AB: Psychotic Disorders Flashcards

1
Q

What is a psychosis formally?

A

(Formally) Disruption in the experience of reality/ reality testing

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2
Q

How does the DSM define psychosis?

A

In terms of positive (adding something) and negative (detracting somethings symptoms) and disorganised.

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3
Q

How are hallucinations defined?

A

Perception-like experiences which occur with our an external stimulus that are

  • Lifelike
  • Full force and impact of normal perceptions
  • Can occur in all modalities
  • Most common: auditory
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4
Q

How may culture impact hallucinations?

A

In some (sub)cultures, hallucinations are normal religious experience

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5
Q

What percentage of the population has audiovisual hallucinations?

A

Children around 8: +/-9%

general population : 5%-28% although very mild

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6
Q

How has the definition for delusions changed from the dsm 4 to the dsm 5? Why is this definition still problematic

A

Changed from erroneous beliefs that usually involve a misinterpretation of perceptions and experiences to being defined as fixed beliefs that are not amendable to change in light of conflicting evidence. This is problematic as it includes religion, anti vaxxers etc

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7
Q

What are the two most common types of delusions according to the slides?

A

Referential- where they believe things are aimed at them that aren’t (perceived messages etc)
Persecutory- The belief that everyone is out to get you

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8
Q

What are some delusions that are less common according to the slides(4)

A

Somatic, grandiosity, erotomania (celebrity x is in love with me) and nihilistic (impending cataostrophe- perhaps if they do or don’t do something)

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9
Q

What is the difference between bizarre and non-bizarre delusions according to the DSM?

A

Delusions are deemed bizarre if they are clearly implausible and not understandable to same-culture peers and do not derive from ordinary life experiences

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10
Q

Name two common negative symptoms of schizophrenia?

A

Reduced expressivity and avolition: reduces self-motivated goal-orientated activities

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11
Q

Name four less common negative symptoms of schizophrenia

A

Alogia: reduced speech production
Anhedonia: reduced enjoyment
A-sociality: reduced interest in social activities.
Blunted effect: difficulty expressing emotions

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12
Q

Give some examples of disorganised symptoms (2)

A

Disorganised speech or catatonic behaviour (disorganised behaviour)

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13
Q

Give four other symptoms

A
  • jumping to conclusions
  • Disrupted self-experience
  • Neurocognitive difficulties
  • Anognosia: Reduced insight into the illness
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14
Q

What problems are presented by the diagnostic criteria of the DSM

A

People can reduce schizophrenia to just these observable symptoms

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15
Q

What is the criterion A for schizophrenia in the DSM5?

A

Duration of 1 month or less if successfully treated.
2 of the following symptoms and 1 must be 1,2 or 3
1) Delusions.
2) Hallucinations.
3) Disorganized speech
4) Grossly disorganized or catatonic behavior.
5) Negative symptoms

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16
Q

What are the criterion B and C for schizophrenia?

A

B: significant impact functioning
C: Continued signs of disturbance for 6 months

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17
Q

What is the general onset of schizophrenia and when does it peak for men and women?

A

16-30 years old
‘Peak’ men- early to mid 20s
‘peak’ women: late 20s

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18
Q

What is schizoaffective disorder?

A

An uninterrupted period of illness during which there is a major mood episode (major depressive or manic) concurrent with criteria of schizophrenia

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19
Q

What is the problem with this definition of a schizoaffective disorder?

A

A schizophrenic disorder must, according to the DSM, not meet the criteria for a major mood disorder. This can also be hard to distinguish in reality; a lot of the time sz/sa is used to describe schizophrenic/schizoaffective

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20
Q

What are the requirements for delusional disorder?

A

A. The presence of one or more delusions with a duration of one month or longer
B. Criterion A for schizophrenia has never been met
C. Apart from the impact of the delusions or its ramifications, functioning is not markedly impaired, and behaviour is not obviously bizarre or odd.
D. If manic or depressive episodes have occurred, these have been brief relative to the duration of the delusional periods

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21
Q

How would you differ diagnoses between delusional disorder and OCD and BDD or mood disorders?

A

even if the belief of catastrophe / body experience is extremely solidified, and there is anosognosia, OCD or BDD fits better than delusional disorder. Similar to schizoaffective disorder, symptoms of mood have to be relatively short compared to symptoms of delusional disorder

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22
Q

What diagnostic tools are often utilised in diagnosing schizophrenia?

A

(Semi) structured interviews which correlate to diagnosis algorithms (charts) and a symptom/ severity profile.
Also a bead task can be used to track a tendency for jumping to conclusions and a digit span test to track neurocognition (working memory.)

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23
Q

Why may a clients answers not fully correlate with the results of his structured interview?

A

clinicians can give an alternate answers to the clients (hearing voices example)

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24
Q

What is the main theory on the etiology of schizophrenia at the minute? What evidence is there for this

A

The dopamine hypothesis (biological neurological perspective)
-Medication implies that dopamine is at the foundation of (positive) symptoms

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25
Q

How does the ethology differ between men and women?

A

◦ A little more men than women

◦ Symptomatology: women have a little more symptoms, but social functioning remains a little better

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26
Q

How is genetics linked to schizophrenia?

A

Strong genetic component; those who have schizophrenia most likely got it genetically but those who have it are more likely to pass on another serious mental disorder then schizophrenia

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27
Q

What effect do anti psychotic medications have?

A

Reduce positive symptoms but doesn’t / barely works on negative symptoms

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28
Q

Briefly describe the aberrant salience model of schizophrenia

A

If schizophrenia causes dopamine irregularities, a sudden shot of it could signal a feeling of importance to the person which could be attributed to a stimulus in the area such as a person, the mind could then try to fill the gaps to make sense of this (ie the person is a spy)

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29
Q

Give two location based risk factors regarding schizophrenia

A

higher chance in urban areas, being a migrant raises risk (moving back decreases)

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30
Q

Is there a link between schizophrenia and drugs?

A

There is a clear link between cannabis and psychosis (especially if you have a predisposition)

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31
Q

What is the link between trauma and psychosis? (3)

A

50-98% of those suffering had previous trauma and 80% of patients experience their psychotic episodes as traumatic too. 19% of people with psychosis have PTSD.

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32
Q

What is mentalising and what link does it have with psychosis

A

Put yourself in other peoples shoes. Deafness/ deprivation impedes development of mentalising and there has been associations found between hearing difficulties, trauma in development and later psychotic symptoms/ disorders. This led to a social defeat hyptheses

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33
Q

What may these risk factors point towards as an overall risk factor for schizophrenia?

A

Social exclusion and inability to relate to other people

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34
Q

Explain the cognitive model of schizophrenia

A

Trigger stimulates an intrusive thought. This increases cognitive dissonance and is misattributed to an external source and experienced as an auditory hallucination which decreases cognitive dissonance. This leads to an appraisal of hallucination which may either be somatic, affective or behavioural and can lead to another intrusive thought.

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35
Q

What are downsides to antipsychotic medication

A

Awful side effects, especially in motor skills (parkinsonism) also stuff like makes you fat, makes you drool etc

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36
Q

How and when should you reduce meds?

A

The odds of relapse 43% with tapering vs 21% with reduced meds

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37
Q

What is the recovery options for someone with schizophrenia?

A

Symptom free is unlikely -20% however undergoing a meaningful personal recovery with the illness is very possible

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38
Q

What (behavioural) risks are associated with schizophrenia? (3)

A

Substance abuse, suicide and their mortality rates are as high or higher than those who smoke

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39
Q

What delusions does the book add regarding our internal thoughts and processes

A

Thought insertion- believing thoughts are placed from an external source
Thought broadcasting- believing that his or her thoughts are broadcast or transmitted
Also believing an external force control their feelings or behaviours

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40
Q

In a study what affected whether hallucinations were perceived to be pleasant or unpleasant?

A

those whose hallucinations were longer, louder, more frequent, and experienced in the third person found the hallucinations unpleasant. Hallucinations that were believed to come from a known person were experienced more positively

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41
Q

What have studies on the brain shown during auditory hallucination?

A

greater activity in Broca’s area and in Wernicke’s area

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42
Q

What is the link between positive and negative symptoms of schizophrenia and episodes of it?

A

The positive episodes are usually expressed in an acute episode while negative symptoms tend to endure beyond an acute episode and have profound effects on the lives of people with schizophrenia.

43
Q

What behaviours were people with schizophrenia found to be more motivated by and equally motivated by?

A

more motivated by goals that had to do with reducing boredom. equally motivated by goals that had to do with relatedness to others and with avoiding a negative outcome (e.g., criticism).

44
Q

What two different types of please exist within the anhedonia construct?

A

Consummatory pleasure- the amount of pleasure experienced in the moment or in the presence of something pleasurable.
Anticipatory pleasure- the amount of expected or anticipated pleasure from future events or activi- ties

45
Q

How do these constructs of anhedonia apply to schizophrenics?

A

People with schizophrenia appear to have a deficit in anticipatory pleasure but not consummatory pleasure

46
Q

How may these negative symptoms be better understood/ represented?

A

Two domains: the motivation and pleasure domain, including motivation, emotional experience and sociality and the expression domain, including outward expression of emotion and vocalisation

47
Q

How may speech be disorganised in a person with schizophrenia?

A

by what are called loose associations, or derailment, in which case the person may be more successful in communicating with a listener but has difficulty sticking to one topic.

48
Q

How may catatonic behaviour manifest?

A

People with this symptom may gesture repeatedly, using peculiar and sometimes complex sequences of finger, hand, and arm movements, which often seem to be purposeful. Some people manifest an unusual increase in their overall level of activity, including much excitement, flailing of the limbs, and great expenditure of energy similar to that seen in mania. At the other end of the spectrum is immobility: people adopt unusual postures and maintain them for very long periods of time

49
Q

Why is catatonia rarely seen in todays schizophrenia?

A

perhaps because medica- tions work effectively on these disturbed movements or postures.

50
Q

Apart from the disorders previously mentioned, describe two other psychotic disorders that are not attributed to specific external sources

A

schizophreniform disorder and brief psychotic disorder. The symptoms of schizophreniform disorder are the same as those of schizophrenia but last only 1 to 6 months. Brief psychotic disorder lasts from 1 day to 1 month and is often brought on by extreme stress, such as bereavement.

51
Q

What are clinical high-risk studies and what debate did this spark regarding psychotic disorders

A

clinical high-risk studies seek to identify young people who are at risk for developing schizophrenia (mild symptoms and family history.) Young people who show these mild symptoms differ from young people who do not in several domains, including their everyday functioning and their rate of conversion to schizophrenia spectrum disorders. (10 and 30% compared to 0.2%) This sparked the debate as to whether this “Attenuated psychosis syndrome” should be added to the DSM

52
Q

What were the arguments for and against this addition? What is the current outcome

A

May help people get treatment and prevent developing further conditions. However reliability and validity is not currently established for inclusion in DSM and there is a high level pf comorbidity in people with promodal symptoms. Thirdly there is the known effects of attaching labels. Ultimately, APS was placed in Section III of DSM-5 that covers conditions in need of further research before being included in the DSM.

53
Q

According to research, do positive or negative symptoms have more of a genetic component?

A

Negative; studies have found that people with schizophrenia in their family histories have more negative symptoms than those whose families are free of schizophrenia

54
Q

What other disorder may schizophrenia share a vulnerability with?

A

Bipolar

55
Q

What is the difference in inheritance between MZ and DZ twins and what does this mean

A

DZ:44.3
MZ: 12.01
The fact is isn’t 100% suggests genetic transmission alone doesn’t account for schizophrenia

56
Q

What is the difference between a family and a facial high risk study?

A

Family studies just inspect families with the disorder in order to ermine heritability while facial high-risk studies begins with one or two biological parents with schizophrenia and follows their off- spring longitudinally to identify how many of these children may de- velop schizophrenia and what types of childhood neurobiological and behavioral factors may predict the disorder’s onset.

57
Q

Name two candidate genes that have been found in association studies and GWAS and what do these genes do?

A

DRD2 which encodes a specific type of dopamine receptor called D2. COMT which is associated with cognitive control processes that rely on the prefrontal cortex

58
Q

What chromosome has COMT been found?

A

on chromosome 22 where rare mutations associated with schizophrenia have been found,

59
Q

what was discovered to be abnormal in people with schizophrenia, in regards to CNVs, through GWAS studies?

A

One GWAS found over 50 rare CNV mutations that were three times more common among people with schizophrenia.Some of the identified gene mutations are known to be associated with other presumed risk factors in the etiology of schizophrenia, including the neurotransmitter glutamate and proteins that promote the proper placement of neurons in the brain during brain development. However they were only found in about 20% of those with schiazophrenia

60
Q

What specific CNV mutations have been observed? More importantly what is significant about these?

A

Reviews of GWAS studies in schizophrenia have identified CNV deletions such as 22q11.21, 15q13.3, and 1q21, many observed CNVs in schizophrenia are also observed in other disorders, including autism spectrum disorder and intellectual disability, suggesting that these CNVs are not specific to schizophrenia

61
Q

How do you read these mutation numbers?

A

22q11.21
22= chromosome 22
q= long arm (p= short arm)
11.21= location on chromosome

62
Q

What else has been observed through GWAS studies apart from CNV’s and candidate genes? (3)

A

Some SNPs associated with schizophrenia are also associated with bipolar disorder. SNP studies, like the familial high-risk studies, suggest that there may be a common genetic vulnerability for both disorders. They also identified 108 different genetic loci containing SNPs that were associated with schizophrenia. Many of the genetic locations involved genes associated with dopamine and glutamate, two neurotrans- mitters associated with schizophrenia

63
Q

What are two key ethological requirements for any GWAS?

A

(a) very large sample sizes, and (b) replication and rigorous statistical tests

64
Q

What three important points can be made about these GWAS findings according to the book?

A

(1) observed mutations are rare: CNVs account for less than 1 percent of genetic variance, and SNPs account for less than 25 percent of genetic variance (Ripke, Sanders, et al., 2011);
(2) only some people with these rare mutations have schizophrenia; and
(3) the mutations are not specific to schizophrenia.

65
Q

What does antipsychotic medication do that lead to the dopamine theory?

A

Antipsychotic drugs fit into and thereby block a type of postsynaptic dopamine receptor called the D2 receptor. From this knowledge about the action of the drugs that help people with schizophrenia, it was natu- ral to conjecture that schizophrenia resulted from excess activity in dopamine.

66
Q

How has the dopamine theory evolved

A

Blocking dopamine receptors in the mesolimbic pathway seemed to help positive symptoms but A revision to the dopamine theory hypothesized that dopamine abnormalities in the prefrontal cortex may account for negative symptoms, but evidence accumulated over the past 25 years does not strongly support this idea. However, research in the past few years has pointed to the important role of dopamine in reward and motivation in the striatum, and this has been linked with motivational deficits in schizophrenia that are part of the negative symptoms

67
Q

What evidence is there to suggest the dopamine theory isn’t as simple (regarding medication.) What is thought to be the reason for this?

A

it takes several weeks for antipsychotic medications to begin lessening the pos- itive symptoms of schizophrenia, although they begin blocking dopamine receptors rapidly. One possibility is that, although antipsychotics do indeed block D2 receptors, their ultimate therapeutic effect may result from the effect this blockade has on other brain areas and other neurotransmitter systems.

68
Q

How have newer drugs developed in regards to neurotransmitters?

A

One possibility is that, although antipsychotics do indeed block D2 receptors (Yilmaz, Zai, et al., 2012), their ulti- mate therapeutic effect may result from the effect this blockade has on other brain areas and other neurotransmitter systems. These newer drugs partially block D2 receptors, but they also work by blocking the serotonin receptor 5HT2

69
Q

What other neurotransmitter transmission is interrupted in people with schizophrenia and why?

A

Dopamine neurons generally modulate the activity of other neural systems; for example, in the prefrontal cortex they regulate gamma-aminobutyric acid (GABA) neurons. Thus, GABA transmission is disrupted in the prefrontal cortex of people with schizophrenia. Similarly, serotonin neurons regulate dopamine neurons in the mesolimbic pathway.

70
Q

Is there any evidence for any other neurotransmitters involved (2+2)

A

Glutamate, though the evidence accumulated over the past 20 years remains suggestive and not definitive. Low levels of glutamate have been found in the cerebrospinal fluid of people with schizophrenia, and postmortem studies have revealed low levels of the enzyme needed to produce glutamate.
Studies have found elevated levels of the amino acid homocysteine, a substance that is known to interact with the NMDA receptor among people with schizophrenia and, during their third trimester, in the blood of pregnant women whose offspring developed schizophrenia as adults. The drugs PCP and ketamine can induce both positive and negative symptoms in people without schizophrenia by interfering with NMDA receptors that are part of the glutamate system.

71
Q

What evidence for this has been found from brain imaging?

A

Newer brain imaging methods, such as SPECT and a specialised form of MRI called proton magnetic resonance spectroscopy, have found evidence for decreased NMDA receptor activity in the prefrontal cortex

72
Q

What brain structure and function abnormalities are commonly found in people with schizophrenia (4)

A

Enlargement of ventricles
Dysfunction of prefrontal and temporal cortex
Problems in communication between brain areas
Faster ageing in the brain (also due to medication)

73
Q

What does the enlarged ventricles suggest?

A

Having larger fluid-filled spaces implies a loss of brain cells.

74
Q

Could this be due to the medication?

A

No, this was studied

75
Q

What are enlarged ventricles correlated with? (3)

A

Large ventricles in people with schizophrenia are correlated with impaired performance on neuropsychological tests, poor functioning prior to the onset of the disorder, and poor response to medication treatment

76
Q

Is this unique to schizophrenia?

A

No can also be seen in disorders such as bipolar with psychotic features

77
Q

What deficits are reported in the prefrontal cortex?

A

MRI studies have shown reductions in gray matter and overall volume (size) in the prefrontal cortex (some contributed by antipsychotic medication.) People with schizophrenia perform more poorly than people without schizophrenia on neuropsychological tests designed to tap functions supported by the pre- frontal region. PET brain-imaging studies find that people with schizophrenia show lower glucose metabolism in the prefrontal cortex when performing neuropsychological tests tapping prefrontal functio

78
Q

What is the cause of this reduction of gray matter in the prefrontal cortex?

A

the number of neurons in this area does not appear to be reduced. More detailed stud- ies indicate that what is lost may be what are called “dendritic spines,” meaning that communication among neurons) is disrupted

79
Q

What is likely to cause this reduction in grey matter?

A

Research has linked these abnormalities in dendritic spines with the candidate genes and CNVs identified in schizophrenia

80
Q

What problems are present in the temporal cortex and surrounding regions? (4)

A

Reduced volume of temporal cortex, hippocampus, basal ganglia and limbic structures, likely due to genetics

81
Q

What makes these findings about the hippocampus more intriguing?

A

the fact that the hypothalamic–pituitary–adrenal (HPA) axis is closely connected to this area of the brain. Chronic stress is associated with reductions in hippocampal volume in other disorders. Although people with schizophrenia do not necessarily experience more stress than people without schizophrenia, they are more reactive to stress.

82
Q

Apart from genetics what is likely to cause reductions in volume of the hippocampus?

A

stress reactivity and a disrupted HPA axis

83
Q

What helps neuroscientists come to the conclusion there is less connectivity in the brain

A

people with schizophrenia have less connectivity in brain white matter than people without schizophrenia in the frontal and temporal cortices and this is associated with the genetic diathesis for schizophrenia

84
Q

What is helpful about measures of brain connectivity in schizophrenia?

A

Measures of brain connectivity in schizophrenia have also been shown to be helpful in pre- dicting who will respond well to antipsychotic medication treatment

85
Q

Name some possible environmental factors which influence the developing brain (2)

A
  • damage during gestation or birth

- . Among people already diagnosed with schizophrenia, cannabis use is associated with a worsening of symptoms

86
Q

If the damage is done early, why would the findings be presented later in life? (2)

A
  • The prefrontal cortex is a brain structure that matures late, typically in adolescence or early adulthood.
  • development of symptoms in adolescence could reflect a loss of synapses due to excessive pruning, the elimination of synaptic connections.
87
Q

What is the relationship between schizophrenia and stress?

A

People with schizophrenia do not appear to experience more stress in daily life than people without schizophrenia however people with schizophrenia were particularly vulnerable to daily stress. Research also shows that, as with many of the disorders, increases in life stress increase the likelihood of a relapse

88
Q

What 3 sociocultural; factors are involved in schizophrenia?

A

Poverty, Urbanicity, and Migration

89
Q

How do families influence schizophrenia?

A

they communicate more vaguely with one another and have higher levels of conflict than families of people without schizophrenia. It is plausible that the conflict and unclear communication are a response to having a family member with schizophrenia. critical comments, hostility, and emotional overinvolvement—led to the creation of the construct called expressed emotion (EE.) This research indicates that the home environment of people with schizophrenia can influence how soon they relapse, with higher expressed emotion predicting relapse.

90
Q

What symptoms often elicit critical comments from which type of people?

A

negative symptoms of schizophrenia are most likely to elicit critical comments, and that the relatives who make the most critical comments are the most likely to view people with schizophrenia as being able to control their symptoms

91
Q

Is this due to high EE causing worse symptoms or worse symptoms causing EE? How can this be explained?

A

Both dawg, One answer to this question involves the effects of stress on the HPA axis and its link to dopamine. Stress activates the HPA axis, causing cortisol to be secreted, which can then increase dopamine activity. Furthermore, heightened dopamine activ- ity itself can increase HPA activation, which may make a person overly sensitive to stress. Thus, there is a bidirectional relationship between HPA activation and dopamine activity.

92
Q

What are people generally like before they develop schizophrenia according to retrospective studies?

A

Lower IQ and higher levels of delinquency.
Boys- more disagreeable
Girls- more passive
Compared with their siblings who did not later develop schizophrenia, the children who later developed schizophrenia as young adults showed poorer motor skills and more expressions of negative emotions.

93
Q

Does this differ from prospective studies?

A

no, especially for low IQ or , impaired cognition, particularly attention and working memory , family members with it and social deficits

94
Q

What problems are presented with facial high risk studies and what is the solution?

A

Large sample sizes makes them hard to locate, because of these difficulties, the clinical high-risk study has been used in more recent research, a design that identifies people with early, attenuated signs of schizophrenia, most often milder forms of hallucinations, delusions, or disorganisation that nonetheless cause impairment

95
Q

What is an issue with any kind of treatment in schizophrenia?

A

some people with schizophrenia lack insight into their impaired condition and refuse any treatment at all

96
Q

Is there a difference in genders in response or insight into treatment?

A

Results from one study suggest that gender (female) and age (older) are predictors of better insight among people in their first episode of the illness, and this may help account for why women with schizophrenia tend to respond better to treatment than men

97
Q

What are extrapyramidal side effects of first generation medication?

A

resemble the symptoms of Parkinson’s disease. People taking antipsychotics may develop tremors of the fingers, a shuffling gait, and drooling.

98
Q

What other side effects are associated with first generation medication

A

sedation, dizziness, blurred vision, restlessness, and sexual dysfunction. dystonia, a state of muscular rigidity, and dyskinesia, an abnormal motion of voluntary and involuntary muscles, producing chewing movements as well as other movements of the lips, fingers, and legs. Another side effect is akasthesia, an inability to remain still; some people on antipsychotics pace constantly and fidget. In a rare muscular disturbance called tardive dyskinesia, the mouth muscles involuntarily make sucking, lip-smacking, and chin-wagging motions. In more severe cases, the whole body can be subject to involuntary motor movements.

99
Q

Compare the effectiveness of first and second generation drugs

A

research suggested that the second-generation antipsychotics were equally as effective as first-generation antipsychotics in reducing positive and disorganised symptoms. some, but not all, second- generation drugs were modestly more effective than the first-generation drugs in reducing negative symptoms and improving cognitive deficits

100
Q

What side effects are associated with second generation medication?

A

extrapyramidal side effects, weight gain. In addition to being unpleasant, weight gain is associated with other serious health problems, such as increased cholesterol and increases in blood glucose, which can cause type 2 diabetes. For example, clozapine and olanzapine have been related to the development of type 2 diabetes (

101
Q

What is often included in family therapy? (6)

A
  • Education about schizophrenia
  • Information about antipsychotic medication
  • Blame avoidance and reduction.
  • Communication and problem-solving skills within the family
  • Social network expansion.
  • Hope.
102
Q

What other psychological treatments are available?

A
Social Skills Training
Cognitive Behavior Therapy
Cognitive Remediation Therapies
Psychoeducation
Residential Treatment
103
Q

What did programmes such as NAVIGATE and RAISE highlight about treatment for schizophrenia?

A

(1) Combined and comprehensive treatments in community settings are important to develop and implement for people with schizophrenia, and (2) the earlier treat- ment begins, the better.