Antipsychotics Flashcards
Four positive symptoms of psychosis
Anhedonia, hallucinations, bizarre behaviour, disorganised thoughts/incomprehensible speech
Five negative symptoms of psychosis
Amotivation, anhedonia, “stuntedness”, poverty of speech, asociality,
Why do we suspect a genetic influence on psychosis risk?
1st degree relatives: 10% chance
identical twins: 50% chance.
The dopamine theory is strengthened by the effectiveness of D2 receptor antagonists. What conversely supports the theory?
D2 agonists like apomorphine or amphetamines or levodopa bring symptoms on.
You start a young male on a first gen antipsychotic. What do you tell him about his chances of responding vs. trying something else?
About 30% of people don’t respond to 1st gen antipsychotics.
What do 1st gen antipschotics famously NOT do?
Help negative symptoms.
What other theories cover aspects of psychosis?
Glutamate theory (psychosis = not enough glutamate) Seratonin hypothesis (psychosis = too much seratonin)
What do the 1st gens end in?
That older toy is the dol you do operations on. 1st gen’s are nastier, they’re like a xena of antipsychotics. Lucky I’m typing because my pen ink can get to thick and I can’t pour out my soul.
- azine
- operidol
- penthixol
What do the first gen drugs end in?
azine
operidol
penthixol
What are the seven 2nd gen antipsychotics .
Keeps you quite. I’m gonna sulk at the parade. Say “the president” in a French accent.
clozapine, aripiprazole, respiradone, olanzapine,
ziprazadone, amisulparide, quetiapine
What are the seven second gen antipsychotics
clozapine, olanzapine, respiridol, aripiprazole, quetiapine, zipresadone, imasulpiride
What makes second gen better? Four things (one’s just a feature)
efficacy for resistant patients
efficacy against negative symptoms
fewer extrapyramidal side effects (and prolactin secretion)
different receptor affinity profile
Four blockades characteristic of antipsychotics in general (one’s not under a blockade heading though)
Alpha
histamine
5HT
antimuscarinic (atropine-like)
What are the associated side effects of: antimuscarinic alpha blockade histamine blockade seratonin blockade
blurred vision, dry mouth, constipation, urinary retention
postural hypertension (peripheral hypotension)
sedation
weight gain
Which of the blockade-heading side effects show tolerance after a short while.
sedative
hypotension
Dopamine inhibits _______ in the _________ system, preventing lactation.
prolactin secretion; TUBEROFUNDIBULAR
What are the four idiosyncratic reactions to antipsychotics
jaundice and blood stuff, antipsychotic malignant syndrome, urticaria
bonus: blood stuff is leukocytopaenia and agranulocytosis
what is antipsychotic malignant syndrome?
an idiosyncratic side effect of antipsychotics.
Bonus: stiff muscles mixed with hypertension and confusion.
ANTIPSYCHOTICS: what are the two brain structures you MUST remember?
Bonus: what’s the lactation one?
mesolimbic (antipsychotic effects) substantia nigra (extrapyramidal effects)
tuberofundibular (lactation)
Where are the antipsychotic effects created in the brain?
mesolimbic
where are the extrapyramidal side effects created in the brain?
nigrostriatal pathway
What is the significance of the mesolimbic system in antipsychotic therapy?
That’s where the antipsychotic dopamine reduction occurs.
What is benztropine and why might you give it alongside an antipsychotic?
It’s an anticholinergic - helps restore some ACh/DA balance in the striatum and reduce extrapyramidal effects.
2nd gen have higher affinities for ACh receptors. What’s the advantage here?
Lower extrapyramidal effects.
What are the early EPSs antipsychotics? Tell me in order of appearance after dosing:
hours-days
weeks
acute dystonias - postural and facial spasms
laryngeal spasm can be life threatening
akithisia - almost restless leg syndrome
Which suptype of EPS can be life threatening?
laryngeal spasming in acute dystonia
What is the long term mega EPS?
When do we expect it to usually occur?
TARDIVE DYSKINESIA
Darting limbs and mega mouth/jaw spasms.
Often precipitates on discontinuation.
Because of upregulated D2 receptors and chronic [inhibitory] D1 block.
What’s behind the tardive diskinesia?
“disuse supersensitivity”
Why would more rapidly dissociating drugs have lower EPS?
More accommodating of brief surges of DA (e.g. in the striatum).
Which 2nd gen is also a partial D2 agonist?
Aripiprazole.
Partial agonism in the mesocortical pathway helps prevent negative symptoms and in the striatum it helps prevent EPS.
