SCA practice case · Video consultation
“I get these sudden terrifying attacks — pounding headache, racing heart, drenching sweats — and my blood pressure’s all over the place”
The candidate brief
This is what you would read in the 3-minute window before the patient connects. Read it once, note two or three hypotheses and one thing you must not miss, then stop.
Patient
Dominic Vasquez · 39 years · male
Setting
Video consultation, with lying and standing BP and the examination (heart, thyroid, fundi) arranged face to face — paroxysmal symptoms with labile hypertension.
Past history
- Labile raised BP at nurse checks
Medication
- None recorded
Allergies
None recorded
Recent notes
Recurrent attacks of headache, palpitations, sweating and pallor for minutes; told it is anxiety.
Reason for contact
“It doesn’t feel like anxiety.”
Practise this case
The full case is in the Hot Seat with the Gold plan. You get a 12-minute timer, a role-player script with facts released only when asked, examiner checkpoints by the three RCGP domains, a model consultation and the guidance behind it.
What this case tests
Show the learning points (spoiler: read after you have practised)
PHAEOCHROMOCYTOMA (a catecholamine-secreting tumour, usually of the adrenal medulla) classically causes PAROXYSMS of the triad — pounding HEADACHE, PALPITATIONS and drenching SWEATING — with pallor, tremor, anxiety/sense of doom, and HYPERTENSION that may be paroxysmal or sustained and is often labile/resistant; the episodic triad with labile BP, especially in a younger patient, should raise the possibility. Consider phaeochromocytoma (and other secondary causes of hypertension) in paroxysmal symptoms, RESISTANT hypertension, YOUNG-ONSET hypertension, hypertensive crises, or a hereditary syndrome, rather than assuming essential hypertension or anxiety — it is rare but important ("the zebra") because it is potentially curable and dangerous if missed. Distinguish the common mimics: anxiety/panic disorder (overlapping symptoms, but phaeochromocytoma has marked objective hypertension/pallor and a stereotyped triad), hyperthyroidism (check TFTs), arrhythmia (ECG), hypoglycaemia, drugs/stimulants and alcohol withdrawal. Investigate biochemically first — plasma free METANEPHRINES or 24-hour urinary fractionated metanephrines (Endocrine Society 2014, international) with TFTs, U&E, glucose/HbA1c and ECG — and, if positive, the specialist images (CT/MRI of the adrenals ± functional imaging) to localise the tumour, with referral to endocrinology (NICE NG136: specialist evaluation for secondary causes under 40; same-day referral if clinic BP is 180/120 mmHg or higher with suspected phaeochromocytoma). A key management principle (specialist-led) is that ALPHA-blockade must precede BETA-blockade, because giving a beta-blocker first or alone can cause unopposed alpha-mediated vasoconstriction and a hypertensive crisis; definitive treatment is surgical removal, which cures most people, though lifelong follow-up is needed because tumours can recur and a minority are malignant; hereditary associations (MEN2, von Hippel-Lindau, NF1, SDH genes) are common, so genetic testing is usually offered and relatives may need screening. The skill is to think of phaeochromocytoma in the paroxysmal-triad/secondary-hypertension patient, test metanephrines, screen mimics and refer — not just label it anxiety.
The guidance behind it
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