Session 12 - psychosis Flashcards
1
Q
what is the definition of psychosis?
A
- presence of hallucinations or delusion but the patients have a lack of insight (don’t believe they’re unwell)
- this isn’t a diagnosis but a set of symptoms
2
Q
what are hallucinations?
A
- the perception of a stimulus without an actual stimulus
- can be in any sensory modality
- auditory = very common
- olfactory = often seen in depression
3
Q
what are visual hallucinations often caused by?
A
they’re usually organic so caused by a problem with the brain or eyes eg. SOL, Lewy body dementia
4
Q
What are hallucinations in the ‘normal’ population known as?
A
- hypnogogic - experienced when going to sleep
- hypnopompic - experienced when waking up
5
Q
what are delusions?
A
- a fixed, false believe which is unshakeable and outside of cultural norms
- eg. think they’re being spied on by the police
- unshakable - even if you showed them proof that what they’re saying isn’t true, they will still believe it
6
Q
who first used the term Schizophrenia?
A
Eugen bleuler
7
Q
what are the first rank symptoms?
A
- auditory hallucinations
- passivity experiences
- thought withdrawal, broadcast or insertion
- delusional perceptions
- somatic hallucinations
8
Q
what are auditory hallucinations?
A
- thought echo - hearing thoughts aloud
- running commentary
- third person - voices referring to the patient in third person and conversing with each other about the patient
9
Q
what are passivity experiences?
A
patient believes an action or feeling is caused by an external force
10
Q
what is thought withdrawal, broadcast or insertion?
A
- thought withdrawal - thoughts are being taken. out of the mind
- thought broadcast - belief that everyone knows what the patient is thinking
- thought insertion - believed that thoughts are being implanted by others
11
Q
what is delusion perception?
A
- attribution of a new meaning to a normally perceived object
- eg. red traffic light means aliens are coming
12
Q
what are somatic hallucinations?
A
- mimics feeling from inside the body
- eg. the sense of being touched when no one is there.
13
Q
what are the positive and negative symptoms and what do these mean?
A
Positive symptoms - something added
- delusions, hallucination, thought disorder (problem with organisation of thoughts), lack of insight
Negative symptoms - symptoms that take away from the patient
- under activity, low motivation, social withdrawal, emotional flattening, self neglect
14
Q
What is the dopamine theory of schizophrenia?
A
- evidence for the involvement of dopamine in schizophrenia
- drugs that increase dopamine levels (eg. amphetamines) induce psychosis
- drugs that antagonise dopamine treat psychosis (esp those acting at D2 receptors - those with the strongest affinity to D2 receptors are most clinically effective)
15
Q
what are the different dopamine pathways in the brain?
A
- mesocortical pathway
- mesolimbic pathway
- nigrostriatal pathway
- tuberoinfundibulnar pathway
16
Q
what is the mesolimbic pathway?
A
- from the ventral tegmental area to the limbic structures and the nucleus accumbens
- overactive in schizophrenia
17
Q
what is the mesocortical pathway?
A
- from the ventral tegmental area to the frontal cortex and the cingulate cortex
- this pathway is responsible for negative symptoms
- it’s underactive in schizophrenia
18
Q
what are the brain changes in schizophrenia?
A
- enlarged ventricles
- reduced grey matter w/ reduced brain weight
- decreased temporal lobe volume → changes in temp lobe → auditory hallucinations
- reduced size of limbic structures and prefrontal cortex
19
Q
what is the neuropathology of schizophrenia?
A
- decreased pre-synaptic markers
- decreased oligodendrocytes
- fewer thalamic neurones
- together these changed lead to a theory of aberrant connectivity which causes schizophrenia
20
Q
apart from changes in the dopamine pathway, what other areas in the brain are affected in schizophrenia?
A
- involvement of the limbic system - they have a role in regulating emotional behaviour
- possible role of the basal ganglia - movement disorder features. even untreated patients can present with motor symptoms
21
Q
what is the nigrostriatal pathway?
A
- it goes from the substania nigra pars compaca to the striatum (caudate nucleus and putamen)
- the basal ganglia is connected to this pathway
22
Q
what type of symptoms does blockage of dopamine in the nigrostriatal pathway cause?
A
- extra pyramidal side effects → parkinsonism
- if taking anti psychotics for a long period of time can get tardive dyskinesia - where the face, body or both make sudden, irregular movements that can’t be controlled - eg. sticking out tongue or blinking excessively
- can also get akathisia - inability to stay still
23
Q
what are the typical antipsychotics and eg?
A
- haloperidol
- they block D2 receptors in ALL CNS dopaminergic pathways
- but their main action as antipsychotics is on the mesolimbic and mesocortical pathways
- side effects come from antagonising D2 receptors in other pathways eg. nigrostriatal - Parkinsonism
24
Q
what are atypical antipsychotics and eg?
A
- clozapine
- lower affinity for D2 receptor
- however milder side effects as they rapidly dissociate from the D2 receptor
- they also block 5HT2 receptors - so have some action on the serotonin pathway
25
why do we get Parkinsonism if we over treat a patient with a typical antipsychotic?
there’s decreased dopamine so increased inhibition on the thalamus so less glutamate going to excite the cortex
26
what are some side effects of antipsychotics?
- **typical antipsychotics** - Parkinsonism because of involvement of substantia nigra. they get rid of postitive symptoms but not negative
- **atypical antipsychotics** - impaired glucose tolerance, weight gain, diabetes, prolonged QT, hypercholesterolaemia, galactorrhea
- sexual dysfunction side effects due to **lack of dopamine to inhibit prolactin production so hyperprolactinaemia**
27
what can happen to the movement of an untreated schizophrenic patients and why does this occur?
- can develop **catatonia** - extreme end of schizophrenia where movement is impoverished
- more than two weeks, one or more of; **stupor/mutism, excitement, posturing, negativism, rigitdity, waxy flexibility, command automatism**
- **less GABA binding so loss of inhibitory effect**
- rarely occurs bc we treat early
28
what is the tuberoinfundibular pathway?
- from the **arcuate and periventricular nuclei** of the **hypothalamus** to the **infundibular region of the hypothalamus**
- in this pathway **dopamine feeds back to the pituitary**
29
why can you get hyperprolactinaemia when taking antipsychotics?
- affects the tuberoinfundibular pathway
- dopamine normally inhibits prolactin release from he pituitary
- DA antagonists which lower dopamine, lead to **loss of dopamine's inhibitory function** and therefore **increased prolactin levels**
- this can lead to - **amenorrhoea, galactorrhoea, decreased fertility, reduced libido and long term can lead to osteopenia/osteoporosis**
30
what are some of the challenges in treating schizophrenia?
- patents tend to **lack insight** - can affect compliance with treatment
- therefore medication can be given in different ways such as a **depot injection** which is **long acting and releases the antipsychotic slowly.**
- it can be also be given **PO or short acting IM**
31
what are the factors associated with good prognosis?
- **no family history**
- good premorbid function
- **actue onset**
- mood disturbance
- **prompt treatments**
- maintenance of motivation
32
what are the long term complications of schizophrenia?
- mortality is twice as high as general population
- shorter life expectancy
- higher incidence of CVS disease, respiratory disease and cancer - partly due to medicine given and also life choices eg. smoking, less likely to have healthy lifestyle
- 9x greater suicide risk that general population
- 2x greater risk of violent death than general population
- substance misuse is common and many patients make (contributing to CVD)
