• Noem ‘n voorbeeld van elk van die drie fenotiasien-subfamilies en sê hoe hulle van mekaar verskil in terme van potensie en newe effekte?
• Watter reseptore word veral deur die tipiese antipsigotiese middels blokkeer?
• Hoe verskil die werkingsmeganisme van die atipiese middels van die van die tipiese middels?
• Watter van die reseptore wat blokkeer word deur die ouer middels verminder die risiko vir ekstrapiramidale newe effekte?
• Watter van die ouer middels het ‘n hoë insidensie van ekstrapiramidale effekte?  Wat is die rede?
• A.g.v. watter reseptorblokkade het die alifatiese groep middels ‘n hoë insidensie van outonome newe effekte?

1) Aliphatic side chain/ compounds (chlorpromazine) and piperidine side chain/ compounds (thioridazine) least potent. Side effects= weight gain, severe sedation, anti-cholinergic effects, a-lytic effects, cardiotoxic (little EPS). Piperazine side chain/ compounds (fluphenazine, perphenazine, trifluoperazine, prochlorperazine) most potent. Side effects= weak anti-cholinergic effects, weak a-lytic effects, less sedation, less cardiovascular effects (high EPS).

2+3) Typical= Blocks Mesolimbic D2 receptors. Atypical= Blocks 5-HT2A receptors more than D2.

4) High D2 binding= high EPS (high affinity= high potency=high EPS). Low/weak D2 binding (low affinity for D2 thus large amount administerted)= low EPS

5) Piperazine side chain/ compounds (fluphenazine, perphenazine, trifluoperazine, prochlorperazine) most potent. (high affinity= high potency=high EPS).

6) Aliphatic side chain/ compounds (chlorpromazine), low potency, Low/weak D2 binding (low affinity for D2 thus large amount administerted)= low EPS