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RB Y3 2 Psychiatry > Schizophrenia > Flashcards

Schizophrenia Flashcards

(79 cards)

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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
does the season of birth have an impact on schizophrenia risk?
seen more in winter births than spring maybe because there are more viruses
26
what happens to the ventricles
enlarged ventricles, to fill gaps left by thinned cortices
27
what happens to the cerebral cortex
becomes thinner and has less tissue in the frontal, temporal lobe and the hippocampus
28
what happens to the grey matter contnet of said areas
decreased
29
what happens to the organization of cortical layers
abnormal layering
30
is there neuronal loss
no, there is decreased arborization meaning there are less dendritic communciations with other neurons
31
when do neuroanatomical differences develop
they are present early in illness, and are likely pre-morbid they progress a bit over disease development
32
in patients with schizophrenia, are symptoms detectable from childhood?
there is identifiable impaired behaviour, motor and intellectual development from infancy but this is present ina lot of kids and means nothing
33
do ventricles continue to enlarge over disease course
no
34
how does amphetamine support the dopamine hypothesis
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
what happens to dopamine signalling
altered - increased in some areas (psychosis - temporal lobe) and decreased in others (negative (hippocampus) and cognitive (frontal) symptoms
36
which neurotransmitters are also affected
glutamine adn serotonin
37
more common in males or females
males
38
onset in males and females
males 15-25 females 25-35
39
incidence in different populations and socioeconomic classes
higher incidence in lower socioeconomic class and urban population
40
does an acute onset confer a good or bad prognosis
good
41
does an older or younger onset confer a good prognosis
older
42
presence of what symptoms is a good prognostic indicator
marked mood disturbance or FH of mood disorder
43
name some poor prognostic indicators
* prolonged prodromal phase and gradual onset * premorbid history of social withdrawal * early onset * male * long duration of untreated psychosis * cognitive impairement * neurological changes
44
course of schizophrenia
45
what is the risk of suicide
10-15%
46
When are the most high risk times for suicide
week after discharge from hospital when insight returns
47
what is the risk of homocide
rare
48
what is one of the most important challenges in managemenet
non adherence due to lack of insight
49
what correlation is there with early treatment and detection and outcomes
beneficial, it reduces the duration of psychosis and predicts more favourable outcomes
50
is co morbidity common
there is an increased frequency of medical illnesses
51
is life span affected
reduced life span
52
what disease is there particuarlly high rates of in schizophrenia
CV diseae
53
why is CVD so high
high smoking rates antipsychotics
54
psychological therapy
CBT is offered to all pt
55
what is the mainstay of action of antipsychotics
block D2 dopamine receptors and others (muscarinic, H1, alpha)
56
how does activity on D2 receptors correlate with antipsychotic potency
runs parallel, but other receptors are used too to reduce EPSE
57
which dopamine pathway do the antipsychotics produce a therapeutic effect by blocking
mesolimbic pathway - relieves the positive symptoms
58
because the drugs are adminstered systemically, they also block dopamine receptors in these pathways: what happens
* 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
how long do the pharmacological and therapeutic effects of antipsychotics take to work
Dopamine receptor blocking activity (pharmacological) is immediate, however therapeutic onset takes a few weeks.
60
what is the main action of typical antipsychotics
block D 2 dopamine receptors - EPSE effects
61
what are the adverse effects caused by blockage of histamine, musarinic, alpha adn serotonin receptors
* 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
what is metabolic syndrome
* Cluster of conditions that occur together and increase your risk of heart disease, stroke and diabetes * Increased abdominal girth, hypertension, hypercholesteremia, T2DM
63
when do acute EPSE commonly occur
first few weeks
64
acute dystonic reaction
painful, involuntary muscle spasm
65
which muscles are most commonly involved in acute dystonic reaction
eye and back and neck muscles e.g. torticollis, protruding tongue, fixed upward gaze
66
who is most susceptible to acute dystonic reaction
young men
67
parkinsonism
* Pharmacological induction of Parkinsonism: bradykinesia, tremor and rigidity
68
akathisia
* An internal restlessness, the patient may feel the need to be constantly moving (subjective) or you may notice them twitching and fidgeting (objective)
69
treatment of acute EPSE
acute dystonic reaction and parkinsonism can be treated with anticholinergics akathisia doesnt respond to them change drug and dose
70
when does tardive dyskinesia develop
after months or years of treatment
71
what are the features of tardive dyskinesia
* Involuntary movements, often of face and tongue, but also of trunk and limb * E.g. grimacing, sticking out tongue, smacking lips etc.
72
can tardive dyskinesia be treated?
often resistant, it also often gets worse when antipsychotic therapy is stopped
73
what drug is shown to be good in treatment resistant patients
clozapine - 50% efficacy in patients tried on 2 antipsychotics already
74
which drug has very little D2 activity
quietapine
75
which receptors does clozapine work on
76
what are the side effects of clozapine
metabolic syndrome, hypersalivation and constipation agranulocytosis and myocarditis
77
what is agranulocytosis
lowering of WBC (mainly neutrophils)
78
what will a blood test show with agranulocytosis
decreased leucocytes
79
what precautions are taken when taking clozapine
* 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

RB Y3 2 Psychiatry (12 decks)

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