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Q1 — Definition and classification (2 min)
Examiner: Define a specific phobia and list the DSM-5 subtypes.
Candidate: A specific phobia is a marked, persistent, excessive or unreasonable fear of a specific object or situation; exposure provokes an immediate anxiety response; the fear is out of proportion to the actual danger, is recognised as excessive (in adults), leads to avoidance or endurance with dread, lasts at least six months, causes impairment, and is not better explained by another mental disorder. The five DSM-5 specifiers are: animal; natural environment; blood-injection-injury; situational; and other.
Q2 — A distinguishing feature (2 min)
Examiner: Which phobia is physiologically unique, and why does it matter?
Candidate: Blood-injection-injury phobia. Unlike every other phobia, where the autonomic response is sympathetic (tachycardia, sweating, tremor), BII phobia produces a biphasic response: a brief initial sympathetic surge followed by vagal overdominance via the Bezold-Jarisch reflex, causing bradycardia, hypotension and vasovagal syncope. It matters because (a) the first-line treatment is APPLIED TENSION, not relaxation — relaxation would worsen the hypotension and faint; and (b) it is highly familial, with heritability around 64 percent.
Q3 — Treatment of choice (3 min)
Examiner: A 19-year-old man has a disabling spider phobia. Walk me through the evidence-based treatment.
Candidate: The treatment of choice is cognitive behavioural therapy with graded in-vivo exposure, which is often curative. The steps are: build a fear hierarchy from least to most anxiety-provoking spider-related stimuli; begin with lower items — pictures, videos, imagined scenes — and progress to real spiders in a graded fashion, remaining with each stimulus until anxiety falls by at least half (habituation); add cognitive restructuring of catastrophic beliefs. A single 2–3 hour intensive (one-session) exposure can cure a simple animal phobia. Flooding — intense immediate exposure — is effective but more distressing with higher dropout. Pharmacotherapy is rarely needed: SSRIs only if severe or comorbid, benzodiazepines should be avoided because they blunt amygdala activation and impair extinction learning, and propranolol only helps performance-related somatic symptoms.
Q4 — Agoraphobia and stepped care (2 min)
Examiner: Define agoraphobia and outline NICE stepped care.
Candidate: Agoraphobia is marked fear or anxiety about two or more of five situations — public transport, open spaces, enclosed spaces, standing in line or in a crowd, and being outside the home alone — because escape might be difficult or help unavailable; it is cued, avoided or endured with dread, out of proportion, persistent for six months, and impairing, and not better explained. DSM-5 explicitly allows agoraphobia with or without a history of panic disorder. NICE stepped care: step 1 — assessment, education, active monitoring; step 2 — low-intensity guided self-help and psychoeducation; step 3 — high-intensity CBT with in-vivo exposure and/or an SSRI (sertraline first-line), with home-based or intensive delivery and a home treatment team for the housebound.
Q5 — A corner question (1 min)
Examiner: What is the molecular basis of fear extinction, and how is it exploited therapeutically?
Candidate: Extinction is not erasure of the fear memory but NEW LEARNING mediated by NMDA-receptor-dependent potentiation in the infralimbic prefrontal cortex, which inhibits amygdala output. Exposure therapy leverages this — repeated safe contact with the feared cue allows the prefrontal cortex to encode a safety memory. D-cycloserine, a partial NMDA agonist, has been studied as augmentation to accelerate extinction during exposure, with mixed evidence. Benzodiazepines, by dampening amygdala activation, impair this NMDA-dependent learning — the mechanistic reason they are discouraged during exposure-based treatment.