Psychosis Flashcards

1
Q

what is psychosis?

A

a state defined by impaired contact with reality, general functioning and well-being OR a loss of contact with reality

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2
Q

Schizophrenia spectrum disorders - what?

A

all psychotic disorders bear similarity with SZ so they all come under the spectrum. SZ is the most prevalent. Most explanations and treatment for SZ are applicable to these too

a) schizoaffective = characterized by symptoms of SZ, and symptoms of a mood disorder, such as bipolar and MDD.
b) Schizotypal personality disorder - less severe form of SZ
c) Schizophreniform - short term SZ

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3
Q

incidence vs prevalence

A

Incidence is the rate of new (or newly diagnosed) cases of the disease

Prevalence is the actual number of cases alive, with the disease either during a period of time (period prevalence) or at a particular date in time (point prevalence)

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4
Q

LowSES & SZ; theory

A

1) Social causation theory -> stress of poverty causes the disorder
BUT it appears in all SES
SO
2) Is it the downward drift theory? = the disorder makes them fall in rank

But: no evidence to support downward drift in long-term data

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5
Q

Positive vs negative delusions & psychomotor symptoms

A

Positive = hallucinations, delusions, disorganised thinking and speech (something added on)

Negative = Poverty of speech, restricted affect, loss of volition & social withdrawal

psychomotor symptoms - awkward movements, repeated grimaces, odd, ritualistic behaviour (OCD link: OCD is a risk factor for SZ)

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6
Q

2 types of SZ (what, effect and cause)

A

People think that there should be 2 types of SZ:
Type 1 = positive symptoms (more likely to improve from the disorder & has biochemical abnormalities)
(relate to DT’s???)

Type 2 = Negative symptoms (more persistent cognitive deficits. May be tied to structural abnormalities) (in MDD theres reduction in blood flow to pfc, seen here too - volition & to reward system = loss of volition)

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7
Q

Biological views of SZ

Genetics

A
    • received the most support

- Genetic factors: high genetic inheritance.

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8
Q

Biochemical abnormalities

A

• Dopamine hypothesis: DOPAMINE NEURONES FIRE TOO OFTEN AND TRANSMIT TOO MANY MESSAGES thus producing the symptoms of SZ (D-2 receptors)
^ the main suggestion for the cause of SZ

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9
Q

Problems with the dopamine hypothesis

A
  • Second generation antipsychotic drugs = more effective than the normal ones
  • The new drugs DO NOT BIND TO D-2 RECEPTORS but also to many D-1, D-4 receptors responsible for serotonin
  • Suggesting that its abnormal activity of DOPAMINE AND OTHER neurotransmitters

**More complex models now also implicate additional (rather than alternative) neurotransmitters (e.g., GABA, serotonin) in the aetiology, rather than just DA alone

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10
Q

Abnormal brain structure

what & why?

A
  • mainly linked to negative symptoms
  • enlarged ventricles: atrophy/ lack of development?
  • reduced reward pathway = MDD. Loss of volition
  • loss of volume in amygdala and pfc = flat affect. MDD have high amyg activity = negative affect

maternal stress, excess dopamine damaging systems environmental factors,– pregnancy and delivery complications

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11
Q

ALWAYS CONSIDER THE DIATHESIS- STRESS MODEL

WHAT

A

The most popular explanation for schizophrenia – the ‘diathesis-stress’ model –>
– inherit a biological predisposition to schizophrenia
– is triggered by later exposure to extreme stress

  1. Disordered neuronal development –> cognitive, motor and social impairments provide vulnerability
  2. Stress leads to over activity of DA system –> pos symptoms (the greater the stress, increased risk of dysregulation and onset)
  3. Prolonged/recurrent stress = degeneration of neurons = structural damage = neg symptoms
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12
Q

Psychosocial factors

A
  • substance use = enhances risk

- Stress

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13
Q

Psychological Views of SZ

A

Cognitive model

  • congruent with bio in that hallucinations and related perceptual difficulties, the sufferers brain is producing strange and unreal sensations –> sensations triggered by bio factors.
  • When people attempt to understand these unusual experiences, more features of the disorder begin to emerge. Misinterpretation of sensory problems
  • Begin to dev delusions
  • “rational path to madness” — tendency to jump to conclusions
  • Dysfunctional schemas (poor self concept + low self esteem)
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14
Q

Cognitive model of delusions

A
  • Delusions are extreme end of a continuum of ‘ordinary thoughts’
  • cognitive distortions/hostility bias in interpretation of events
  • the core of the model is an account of the way that causal attributions influence self-representations, which in turn influence future attributions: the attribution–self-representation cycle.
  • We argue that biases in this cycle cause negative events to be attributed to external agents and hence contribute to the building of a paranoid world view
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15
Q

ToM in delusions

WHAT & evidence

A

• Difficulties monitoring own and representing other’s mental states
– May lead to delusions of paranoia and reference

– Reduced understanding of ToM (deception) jokes
(Marjoram et al., 2005)
– Reduced understanding of irony in SZ (diss)
– Deficits in inference of intentions and detection of
cognitive emotions (Craig et al., 2014)
BUT: show shame and awareness of others perceptions suggesting some ToM (McCabe et al., 2004)

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16
Q

Hallucinations = a failure of attention?

A

• impairment in automatic processing of sensory input
- hallucinations + delusions = stem from sensory overload
– impose meaning on confusing internal and external inputs =Delusions

-• explains pos symptoms, and neg symptoms (withdrawal, flat affect) are a consequence of this sensory overload

17
Q

Sociocultural Views

AA & rates of recovery

A

rates of SZ differ between racial and ethnic groups – mainly between blacks vs whites
WHY?
a) They are actually more prone
b) Majority are unintentionally biased in their diagnoses or misread cultural differences
c) Economic sphere; AA are more likely to be poor. When ££ is controlled for then the gap closes

Rates of SZ vary from country to country in key ways

a) Course and outcome varies considerably
b) Developing countries have a better rate of SZ recovery vs developed countries + less likely to have impaired social functioning, cont symptoms, require meds or hospitals

18
Q

family dysfunction + SZ

what , effects + therapy

A
  • family stress
  • display more conflict, poor communication + critical and over involved
  • high in negative expressed emotion (NEE) (over involvement)
    a) SZ are 4x more likely to relapse if they live with a family high vs low in expressed emotion
    • BIDIRECTIONAL = families can influence SZ but SZ can influence families

Family intervention and psycho-educational programmes aim to reduce NEE are highly successful
– Educate about role of family in triggering episodes and address family problem solving skills
**diathesis stress model

19
Q

Treatment for SZ (5)

A

1) Milieu therapy – institution that promotes self respect.
BUT
many do remain impaired and have to live in shelters on their release

2) token economy – operant conditioning
BUT
is this just teaching people to imitate behavior rather than actually changing it; “performing”

3) antipsychotic drugs - most used
4) CBT - helps people try and view their hallucinations in different ways; does seem to reduce stress.

5) Avatar therapy –
fight back with face. after 30 mins found a reduction in stress and had less intense auditory hallucinations
- gave patients a sense of control of the voices
- reduction of distress
- Disconfirmation of maladaptive beliefs about the voice
** The mechanism may be anxiety related: the therapy may be reducing cognitive avoidance of fear-relevant information and also reducing anxiety as a direct consequence of exposure
CHALLENGE = keeping it realistic but keeping them safe

20
Q

is psychosis normal?

A
  • 5% of people have psychotic experiences
  • some people report positive experiences of hearing voices.
    • some theorists argue that delusions differ from beliefs held by the general population only by the strength of the belief, and their cultural acceptability
  • distress caused by these voices = diagnosis. Some voices are v distressing for people and tell them to do bad things
21
Q

SZ & diagnosis

A
  • huge variability in symptoms
  • –> some clinicians argue that SZ is actually a group of distinct, but related, disorders that share common features
  • Diagnosis largely ignores the existence of a continuum of experience of psychotic symptoms in the psychiatric and general population. –> schizotypy (DIMENSIONAL PERSPECTIVE)
  • should see it as a combo of many small problems
22
Q

Diathesis stress model - evidence w cortisol

A

Stress –> abnormalities in HPA –> cortisol/dysregulation –> psychosis

1) the absence or the presence of specific life stressors could be the best explanation why there are other people who are not genetically vulnerable of developing the brain disorder which is schizophrenia.
2) elevated cortisol NOT a consequence of psychosis cos - when treatment of corticosteriods is used (auto-immune disorder) = high rate of psychosis like symptoms
3) social support = resilience factor; see family systems

CAVEATS

  • subjective accounts of stressors & NEED preclinical stress in SZ
  • SES differences
23
Q

obsession vs delusion?

A
  • To the lived experience their both real
  • Obsession = intrusive
  • What triggers them
24
Q

How many diagnoses can you think of which might feature psychosis as a symptom?

A
OCD
PTSD
MDD + BIPOLAR
SUD
PD(?)
25
Q

How useful is the DSM 5 IN SZ diagnosis

A
  • Can help people (treatment/closure)
    • Some theorists argue that once you’ve been diagnosed =self-fulfilling prophecy
  • Can mess people around cos its so broad + has loads of related symptoms
  • Can show societal regression
  • Need to section; need diagnosis