Schizophrenia Flashcards

1
Q

how long must symptoms be presnent for for a diagnosis to be made

A

for at least one month an associated 6 month period of functional decline

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2
Q

what criteria is used to define first and second rank symptoms

A

Schneider’s criteria

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3
Q

when does schizophrenia usually present

A

can present at any time, although rarely before puberty

late teens/early 20s

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4
Q

what is the most common type of schizophrenia

A

paranoid schizophrenia

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5
Q

which symptoms predominate in paranoid schizophrenia

A

first rank symptoms

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6
Q

what is hebephrenic schizophrenia associated with

A

immature, silly, frivility, agitation

changes in mood are common

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7
Q

what predominates in catatonic schizophrenia

A

movement disorder

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8
Q

what are negative symptoms

A

Refer to a decrease/loss of mental function

Demotivation, self-neglect, apathy, anhedonia, reduced social interaction, blunting of affect (reduced range of emotions), avolition (inability to initiate and persist in goal directed behaviour), alogia (quantitative and qualitative decrease in speech)

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9
Q

which cognitive domains are affected

A

all

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10
Q

what is the primary negative symptom

A

affective blunting

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11
Q

when are depression/elation common in schizophrenia

A

often after an acute psychotic exacerbation

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12
Q

what is the most dangerous cmplication of schizophrenia

A

suicidal tendency

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13
Q

what is the predominant feature f the prodromal phase

A

the predominant feature is cognitive symptoms

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14
Q

what is the typical natural history of a pt before they rpesent with schizophrenia

A

patient typically performs fine until teens, when school performance etc declines

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15
Q

what is the underlying aetiology

A

Neurodevelopmental disconnection caused by an interaction of genetic and multiple environmental factors (stress diathesis).

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16
Q

what are the underlying genetics of schizophrenia

A

polygenic and likely non mendelian inheritance

family history is a risk

there are some known high risk mutations

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17
Q

what is a high risk mutation

A

22q11

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18
Q

what is the risk of schizophrenia if both parents/MZ twin has it

A

50%

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19
Q

which disorders are often also present in families with some schizophrenia

A

BAD

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20
Q

which drug is particularly implicated in schizophrenia development

A

cannabis

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21
Q

which pre natal factors increase risk

A

pre natal exposure to viruses - this increases risk by 50%

live virus, chemical mediators of infection or fever can all affect brain development

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22
Q

in which trimester does a viral infection have the highest risk on development of schizophrenia

A

2nd trimester

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23
Q

do obstetric problems cause schizophrenia

A

cause and effect??

there is a higher rate of birth complications eg emergency C section, pre eclampsia, fetal hypoxia

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24
Q

what neuranatomical differences are seen in schizophrenia

A

decreased size of cerebral cortex in particular frontal lobe, some temporal lobe too. enlarged ventricles and thinned cortices

altered dopamine signalling - overactivity?

glutamine and serotonin neurotransmission also altered

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25
Q

does the season of birth have an impact on schizophrenia risk?

A

seen more in winter births than spring

maybe because there are more viruses

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26
Q

what happens to the ventricles

A

enlarged ventricles, to fill gaps left by thinned cortices

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27
Q

what happens to the cerebral cortex

A

becomes thinner and has less tissue in the frontal, temporal lobe and the hippocampus

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28
Q

what happens to the grey matter contnet of said areas

A

decreased

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29
Q

what happens to the organization of cortical layers

A

abnormal layering

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30
Q

is there neuronal loss

A

no, there is decreased arborization meaning there are less dendritic communciations with other neurons

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31
Q

when do neuroanatomical differences develop

A

they are present early in illness, and are likely pre-morbid

they progress a bit over disease development

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32
Q

in patients with schizophrenia, are symptoms detectable from childhood?

A

there is identifiable impaired behaviour, motor and intellectual development from infancy

but this is present ina lot of kids and means nothing

33
Q

do ventricles continue to enlarge over disease course

A

no

34
Q

how does amphetamine support the dopamine hypothesis

A

schizophrenia is thought to be due to dopamine overactivity

release dopamine in the brain and worsens the symptoms of schizophrenia and can induce a similar behaivoural syndrome

35
Q

what happens to dopamine signalling

A

altered - increased in some areas (psychosis - temporal lobe) and decreased in others (negative (hippocampus) and cognitive (frontal) symptoms

36
Q

which neurotransmitters are also affected

A

glutamine adn serotonin

37
Q

more common in males or females

A

males

38
Q

onset in males and females

A

males 15-25

females 25-35

39
Q

incidence in different populations and socioeconomic classes

A

higher incidence in lower socioeconomic class and urban population

40
Q

does an acute onset confer a good or bad prognosis

A

good

41
Q

does an older or younger onset confer a good prognosis

A

older

42
Q

presence of what symptoms is a good prognostic indicator

A

marked mood disturbance or FH of mood disorder

43
Q

name some poor prognostic indicators

A
  • prolonged prodromal phase and gradual onset
    • premorbid history of social withdrawal
  • early onset
  • male
  • long duration of untreated psychosis
  • cognitive impairement
  • neurological changes
44
Q

course of schizophrenia

A
45
Q

what is the risk of suicide

A

10-15%

46
Q

When are the most high risk times for suicide

A

week after discharge from hospital

when insight returns

47
Q

what is the risk of homocide

A

rare

48
Q

what is one of the most important challenges in managemenet

A

non adherence due to lack of insight

49
Q

what correlation is there with early treatment and detection and outcomes

A

beneficial, it reduces the duration of psychosis and predicts more favourable outcomes

50
Q

is co morbidity common

A

there is an increased frequency of medical illnesses

51
Q

is life span affected

A

reduced life span

52
Q

what disease is there particuarlly high rates of in schizophrenia

A

CV diseae

53
Q

why is CVD so high

A

high smoking rates

antipsychotics

54
Q

psychological therapy

A

CBT is offered to all pt

55
Q

what is the mainstay of action of antipsychotics

A

block D2 dopamine receptors and others (muscarinic, H1, alpha)

56
Q

how does activity on D2 receptors correlate with antipsychotic potency

A

runs parallel, but other receptors are used too to reduce EPSE

57
Q

which dopamine pathway do the antipsychotics produce a therapeutic effect by blocking

A

mesolimbic pathway - relieves the positive symptoms

58
Q

because the drugs are adminstered systemically, they also block dopamine receptors in these pathways: what happens

A
  • Blockage in nigrostatial pathway: extra-pyramidal side effects
  • Blockage in pituitary pathway: increased PRL – galactorrhoea, gynaecomastia, sexual dysfunction, amenorrhoea, infertility. Can lead to osteoporosis.
  • Blockage in reward component of mesolimbic pathway: reduced pleasure
59
Q

how long do the pharmacological and therapeutic effects of antipsychotics take to work

A

Dopamine receptor blocking activity (pharmacological) is immediate, however therapeutic onset takes a few weeks.

60
Q

what is the main action of typical antipsychotics

A

block D 2 dopamine receptors - EPSE effects

61
Q

what are the adverse effects caused by blockage of histamine, musarinic, alpha adn serotonin receptors

A
  • Antihistamine activity: drowsiness and sedation, increased appetite
  • Blockage of muscarinic receptors (anticholinergic symptoms)
  • Blockage of alpha receptors: postural hypotension, interrupts the baroreflex response
    • Dizziness, light headedness, fainting
  • Blockage of serotonin receptors: metabolic syndrome
62
Q

what is metabolic syndrome

A
  • Cluster of conditions that occur together and increase your risk of heart disease, stroke and diabetes
  • Increased abdominal girth, hypertension, hypercholesteremia, T2DM
63
Q

when do acute EPSE commonly occur

A

first few weeks

64
Q

acute dystonic reaction

A

painful, involuntary muscle spasm

65
Q

which muscles are most commonly involved in acute dystonic reaction

A

eye and back and neck muscles e.g. torticollis, protruding tongue, fixed upward gaze

66
Q

who is most susceptible to acute dystonic reaction

A

young men

67
Q

parkinsonism

A
  • Pharmacological induction of Parkinsonism: bradykinesia, tremor and rigidity
68
Q

akathisia

A
  • An internal restlessness, the patient may feel the need to be constantly moving (subjective) or you may notice them twitching and fidgeting (objective)
69
Q

treatment of acute EPSE

A

acute dystonic reaction and parkinsonism can be treated with anticholinergics

akathisia doesnt respond to them

change drug and dose

70
Q

when does tardive dyskinesia develop

A

after months or years of treatment

71
Q

what are the features of tardive dyskinesia

A
  • Involuntary movements, often of face and tongue, but also of trunk and limb
  • E.g. grimacing, sticking out tongue, smacking lips etc.
72
Q

can tardive dyskinesia be treated?

A

often resistant, it also often gets worse when antipsychotic therapy is stopped

73
Q

what drug is shown to be good in treatment resistant patients

A

clozapine - 50% efficacy in patients tried on 2 antipsychotics already

74
Q

which drug has very little D2 activity

A

quietapine

75
Q

which receptors does clozapine work on

A
76
Q

what are the side effects of clozapine

A

metabolic syndrome, hypersalivation and constipation

agranulocytosis and myocarditis

77
Q

what is agranulocytosis

A

lowering of WBC (mainly neutrophils)

78
Q

what will a blood test show with agranulocytosis

A

decreased leucocytes

79
Q

what precautions are taken when taking clozapine

A
  • FBC must be monitored: weekly for first 6 months, 2weekly for next 6 months, every 4 weeks thereafter, and one month after cessation
  • FBC if patient gets ill
  • watch out for sore throat
  • start drug in hospital and monior ECG, BP and pulse for myocarditis