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MTB x > week 10 part 1 > Flashcards

week 10 part 1 Flashcards

1
Q

Define Schizophrenia

A

A disorder characterised by loss of contact with the environment

  1. Disintegration in the level of functioning in everyday life
  2. Disintegration of personality
  3. Expressed as a disorder of feeling, thought, perception and behaviour
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2
Q

What is the definition and schizophrenia studied by?

A

Behavioural neuroscience

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3
Q

When was it thought that schizophrenia was a disease of a mind?

A

Last 50 years

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4
Q

What is the prevalence of schizophrenia?

A
  1. Most common mental illness

2. 1-2% of the population

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5
Q

Who has schizophrenia?

A
  1. 12.5% 3rd-degree relatives
  2. 25% 2nd-degree relatives
  3. 50% 1st-degree relatives
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6
Q

What does demographics of schizophrenia tell us?

A

A little bit about the origin of the disease

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7
Q

Where is schizophrenia common in?

A
  1. All cultures, genders and race

2. Men tend to develop symptoms earlier

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8
Q

What is the peak onset of schizophrenia?

A

Age group: 18-25 years

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9
Q

What are the symptoms for schizophrenia

A
  1. Adapted from DSM-V
  2. Describe clinical symptoms of behaviour which are either an exaggerating of existence characteristics of trait or reduction or duration of behaviours
  3. Positive and Negative symptoms
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10
Q

What are the positive symptoms of schizophrenia?

A
  1. exaggerations or distortions of normal processes or behaviours
  2. Delusions
  3. Hallucination
  4. Disorganised thinking
  5. Inappropriate behaviour
  6. Catatonia
  7. Include cognitive and mood symptoms
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11
Q

What are the negative symptoms of schizophrenia?

A
  1. Flat effect - absence of normal behaviour or emotion
  2. Social withdrawal
  3. Absence of emotion and expression
  4. Reduced energy, motivation and activity
  5. poor hygiene
  6. Include cognitive and mood symptoms
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12
Q

Positive symptoms

A
  1. Delusion (often paranoid)
  2. Hallucinations
  3. Disorganised speech
  4. Disorganised or catatonic behaviour
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13
Q

Negative symptoms

A
  1. Social withdrawal
  2. Flat emotional response
  3. Anhedonia
  4. Lack of motivation
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14
Q

What are more responsive to therapeutic drugs?

A

Postive symptoms

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15
Q

Which symptom is more difficult to treat?

A

Negative symptoms

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16
Q

What does positive symptoms refer to?

A

Mental disturbances in the patient’s perception of reality that do not exist objectively

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17
Q

Hallucination

A

Tend to be in auditory mode rather visual mode

Take form of voices being heard in the head or thinking their thoughts are being broadcast

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18
Q

What is catatonic behaviour

A
  1. Abnormality of movement and behaviour due to disturbed mental state
  2. Withdrawn from society
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19
Q

What does negative symptoms refer to?

A

Mental abilities which the patient has lost or abilities that the patient can no longer perform

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20
Q

What is flat emotional response?

A

inappropriate response to emotion such as someone laughing when there is a funerial

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21
Q

What is anhedonia?

A

When a person doesn’t experience pleasure in anything

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22
Q

What are key symptoms of depression?

A
  1. Anhedonia

2. Lack of motivation

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23
Q

What is aetiology?

A
  1. Cause, or set of causes, or manner of causation of a disease or condition
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24
Q

What is the early stage of schizophrenia aetiology called?

A

Prenatal childhood

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25
Q

What is early stage (aetiology) of schizophrenia?

A

Genetic predisposition and gene expression + Environmental insult including viruses, toxins, poor nutrition, birth complications

give rise to neurodevelopmental abnormalities from conception to early adulthood including:

  1. neuron formation
  2. migration
  3. synaptogenesis
  4. pruning
  5. apoptosis
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26
Q

What is the latent stage of schizophrenia aetiology called?

A

Puberty adolescence

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27
Q

What is the latent stage (aetiology) of schizophrenia?

A

Early subtle signs predicting schizophrenia including:

  1. motor abnormalities
  2. Apathy
  3. Social withdrawal
  4. Deficit in attentional and information-processing task
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28
Q

What is late stage of schizophrenia aetiology called?

A

Young adulthood

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29
Q

What is the late stage (aetiology) of schizophrenia?

A

Excessive synaptic pruning in adolescence leads to abnormal neuronal connectivity and function + later environmental insult such as stress, substance use, and HPA axis dysfunction

lead to greater impairment of cognitive function including:

  1. Deficit in attention
  2. Memory
  3. Executive function
  4. Positive symptoms including hallucination, delusion, disorganization
  5. Worsening of negative symptoms including deficit in motivation and emotion, isolation and anhedonia
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30
Q

What is the theories on the origin of schizophrenia

A
  1. Dopamine Hypothesis
  2. Glutamate hypothesis
  3. Immunological theory
  4. Neural development hypothesis
  5. Membrane hypothesis
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31
Q

What is dopamine hypothesis?

A

Overstimulation of dopaminergic pathways in cortical and limbic areas

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32
Q

What is immunological theory?

A

Abnormal immunological finding in subgroup schizophrenic patients

  1. Neurodegeneration
  2. Viral Infections
  3. Microglial activation
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33
Q

What is Glutamate hypothesis?

A

NMDAR hypofunction

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34
Q

What was schizophrenia called in 1800?

A

Premature madness

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35
Q

What did Carlsson and Lindqvist establish?

A
  1. Dopaminergic transmission altered in schizophrenia
  2. Attempt to identify compound that help motor symptoms of PD
  3. Discovered antipsychotic drugs
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36
Q

What drugs had an effect on the dopaminergic system and all replicated psychotic symptoms of schizophrenia?

A
  1. Largactil (Chlorpromazine)
  2. Reserpine
  3. Amphetamine
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37
Q

What is Largactil?

A

Commonly produce dyskinesia , parkinsonism

38
Q

What is largactil name given to?

A

Drug called Chlorpromazine which was initially developed in 1950 as a drug for anaesthesia - calming effects of individual

39
Q

What is Reserpine?

A

Effective for treating psychosis

Block the re-uptake of dopamine and other monoamines

40
Q

What is Amphetamine?

A

Increase synaptic monoamine levels

Can induce psychotic symptoms

41
Q

What do all these drugs have?

A

High affinity for dopamine D2 receptor

42
Q

What further supported the role of dopamine in mental function?

A

Amphetamines or L-dopa may lead to disturbances, mimicking paranoid schizophrenia

43
Q

What do different receptors have?

A

Different distribution in the brain

44
Q

What happens when D1 receptor bind to dopamine?

A

Produce excitatory effects

45
Q

What happens in D2 receptor?

A

Produce inhibitory effect on neurotransmission of dopamine

46
Q

What is the brain distribution of D1?

A

Predominantly cortical

47
Q

What is the brain distribution of D2?

A

Predominantly subcortical/STRIATAL

48
Q

What can the effects of abnormalities in dopamine function vary by?

A

Brain region

49
Q

What does hypoactivity in one region explain?

A

Hyperactivity in another region which will explain positive and negative symptoms

50
Q

Where are there drops in level of dopamine?

A

prefrontal cortex

51
Q

What is the hypofunction on a feedback loop with?

A

Stratium

52
Q

in normal state, where are there dopaminergic neurons?

A

Ventral tegmental area projecting to PFC and nucleus accumbens

53
Q

what happens in schizophrenia state?

A

There is inhibitory feedback
sends reduced inhibitory signals to stratium
limbic system becomes hyperactive

54
Q

Where was dopamine metabolites not universally elevated in?

A
  1. CSF

2. Serum of patients with schizophrenia

55
Q

What was the paradox of dopamine metabolite measured?

A

Reduced in some patients with schizophrenia while still correlating with symptom severity and response to antipsychotic drugs

56
Q

What was hypofrontality in these studies directly correlated with?

A

Low CSF dopamine metabolite levels

57
Q

What does CSF dopamine metabolite level reflect?

A

cortical dopamine metabolism

58
Q

What indicates low frontal dopamine levels?

A

The relationship between hypofrontality and low CSF dopamine metabolite levels

59
Q

What did lesions of dopamine neurons in PFC result in?

A

Increased levels of dopamine and its metabolite and D2 receptor density in stratium

60
Q

What did application of dopamine agonist to prefrontal areas reduce

A

Dopamine metabolite levels in the stratium

61
Q

What is schizophrenia characterised by?

A
  1. Frontal hypodopaminergia resulting in stratial hyperdopaminergia
62
Q

What did Davis et al hypothesise

A

gative symptoms of schizophrenia resulted from frontal hypodopaminergia, based on the similarities between the behavior exhibited by animals and humans with frontal lobe lesionsand the negative symptoms of schizophrenia

63
Q

What did postive symptoms hypothesized to result from?

A

striatal hyperdopaminergia, based on the findings that higher dopamine metabolite levels are related to greater positive symptoms and response to antipsychotic drug treatment.

64
Q

What is the rule for wisconsin card sorting?

A
  1. The number of item on the card
  2. The colour
  3. What the card actually is
65
Q

What is positive symptoms due to?

A

Overactivity in mesolimbic symptoms

66
Q

What are negative symptoms associated with?

A

Hypofrontality (reduced dopamine in the frontal cortex)

67
Q

What is the prototypical compound for atypical antipsychotic?

A

Clozapine

68
Q

What does atypical antipsychotics have

A
  • A better therapeutic and side effect profile than the typical antipsychotics-1st generation (FEWER side-effects)
  • Affinity for a number of receptors
  • Lower affinity for the dopamine D2 receptor
69
Q

What are examples of atypical antipsychotics?

A
  1. Clozapine - low motor disorders
  2. Olanzapine - very low
  3. Risperidone - low
  4. Quetiapine - very low
  5. Ziprasidone - very low
70
Q

Glutamatergic models

A

are based upon the observation that the psychotomimetic agents such as phencyclidine (PCP) and ketamine induce psychotic symptoms and neurocognitive disturbances similar to those of schizophrenia by blocking neurotransmission at N-methyl-D-aspartate (NMDA)-type glutamate receptor

71
Q

What do we need to consider when we consider it as a neurodevelopmental disease?

A

The process of maturation in the brain

72
Q

What 3 things start from moment of fertilization?

A
  1. Neuronal proliferation
  2. Migration arborization
  3. Myelination
73
Q

What is the cortical development in Schizophrenia?

A
  1. Reduced interneuron activity
  2. Excessive excitatory pruning
  3. Deficient myelination
74
Q

step 1 of environment stress in schizophrenia?

A

The risk of people living in rural areas is taken as a baseline

75
Q

step 2 of environment stress in schizophrenia

A

People living in large city are twice as likely to develop schizophrenia as people living in the countryside

76
Q

step 3 of environment stress in schizophrenia

A

The risk of schizophrenia for people living in smaller cities is somewhere in between

77
Q

step 4 of environment stress in schizophrenia

A

Children who move to city later in life have a lower risk than children who move to the city earlier in life

78
Q

Who has greater risk of developing sz to those that are born in a different time of year

A

People that born in early spring

79
Q

What increases the rate of mental health problems for individuals as young adults?

A

Poverty during early development

80
Q

Family-level stress

A 
–	Parental stress
–	parental psychopathology
–	low parental warmth or investment
–	hostile and inconsistent parenting
–	child abuse and neglect.
81
Q

Individual level stress

A

– stressful life events (financial)
– hypothalamic-pituitary-adrenal (HPA) axis changes → stress physiology altered
– poor prenatal health and birth outcomes → maternal stress / in-utro stress
– inadequate nutrition and toxin exposure

82
Q

Poverty in adulthood

A

– Higher rates of depressive disorders, anxiety disorders, psychological distress, and suicide. → studies shows in certain underprivilege communities in London there was a greater risk for sz for depression and suicide than the larger population

83
Q

Who has an increase risk to develop schizophrenia

A

Children and young adult that suffer from Asthma

84
Q

What increases risk for SZ and Asthma?

A
  1. Maternal inflammation during pregnancy
  • Increase activity of microglia in PET scans in young people predicts elevated risk to develop SZ.
  • Microglia are also found to be increased when there is neuroinflammation
85
Q

What is severity of schizophrenia linked to?

A

Activation of microglia

• Elevated inflammation during pregnancy or adolescence might increase risk for SZ

86
Q

What is component 4 associated with?

A

excessive pruning of synapses and also with inflammation and activation of microglia

87
Q

What is excessive synaptic pruning caused by?

A

Variant of C4 gene

88
Q

What might trigger hyperactivation of microglia and an inflammatory phenotype of the brain

A

poverty or social isolation or the excessive consumption of drugs

89
Q

post mortem brain

A

imbalances on dopamine concentration, been found to have imbalances on GABAergic synapses, been found to have activated microglia and been found to have higher level of inflammation

90
Q

What is a poor model for schizophrenia?

A

Rodents

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