First-generation antipsychotics — consultant viva

Station structure

Time: 8–10 minutes. Depth: consultant teaching registrar. Expect named trials, potency map, occupancy teaching, emergency EPS/NMS steps, Carbon TD nuance, and TRRIP — not undergraduate “typicals cause EPS” only.[1][2][3][6][8]

Core questions and model points

1. Define FGA and classify. D2-dominant typical antipsychotics; chemical families (phenothiazines, thioxanthenes, butyrophenones); high vs low potency adverse-effect trade-off.[4]

2. Are SGAs always better? CATIE: perphenazine comparable to several SGAs on effectiveness. CUtLASS: no QoL win for SGAs. EUFEST: FEP — higher haloperidol discontinuation. Leucht NMA: small efficacy differences, large tolerability differences.[1][2][3][4]

3. Mechanism. Striatal D2 occupancy efficacy zone ~65–80%; EPS risk rises near/above ~80%; Kapur–Seeman fast-off contrast with some atypicals; circuit map (mesolimbic vs nigrostriatal vs tuberoinfundibular).[5]

4. Akathisia vs agitation. Barnes scale concept; do not escalate antipsychotic; reduce/switch/treat restlessness.[7]

5. Dystonia and NMS. Parenteral anticholinergic (+ airway if laryngeal); NMS = stop dopamine antagonists, support, ICU.[7]

6. TD. Carbon: higher with FGAs than SGAs; SGAs not zero; AIMS; minimise unnecessary exposure; clozapine if TRS.[6][8]

7. Depot and TRS. Oral tolerability first; oil depot for adherence; TRRIP — do not delay clozapine after two adequate failures.[8]

Examiner traps

• Claiming CATIE proved all FGAs inferior.
• Using EUFEST to ban all FGA use in multi-episode patients.
• Escalating dose for akathisia.
• “SGAs never cause TD.”
• Depot instead of clozapine for clear TRS. [1]

These traps reverse the CATIE/CUtLASS nuance, Carbon TD differential, Barnes akathisia teaching, and TRRIP pathway.[1][2][6][7][8]