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Psychiatry > Neurobiology of Psychosis and Schizophrenia > Flashcards

Neurobiology of Psychosis and Schizophrenia Flashcards

1
Q

hertability in schizophrenia?

A

78%

45% lifetime risk if both parents or MZ twin affected

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2
Q

what is heritability?

A

proportion of observable differences in a trait between individuals in a population that is due to genetic differences

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3
Q

what problems during pregnancy can increase chance of schizophrenia in later life?

A 
2nd trimester viral illness
pre-eclampsia
fetal hypoxia
emergency C section
(also childhood viral CNS infection)
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4
Q

which drug is highly associated with schizophrenia?

A

cannabis

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5
Q

differences in the brain of people with schizophrenia?

A

reduced frontal lobe volume
reduced frontal lobe grey matter
enlarged lateral ventricle volume
overall reduction in grey matter volume

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6
Q

main points about grey matter changes in schizophrenia?

A

associated with widely distributed grey matter abnormalities
abnormalities present in early illness and likely before onset of illness
grey matter reductions due to reduced arborisation and not neuron loss
grey matter reductions likely progressive in initial years of illness

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7
Q

how is white matter affected in schizophrenia?

A

hypothesis of abnormal neural integration in schizophrenia

- white matter connects different brain regions therefore white matter abnormalities hypothesised

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8
Q

how can white matter abnormalities be investigated?

A

diffusion tensor imaging (DTI) - type of MRI which shows tracts
2 measures most often reported
- fractional anisotropy (FA) - high numbers = healthy white matter
- mean diffusivity (MD) - high numbers = less healthy white matter

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9
Q

what findings on DTI would be most consistent with schizophrenia?

A

FA reduced and MD increased

- higher FA = more severe psychotic symptoms

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10
Q

describe the neurodevelopmental model for schizophrenia?

A

environmental risk factors act in utero
children who later develop schizophrenia have identifiable impaired behaviour, motor and intellectual development from infancy
ventricular enlargement is already present at diagnosis and is not progressive
disruption of normal cerebral cortical cytoarchitecture

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11
Q

how is dopamine affected in schizophrenia?

A

drugs which release dopamine (amphetamines) in the brain or D2 receptor agonists (apomorphine etc) produce a psychotic state
dopamine receptor antagonists are therefore used to treat schizophrenia symptoms
assumed that schizophrenia is related to overactivity of dopamine pathways in the brain

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12
Q

what are the 3 dopaminergic pathways in the brain?

A 
tuberoinfundibular = control of prolactin release
mesolimbic/cortical = motivation and reward
nigrostriatal = extrapyramidal motor system
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13
Q

how do amphetamines effect dopamine synapse?

A

increase dopamine transmission

antipsychotics have the opposite effect

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14
Q

components and function of D1 dopamine receptor family?

A

D1 and D5

stimulate cAMP

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15
Q

components and function of D2 receptor family?

A

D2, D3 and D4
inhibit adenylyl cyclase
inhibit voltage activated calcium channels
open potassium channels

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16
Q

describe the distribution of dopamine receptors in the brain?

A

D1 and D2 in both limbic and striatal areas
D1 most abundant
D2 most pharmacologically important in CNS
other subtypes in smaller numbers and more discrete distribution

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17
Q

which abnormalities in dopaminergic system cause which symptoms in schizophrenia?

A

subcortical dopamine hyperactivity = psychosis

mesocortical dopamine hypoactivity = negative and cognitive symptoms

18
Q

what other neurotransmitters may be involved in schizophrenia?

A

glutamate
- altered NMDA receptor subunit expression
serotonin
- abnormalities in serotonin 2A binding potential in frontal cortex index significantly smaller in patients with schizophrenia

19
Q

what may cause the bran pathology seen in schizophrenia?

A

gene alterations

  • neuregulin (signalling protein that mediates cell interactions and plays critical role in growth and development of multiple organ systems)
  • dysbindin (essential for adaptive neural plasticity)
  • DISC-1 (involved in neurite overgrowth and cortical development through its interactions with other proteins)
20
Q

5 examples of typical antipsychotics?

A 
chlorpromazine
thioridazine
fluphenazine
haloperidol
zuclopentixol
21
Q

main feature of typical antipsychotics?

A

D2 receptor inhibition

22
Q

what correlation is seen between average dose of antipsychotic required to improve symptoms and D2 receptor binding activity?

A

larger dose causes reduced binding at D2 receptors
however, a delay in clinical effect is seen which indicates that neuronal adaptation to the D2 blockade is needed before symptoms improve
(i.e same reason that amphetamines affect dopamine transmission immediately but onyl get psychotic symptoms with continued use)

23
Q

definition of atypical antipsychotics?

A

high 5-HT2A to D2 ratio (affect both receptors)
less likely to cause extra-pyramidal side effects
better efficacy against negative symptoms
effective in patients unresponsive to typical drugs

24
Q

examples of atypical antipsychotics?

A 
olazapine
risperidone
quetiapine
clozapine
aripiprazole
amisulpride
25
Q

how do antipsychotics cause parkinsons symptoms?

A

block D2 dopamine receptors in nigrostriatum

parkinsons is also due to loss of dopaminergic neurons here so causes same symptoms

26
Q

what occurs in an acute dystonic reaction to antipsychotics?

A

muscle spasms

- takes hours to days

27
Q

how is an acute dystonic reaction managed?

A

prochlorperazine
procyclidine
orphphenadrine
(i.e all acetylcholine antagonists)

28
Q

how long do parkinsonism symptoms take to occur in antipsychotic treatment?

A

days to months

29
Q

features of akathesia as a result of antipsychotic treatment?

A 
internal restlessness
(fidgeting, wriggling, pacing etc)
30
Q

features of tardive dyskinesia?

A

repetitive involuntary purposeless movements
- grimacing, sticking tongue out, lip smacking, pursing lips, blinking etc
usually takes years to develop and continues after stopping medication

31
Q

endocrine effects of antipsychotics?

A

dopamine inhibits prolactin production, so D2 blockade cause hyperprolactinaemia

  • sexual dysfunction
  • galactorrhoea/gynaecomastia
  • amenorrhoea
  • infertility
  • low oestrogen/testosterone which can lead to osteoporosis
32
Q

how do hallucinogenic drugs cause psychosis?

A

high affinity for 5-HT2 receptors causing pure 5-HT2 antagonism (antipsychotics dont cause PURE antagonism)
some evidence of reduced 5-HT2A receptor binding in people at risk of schizophrenia

33
Q

which type of antipsychotic is more likely to cause a netabolic syndrome and how?

A

atypicals
interactions at specific serotonin receptors may modulate aspects of the immune response and inflammation as well as weight gain

34
Q

what is metabolic syndrome?

A

cluster of conditions which occur together to cause increased risk of heart disease, stroke and type 2 diabetes (hypertension etc)

35
Q

histamine blockade causes which 2 symptoms?

A

sedation

increased appetite

36
Q

what are the effects of the alpha adrenergic blockade caused by snatipsychotics?

A

causes hypotension and interrupts the baroreflex response leading to dizziness, lightheadedness and fainting on rising from lying/sitting (orthostatic hypotension)

37
Q

effect of antispychotics on muscarinic receptors?

A 
blockade
muscarinic receptors are the target of parasympathetic nervous system
causes anti-cholinergic effects:
- blurred vision
- dry mouth
- constipation
- urinary retention
- sedation and confusion
38
Q

which effect of antisychotics is most likely to cause better sleep?

A

histamine blockade

39
Q

which neuroreceptors are involved with muscular stiffness and tremor?

A

dopamine

40
Q

which antipsychotic is least likely to cause parkinsonism?

A

quetiapine

41
Q

potential dangerous side effect of clozapine?

A

agranulocytosis

42
Q

how is clozapine monitored?

A

FBC weekly for first 6 months, then fortnightly for next 6 months, every 4 weeks thereafter
keep monitoring for 1 month after stopping drug
do FBC immediately in patient taking clozapine with a sore throat
monitor ECG, BP and pulse before starting (myocarditis risk)

Psychiatry (36 decks)

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