Biological Bases of Behavior and Psychopharmacology
What this domain tests
This domain tests whether you understand mechanisms, expected effects, and adverse effects well enough to recognise them clinically and coordinate with psychiatry - not to prescribe.
Core rules
- Know the major systems: dopaminergic pathways in psychosis and reward, serotonergic modulation, GABAergic inhibition, glutamatergic excitation, and HPA-axis stress regulation.
- SSRIs and SNRIs are first-line for many depressive and anxiety disorders; benefit usually emerges over two to four weeks; short half-life agents produce discontinuation syndromes if stopped abruptly.
- Lithium has a narrow therapeutic index, with maintenance levels commonly around 0.6–1.0 mmol/L; toxicity risk rises with dehydration, NSAIDs, ACE inhibitors, and thiazides. Monitor renal and thyroid function.
- Atypical antipsychotics require metabolic monitoring: weight, waist, glucose, lipids. Clozapine requires regular blood counts because of agranulocytosis risk.
- Distinguish akathisia from worsening anxiety, and drug-induced parkinsonism from depression with psychomotor slowing.
Worked example
A patient stable on lithium takes ibuprofen for back pain and presents with coarse tremor, vomiting, ataxia, and confusion. Reasoning: NSAIDs reduce renal lithium clearance, so this is suspected lithium toxicity. Action: hold the lithium, arrange an urgent serum level and renal function, ensure hydration, and contact the prescriber. The psychological point is that a new physical symptom in a patient on lithium is a medical question first.
Traps that cost marks
Assuming a psychologist adjusts doses; raising an antipsychotic because akathisia was read as agitation; forgetting over-the-counter and herbal interactions such as St John's wort; and missing serotonin syndrome's triad of autonomic instability, clonus, and altered mental state.