Occupational Medicine Core Clinical Practice
What this domain tests
Core clinical practice asks you to reason from exposure to health effect, and back again. Candidates must know the main occupational lung diseases (silicosis, coal workers' pneumoconiosis, asbestos-related disease, occupational asthma, hypersensitivity pneumonitis, COPD from dusts), noise-induced hearing loss, hand-arm vibration syndrome, musculoskeletal and work-related stress presentations, occupational dermatoses, and the classic toxicology of lead, mercury, solvents, pesticides and carbon monoxide. Be comfortable with the hierarchy of exposure controls and with surveillance: spirometry, audiometry, biological monitoring and skin checks.
Concepts to hold
Understand latency: pneumoconioses and asbestos-related malignancy take decades, occupational asthma often takes months to years of sensitisation, acute irritant effects are immediate. Know dose-response and the difference between sensitising and irritant asthma. For noise, distinguish temporary threshold shift from permanent 4 kHz notch and know that hearing loss is sensorineural. For vibration, know the Stockholm Workshop scale logic and that vascular and neurological components differ.
Traps
Questions love the plausible-but-wrong attribution: blaming a pre-existing condition on work without temporality, or attributing a disease to the wrong exposure (e.g. asbestos vs silica vs coal). Watch for 'most likely' wording, which rewards the commonest cause, not the most dramatic. Remember that a normal examination does not exclude early occupational disease, and that biological monitoring measures exposure or body burden, not always health effect.
Worked rule of thumb
For any suspected occupational disease, run the sequence: is there a recognised causal agent, was exposure credible in dose and timing, does the clinical picture fit, and is there a temporal relationship with work? If all four line up, attribute; if one fails, investigate further rather than dismissing.
Example
A 55-year-old with progressive dyspnoea and bilateral upper-zone fibrosis and a history of sandblasting: think silicosis, and remember increased TB risk.