Week 11 - psychotic disorders Flashcards

1
Q

What are some clinical manifestations of schizophrenia?

A

Major disturbances in thought, emotion and behaviour

  • Disordered thinking
  • Lack of emotional expressiveness
  • Disturbances in movement or behaviour

Can disrupt interpersonal relationships, diminish the capacity to work or live independently

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2
Q

What is the lifetime prevalence of schizophrenia?

A

1%

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3
Q

When does onset of schizophrenia typically occur?

A

Late adolescence or early adulthood

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4
Q

What are the positive symptoms of schizophrenia?

A

Delusions

Hallucinations

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5
Q

What are the negative symptoms of schizophrenia?

A

Avolition

Alogia

Anhedonia

Blunted affect

Asociality

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6
Q

What are the disorganised symptoms of schizophrenia?

A

disorganised behaviour

disorganised speech

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7
Q

What are the different types of delusions?

A

Persecutory

Thought insertion

Thought broadcasting

Outside control

Grandiose delusions

Ideas of reference

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8
Q

What are the different types of hallucinations?

A

Auditory

Visual

Hearing voices

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9
Q

What are the two domains of the negative symptoms of schizophrenia?

A

Experience domain

  • Motivation
  • Emotional experience
  • Sociality

Expression domain

  • Expression of emotion
  • Vocalisations
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10
Q

What is thought to cause the positive symptoms of schizophrenia?

A

An excess of dopamine in the mesolimbic pathway, although the reasons for this increase are not known

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11
Q

What may be therapeutic to the positive symptoms of schizophrenia?

A

Decreasing the dopamine in the mesolimbic pathway

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12
Q

What is thought to cause the negative and cognitive symptoms of schizophrenia?

A

A shortage of dopamine in the mesocortical pathway

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13
Q

What may be therapeutic for the negative and cortical symptoms of schizophrenia?

A

Increasing dopamine in the mesocortical pathway

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14
Q

What happens when you treat schizophrenia with a D2 antagonist antipsychotic?

A

Can successfully treat positive symptoms by reducing dopamine signalling in the mesolimbic pathway

However, the dopamine antagonist also reduces signalling in the mesocortical pathway meaning that the negative and cognitive symptoms are not addressed, and in some cases, can be worsened

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15
Q

What happens when you treat schizophrenia with an atypical D2 partial agnoist antipsychotic?

A

Works to reduce the excess dopamine in the mesolimbic pathway, treating the positive symptoms

Simultaneously, within the mesocortical pathway a dopamine partial agonist will act to enhance dopamine signalling, meaning that the negative and cognitive symptoms of schizophrenia could be improved as well

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16
Q

What is the glutamate hypothesis?

A

Glutamate is the predominant ‘go’ neurotransmitter in the brain

There are many lines of evidence implicating glutamate NMDA receptors in schizophrenia

17
Q

What does the evidence implicate regarding glutamate NMDA receptors in schizophrenia?

A

Post mortem changes in NMDA receptors in the brains of patients with schizophrenia

NMDA-receptor antagonists can cause psychotic symptoms in humans

Some glutamatergic drugs have shown promise in treating schizophrenia

18
Q

Describe the interactions between glutamate and dopaminergic pathways.

A

Reduced NMDA receptor availability/functioning on GABAergic interneurons >

Disinhibition of glutamatergic projections onto midbrain dopamine neurons >

Increased glutamate release >

Increase activation of dopaminergic neurons

19
Q

What is ventricular enlargement correlated with?

A

Poor performance on cognitive tests

Poor premorbid adjustment

Poor response to treatment

20
Q

Describe schizophrenia vs treatment-resistance schizophrenia (TRS)

A

TRS may represent a distinct pathophysiological entity

21
Q

What differences have brain imaging techniques highlighted regarding the brain structures of TRS and treatment-responsive schizophrenia?

A

Widespread grey matter volume reductions in several lobes of the brain

22
Q

How does brain connectivity differ for patients with treatment-resistant schizophrenia?

A

Reduced connectivity in certain key brain regions and a reduced total density of dopaminergic synapses, compared to treatment-responsive schizophrenia and the control population

23
Q

When does psychosis emerge?

A

Late adolescence or early adulthood with a peak between the ages of 18 and 25, when the prefrontal cortex is still developing

24
Q

In the neurodevelopmental model of schizophrenia, what is observed with longitudinal neuroimaging?

A

A progressive reduction of grey-matter volume with age

The combined effects of pruning of the neuronal arbour and myelin deposition are thought to account for this

25
Q

What does normal cortical development involve?

A

Proliferation

Migration of cells

Dendritic aborisation

Myelination

The first two processes occurring mostly during prenatal life and the latter two continuing through the first two post-natal decades

26
Q

What is the evidence that the immune system is linked to the pathology of schizophrenia?

A

Elevated cytokines and microglial activation

27
Q

How has PET imaging been used?

A

To examine immune system activity in patients with schizophrenia

28
Q

In comparison of 16 patients with schizophrenia and 16 controls, what differences were found in oropharynx flora?

A

Patients with schizophrenia were dominated by a greater number of microbiome species

Patients with schizophrenia had greater abundance of lactic acid bacteria

There were difference in the metabolic pathways controlling glutamate and B12 transport (increase in schizophrenia) and carbohydrate and lipid metabolism (decreased in schizophrenia

29
Q

What have epidemiological studies and twin studies identified about environmental factors and schizophrenia?

A

Prenatal exposure to viral infections

Poor pre-natal nutrition

Adverse obstetric events

Cannabis smoking during adolescence

30
Q

What have numerous studies found about the genetic factors of schizophrenia?

A

Developing schizophrenia is greater in the relatives of patients with schizophrenia

Susceptibility genes may result in an increased risk of schizophrenia