Antipsychotics Flashcards Preview

Neuro Block 5 > Antipsychotics > Flashcards

Flashcards in Antipsychotics Deck (24)
Loading flashcards...

Why are Psychosis and parkinsonism two sides of the same coin?

they stem from opposite issues with dopamine

treatment of psychois involves blocking DA receptors and has parkinsonism as a negative effect

Parkinsonisn treatment involves increasing DA levels and has psychosis as a negative effect


What is the dopamine hypothesis for schizophrenia?

psycosis is due to a hyperactive dopaminergic system, particularly with increased DA production and increased acvity at the D2 receptor subtype


What is the evidence supporting the dopamine hypothesis for schizophrenia?

1. amphetamines work by causing the brain to produce more dopamine and have been shown to produce psychotic-like symptoms

2. 1st gen anti-psychotics like haloperidol act by blocking dopamine receptors in the brain


What are the two weaknesses of the dopamine hypothesis for schizophrenia?

1. amphatamines only mimic the POSITIVE symptoms of schizophrenia

2. first generation antipsychotic drugs are only effective on the POSITIVE symptoms of the disease


What are the four DA pathways in the brain?

1. mesolimbic

2. mesocortical

3. nigrostriatal

4. tuberoinfundibular


Where does the mesolimbic pathway go to?

What symptoms of schizophrenia doe sit mediate?

it runs form the tegmentum (VTA) to the nucleus accumbens in the limbic system

it's the proposed area of the brain that mediates the positive symptoms of schizophrenia

If you block the D2 DA receptors in this area you have a decrease in the positive symptoms


Where does the mesocortical pathway go? What symptoms of schizophrenia does it mediate?

it runs form the tegmentum to the frontal and limbic cortices

proposed to mediate the negative (and maybe cognitive) symptoms of schizophrenia



Oddly enough, decreaseing DA levels or activity in the mesocortical pathway may _______ negative symptoms of schizophrenia.

What is this likely due to?

it actually produces or worsens the negative symptoms!!

It's probably due to an increase in 5HT, which inhibits DA release here

this explains why negative symptoms are unaffected or worsened by antipsychotics that only block DA receptors


Why are 2nd generation antipsychotics more beneficial in treating negative symptoms?

they block both DA and 5HT receptors, not just DA receptors


Where does the nigrostriatal pathway run?

What is the effect on this area form the first generation antipsychotics?

it runs form the substantia nigra to the basal nuclei - they regulate posture and voluntary movement

the first gens block DA receptors in the stratum, so you get a parkinsonism like syndrome. SGAs are less likely to produce these


Where does the tuberoinfundibular pathway run? How is this affected by FGAs?

it runs from the hypothalamus to the anterior pituitary, where DA inhibits prolacting secretion

With FGAs, female patients can experience galactorrhea, amenorrhea and sexual dysfunction


FGAs block what receptors? What symptoms are they good for?

they all block D2 receptors in the limbic system

most effective against positive symptoms

(may also affect muscarinic, adrenergic, and histaminergic receptors too)


What receptors are blocked by the second gen antipsychotics?

DA and 5HT


Why is affecting both DA and 5HT receptors better than just DA?

presynaptic 5HT receptors regulate DA release

- activating them blocks the release of DA

-Inhiting them increases the release of DA


Why do the SGAs have fewer extrapyramidal symptoms than the FGAs?

they block 5HT receptors in the stratum, so you get increased DA release in the nigrostratal pathway, counteracting the DA receptor blockade and avoiding the parkinsonism symptoms


Why do SGAs have better action against the negative symptoms than the FGAs?

they actually increase dopamine release int he mesocortical pathway by binding to teh 5HT receptors

this improves negative symptoms


If SGAs help the negative symptoms by increasing release of DA, how can they also help the positive symptoms if excess dopamine is causing the positive symptoms in the firs tplace?

Oddly enough, in the mesolimbic pathway (which mediates the postivie symptoms), 5HT has less of an effect on DA release than in the other 3 pathways

this means that SGAs binding to 5HT does NOT increase DA release here and they stil lbind to DA receptors like the FGAs do, so they still work for the positive symptoms


What are the negative effects of the SGAs?

weight gain (most frequently with clozapine and olanzapine)

increased incidence of type 2 diabetes

increased lipid levels - associated with onset of myocarditis and cardiomyopathies


How is tardive dyskinesia different from the extrapyramidal symptoms?

EPS can dissipate when drug is discontinued

tardive dyskinesia may be irreversible or take years to go away


What is the only antipsychotic where the incience of tardive dyskinesia is 0?


(so it's the drug of choice in schizophrenia patients with mod to severe dyskinesias)


What is the most common reason for poor compliance with the SGAs?

weight gain

(clozapine and olanzapine are the worst for this, ziprasidone and aripiprazole are better)


At what point does the American DIabetes Association recommend a change in antipsychotic drugs to avoid type 2 diabese?

when a patient gains more than 5% of baseline weight while on the SGA


Which group is more at risk for developing tardive dyskinesia?


in FGAs is may be as high as 53%

in SGAs, about 5%