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psychosis Flashcards

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1
Q

main 4 symptoms of psychosis

A

delusions, disordered thoughts, hallucinations and catatonia

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2
Q

what causes schizophrenia

A

schizophrenia
bipolar disorder
illegal drugs
prescription drugs
PTSD
sleep deprivation
caffeine intoxication
Alzheimer’s disease

-part of other conditions- can have causes that are not directly related to an illness

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3
Q

normal experience with first episode of psychosis

A

First episode usually unexpected

cannot usually be immediately diagnosed with particular causal disorder

definitive diagnosis may come later

may be designated as having experienced ‘brief psychotic episode’

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4
Q

what is a ‘brief psychotic episode?

A

period of psychosis not caused by a mental health disorder

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5
Q

what are psychotic episodes frequently predicted by

A

prodromal phase

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6
Q

what is predromal phase? How long does it last?

A

changes in behaviour: irritability, difficulty concentrating, memory problems, anxiety, depression

can last months to years

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7
Q

why may there be a delay in treatment when acute phase begins?

A

person suffering doesn’t recognise they are ill? Friends/ relatives do not understand what’s happening?

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8
Q

what is the effect of delayed treatment

A

worse outcomes

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9
Q

what can help a person receive speed intervention?

A

If person has experiences psychosis because of an underlying mental health condition, they may recognise prodromal symptoms and receive speed intervention before their next episode

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10
Q

three types of symptoms of schizophrenia

A

cognitive, positive and negative

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11
Q

positive symptoms of schizophrenia

A

hallucinations, delusions, disorganised speech, disorganised behaviour or catatonia

symptoms that a person with schizophrenia has that a normal individual does not

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12
Q

negative symptoms of schizophrenia

A

loss of emotional response, anhedonia and apathy

symptoms that a person with schizophrenia lacks, that a normal person has

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13
Q

requirements for a schizophrenia diagnosis

A

two positive symptoms, or a positive and negative symptoms

must impact significantly

continuous signs of disturbance in behaviour for at least 6 months

not explained by something else

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14
Q

schizoaffective disorder

A

meets the criteria for schizophrenia and a major mood episode (mania or depression)

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15
Q

three types of schizoaffective disorder

A

bipolar type, depressive type and mixed

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16
Q

bipolar type schizoaffective disorder

A

manic and depressive episodes

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17
Q

depressive type schizoaffective disorder

A

depressive only

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18
Q

mixed schizoaffective disorder

A

manic and depressed simultaneously

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19
Q

epidemiology of schizophrenia

A

Around 1% of the population

Males 1.4x female (more frequent in males)

Strikes at an early age
Males: late teens
Females: late twenties
second female peak around the age of menopause

Highly disabling
no cure

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20
Q

suicide and schizophrenia

A

Much higher rate of suicide in schizophrenia than depression

5% of those suffering will take their own life

(double the rate of people with depression, while 10-15% of people with bipolar disorder type 1 commit suicide)

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21
Q

obesity and antipsychotics

A

Many antipsychotics can produce significant increases in BMI
-likely due to actions at H1 and 5HT receptors. Because obesity is associated with T2DM,

increased BMI is likely to be a major reason why the risk of diabetes is higher in people on antipsychotic drugs.

the negative symptoms of schizophrenia and the sedative effects of antipsychotics may also contribute to weight gain

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22
Q

antipsychotics and insulin resistance

A

can induce insulin-resistance independent of their effects on BMI:
this effect can occur with drugs that do not produce marked changes in appetite.

Antipsychotics are thought to cause insulin resistance by inhibiting a component of the insulin signalling cascade, Akt,

and by decreasing the phosphorylation of one of the targets of the insulin receptor kinase activity, insulin receptor substrate 1 (IRS-1)

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23
Q

Antipsychotics and beta cells

A

direct effect on beta cells

can cause pancreatic beta cell dysfunction in several ways

acting on muscarinic dopamine, adrenergic and serotonergic receptors they can decrease insulin secretion

may also decrease cellular concentrations of ATP which would also decrease insulin secretion

may damage beta cells and induce apoptosis

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24
Q

mental health act 1983

A

allows for compulsory hospitalisation and treatments

gives power to medical professionals, social workers and the police

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25
Q

section 2 mental health act

A

28 day assessment and treatment order

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26
Q

section 2 mental health act

A

28 day assessment and treatment order

27
Q

section 3 mental health act

A

6 month treatment order

can be renewed

usually have a pre-diagnosed mental health disorder that has worsened, therefore doctors are sure that keeping them for an extended time is of benefit

28
Q

sectioning

A

approved mental health professional or nearest relative

must be seen by two doctors
-one must be a psychiatrist
-one has to know the patient
and an approved mental health professional

cannot refuse treatment (except ECT)

29
Q

genetic factors of schizophrenia

A

1% in general population

8-10% if near relative affected

50% in twin studies (concordance rate)
–Probably influence of many “tendency” genes, which may have a small impact individually (unlikely to be due to a single schizophrenia gene). eg. DISC1 – disrupted in schizophrenia 1
–Many of these tendency genes may require an environmental impact too

30
Q

gene disrupted in schizophrenia 1

A

DISC 1

31
Q

Environmental factors

A

winter birth

substance abuse: cannabis, amphetamine

32
Q

winter birth as an environmental for schizophrenia?

A

maternal exposure to viruses?
controversial risk factor, many think it is a myth

33
Q

amphetamine as an environmental factor for schizophrenia

A

causes psychosis

can worsen the psychosis of someone who already have schizophrenia, or cause them to have a relapse

34
Q

cannabis as an environmental factor of schizophrenia

A

heavy cannabis use can increase the risk of development about schizophrenia

35
Q

why is it controversial that substance abuse may cause schizophrenia?

A

cause or effect? schizophrenics have a high risk for substance abuse

36
Q

what does AKT1 code for?

A

kinase that inactivates enzyme glycogen synthase kinase

involved in signalling via dopamine D2 receptors

37
Q

example that genetic factors may require some influence of the environment

A

increased risk of schizophrenia in those homozygous for mutant ATK 1 when they use cannabis everyday,
but not if they used cannabis at week ends or less, or never used cannabis

38
Q

social factors influencing schizophrenia

A

difficult childhood conditions:
-discrimination
-dysfunctional families
-abuse/ trauma

epigenetic changes?

39
Q

evidence schizophrenia may be a neurodevelopmental disorder

A

Age of onset (teenage/early adult)
-around time where the brain is changing quite a lot

Structural differences in the brain between schizophrenic and healthy individuals

40
Q

evidence that schizophrenia is a neurodegenerative disorder

A

Progression of disease in many cases, particularly true if it is not treated early

Reductions in brain volume

Excitotoxicity? could be that glutamate is one of the major factors

41
Q

T gondii

A

Risk factor suggested for schizophrenia and bipolar

Estimated that up to 30% of the world’s population is infected with T gondii

Once infected, impossible to get rid of

Migrates to tissues (brain) , where it forms cysts

Known to manipulate the behaviour of rodents to increase their chances of being eaten by cats (a necessary part of the parasite’s life cycle)

Has been suggested that it may also be able to influence human behaviour

42
Q

original form of dopamine hypothesis of schizophrenia

A

due to hyperactivity of the mesolimbic pathway (VTA to ventral striatum)

unlikely to describe the root cause of schizophrenia but may be a ‘final common pathway’

43
Q

what is a final common pathway

A

system on which several different causal factors converge on to produce the symptoms of a disease

44
Q

evidence for the dopamine hypothesis

A

reserpine depletes dopamine, leads to improvement in positive symptoms
-hallucinations and delusions lessen

amphetamine releases dopamine, amphetamine can cause psychosis

L-DOPA and dopamine agonists can cause psychosis if given at high doses

altered dopaminergic activity (hyperactivity) in certain brain areas may play a role in schizophrenia

45
Q

D1 like receptors

A

D1, D5

46
Q

D2 like receptors

A

D2, D3, D4

47
Q

correlation of therapeutic concentration of antipsychotics with the concentration needed to occupy 75% of D2 receptors

A

almost 1:1 relationship
indicates that activity at D2 receptors is important for antipsychotic activity

48
Q

increased dopamine transmission in mesolimbic pathway

A

mesolimbic pathway involved in emotion, fear and motivation
important in positive symptoms

49
Q

suggested importance of mesocortical pathway in schizophrenia

A

Decreased dopaminergic transmission in mesocortical pathway, important in negative symptoms

50
Q

dopaminergic pathways seen as being important in side effects

A

tuberhypophyseal (HT/Pituitary) - hormone release from the pituitary

nigrostriatal - motor control. important in Parkinson’s disease

51
Q

modern view of dopaminergic pathways

A

excess of dopaminergic activity in the nigrostriatal pathway going to the associative pathway
-explains positive symptoms

normal ore reduced DA activity in the mesolimbic pathway to ventral striatum
-cause of negative symptoms?

52
Q

detail of associative striatum DA hypothesis of schizophrenia

A

Associative striatum (AS) involved in assigning salience to stimuli e.g. threat level

Excess noise in AS dopaminergic signalling
-increased salience assigned to unimportant stimuli
-May lead to the positive symptoms

Cognitive impairments
-hypodopaminergic cortical function
-possibly driven by striatal hyperdopaminergic signalling

Negative symptoms
-impaired reward based learning
-not able to assign importance to things should be important
–decreasing reward we get from those stimuli
–possibly leading to apathy and anhedonia
?driven by striatal hyperdopaminergic signalling

53
Q

involvement of other receptors in schizophrenia (not dopamine)

A

NMDA receptor dysfunction
serotonin receptors
muscarinic receptors

54
Q

NMDA receptor dysfunction? in schizophrenia

A

glutamate dysfunction may be the root cause

NMDA antagonists cause psychosis e.g. ketamine

suggests that positive allosteric modulators of glutamate receptors could be a new therapeutic approach - AMPAkines?

55
Q

Serotonin receptors and schizophrenia

A

LSD causes psychosis

apathy and avolition in schizophrenia superficially similar to depression?

probably not the root cause, but 5HT receptor activity seems to give a better therapeutic profile

56
Q

muscarinic receptors and schizophrenia

A

mAChR antagonists worsen negative + cognitive symptoms

Scopolamine (non-selective mAChR antagonist) can cause psychosis

? muscarinic agonists useful

but mAChR antagonist activity gives better side effect profile
-with antipsychtic drugs that don’t have activity at muscarinic receptors, you sometimes see very serious movement disorders as an unwanted effect- drugs that have muscarinic antagonistic activity seem to avoid this problem

may be useful to develop subtype selective allosteric modulators
-difficult to do as the sites of muscarinic receptors don’t differ much between receptor subtypes but may be possible to develop allosteric modulators of individual subtypes
-allosteric site on muscarinic receptors is much less conserved so it may be a viable therapeutic approach

57
Q

antipsychotics : dirty drugs

A

dopamine D2 antagonists/ partial agonists
-actions at many different receptor types
-lack of selectivity = side effects

dirty nature may also give rise to therapeutic benefits
e.g. actions at 5HTR

58
Q

common side effects of antipsychotics

A

extrapyramidal effects (esp in older)
galactorrhea
cognitive impairment
sedation
weight gain
anti-muscarinic effects

59
Q

what are extrapyramidal effects? what causes them?

A

Movement disorders

dystonia: involuntary muscle contraction and spasms
tardive dyskinesia: face, body/ both make sudden irregular movements - can be permenant

probably interfering with the function of D2 receptors in the motor striatum

60
Q

what is galactorrhea? what causes it?

A

inappropriate milk production in women who haven’t given birth

tuberohypophyseal D2 receptors inhibit prolactin release. When these are inhibited it causes hyperprolactinemia

61
Q

what causes cognitive impairment (antipsychotics)

A

D2 inhibition in cortex?

effects at other receptors (anti-muscarinic effects probably produce cognitive impairment too

62
Q

why do antipsychotics cause sedation?

A

Histamine H1 antagonism ?

63
Q

why do antipsychotics cause weight gain?

A

H1 and 5HTR antagonism?

64
Q

what are anti-muscarinic side effects?

A

dry mouth, blurred vision, memory problems (cog impairment), cardiac problems

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