Schizophrenia Flashcards

1
Q

What is schizophrenia?

A

Separation between perception, memory, personality and cognition

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2
Q

What is the impact of schizophrenia?

A
  • Typically occurs between 15-45 years of age
  • High suicide rate
  • Many having to live in assisted care/with families
  • Only 25% recover
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3
Q

What are the positive symptoms of schizophrenia?

A

Acute -> respond to treatment

  • Hallucinations (auditory, visual, olfactory)
  • Delusions (grandeur, paranoia)
  • Thought disorder
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4
Q

What are the negative symptoms of schizophrenia?

A
  • Affective flattening
  • Apathy and social withdrawal
  • Alogia (lack of speech)
  • Anhedonia (inability to experience pleasure)
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5
Q

What are the different subtypes of schizophrenia?

A

Paranoid - Delusions of persecution
Disorganised - Early onset with personality deterioration
Catatonic - Mutism and abnormal postures (rare)

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6
Q

What are the causes of schizophrenia?

A

Genetic - however not full story as only co-occurance of 50% of monozygotic twins
Environmental factors - such as drug use in developmental years and prenatal stressors

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7
Q

What is the pathology of schizophrenia?

A

Evidence of neurodeveopmental disorder with defects in cortex (atrophy) and enlarged cortices
HOWEVER NO CLEAR PATHOLOGY

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8
Q

What is the dopamine hypothesis of schizophrenia?

A
  • Over activity of the dopaminergic neurons innervating the mesolimbic and mesocortical pathways
  • Mesolimbic cortex associated with emotions and memory (positive symptoms?)
  • Prefrontal cortex involved in organisation of behaviour, motivation, planning, attention, and social behaviour (negative symptoms?)
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9
Q

What is the evidence supporting the dopamine hypothesis?

A
  • Drugs acting as dopamine agonists induce psychosis (e.g cocaine)
  • Antipsychotic drugs tend to block dopamine receptors
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10
Q

What were the first drugs used to treat scizophrenia?

A

Antipsychotics e.g chloropromazine which had sedative effect

  • Later found to be dopamine antagonist
  • However 15-30% of patients ‘drug resistant’
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11
Q

What are the ‘atypical’ second generation drugs to treat schizophrenia?

A

e. g Clozapine
- Less side effects
- Better treatment of negative symptoms

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12
Q

Which receptors do the typical schizophrenia drugs act on?

A
  • High affinity for D2 present in limbic system but also nigrostriatal pathway (cause parkinsons-like symptoms)
  • Occupancy of histamine receptors associated with sedative effect
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13
Q

What receptors do the atypical schizophrenia drugs act on?

A
  • Bind to many receptors
  • Affect D3 and D4 receptors in the cortex creating less Parkinsons-like effect
  • Possible increased 5-HT activation may be decreasign negative symptoms
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14
Q

What are etrapyramidal motor disturbances?

A
  • Associated with block of D2
  • Involuntary movements, rigidity (Parkinson’s-like) typically disapear after first weeks of treatment
  • Tarditive dyskinesia (involuntary movements in face/body trunk) can occur in 20-40% of patients for months or years of treatment relating to adaptive hypersensitivity of nigrostriatal pathways that can be irreversible
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15
Q

What are the endocrine side effects of schizophrenic treatment?

A

D2 usually inhibits prolactin, inhibition can therefore lead to breast swelling and lactation in men and women

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16
Q

What additional side effects can occur in response to schizophrenia treatment?

A
  • Peripheral effects: blurred vision, dry mouth and constipation due to muscarninc blocking
  • Hypertension due to blocking of adrenoreceptors
  • Weight gain due to 5-HT blocking
17
Q

Why is their skepticism for the dopamine hypothesis of schizophrenia?

A

Dopamine block is rapid, but anti-psychotic effects often take a long time to be treated

18
Q

What is the glutamate theory?

A
  • Schizophrenia related to NMDA receptors (agonists of this e.g Ketamine also produce scizophrenia like symptoms)
  • Proteins at glutamatergic synapses are a hub of schizophrenia-susceptibility proteins
  • Reduced glutamate levels and glutamate receptors in schizophrenia-affected brain.
    Should we try to reduce glutamate receptor levels?