L24: Schizophrenia Flashcards

1
Q

Who are the two people involved in the history of schizo?

A

Emil Kraepelin- Dementia praecox, onset in adolescence, chronic deteriorating course, permanent and pervasive functional deficits, core symptoms are loss of cognitive functions (memory and planning)

Eugen Bleuler- schizophrenia, hallucination and delusions are secondary features and primary symptoms include ambivalence, loosening of associations, incongruous affect, autism

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2
Q

What is the DSM-5 criteria for schizo?

A

A. 2 or more of the following or a significant proportion of time over a one month period (delusions, hallucinations, disorganized speech, disorganized or catatonic behaviour, negative symptoms)
B. Significant social/ occupational disturbance
C. Signs of disturbance present over 6 mths
D. Not due to schizoaffective disorder or exclusively occurring during course of mood disorder
E. Not due to substance or gen med condition
F. If pervasive developmental disorder is present, prominent delusions or hallucinations are present for a month

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3
Q

What are hallucinations?

A

A perception in a conscious state in the absence of a stimulus (nothing there but brain thinks there is)
Illusion: a misperception of a stimulus, something there but brain screws it up
Can be in any sensory domain (auditory, visual, olfactory, gustatory, tactile like formication, nociceptive, chronoceptive)
Auditory hallucinations most common with schizo and visual more common with substance use
Other causes: substances, dementia, delirium, migraine, epilepsy, infection and tumor, associated with sleep

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4
Q

What are delusions? What are the 6 types?

A

Fixed, false belief not in keeping with an individuals culture
Bizarre when not possible or patently untrue
Paranoid (you are in danger/ being targeted)
Grandiose (you have special powers or abilities)
Nihilistic (you are dead or do not exist)
Reference (things around you have special meaning or are meant for you)
Erotomanic (someone is in love with you)
Somatic (there is something wrong with you biologically or mentally)

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5
Q

What are negative symptoms?

A

Deficit symptoms in schizo (5 As)
Apathy, Anhedonia, Antisocial, Amotivation, Alogia
Contribute more to functional impairment than hallucinations or delusions and less amenable to treatment

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6
Q

What are some cognitive symptoms of schizo?(6)

A

Slowed processing speed
Impaired attention
Impaired memory
Impaired executive function
Impaired social cognition
Impaired verbal comprehension

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7
Q

What is involved in the clinical course of schizo?

A

It is a chronic illness
Age of onset for males is around 15-25 and women is 25-35 and onset before 15 or after 50 is rare
Patients are normally diagnosed when they begin to exhibit disorganized behaviour or hallucinations/delusions
Over course of lifetime, positive symptoms become less prominent, but negative and cognitive functions persist.
Best predictor of future functional impairment is the level of function after the first episode
Men with schizo are less likely to marry and have WORSE prognosis than females with schizo

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8
Q

What are the three phases of schizo?

A
  1. Initial prodromal phase: attenuated symptoms (not hallucinations or delusions, maybe odd ideas or sensory misperceptions), anxiety, sleep disturbances, mood problems, functional decline, preceded psychosis by 1 year, diagnoses retrospectively
  2. First episode of psychosis: treatment results in remission of positive symptoms
  3. Residual symptoms: 50% of patients require social supports, negative and cognitive symptoms persist
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9
Q

What is the epidemiology of schizo?

A

1:1 male to female ratio, maybe slightly higher for males
Annual incidence is 1/10000, and lifetime prevalence is 0.7-1%

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10
Q

What are some risk factors for schizo?

A

Family history (MZ have 40-50% concordance)
Urban birth, first generation immigrant, winter birth, prenatal infection or malnutrition, obstetrical complications, increasing paternal age

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11
Q

What is an Ultra High Risk Phenotype?

A

Most commonly defined as family history of psychosis and at least 1 of: attenuated + symptoms, brief psychotic symptoms, functional decline
About 50% of these individuals will present with symptoms of schizo within a year of identification
Show executive dysfunction, working memory problems

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12
Q

What is involved in the etiology (causes) of schizo?

A

No evidence of refrigerator mothers
Genetics: 22q11 deletion (velocardiofacial syndrome), identified through linkage analysis showing up to 4000 genes mostly in development, DA, or Glu pathways, many candidate genes (COMT, neuregulin 1, dysbindin, DA and Glu receptors)
Neurodevelopmental and neurodegenerative theories

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13
Q

What is the neurodevelopmental theory and the neurodegenerative theory of schizo? Which one is the prevailing theory?

A

Neurodevelopmental: predisposition to schizo based on abnormal neural development in childhood and adolescence
Neurodegenerative: thought that individuals with schizo has typical brain development before an incident that led to the disease onset
NEURODEVELOPMENTAL IS PREVAILING THEORY

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14
Q

What are some brain changes in schizo?

A

Brain volume changes: increased ventricular size, temporal lobe asymmetry, loss of frontal grey matter
NO evidence of gliosis on pathology (scaring)

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15
Q

What is the relationship between cannabis and schizo? What about other substances?

A

Was thought to be an independent risk factor for schizo
Now thought that cannabis can precipitate psychosis in individuals with specific genetic risk factors (like COMT polymorphism)
Amphetamines and cocaine; agitation, illusions, paranoia during withdrawal and tactile hallucinations
Phencyclidine: PCP, bet substance model of schizo, causes hallucinations, delusions, and negative symptoms

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16
Q

What is the dopamine hypothesis of schizo?

A

Initially thought that excess DA was responsible for symptoms
Amphetamines induced psychotic symptoms
First gen antipsychotics act as D2 receptor antagonists
PET scanning shows increased DA activity in striatum, proportional to the severity of psychosis

17
Q

What is the glutamate hypothesis?

A

Antagonists of NMDA-type glutamate receptors induce psychotic symptoms
Individuals with schizo demonstrate a glutaminergic deficit in temporal and striatal regions

18
Q

What are negative symptoms associated with?

A

Cholinergic deficits, and serotonergic deficits particularly in prefrontal cortex (not DA)
Antipsychotics with D4 receptor antagonism and 5HT receptor activity have better effects on negative symptoms
PET scanning shows decreased metabolism in prefrontal cortex

19
Q

What are the two different types of treatments for schizo?

A

Biological treatments: antipsychotics and ECT
Psychosocial treatments: cognitive, family and occupational interventions

20
Q

How are antipsychotics used to treat schizo? What are the two types and differences between them?

A

Found when looking for new surgical anesthetics
Divided into first (typical) and second gen (atypical)

First gen: typical, DA blockers, high/ mid/ low potency, higher D2 binding affinity than atypicals, higher risk of akathisia, parkinsonism, dystonias, tardive dyskinesias

Second gen: atypical, less D2 binding and more D4 5HT binding, better for negative symptoms and common side effects are weight gain, sedation, erectile dysfunction