Regarding the pharmacological properties of antipsychotics, all of the following statements are correct EXCEPT:

Explanation

## Analysis of Antipsychotic Pharmacology ### The Incorrect Statement (Option D) **Key Point:** Aripiprazole is a **partial D2 agonist** — it does NOT selectively act as a dopamine agonist at mesolimbic receptors while blocking dopamine at mesocortical receptors. Its partial agonist activity means it acts as a **functional antagonist** in hyperdopaminergic states (mesolimbic pathway, relevant to positive symptoms) and as a **functional agonist** in hypodopaminergic states (mesocortical pathway, relevant to negative/cognitive symptoms). However, this is a pharmacodynamic consequence of partial agonism at a single receptor type — aripiprazole does NOT have differential receptor selectivity between these two pathways. The description in Option D incorrectly implies pathway-specific agonist vs. antagonist receptor selectivity, which is mechanistically inaccurate. ### Why the Other Statements Are Correct | Statement | Mechanism | Citation | |-----------|-----------|----------| | **Option A: FGA D2 affinity** | FGAs (e.g., haloperidol) generally have higher D2 receptor binding affinity than most SGAs; the key additional distinction is slower dissociation kinetics ("fast-off" theory for SGAs) | KD Tripathi 8e Ch 13 | | **Option B: Risperidone & prolactin** | Risperidone has high D2 blockade in the tuberoinfundibular pathway; quetiapine has lower D2 occupancy → less prolactin elevation | Harrison 21e Ch 397 | | **Option C: Clozapine & tardive dyskinesia** | Clozapine's rapid dissociation from D2 receptors ("fast-off" kinetics) + low striatal D2 occupancy + 5-HT2A blockade = markedly reduced risk of tardive dyskinesia vs. haloperidol | KD Tripathi 8e Ch 13 | ### Clinical Pearl **High-Yield:** Aripiprazole is a **partial D2 agonist** (and partial 5-HT1A agonist + 5-HT2A antagonist). Its net effect depends on the prevailing dopamine tone in a given pathway — functional antagonism where dopamine is high (mesolimbic), functional agonism where dopamine is low (mesocortical) — but this is a consequence of partial agonism, NOT differential receptor selectivity between pathways. This distinction is frequently tested in NEET PG pharmacology (KD Tripathi 8e, Ch 13).