How do typical and atypical antipsychotics differ in mechanism and adverse effects?

• A. Typical antipsychotics primarily block dopamine D2 receptors and have a higher risk of extrapyramidal symptoms; atypical antipsychotics block D2 and 5-HT2A receptors, with lower EPS risk but higher metabolic side effects.
• B. Typical antipsychotics block only 5-HT2A receptors; atypical block only D2 receptors and have less metabolic risk.
• C. Both types block D2 receptors but atypicals cause more EPS.
• D. Typical antipsychotics primarily enhance dopamine signaling; atypicals suppress dopamine globally.

Answer: (C)

At the heart of their differences is receptor targets and how that shapes both benefits and side effects. Typical antipsychotics mainly block dopamine D2 receptors, especially in pathways tied to psychosis, which helps reduce positive symptoms. But this same D2 blockade in motor circuits leads to extrapyramidal symptoms such as dystonia, akathisia, parkinsonism, and can raise prolactin levels.

Atypical antipsychotics also block D2 receptors, but they add strong antagonism of 5-HT2A receptors. This serotonin blockade modulates dopamine release in several brain regions, which lowers the risk of movement-related side effects and can help with negative symptoms and mood. The trade-off is a higher likelihood of metabolic side effects like weight gain, dyslipidemia, and insulin resistance with many of these agents.

So the best synthesis is that both classes block D2, but atypicals’ additional 5-HT2A antagonism reduces extrapyramidal symptoms while increasing metabolic risks. The other statements mischaracterize the primary targets or the direction of the side-effect profiles.