Pharmacology - An introduction to Psychopharmacology Flashcards
chloropromazine, haloperidol, sulpride, clopixol and fluphenazine are examples of what
a.first generation antipsychotics (typical)
b.second generation antipsychotics (atypical)
a.first generation antipsychotics (typical)
lurasidone,olanzapine, quetiapine, risperidone, aripiprazole, amisulpride and clozapine are examples of what
a.first generation antipsychotics (typical)
b.second generation antipsychotics (atypical)
what causes positive symptoms in schizophrenia (positive symptoms – any change in behaviour or thoughts, such as hallucinations or delusions)
a.overactivity of the mesolimbic pathway
b.underactivity of the mesolimbic pathway
c.mesocortical pathway dysfunction
a.overactivity of the mesolimbic pathway
what causes the negative symptoms of schizophrenia
negative symptoms – where people appear to withdraw from the world around then, take no interest in everyday social interactions, and often appear emotionless and flat
a.overactivity of the mesolimbic pathway
b.underactivity of the mesolimbic pathway
c.mesocortical pathway dysfunction
c.mesocortical pathway dysfunction
antipsychotics are antagonists of the receptors for which neurotransmitter
a. GABA
b.dopamine
c.glutamate
d.5HT
b.dopamine
antipsychotics are antagonists to which dopamine receptor
a.D1
b.D2
c.D3
d.D4
e.D12
b.D2
ANTIPSYCHOTICS ARE ……………….. to D2 dopamine receptors
a.agonists
d.antagonists
d.antagonists
which schizophrenia symptoms are improved by antipsychotics
a.positive symptoms
b.negative symptoms
a.positive symptoms
psychotic symptoms eg. hallucinations and delusions
prolactin elevation as a side effect of antipsychotics is due to dopamine antagonism in which area
a.nigrostriatal tract
b.corticospinal tract
c.HPA axis
d.tuberoinfundibular system
d.tuberoinfundibular system
extra pyrimidal side effects of antipsychotics are mediated by dopamine antagonism at which area
a.nigrostriatal tract
b.corticospinal tract
c.HPA axis
d.tuberoinfundibular system
a.nigrostriatal tract
acute dystonia, parkinsonism, akathisia and tardive dyskinesia are examples of extra pyrimidal side effects of antipsychotics these are due to dopamine antagonism in which area
a.nigrostriatal tract
b.corticospinal tract
c.HPA axis
d.tuberoinfundibular system
a.nigrostriatal tract
akathisia
inability to keep still
metabolic side effects are more common with which type of antipsychotics
a.first generation - typical
b.second generation - atypical
b.second generation - atypical
which of these drugs is most likely to have metabolic side effects
a. quetiapine
b.chloropromazine
c.haloperidol
d.sulpride
e.clopixol
a. quetiapine
increased risk with second gen especially quetiapine, olanzapine, clozapine
all the rest are first gen
which of these drugs is most likely to have metabolic side effects
a. olanzapine
b.chloropromazine
c.haloperidol
d.sulpride
e.clopixol
a. olanzapine
increased risk with second gen especially quetiapine, olanzapine, clozapine
all the rest are first gen
which of these drugs is most likely to have metabolic side effects
a.clozapine
b.chloropromazine
c.haloperidol
d.sulpride
e.clopixol
a.clozapine
increased risk with second gen especially quetiapine, olanzapine, clozapine
all the rest are first gen
3 metabolic side effects of antipsychotics …
weight gain
dyslipidaemia
type 2 diabetes
which metabolic side effect of antipsychotics is associated with 5HT2C, 5HT1A and H1 antagonism
a.weight gain
b.dyslipidaemia
c.type 2 diabetes
a.weight gain
dyslipidaemia - associated with weight gain and lifestyle factors
type 2 diabetes- associated with lifestyle, weight gain and direct effects
true or false people with schizophrenia have a normal life expectancy
a.false
reduced life expectancy
due to..
negative symptoms of illness
lifestyle factors
less likely to attend GP
less likely to be offered interventions
SSRIs, SNRIs, NASSAs , MAOIs and TCAs are alll examples of what
a.antipsychotics
b.anti depressants
b.anti depressants
SSRIs
selective serotonin reuptake inhibitors
SNRIs
serotonin and noradrenaline reuptake inhibitors
NASSAs
Noradrenergic and specific serotinergic antidepressants
MAOIs
monoamine oxidase inhibitors
TCAs
tricyclic antidepressants
SSRIs stop reuptake of serotonin into which neurons
a.pre synaptic
b.post synaptic
a.pre synaptic
problems with the monoamine hypothesis
(depression caused by a functional deficiency of monamines - serotonin and noradrenaline , derived from observation that antidepressants increased levels of serotonin and nor.)
antidepressants increases availability of monoamines immediately , however onset of action is delayed 2-3 weeks
evidence for serotonin in depression is conflicting
more detailed knowledge about neurotransmitter systems in the brain
novel antidepressants do not impact serotinergic systems eg ketamine