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cns > Session 12 - psychosis > Flashcards

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
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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
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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

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4
Q

What are hallucinations in the ‘normal’ population known as?

A
  • hypnogogic - experienced when going to sleep
  • hypnopompic - experienced when waking up
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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
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6
Q

who first used the term Schizophrenia?

A

Eugen bleuler

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7
Q

what are the first rank symptoms?

A
  • auditory hallucinations
  • passivity experiences
  • thought withdrawal, broadcast or insertion
  • delusional perceptions
  • somatic hallucinations
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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
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9
Q

what are passivity experiences?

A

patient believes an action or feeling is caused by an external force

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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
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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
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12
Q

what are somatic hallucinations?

A
  • mimics feeling from inside the body
  • eg. the sense of being touched when no one is there.
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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
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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)
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15
Q

what are the different dopamine pathways in the brain?

A
  • mesocortical pathway
  • mesolimbic pathway
  • nigrostriatal pathway
  • tuberoinfundibulnar pathway
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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
Q

why do we get Parkinsonism if we over treat a patient with a typical antipsychotic?

A

there’s decreased dopamine so increased inhibition on the thalamus so less glutamate going to excite the cortex

26
Q

what are some side effects of antipsychotics?

A
  • 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
Q

what can happen to the movement of an untreated schizophrenic patients and why does this occur?

A
  • 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
Q

what is the tuberoinfundibular pathway?

A
  • 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
Q

why can you get hyperprolactinaemia when taking antipsychotics?

A
  • 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
Q

what are some of the challenges in treating schizophrenia?

A
  • 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
Q

what are the factors associated with good prognosis?

A
  • no family history
  • good premorbid function
  • actue onset
  • mood disturbance
  • prompt treatments
  • maintenance of motivation
32
Q

what are the long term complications of schizophrenia?

A
  • 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)

cns (7 decks)

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