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Folio edition · Set in Instrument Serif & Archivo

Psych VivasFoundations — neurotransmitters receptors signalling

Psych Vivas · Foundations — neurotransmitters receptors signalling

Neurotransmitters, receptors and signalling — viva

Fellowship viva on monoamine, GABA, glutamate and ACh systems; GPCR cascades; drug-class mapping; serotonin toxicity vs NMS; delayed antidepressant onset.

clinical
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Target exams

FRANZCPMRCPsychABPNMD-DNB

Target exams

FRANZCPMRCPsychABPNMD-DNB
Prompt
Examiner draws a blank synapse on the whiteboard and says: 'Fill in transmitters, receptors, second messengers, then hang six drug classes and two toxidromes on your diagram.'

Station structure

Time: 8–10 minutes. Depth: consultant teaching registrar. Expect clean definitions, pathway tables, and safe toxidrome discrimination without undergraduate slogans.[1][3]

Core questions and model points

  1. Ionotropic vs metabotropic. Ionotropic = ligand-gated ion channel (GABA-A, NMDA, 5-HT3, nicotinic). Metabotropic = GPCR with second messengers (most monoamine receptors, muscarinic, GABA-B, mGluR).[2][5]

  2. Four dopamine pathways. Mesolimbic efficacy; mesocortical secondary negatives risk; nigrostriatal EPS; tuberoinfundibular prolactin. Version III: striatal dysregulation as final common pathway.[1]

  3. 5-HT clinical map. Name 1A, 2A, 2C, 3 with hooks (anxiolytic cascade teaching; SGA/psychedelic; metabolic/appetite; nausea).[2]

  4. Why SSRIs take weeks. Initiation (SERT block) vs adaptation (receptors, cascades, circuits) — Hyman–Nestler.[3]

  5. BZD mechanism. GABA-A PAM, not direct agonist; dependence/withdrawal as chronic PAM exposure problem.[6]

  6. Glutamate exam hooks. NMDA hypofunction/PCP model of psychosis; ketamine rapid antidepressant cascade language.[5]

  7. Toxidromes. Serotonin toxicity (Hunter, clonus) vs NMS (dopamine hypofunction, rigidity).[4]

Pass criteria

  • Accurate ionotropic/metabotropic distinction.[2]
  • Pathway–side-effect dopamine map correct.[1]
  • Delayed AD onset explained as adaptation, not “levels rising slowly.”[3]
  • Serotonin toxicity vs NMS not confused.[4]
  • At least one non-monoamine system (GABA or glutamate or ACh) used correctly in a clinical example.[5][6]

References

  1. [1]Howes OD, Kapur S The dopamine hypothesis of schizophrenia: version III--the final common pathway Schizophr Bull, 2009.PMID 19325164
  2. [2]Barnes NM, Sharp T A review of central 5-HT receptors and their function Neuropharmacology, 1999.PMID 10462127
  3. [3]Hyman SE, Nestler EJ Initiation and adaptation: a paradigm for understanding psychotropic drug action Am J Psychiatry, 1996.PMID 8561194
  4. [4]Dunkley EJ, Isbister GK, Sibbritt D, et al. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity QJM, 2003.PMID 12925718
  5. [5]Javitt DC, Zukin SR Recent advances in the phencyclidine model of schizophrenia Am J Psychiatry, 1991.PMID 1654746
  6. [6]Soyka M Treatment of Benzodiazepine Dependence N Engl J Med, 2017.PMID 28328330