L5+6 - Schizophrenia & the Psychoses Flashcards

1
Q

treatment for catatonia?

A

ECT

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2
Q

DSM-5 symptoms of schizophrenia?

A

The presence of two or more characteristic symptoms which must be present for a significant proportion of time during a one month period (or less if successfully treated). At least one of these must be 1,2 or 3 of:

Delusions Hallucinations
Disorganised speech (i.e. frequent derailment or incoherence)
Grossly disorganised or catatonic behaviour
Negative symptoms (i.e. diminished emotional expression or avolition)

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3
Q

What is the pattern of onset for schizophrenia

A

delusions and hallucinations are usually at first presentation, then moves onto negative symptoms - chronic disease state.

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4
Q

concordance for scz in twins?

A

50% - pretty high

indicates that psychologycal and enviro factors probably contribute 50%

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5
Q

Marijuana and SCZ?

A

There is a clear link….
drug nduced psychosis should dissipate as soon as drug is gone.

maybe someone with non-onset scz is more likely to smoke.

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6
Q

does psychosis indicate schizophrenia?

A

no.

many people report subclinical psychotic experiences but do not go onto get the diagnosis..

however, you need to have psychosis to get schizophrenia diagnosis.

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7
Q

What is the schizophrenia spectrum?

A
  • demonstrates that some people who have subclinical, isolated psychotic symptoms will not go on to develop schizophrenia.

isolated symptoms –> prodromal symptoms –> schizophrenia

  • The more sophisticated the person, the more sophisticated the delusion.
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8
Q

What is the hypothetical path from gene to behaviour?

A

genotype –> subtle molecular abnormality –> abnormal information processing as a biological endophenotype –> abnormal behaviour with complex functional interactions and emergent phenomena (symptom phenotype)

aka someone with the risk gene can have the underlying changed biological system, but ultimately, it is their personalty and coping skills and interactions with the environment that will determine whether psychiatric symptoms develop

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9
Q

What are some scz risk genes

A

COMT
FKBPS SNPs
AKTI SNPs

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10
Q

How much earlier is onset in men that women

A

3-5 years

usually related to some type of stressful event

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11
Q

Describe the course of schizophrenia

A

prodomal phase (subclinical phenomena) associated with a delusion –> psychosis –> remittance –> relapse –> deficits

15-20% make complete recovery
15% never recover
most patients will recover at least partially

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12
Q

Positive symptoms?

A
  • Hallucinations
  • Delusions
  • Bizarre behaviours
  • Thought disorder e.g. neologism, incoherence, loose associations
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13
Q

Negative symptoms?

A
  • different to ‘affective symptoms’
  • flattened affect - no stimulus elicits emotional response
  • alogia - decrease in speech flow
  • avolition
  • anhedonia
  • attention deficit
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14
Q

Dopamine hypothesis?

A
  • hypothesises the the overactivity of one of three dopamine transmitter systems in the brain.
  • Antipsychotics inhibit this system
  • POSITIVE SYMPTOMS due to increased activity in mesolimbic DA pathway
  • NEGATIVE SYMPTOMS due to decreased activity in the mesocortical pathway (impairment of reward pathway)

glutamate may be involved in both negative and positive symptoms, and cog impairments

  • holinergic and GABA changes are important in cog changes
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15
Q

What did atypical antipsychotics do

A

serotonin

did not produce movement disorder

e.g. haloperidol

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16
Q

Glutamate hypoersis?

A
  • it may be an effective therapeutic targic
  • abnormal NMDA and AMPA mRNA in hippocampus….

therefore treatment resistent patients may have diff underlying pathology.

17
Q

What are negative symptoms theorised to be due to?

A

mesocortical - preforntal cortex circuitry malfunction

18
Q

What are positive symptoms thought to be due to?

A

mesolimbic pathway malfunction - OVERACTIVATION

19
Q

What are affective symptoms thought to be due to

A

mesocortical - Ventromedial PFC circuitry malfunction

20
Q

What are aggressive symptoms thought to be due to?

A

orbitofrontal cortex and amygdala malfunction

21
Q

What are cognitive symptoms thought to be due to?

A

Dorsolateral PFC malfnction

22
Q

Which dopamine pathways are thought to be fine in scz?

A

nigrostriatal and tuberfundibular pathways.

23
Q

what is the function or orbitoPFC

A

inhibition, control, emotion processing

24
Q

What is DLPFC thought to do

A

behavioural activation, planning, getting things under way

25
Q

What can a pure d2 agontagonist do to help

A

decrease positive symptoms by dampening the overactive mesolimbic pathway..

HOWEVER…

this will cause a lack of pleasure - anhedonia

26
Q

Arguments against dopamine hypothesis?

A
  1. time course between administration of dopamine blocker and clinical response
  2. DA agonists have inconsistent effect on psychosis
  3. direct evidence of increased DA activity is poor.
27
Q

“two types of schizophrenia” - what are they

A

type 1 - mostly positive symps

type 2 - mostly negative symps

Dopamine antipyshotics are best at type 1 stuff not type 2

28
Q

What were liddle’s three symdromes model of schizophrenia broken down into?

A
  • hallucinations and delucions
  • negative symptoms
  • behavioural disorganisation
29
Q

Brain changes associated with SCZ

A

Changes are thought to FOLLOW the diagnosis.

  • Ventricular dilatation
  • loss of grey matter (ight temporal, inferior frontal cortex, cingulate, left medial temporal, left OPFC, cerebellum)
  • PFC changes
  • ## corpus callosum
30
Q

If SCZ could be localised, where would it be?

A
  • temporal lobe

- Frontal love

31
Q

Changes in hippocampus in SCZ?

A
  • pyramidal cells are disorganised
  • hippocampal atrophy

makes sense that people with scz have memory deficit, especially those with negative symp

32
Q

What could glucocorticoids have to do with the brain pathology in SCZ?

A

chronic stress hormone causing cell death

stressful life event usually with onset of schizophrenia

33
Q

what cognitive areas are impaired in SCZ?

A

GLOBAL

  • attention
  • affect - little like ASD, processing of social info is compromised. poor at expressing too.
  • language - clanging, word salad
  • memory
  • spatial abilities
  • frontal functions
  • processing speed
  • fine motor function
34
Q

What do changes in the DLPFC do

A

negative symps (DECREASED ACTIVITY)

35
Q

What do changes in the inferior parietal cortex do

A

DECREASED

negative symps - psychomotor poverty

36
Q

What do changes in the superior temporal gyrus do

A

auditory hallucinations

INCREASED

37
Q

What do changes in Broca’s area do

A

incerased

auditory hallucinations

38
Q

What do changes in the amygdala do

A

persecutory delusions

INCREASD

39
Q

What do changes in the Hippocampus du

A

first rank and positive symptoms