eyetracking and schizphrenia tend to be traited together because they likely happen to be on genes close together.

21
Q

What is the pyramid of brain structure and function?

A

brain structure and function is atypical. Certain types of cells tend to line up with each other and be at certain levels. Grey matter in certain places, white matter in certain places and they tend to line up in normal people. This is not rhe case in people with schizophrenia.

not understanding whats going on socially

fewer connections

impaired social cognition

attentional and working memory deficits

loss of white matter (fewer connections)

Loss of gray matter (cell bodies are dying)

disrupted brain development in adolescence

disorganized cytoarchitecture

22
Q

what is the brain structure of people with schizophrenia?

A
  • decreased brain volume
  • enlarged ventricles (negative symptoms)

we’re thinking this is probably related to negative symptoms because we are losing matter, we are losing brain,. One of the big reasons we want early intervention.

we see decreased brain volume, cells are dying. Someone with schizophrenia, the ventircles are getting bigger. These arethespaces in the brain that hold fluid. They get bigger because the grey matter is dying.

Reduced volume of the thalamus
Gateway for processing all incoming sensory info
Disorganized perception & thoughts?

(the thalamus is like the call directing centre. Like this is whats happening and I’m giving it to you etc. If the thalamus is smaller it probably isnt as effective. )

Abnormalities in temporal lobe areas
(e.g., reduced volume of hippocampus & amygdala)

(none of these things are found in everybody but as far as tests go just assume this is the answer)

But…not found in all patients

23
Q

What is the brain function of people with schizophrenia?

A

Hypofrontality

Reduced neural connectivity
(excessive synaptic pruning?)

(hypo is less meaning less activity in the frontal lobe, less neural connectivity. Could this be high synaptic pruning early on?)

Negative symptoms?
Major DA pathway
(PFC inhibits DA in limbic system)

Working memory
(major dopamine pathway connected to the limbic system and dopamine plays a huge role in schizophrenia.)

Representing sensory info to guide behavior

Disorganized behavior & speech, thought disorder

Brain Function:
- temporal cortex, language areas (which is active during auditory hallucinations?)

  • Broca’s area speech production (speaking)

Wernicke’s area: Language comprehension (hearing)

understanding language and taking in the info.

24
Q

For auditory hallucinations which part of the brain is activated?

A

Broca’s area.

Not recognizing internal voice?

25
Q

What is the original DA hypothesis for Schizophrenia?

A

Schizophrenia goes to DA excess

dopamine hypothesis is huge. THe original hypothesis was that schizophrenia is too much dopamine because when you take a bunch of drug you can imitate a bunchoof symptoms of schizophrenia. Drugs that reduce dopamin in the system take away schizophrenia like behaviour.
Drugs

Drugs increase DA
Result in schizophrenia-like behaviour
e.g., Amphetamine, L-Dopa for Parkinson’s disease
Drugs decreases DA

Reduce schizophrenia-like behaviour
e.g., Neuroleptics
Do not treat negative symptoms

26
Q
A

Negative symptoms
- decreases DA in cortical regions
* underactivity at D1 receptors

(but it doesn;t explain negative systems so they revised it. Less dopamine in the cortical regions. Underactivity at the D 1 receptors)

Positive symptoms
increases DA in subcortical regions
* pre-synaptic
* too much produced and released into synapse
→ overactivity at D2 receptors
* post-synaptic
* some findings of too many D2 receptors

(positive symptoms seem to be related to increased dopamine activity in subcoritical areas like the limbic system.)

27
Q

What are the dopaminergic Pathways?

A

Mesolimbic Pathway (positive symptoms)

we have basically this is where a ton of the dopamine is produced and its sending it to the nucleus accumbems and othertings like the limibc system.

Nucleus Accumbens (NA)

Ventral Tegmental Area (VTA)

Mesocortical Pathway (negative symtptoms)

frontal cortex

when theres more dopamine up here it says you’re solid you don’t need to produce it.

the reduced activity means the frontal cortex allows the VTA to keep producing it still.

28
Q

What is the Glutamate Hypothesis?

A

decreased glutamate

(PCP & ketamine → schizophrenia-like behavior)

Underactivity at NMDA receptors

DA receptors also inhibit glutamate activity, so…
Too ↑ DA activity → too ↓ glutamate activity

Glutamate plays a role in learning, memory, neural
processing

  • Explain problems with attention, working
    memory, executive function?
29
Q

What is the neurodevelopmental Hypothesis?

A

“silent lesion”

this is the best theory and it will be on the test.

Abnormalities lie dormant until normal developmental processes expose problems

you are born and things are ownky but they are dormant until normal developmental processes happen and you aren’t able to process things.

So…neuropathology before SCZ onset

(so the pathology/the problems in the system are thre way before you see the symptoms. )

30
Q

What are the neurodevelpomental things associated with Schizophrenia?

A

Neuromotor,
cognitive &
behavioral
abnormalities

Smaller head circumference at birth

Slower to reach developmental milestones

Higher rates of left-handedness

  • Congenital
    minor
    physical &
    craniofacial
    anomaliesVelocardial Facial
    Syndrome
31
Q

How does gestational and perinatal exposures?

A
  • Viral infection
  • Early nutritional deficiencies & maternal
  • Pregnancy & birth complications

Gestational & perinatal

Maternal starvation (1st trimester)

Dutch Hunger Winter of 1944/1945
2x risk

(this is when Nazis were ruling areas and they prevented food supplies from getting to these people. women in their first trimeste were more likely to have kids that develop schizophrenia)

Obstetric complications
Premature birth, hypoxia

(relating to less oxygen availability. Cell death happens at this point and we are losing pieces.)

Maternal viral infections
1957 Helsinki influenza (2nd trimes
Mother fever > 38ºC → 3.7x risk

(if a mom was in her second trimester and had a really bad fever she had more risk of her baby having schizophrenia.. Proteins are denaturing/things are dying and not functinoing. )

32
Q

What is a later environmental stressor for Schizophrenia?

A

Cannabis

People with schizophrenia are 2x as likely as the
general population to smoke cannabis

they use it more to deal with their schizophrenia. BUT also if people use a shit ton of weed at the age of 14, that was the age that conferred the most risk later/ The stud was done decades ago. Weed now is not the same. Weed now is way more intense. We are starting to see more adolescents coming in with first onset psychoses.

33
Q

What is the cannabis diathesis-stress model?

A

COMT gene
Breaks down proteins
(incl. DA, NE, etc.)
* 2 alleles
* Met → high DA
* Val → lower DA

we have this gene and 2 alleles for it. The met allele gives you high dopamine and the val gives you low dopamine. If you have the met met gene and you don’t use weed vs you do use weed in adolescence. Whats the difference. If you have one val and one met, what would you tell your friend to do. Don’t use it. If they have the val val gene don’t do it. Way worse.

34
Q

What is the general diathesis-stress model

A

genetic factors and prenatal perinatal Events

goes to Brain Vulnerability

goes to stress and developmental maturation processes

goes to psychosis

35
Q

What is the neurodevelopmental hypothesis?

A

but… “doomed from the womb?

No environmental factor necessary or sufficient

you can have a whole bunch of genes and still not develop it. You need environmental stressors.

36
Q

What is the Etiology: “Mutliple-Hit” Model?

A

Brain development from conception to early adulthood
(e.g., neuron formation, migration, synaptic pruning)

Anatomical & functional disruption in neuronal connectivity & communication
Cognitive dysmetria (dysregulation of information processing in the brain)

Impairments in higher-order cognitive processes
(e.g., attention, memory, language, emotion)

Symptoms of schizophrenia (e.g., hallucinations, delusions,
negative symptoms, disorganized speech)

these are our cognitive symptoms that we’re starting to see.

this leads to higher order problems in cognitions.

psycho etiology is in this slide.

37
Q

What is the psychosocial etiology of schizophrenia?

A

(psychological stress tends to lead more to relapse than onset.)

Psychological Stress
increase
Relapse rate
* Migration
* Urbanization
* Lowest SES (it comes from your SES or you end up in that SES. )

Sociogenic hypothesis
Social-selection theory
“downward drift”

38
Q

How does migration to Western Countries impact schizophrenia?

A

Risk for developing schizophrenia:

1st generation migrants: 2.7 (risk for schizophrenia is about double. as a second gen migrant.)

2nd generation migrants: 4.5 (first gen migrants tend to come into social circles that have more than them and they haie kids are more in betwee nand have less ingroup memebers.)

From developing vs. developed countries: 3.3

(migrants from developing countries are more at risk. )

From areas with predominantly black population: 4.8

(racism. If you are coming from a place with a predominantly black population and going into a place where this is not the case you are likely to experience a ton of racism. Chronic stress. )

Potential explanations?

Diagnostic bias? No

Selective migration? No

Discrimination and social defeat?

(chronic stressful experience of outsider status)

39
Q

What is the psychosocial etiology?

A

Family

Outdated
“Schizophrenogenic mother”

Current (relapse rartes are higher with expressed emotion)

Expressed emotion – relapse (3.7x)
- Criticism
- Hostility
- Emotional over-involvement

40
Q

What is the treatment response for schizophrenia?

A

33% continue to have symptoms and problems even after
treatment

12% need long-term institutional care

38% function well 15-25 years later
(i.e., can manage symptoms)

10-15% fully recover
(symptoms remit > 2 yrs, good social functioning) (this doesn’t mean its gone. )

No “cure”

41
Q

What is the historical bio treatment?

A

Prefrontal lobotomy

Controversy about cognitive deficits

Institutionalization

Insulin coma

ECT

42
Q

What is the current Bio (Current)?

A

Antipsychotic

Medication

Mechanism: Block DA receptors

(2 kinds both count for the grid. So this could be the whole grid.)

  • 1st generation
    “Conventional” antipsychotics
  • 2nd generation
    “Atypical” antipsychotics
43
Q

What are the ranges of response for psychotic episodes?

A

1+ psychotic episodes

  • Episode has relatively rapid return to normal
    functioning
  • Good prospects for recovery

(if you get back to your normal functioning quickly you have a better prognosis)

Years of recurrent psychotic relapses

  • Periods of remission
  • Varying degrees of residual impairment
    Failure to respond
43
Q

What is the psychosocial treatment for Schizophrenia?

A

CBT (you need the meds. YOu aren’t gonna great it wit hthese things. This is a severe mental illness meaning you NEED the medication but psychological stuff on top of it improves. )

  • Reframe positive symptoms (trying to help create a tiny little space of consideration that the things they are seeing, hearing, smelling, beheliving migh t be true. )
  • Identify triggers for symptoms
  • Improve social skills (people often become depressed because they know whats coming.)
  • Reduce relapse

*Not helpful for negative symptoms

Cognitive remediation
* Improve cognitive functioning

Other individual
* CBT + life skills

43
Q

What is the psychosocial treatment for schizophrenia?

A

Family Therapy
Communication skills

Decreased expressed emotion

getting families to be less hostile and less critical.

Case Management

Social and Living Skills Training

Vocational rehabilitation