Basic Sciences Relevant to Psychiatry
What the exam tests
This domain asks you to connect clinical signs to neuroanatomy, neurophysiology, neurotransmitter systems, drug mechanisms and genetic architecture. Expect short vignettes about drug side-effects, lesion effects and inheritance patterns.
Core rules
- Prefrontal and limbic circuits mediate executive function, affect regulation and memory; hippocampal and amygdala dysfunction maps onto memory and fear processing.
- Dopamine: mesolimbic overactivity is linked to positive symptoms; tuberoinfundibular blockade raises prolactin; nigrostriatal blockade causes extrapyramidal signs.
- Serotonin, noradrenaline, GABA and glutamate explain antidepressant, anxiolytic and mood-stabilizer actions; glutamate models inform psychosis research.
- Antipsychotic D2 occupancy around 60-80% is usually therapeutic, while occupancy above about 80% increases extrapyramidal risk.
- Psychiatric genetics is polygenic; heritability is not destiny, and copy-number variants are rare but high-impact.
Worked example
A man with schizophrenia develops breast enlargement and milky discharge after starting risperidone. The reasoning is not 'hormonal imbalance' but dopamine D2 blockade in the tuberoinfundibular pathway, which removes tonic inhibition of prolactin release. Prolactin rises; sexual side-effects and osteoporosis risk follow. Checking prolactin, reviewing the drug and considering a prolactin-sparing agent are appropriate.
Traps that cost marks
Do not confuse potency with efficacy; haloperidol is potent but not more effective than other antipsychotics. Do not attribute all extrapyramidal signs to 'anxiety'. Remember that clozapine's agranulocytosis risk requires blood monitoring, and that CYP interactions can change drug levels without changing dose.