Schizophrenia Flashcards
how long must symptoms be presnent for for a diagnosis to be made
for at least one month an associated 6 month period of functional decline
what criteria is used to define first and second rank symptoms
Schneider’s criteria
when does schizophrenia usually present
can present at any time, although rarely before puberty
late teens/early 20s
what is the most common type of schizophrenia
paranoid schizophrenia
which symptoms predominate in paranoid schizophrenia
first rank symptoms
what is hebephrenic schizophrenia associated with
immature, silly, frivility, agitation
changes in mood are common
what predominates in catatonic schizophrenia
movement disorder
what are negative symptoms
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)
which cognitive domains are affected
all
what is the primary negative symptom
affective blunting
when are depression/elation common in schizophrenia
often after an acute psychotic exacerbation
what is the most dangerous cmplication of schizophrenia
suicidal tendency
what is the predominant feature f the prodromal phase
the predominant feature is cognitive symptoms
what is the typical natural history of a pt before they rpesent with schizophrenia
patient typically performs fine until teens, when school performance etc declines
what is the underlying aetiology
Neurodevelopmental disconnection caused by an interaction of genetic and multiple environmental factors (stress diathesis).
what are the underlying genetics of schizophrenia
polygenic and likely non mendelian inheritance
family history is a risk
there are some known high risk mutations
what is a high risk mutation
22q11
what is the risk of schizophrenia if both parents/MZ twin has it
50%
which disorders are often also present in families with some schizophrenia
BAD
which drug is particularly implicated in schizophrenia development
cannabis
which pre natal factors increase risk
pre natal exposure to viruses - this increases risk by 50%
live virus, chemical mediators of infection or fever can all affect brain development
in which trimester does a viral infection have the highest risk on development of schizophrenia
2nd trimester
do obstetric problems cause schizophrenia
cause and effect??
there is a higher rate of birth complications eg emergency C section, pre eclampsia, fetal hypoxia
what neuranatomical differences are seen in schizophrenia
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
does the season of birth have an impact on schizophrenia risk?
seen more in winter births than spring
maybe because there are more viruses
what happens to the ventricles
enlarged ventricles, to fill gaps left by thinned cortices
what happens to the cerebral cortex
becomes thinner and has less tissue in the frontal, temporal lobe and the hippocampus
what happens to the grey matter contnet of said areas
decreased
what happens to the organization of cortical layers
abnormal layering
is there neuronal loss
no, there is decreased arborization meaning there are less dendritic communciations with other neurons
when do neuroanatomical differences develop
they are present early in illness, and are likely pre-morbid
they progress a bit over disease development
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
do ventricles continue to enlarge over disease course
no
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
what happens to dopamine signalling
altered - increased in some areas (psychosis - temporal lobe) and decreased in others (negative (hippocampus) and cognitive (frontal) symptoms
which neurotransmitters are also affected
glutamine adn serotonin
more common in males or females
males
onset in males and females
males 15-25
females 25-35
incidence in different populations and socioeconomic classes
higher incidence in lower socioeconomic class and urban population
does an acute onset confer a good or bad prognosis
good
does an older or younger onset confer a good prognosis
older
presence of what symptoms is a good prognostic indicator
marked mood disturbance or FH of mood disorder
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
course of schizophrenia
what is the risk of suicide
10-15%
When are the most high risk times for suicide
week after discharge from hospital
when insight returns
what is the risk of homocide
rare
what is one of the most important challenges in managemenet
non adherence due to lack of insight
what correlation is there with early treatment and detection and outcomes
beneficial, it reduces the duration of psychosis and predicts more favourable outcomes
is co morbidity common
there is an increased frequency of medical illnesses
is life span affected
reduced life span
what disease is there particuarlly high rates of in schizophrenia
CV diseae
why is CVD so high
high smoking rates
antipsychotics
psychological therapy
CBT is offered to all pt
what is the mainstay of action of antipsychotics
block D2 dopamine receptors and others (muscarinic, H1, alpha)
how does activity on D2 receptors correlate with antipsychotic potency
runs parallel, but other receptors are used too to reduce EPSE
which dopamine pathway do the antipsychotics produce a therapeutic effect by blocking
mesolimbic pathway - relieves the positive symptoms
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
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.
what is the main action of typical antipsychotics
block D 2 dopamine receptors - EPSE effects
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
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
when do acute EPSE commonly occur
first few weeks
acute dystonic reaction
painful, involuntary muscle spasm
which muscles are most commonly involved in acute dystonic reaction
eye and back and neck muscles e.g. torticollis, protruding tongue, fixed upward gaze
who is most susceptible to acute dystonic reaction
young men
parkinsonism
- Pharmacological induction of Parkinsonism: bradykinesia, tremor and rigidity
akathisia
- An internal restlessness, the patient may feel the need to be constantly moving (subjective) or you may notice them twitching and fidgeting (objective)
treatment of acute EPSE
acute dystonic reaction and parkinsonism can be treated with anticholinergics
akathisia doesnt respond to them
change drug and dose
when does tardive dyskinesia develop
after months or years of treatment
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.
can tardive dyskinesia be treated?
often resistant, it also often gets worse when antipsychotic therapy is stopped
what drug is shown to be good in treatment resistant patients
clozapine - 50% efficacy in patients tried on 2 antipsychotics already
which drug has very little D2 activity
quietapine
which receptors does clozapine work on
what are the side effects of clozapine
metabolic syndrome, hypersalivation and constipation
agranulocytosis and myocarditis
what is agranulocytosis
lowering of WBC (mainly neutrophils)
what will a blood test show with agranulocytosis
decreased leucocytes
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
