schizo Flashcards

1
Q

what is defining features in psychotic disorders

A

patients experience delusions or hallucinations but have lost insight into condition

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2
Q

how are psychotic disorders treated

A

all psychotic disorders are treated with neuroleptics (antipsychotics)

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3
Q

what are positive/ negative symptoms of schizo

A

positive (caused by excess excitatory neurotransmission): abnormal thoughts, perceptions, language and behaviour; including delusions, hallucinations and catatonic behaviour

negative (excess inhibitory neurotransmission): restrictions in range and intensity of emotional expression, communication, body language and lack of interest in activities that were once enjoyable

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4
Q

what are possible neuronal origins of scz

A

different theories:

excessive 5HT transmission in brain; all drugs which activate 5HT (2A/2C) receptors are hallucinogenic e.g LSD

excessive dopaminergic transmission in brain:

all neuroleptic drugs show some degree of D2 antagonism, however no good evidence for overactive DA function in schizo

amphetamine induced psychosis strongly resembles schizo, amphetamine causes increase in concentrations in dopamine, it is possible that dopamine simply mediates effects/ symptoms caused by other malfunctions

glutamate is also implicated:
NMDA receptor antagonists such as ketamine and phencyclidine produce symptoms very similar to schizo, phencyclidine is regarded as best research tool in animal models of schizo

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5
Q

what are neuronal targets of schizo treatment

A

it is generally assumed neuroleptics act primarily by antagonising the action of dopamine in its mesolimbic and mesocortical pathways, these are targets for drug action

neuroleptics also disrupt other dopaminergic pathways in brain

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6
Q

what are side effects of all neuroleptics

A

extrapyramidal side effects that emulate parkinsonism (pseudo-parkinsonism) which include release of prolactin

older/typical neuroleptics tendency to produce these side effects increases with antipsychotic potency and selectivity for D2 antagonism
however there are a few exceptions

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7
Q

what are examples of typical neuroleptics

A

most neuroleptics are typical neuroleptics
they are:

most phenothiazines e.g chlorpromazine

thioxanthines e.g flupenthixol

butyrophenones e.g haloperidol

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8
Q

what are advantages/disadvantages of typical neuroleptics

A

advantages: relieve positive symptoms, have sedative effect (may be disadvantage)

disadvantages:
ineffective against negative symptoms

extrapyramidal side effects such as dystonia and akathisia,

tardive dyskinesia (repetitive stereotyped movements which can endure after drug treatment has stopped)

hyperlactinaemia: leading to galactorrhea, and amenorrhea (reduced gonadal function resulting in impotence or absence of menstruation)

aplastic anaemia

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9
Q

what is pharmacological profile of typical neuroleptics

A

antagonists of D2 receptors, H1 receptors, muscarinic receptors and alpha adrenoceptors

specific binding pattern of drug to each receptor determines efficacy and side effects

binding to H1 receptors could explain sedative effects

antagonism of alpha 1 causes hypotension

muscarinic antagonism produces anti cholinergic effects but can also help relieve pseudo parkinsonism caused by dopamine antagonism

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10
Q

what are examples of atypical neuroleptics

A

dibenzazepine derivates e.g: clozapine

benzisoxazole derivatives e.g risperidone

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11
Q

what are advantages and disadvantages of atypical neuroleptics

A

advantages: relieve both positive and negative symptoms, can relieve psychosis resistant to typical neuroleptics,

much lower incidence of extrapyramidal side effects and tardive dyskinesia than typical neuroleptics

disadvantages:
dribbling

agranulocytosis (clozapine)

weight gain especially of systematic fat which leads to diabetes and CV disease

concern in fat increase is regarded by some as more problematic than extrapyramidal side effects associated with typical neuroleptics in terms of morbidity and patient compliance

prolongation of cardiac QT interval

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12
Q

what is pharmacological profile of atypical neuroleptics

A

clozapine:

clozapine shows relatively weak binding to D2 receptors, although it is still effective suggesting D2 antagonism may not be key factor

clozapine is 5HT 2a/2c receptor antagonist, could contribute to antipsychotic effect, also may account for increase in fat

weak partial agonist of 5HT1a receptors, leads to increase of dopamine from mesocortical neurones projecting to frontal cortex, could account for relief of negative symptoms

muscarinic and alpha 2 antagonism: these actions are thought to contribute to the lower incidence of extrapyramidal side effects

atypical neuroleptics only occupy 30% of D2 receptors (weak antagonism)

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13
Q

give and example of a 3rd gen neuroleptic and its effects on receptors

A

aripiprazole is a 3rd gen neuroleptic

D2 partial agonist (high affinity but low intrinsic activity) so may have physiological antagonistic effects

5HT1a partial agonist

5HT2a weak agonist

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14
Q

what are advantages and disadvantages of a 3rd gen neuroleptic

A

advantages:
few extrapyramidal side effects (no difference from placebo)

little weight gain and few CV abnormalities

safe in overdose

disadvantages:

hyperprolactinaemia
hypercholesterolaemia
akathisia

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