Schizophrenia Flashcards

1
Q

What is Schizophrenia?

A

A type of psychosis/severe mental disorder categorised by a profound amount of disruption of cognition and emotion. Contact with external reality and insight are impaired. Affects a person’s language through perception, emotions and sense of self.

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2
Q

How many people are affected by Schizophrenia at one point in their life?

A

1% of the population. No more than 1 in 5 completely recover.

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3
Q

Definition of Positive Symptoms

A

Aren’t called positive because they are good but because they add something which ‘normal’ people don;t have.

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4
Q

What are some examples of Positive symptoms?

A
  1. Hallucinations
  2. Delusions/paranoia/grandeur
  3. Disorganised speech
  4. Disorganised/catatonic behaviour
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5
Q

What are hallucinations?

A

Disturbances of reality in any of the sense. False perceptions that either have no base in reality or are distorted perceptions of things that are. Most common are auditory hallucinations.

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6
Q

What are delusions?

A

Firmly held irrational beliefs that have no basis in reality. Common types:

  • Delusions of persecution
  • Delusions of grandeur
  • Delusions of control
  • Delusions of reference
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7
Q

Definition of negative symptoms

A

Known as ‘deficits’ if they’re present for at least a yea, and are something someone has lost.

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8
Q

Examples of negative symptoms

A
  1. Avolition
  2. Speech Poverty (Alogia)
  3. Affective Flattening
  4. Anhedonia
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9
Q

What is Avolition?

A

Lack of purposeful, willed behaviour. Reduction, difficulty or instability to start or continue with goal-directed behaviour. People with SZ often have a sharply reduced motivation to carry out a range of activities and results in lowered activity.

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10
Q

What is Speech Poverty (Alogia)?

A

Limited speech output with limited, often repetitive, content. Involves reduced frequency and quality of speech.

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11
Q

What is Anhedonia?

A

Loss of interest/pleasure, or reduced emotions to things that are pleasurable. Social aspect confused with depression - only physical anhedonia is reliable for SZ.

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12
Q

Who conducted the ‘Sane in Insane Places’ study?

A

Rosenhan (1973)

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13
Q

What was the ‘Sane in Insane Places study?

A
  • Covert ppt observation
  • Students reported a ‘dull thud’ which was not an actual symptom according to the DSM II
  • All were diagnosed with SZ and hospitalised
  • They were given meds/treatments and not allowed to leave until the university intervened, sometimes up to 2 months
  • Rosenhan later phoned and said he was sending more fake patients. Over the next few weeks, 21% were diagnosed as ‘pseudopatients’ and sent home.
  • He never actually sent any over.
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14
Q

The role of Dopamine Receptor Genes in SZ

A

(D2, DR2)

  • Affects a number of dopamine receptor sites and transports proteins for dopamine
  • Associated with negative and positive symptoms (Davis & Khan 1991)
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15
Q

The role of Glutamate Receptor Genes in SZ

A

(NMDA, AMPA)

  • Affects a number of glutamate receptor sites. Especially important in the ventral striatum
  • Associated with negative symptoms (Sorg et al 2013)
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16
Q

The role of GRK in SZ

A

(G-Protein Coupled Receptor Kinase)
- Makes epigenetic and sensitivity changes to receptors for a number of excitatory neurotransmitters. Higher levels increase effects (Funk et al 2014)

17
Q

Gottesman’s study on SZ in families

A
(1991)
Studied concordance rates in children with SZ parents or siblings
2x SZ parents: 46% concordance
1x SZ parent: 13% concordance
1x SZ sibling: 9% concordance
18
Q

Joseph’s study on SZ in twins

A

(2004)
Meta analysis of data on MZ vs DZ twin concordance with SZ
MZ concordance: 40.4%
DZ concordance: 7.4%
Modern studies use ‘blind’ researchers. They show a lower but still big difference

19
Q

Tienari’s study on SZ in adoptive families

A

(2000)
Compared siblings raised together vs apart
164 had SZ mothers = 6.7% developed SZ
197 were in a ‘control group’ = 2% developed SZ
Conclusion = genetic liability for SZ is ‘decisively confirmed’

20
Q

What is the Dopamine Hypothesis?

A

States that SZ is caused by an imbalance of dopamine, either:

  • They have too many D2 receptors
  • Their D2 receptors are too sensitive/fire too often
  • They produce too much dopamine
21
Q

What is Dopaminergia?

A

Dopamine’s actions in the brain. If there is too much, it’s known as hyperdopaminergia. If there is too little, it’s known as hypodopaminergia.

22
Q

What does Hyperdopaminergia cause in the subcortex?

A

It’s associated with positive symptoms. Broca’s area produces speech and too much dopamine here leads to the speech and hearing-related symptoms

23
Q

What does Hypodopaminergia cause in the subcortex?

A

Associated with negative symptoms. PFC is the central executive and too little here leads to avolition/catatonia.

24
Q

What are drugs that increase dopamine activity?

A
  • Amphetamines

- L-dopa

25
Q

What are drugs that decrease dopamine activity?

A
  • Chlorpromazine

- Clozapine

26
Q

What did Davis & Khan theorise about Dopamine in SZ?

A
  • Too much in mesolimbic pathway > positive symptoms

- Too little in PFC > negative symptoms

27
Q

What is the Double Bind Theory?

A

Bateson et al (1956): contradictory messages are responsible for children having/developing SZ. The parenting type is known as the ‘Schizophrenogenic Mother’

28
Q

What did Kuipers et al say about Expressed Emotion?

A
  • Families with high expressed emotion can trigger psychotic episodes
  • These families describe SZ relatives in hostile, critical terms
  • EE levels in family/friends is strongly correlated with relapse rates
29
Q

What did Noll et al say about Expressed Emotion?

A
  • Negative emotions can trigger SZ episodes in vulnerable people. Supportive environments may be protective. This is a diathesis-stress model.
30
Q

What are the three stages of Beck & Rector’s Cognitive Model?

A

Stage 1: Cognitive Processing Biases
Stage 2: Misattribution of consequences to causes
Stage 3: Failure to test reality with memory or logic

31
Q

What is the cognitive process of Delusions?

A

Inadequate information processing > Egocentric Biases > Failure to contextualise events