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Q1: Definition and the primary/secondary distinction (3 min)
Examiner: Define Raynaud phenomenon and distinguish primary from secondary.
Expected answer:
- Raynaud phenomenon is episodic, REVERSIBLE vasospasm of the digital arteries and cutaneous arterioles, triggered by cold or emotional stress, producing the classical TRIPHASIC colour change: WHITE (ischaemia) → BLUE (cyanosis) → RED (reperfusion hyperaemia).
- PRIMARY (Raynaud disease): young (onset under 30), female, bilateral and symmetric, normal nailfold capillaries, ANA negative, no tissue loss (no ulcers, no pitting scars), family history; benign, functional.
- SECONDARY (Raynaud phenomenon): older onset (over 30), asymmetric/unilateral, abnormal nailfold capillaries (dilated loops, dropout), positive ANA, digital ulcers/pitting scars/gangrene, associated with a systemic disease (systemic sclerosis is the commonest cause).
Q2: Investigations (3 min)
Examiner: How do you investigate a patient with Raynaud phenomenon?
Expected answer:
- The diagnosis is CLINICAL. Investigations aim to separate primary from secondary and to screen for underlying disease.
- Nailfold capillaroscopy (or bedside dermoscopy with immersion oil at the proximal nailfold) — the single most useful discriminator: normal in primary, abnormal (dilated tortuous loops, bushy capillaries, avascular dropout) in secondary, and predictive of evolution to systemic sclerosis.
- Autoantibodies: ANA (screen for connective tissue disease); if positive, anti-centromere (limited cutaneous SSc/CREST), anti-Scl-70 / anti-topoisomerase I (diffuse SSc), anti-RNA polymerase III (renal crisis), anti-U1-RNP (MCTD).
- Routine bloods: FBC, ESR/CRP (raised in inflammatory/secondary), U&E, LFTs, TFTs (autoimmune thyroid association), CK (myositis), immunoglobulins, complement/cryoglobulins if indicated.
- Organ screen in suspected systemic sclerosis: pulmonary function tests (DLCO falls early — ILD/PAH), high-resolution CT chest, echocardiogram (pulmonary arterial hypertension), ECG.
Q3: Management (3 min)
Examiner: Outline the management of Raynaud phenomenon.
Expected answer:
- General (all patients): cold avoidance, hand and whole-body warming (gloves, heated clothing), smoking cessation, reduce caffeine/stress, and AVOID beta-blockers and decongestants (unopposed α vasoconstriction worsens attacks).
- PRIMARY: reassure (benign); lifestyle alone often suffices; if symptomatic, a calcium-channel blocker is first-line — nifedipine modified-release or amlodipine. Alternatives: losartan, fluoxetine.
- SECONDARY: treat the underlying disease AND aggressive vasodilation — high-dose CCB, add a PDE-5 inhibitor (sildenafil, tadalafil), topical nitrates; for severe/refractory disease IV prostacyclin (iloprost) in hospital; the endothelin-receptor antagonist bosentan reduces the number of NEW digital ulcers in systemic sclerosis.
- Critical ischaemia / acute severe attack: admit, warm, IV iloprost, analgesia, wound care, treat the underlying disease; botulinum toxin injection or digital sympathectomy for refractory cases; amputation for irreversible necrosis.
Q4: Complications, prognosis and follow-up (2 min)
Examiner: What complications can occur, and what is the prognosis?
Expected answer:
- Complications: digital ulcers (painful, slow to heal, become infected), pitting scars (digital pulp 'ice-pick' scars from prior microinfarction), critical ischaemia with gangrene requiring amputation (mainly severe secondary Raynaud), sclerodactyly and contractures.
- PRIMARY prognosis: benign; attacks reduce with age and warming; normal life expectancy.
- 5-20% of patients initially labelled 'primary' evolve into a connective tissue disease — most often systemic sclerosis within 2-5 years; abnormal nailfold capillaroscopy plus positive ANA identifies this at-risk subgroup.
- SECONDARY prognosis is driven by the underlying disease (systemic-sclerosis ILD/PAH drive mortality); early nailfold + autoantibody screening and organ surveillance allow detection before organ disease declares itself.