I have a case of systemic sclerosis give me favourite examiner questions and answers ( cut the basic what is your diagnosis kind of questions) like differentials of raynaud phenomenon or diff between acrocynosis and raynaud
Reading File
Reading File
Searching the Web
systemic sclerosis Raynaud phenomenon acrocyanosis differential diagnosis review
Searching PubMed
systemic sclerosis Raynaud phenomenon
Reading File
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Reading File
Finding Sources
Systemic sclerosis viva: high-yield examiner questions with model answers
Use a structured answer: clinical feature -> interpretation -> why it matters. Avoid simply listing signs.
1. “What are the differentials of Raynaud phenomenon?”
Answer:
I would divide them into:
I would divide them into:
-
Primary Raynaud phenomenon
- Young woman, onset usually before 30 years
- Symmetrical episodic attacks
- No ulcers, gangrene, pitting scars, or tissue loss
- Normal pulses, normal nailfold capillaries, negative or low-titre ANA
-
Secondary Raynaud phenomenon
- Connective-tissue diseases: especially systemic sclerosis, also SLE, mixed connective-tissue disease, dermatomyositis, Sjögren syndrome, rheumatoid arthritis, vasculitis
- Arterial disease: atherosclerosis, embolic disease, thoracic outlet syndrome, Buerger disease
- Occupational: vibration-induced white finger
- Drugs and toxins: beta-blockers, non-selective sympathomimetics, amphetamines, cocaine, ergot derivatives, some chemotherapy
- Haematological or hyperviscosity disorders: cryoglobulinaemia, cold agglutinin disease, paraproteinaemia
- Endocrine/metabolic: hypothyroidism
Features strongly favouring secondary Raynaud/systemic sclerosis: onset after 30 years, severe painful attacks, asymmetry, thumb involvement, digital pitting or ulcers, abnormal capillaroscopy, positive ANA or disease-specific antibodies.
2. “Differentiate Raynaud phenomenon from acrocyanosis.”
| Feature | Raynaud phenomenon | Acrocyanosis |
|---|---|---|
| Pattern | Episodic vasospasm | Persistent discoloration |
| Colour | Classically white -> blue -> red, though not all phases are required | Persistent symmetrical blue or violaceous hands/feet |
| Trigger | Cold or emotional stress | Cold worsens it, but cyanosis persists |
| Symptoms | Numbness, tingling, pain on reperfusion | Usually painless, sometimes sweating/coldness |
| Demarcation | Sharply demarcated digits | Diffuse, mottled distal cyanosis |
| Tissue injury | Possible in secondary disease: ulcers, pitting, gangrene | No trophic change, ulcers, or gangrene in primary acrocyanosis |
| Typical patient | Any age, assess for secondary cause | Often young women |
| Capillaroscopy | May be abnormal in secondary Raynaud | Normal in primary acrocyanosis |
A short examiner answer: “Acrocyanosis is persistent, painless, symmetrical cyanosis; Raynaud is a reversible, episodic, cold-triggered vasospastic colour change, and secondary Raynaud may cause digital ischemia.” Bailey & Love describes acrocyanosis as painless and non-episodic, commonly affecting young women. Bailey & Love's Short Practice of Surgery, 28th ed., p. 1046.
3. “How do you distinguish primary from secondary Raynaud phenomenon?”
Answer:
Primary Raynaud is benign functional vasospasm. Secondary Raynaud reflects structural microvascular disease or arterial pathology.
Primary Raynaud is benign functional vasospasm. Secondary Raynaud reflects structural microvascular disease or arterial pathology.
| Finding | Primary | Secondary |
|---|---|---|
| Age at onset | Usually <30 years | Often >30 years |
| Symmetry | Symmetrical | May be asymmetric |
| Attack severity | Mild | Severe, frequent, painful |
| Ischaemic complications | Absent | Pitting scars, ulcers, gangrene may occur |
| Pulses | Normal | May be reduced if macrovascular disease |
| Nailfold capillaroscopy | Normal | Abnormal, especially in systemic sclerosis |
| Serology | ANA negative/low titre | ANA and disease-specific antibodies may be positive |
| Systemic symptoms | None | Skin thickening, reflux, dyspnoea, arthralgia, myositis etc. |
4. “What are your clinical clues that Raynaud is due to systemic sclerosis?”
Answer:
I would look for:
I would look for:
- Puffy fingers progressing to sclerodactyly
- Digital pitting scars, fingertip ulcers, pulp loss, acro-osteolysis
- Telangiectasia
- Calcinosis
- Tight facial skin, reduced oral aperture, radial perioral furrows
- Abnormal nailfold capillaries
- Reflux, dysphagia, bloating or diarrhoea from gastrointestinal dysmotility
- Breathlessness from ILD or pulmonary arterial hypertension
- Tendon friction rubs, joint contractures
- Raised blood pressure or renal dysfunction suggesting scleroderma renal crisis
Long-standing limited cutaneous disease often has prominent vascular disease with Raynaud and fingertip ischemic ulcers. Goldman-Cecil Medicine, systemic sclerosis section.
5. “What will you look for in the hands of a patient with systemic sclerosis?”
Answer:
I would inspect for:
I would inspect for:
- Puffy hands in early disease
- Sclerodactyly: tight, shiny, tapering fingers
- Reduced skin folds and reduced ability to pinch skin
- Fixed flexion contractures
- Digital-tip pitting scars
- Active digital ulcers: distinguish ischemic pulp ulcers from ulcers over calcinosis or extensor surfaces
- Loss of finger pulp and terminal phalanx resorption
- Calcinosis deposits, especially on finger pads
- Telangiectasia
- Nailfold capillary abnormalities
- Evidence of infection around an ulcer
- Signs of inflammatory arthritis or myositis suggesting overlap disease
A useful interpretation is: “Pitting scars and pulp ulcers indicate chronic digital ischemia; extensor ulcers may result from trauma over tight atrophic skin; chalky discharge suggests calcinosis.”
6. “Describe the nailfold capillaroscopy findings in systemic sclerosis.”
Answer:
Typical scleroderma-pattern changes are:
Typical scleroderma-pattern changes are:
- Giant capillaries
- Dilated capillary loops
- Microhaemorrhages
- Capillary dropout or avascular areas
- Disorganised architecture
- Neoangiogenesis with bushy or ramified capillaries in later disease
This helps distinguish primary Raynaud, where capillary architecture is typically normal, from secondary Raynaud due to systemic sclerosis-spectrum disease. Nailfold examination is a key test in someone with Raynaud plus puffy fingers or positive ANA.
7. “What are the cutaneous subsets of systemic sclerosis, and why do they matter?”
Answer:
| Feature | Limited cutaneous SSc | Diffuse cutaneous SSc |
|---|---|---|
| Skin distribution | Distal to elbows/knees, often face | Trunk plus proximal limbs and distal limbs |
| Raynaud | Often long preceding history | May occur with or after skin disease begins |
| Antibody association | Anti-centromere | Anti-topoisomerase I or anti-RNA polymerase III |
| Important risks | PAH, digital ischemia, calcinosis, telangiectasia | Early ILD, renal crisis, cardiac disease, rapidly progressive skin fibrosis |
| Course | Often more indolent | Early years may be rapidly progressive |
Diffuse disease commonly begins with puffy, itchy fingers and evolves into skin induration, followed by hyperpigmentation, loss of hair and impaired sweating. Goldman-Cecil Medicine, systemic sclerosis section.
Exam trap: Limited does not mean mild. Late pulmonary arterial hypertension and severe digital vasculopathy can be life-threatening.
8. “Explain CREST syndrome. Is it still useful?”
Answer:
CREST refers to:
CREST refers to:
- Calcinosis
- Raynaud phenomenon
- Esophageal dysmotility
- Sclerodactyly
- Telangiectasia
It is a useful bedside mnemonic for a phenotype that often overlaps with limited cutaneous systemic sclerosis. However, I would not use CREST as a substitute for assessing the full disease extent, because patients may have internal-organ involvement regardless of whether all five features are present.
9. “Which antibodies do you request, and how do they guide prognosis?”
Answer:
- ANA: screening test, usually positive, but not diagnostic alone.
- Anti-centromere antibody: limited cutaneous disease; increased risk of pulmonary arterial hypertension.
- Anti-topoisomerase I (anti-Scl-70): diffuse disease and higher risk of interstitial lung disease.
- Anti-RNA polymerase III: rapidly progressive diffuse skin disease and strong association with scleroderma renal crisis. Assess carefully for concurrent malignancy according to local practice.
- Anti-PM/Scl: scleroderma-myositis overlap.
- Anti-U1 RNP: may suggest mixed connective-tissue disease or overlap phenotype.
- Anti-U3 RNP/fibrillarin: diffuse disease, often severe visceral involvement in some populations.
Key viva sentence: “Antibodies do not replace organ screening, but they help risk-stratify the patient.”
10. “How would you assess severity of skin involvement?”
Answer:
I would use the modified Rodnan skin score (mRSS). It grades skin thickness from 0 to 3 at 17 body sites, giving a maximum score of 51.
I would use the modified Rodnan skin score (mRSS). It grades skin thickness from 0 to 3 at 17 body sites, giving a maximum score of 51.
It is most useful in diffuse cutaneous disease to document baseline severity and progression, and to monitor response over time. It should be interpreted alongside function, joint contractures, tendon friction rubs, and internal-organ involvement.
11. “What causes digital ulcers in systemic sclerosis, and how do you classify them?”
Answer:
Digital ulcers result from a combination of vasospasm, fixed obliterative microangiopathy, impaired tissue repair, trauma, tight atrophic skin and sometimes calcinosis.
Digital ulcers result from a combination of vasospasm, fixed obliterative microangiopathy, impaired tissue repair, trauma, tight atrophic skin and sometimes calcinosis.
I would classify them clinically as:
- Ischaemic ulcers: often at the fingertip/pulp, painful, associated with pitting scars and poor perfusion.
- Mechanical/traumatic ulcers: over extensor surfaces, bony prominences or contractures.
- Calcinosis-associated ulcers: may extrude chalky white material.
- Infected ulcers: increasing pain, erythema, discharge, cellulitis or systemic features.
Fingertip ischemic ulceration can heal with digital pitting, become infected, and may be associated with acro-osteolysis. Goldman-Cecil Medicine, systemic sclerosis section.
12. “How will you manage severe Raynaud or an active ischemic digital ulcer?”
Answer:
First, I would assess whether this is threatened digital ischemia requiring urgent specialist input.
First, I would assess whether this is threatened digital ischemia requiring urgent specialist input.
General measures
- Avoid cold exposure, nicotine and vasoconstricting drugs
- Keep the whole body warm, not only the hands
- Manage pain
- Wound care and culture/treat infection when indicated
- Check peripheral pulses and consider arterial imaging if asymmetry, reduced pulses or severe ischemia suggests macrovascular disease
Vasodilator therapy
- A dihydropyridine calcium-channel blocker, commonly nifedipine, is usually first-line.
- PDE-5 inhibitor can be used for persistent severe Raynaud.
- Intravenous prostanoid therapy, such as iloprost, is considered for severe refractory Raynaud or active digital ischemia/ulcers.
- Bosentan can reduce new digital-ulcer formation in selected recurrent-ulcer cases, but does not heal an established ulcer.
A recent systematic review informing recommendations for SSc-associated Raynaud and digital ulcers supports a stepwise vasodilator approach, including calcium-channel blockers, PDE-5 inhibitors and prostanoids when needed (2024 systematic review, PMID 38306796).
13. “How do you screen for interstitial lung disease in systemic sclerosis?”
Answer:
Every patient needs baseline assessment because ILD may be early and asymptomatic.
Every patient needs baseline assessment because ILD may be early and asymptomatic.
- Detailed respiratory history and examination
- Pulmonary function tests: FVC and DLCO
- High-resolution CT chest: most sensitive test for ILD and often needed at baseline
- Repeat PFTs serially to detect progression
- Consider echocardiography as dyspnoea may also be due to PAH, cardiac disease, anaemia or deconditioning
SSc-ILD most commonly shows an NSIP pattern, while UIP is less common than in idiopathic pulmonary fibrosis. Harrison's Principles of Internal Medicine, 22nd ed., p. 2909.
14. “Differentiate ILD from pulmonary arterial hypertension in systemic sclerosis.”
| Feature | SSc-associated ILD | SSc-associated PAH |
|---|---|---|
| Usual timing | Often early, especially diffuse disease | Often later, particularly limited disease |
| Symptoms | Progressive exertional dyspnoea, cough | Progressive exertional dyspnoea, fatigue, syncope, chest discomfort |
| Examination | Fine bibasal crackles | Loud P2, RV heave, raised JVP, peripheral oedema late |
| PFT | FVC reduced, DLCO reduced | Disproportionately low DLCO with relatively preserved FVC |
| HRCT | Interstitial changes/fibrosis | May be relatively normal or show vascular changes |
| Confirmation | HRCT plus PFT trajectory | Right-heart catheterisation |
Exam point: In SSc, dyspnoea should never automatically be attributed to fibrosis. Evaluate for both ILD and PAH.
15. “What is scleroderma renal crisis?”
Answer:
Scleroderma renal crisis is an acute, potentially life-threatening renal vasculopathy, classically presenting with:
Scleroderma renal crisis is an acute, potentially life-threatening renal vasculopathy, classically presenting with:
- Abrupt new severe hypertension
- Rapid acute kidney injury
- Headache, visual symptoms, encephalopathy or seizures
- Microangiopathic haemolytic anaemia and thrombocytopenia may occur
- Urinalysis often shows only mild proteinuria/haematuria compared with other glomerular diseases
It is more strongly associated with diffuse cutaneous disease, early rapidly progressive skin disease, anti-RNA polymerase III antibody, tendon friction rubs and exposure to moderate or high-dose glucocorticoids.
Immediate treatment: start an ACE inhibitor promptly, usually captopril in an acute setting, then titrate aggressively while monitoring blood pressure and renal function. Do not withhold ACE inhibition merely because creatinine rises initially.
16. “Why are steroids a difficult issue in systemic sclerosis?”
Answer:
Glucocorticoids may be needed for overlap inflammatory arthritis, myositis or another clear indication, but moderate-to-high doses increase the risk of scleroderma renal crisis. Therefore I would use the lowest effective dose, avoid routine steroids for skin fibrosis, monitor blood pressure closely, and involve rheumatology early.
Glucocorticoids may be needed for overlap inflammatory arthritis, myositis or another clear indication, but moderate-to-high doses increase the risk of scleroderma renal crisis. Therefore I would use the lowest effective dose, avoid routine steroids for skin fibrosis, monitor blood pressure closely, and involve rheumatology early.
17. “What gastrointestinal questions would you ask?”
Answer:
I would specifically ask about:
I would specifically ask about:
- Reflux, heartburn and regurgitation
- Dysphagia: solids, liquids, progressive or intermittent
- Early satiety, nausea, vomiting or gastroparesis symptoms
- Bloating, diarrhoea, steatorrhoea or weight loss suggesting small-bowel bacterial overgrowth
- Constipation, faecal incontinence or pseudo-obstruction symptoms
- Iron-deficiency anaemia or melaena, which may suggest gastric antral vascular ectasia
The mechanism is smooth-muscle atrophy/fibrosis and dysmotility. The lower oesophagus is commonly involved, leading to reduced peristalsis and reflux. Harrison's Principles of Internal Medicine, 22nd ed., p. 2909.
18. “What is the differential diagnosis of sclerodactyly?”
Answer:
Important differentials include:
Important differentials include:
- Systemic sclerosis
- Scleroderma overlap syndromes
- Mixed connective-tissue disease
- Eosinophilic fasciitis: often spares fingers, may have groove sign
- Diabetic cheiroarthropathy
- Chronic graft-versus-host disease
- Nephrogenic systemic fibrosis in advanced renal failure with gadolinium exposure
- Scleromyxoedema
- Myxoedema/hypothyroidism
- Occupational or toxic exposures, for example vinyl chloride
- Localised scleroderma/morphoea, though this usually lacks Raynaud and systemic features
High-yield discriminator: true systemic sclerosis is suggested by Raynaud, nailfold microangiopathy, sclerodactyly, disease-specific autoantibodies and internal-organ disease.
19. “How do you distinguish systemic sclerosis from eosinophilic fasciitis?”
Answer:
| Feature | Systemic sclerosis | Eosinophilic fasciitis |
|---|---|---|
| Raynaud phenomenon | Common | Usually absent |
| Fingers and face | Often involved | Usually spared |
| Skin | Sclerodactyly, facial tightening, telangiectasia | Woody induration of limbs, peau d’orange |
| Groove sign | Not typical | Can occur along superficial veins |
| Nailfold capillaries | Abnormal in many cases | Usually normal |
| Blood eosinophilia | Not characteristic | May be present early |
| Internal organ disease | Can affect lungs, kidneys, gut, heart | Uncommon |
20. “What is the most important safety-net advice for this patient?”
Answer:
I would advise urgent assessment for:
I would advise urgent assessment for:
- A new or rapidly worsening digital ulcer, black fingertip, severe persistent digital pain or suspected infection
- New severe headache, visual disturbance, confusion, breathlessness or abrupt hypertension: consider renal crisis
- New progressive dyspnoea, syncope, chest pain or leg swelling: consider PAH, ILD or cardiac involvement
- Dysphagia with weight loss, persistent vomiting, abdominal distension or inability to pass stool/flatus
- Fever or a nonhealing ulcer
Quick one-line examiner answers
-
“What is digital pitting?”
A depressed scar at the fingertip caused by recurrent ischemic tissue loss. -
“What is acro-osteolysis?”
Resorption of the distal phalanges, often associated with severe chronic digital ischemia in systemic sclerosis. -
“Why does the mouth become small?”
Perioral skin fibrosis causes radial furrowing and reduced oral aperture, termed microstomia. -
“Why does reflux occur?”
Fibrosis and atrophy of oesophageal smooth muscle cause hypomotility and reduced lower-oesophageal sphincter competence. -
“What does a disproportionately low DLCO suggest?”
Pulmonary vascular disease or PAH, though ILD and anaemia must also be considered. -
“What is the first drug you avoid or question in diffuse SSc?”
Moderate-to-high-dose glucocorticoids because of renal-crisis risk. -
“Can a patient with limited SSc develop serious organ disease?”
Yes. Limited disease carries significant risk of PAH, digital vasculopathy and gastrointestinal involvement. -
“What is the most useful bedside clue to secondary Raynaud?”
Digital pitting scars or ulcers, particularly with abnormal nailfold capillaries.
What are differentials of erythromelalgia
Reading File
Finding Sources
Searching PubMed
erythromelalgia differential diagnosis
Searching the Web
erythromelalgia differential diagnosis clinical features red hot painful extremities
Reading File
Reading File
Finding Sources
Erythromelalgia is episodic burning pain, erythema and increased warmth, usually of the feet, triggered by heat, exercise, standing or limb dependency, and relieved by cooling/elevation.
Differentials of erythromelalgia
| Differential | How to distinguish it from erythromelalgia |
|---|---|
| Complex regional pain syndrome (CRPS) | Often follows trauma, fracture or surgery; usually unilateral; allodynia, hyperalgesia, swelling, sweating and trophic changes may occur. It is not consistently heat-triggered and cooling-relieved, and tends to be more persistent than episodic. |
| Peripheral neuropathy / small-fibre neuropathy | Burning pain and sensory loss in a stocking distribution, but usually no striking episodic erythema and warmth. Consider diabetes, alcohol, B12 deficiency, chemotherapy and autoimmune neuropathy. |
| Raynaud phenomenon, especially reactive hyperaemic phase | Raynaud is cold/stress triggered and starts with pallor or cyanosis, followed by redness on rewarming. Erythromelalgia is heat/exercise triggered, with red hot painful extremities from the outset. |
| Acrocyanosis | Persistent, painless or minimally symptomatic blue-purple discoloration, worsened by cold. It is not a burning red-hot episodic syndrome. |
| Perniosis (chilblains) | Cold/damp exposure produces persistent pruritic or painful erythematous-violaceous papules or plaques that last days to weeks, rather than heat-induced attacks relieved by cooling. |
| Cellulitis / erysipelas | Usually unilateral, persistent and progressively painful, with an infective focus, possible fever, lymphangitis and raised inflammatory markers. Erythromelalgia is recurrent and often bilateral/symmetrical. |
| Deep-vein thrombosis or superficial thrombophlebitis | Unilateral limb swelling, tenderness and venous distribution, rather than recurrent distal burning attacks. Investigate urgently when suspected. |
| Venous insufficiency / stasis dermatitis | Chronic dependent oedema, varicosities, hyperpigmentation and eczematous skin changes. Symptoms improve with elevation but lack the stereotyped burning hot red attacks. |
| Peripheral arterial disease or acute limb ischaemia | Reduced/absent pulses, cool limb, claudication/rest pain, pallor or cyanosis. Erythromelalgia usually has normal or bounding pulses and a warm erythematous limb during an attack. |
| Vasculitis / connective-tissue disease | Purpura, ulcers, livedo, systemic symptoms, renal/neurological involvement, abnormal inflammatory markers or autoantibodies may point to vasculitis or diseases such as SLE. |
| Fabry disease | Burning acropain beginning in childhood/adolescence, often heat/exercise triggered, but look for angiokeratomas, hypohidrosis, corneal verticillata, gastrointestinal symptoms, renal and cardiac disease. |
| Gout or inflammatory arthritis | Localised acutely inflamed joint with reduced joint movement and tenderness. Not usually diffuse episodic erythema/warmth involving the whole foot or hand. |
| Contact dermatitis / red-foot syndrome | Exposure-related itch, scaling, vesicles or clear contact distribution rather than severe heat-provoked burning pain. |
A good viva answer
“The important differentials are CRPS, peripheral or small-fibre neuropathy, Raynaud phenomenon during its hyperaemic phase, acrocyanosis, perniosis, cellulitis, venous disease or DVT, peripheral arterial disease, vasculitis, Fabry disease and inflammatory arthritis. Erythromelalgia is favoured by recurrent bilateral burning red hot extremities precipitated by warmth, exercise or dependency and relieved by cooling and elevation.”
Dermatology texts particularly highlight CRPS, peripheral neuropathy and the hyperaemic phase of Raynaud phenomenon as important mimics. Dermatology, 5th ed., p. 2224.
Examiner extension: “What secondary causes must you actively look for?”
Do not confuse these with mimics. These are causes/associations of secondary erythromelalgia:
- Myeloproliferative neoplasms, especially essential thrombocythaemia and polycythaemia vera
- Ask about headache, visual disturbance, aquagenic pruritus, thrombosis and splenomegaly.
- Check FBC with platelet count and haematocrit, then investigate for JAK2/CALR/MPL as appropriate.
- Diabetes and peripheral neuropathy
- Autoimmune connective-tissue disease, including SLE
- Vasculitis
- Peripheral arterial disease
- Myelodysplastic syndromes
- Drugs, occasionally including calcium-channel blockers and some platelet-active agents
A particularly aspirin-responsive erythromelalgia syndrome should raise suspicion for a platelet-mediated myeloproliferative disorder. Dermatology, 5th ed., p. 2224.
Safety point: Do not advise prolonged ice-water immersion. It can cause maceration, ulceration and cold injury.
What is the cause of salt and pepper pigmentation in systemic sclerosis
Reading File
Finding Sources
Searching PubMed
systemic sclerosis salt pepper pigmentation
Searching the Web
systemic sclerosis salt and pepper pigmentation mechanism perifollicular sparing
Salt-and-pepper pigmentation in systemic sclerosis is due to a mixture of:
- Hypopigmentation/depigmentation from melanocyte damage or loss, probably related to oxidative stress and skin fibrosis.
- Relative preservation of melanocytes around hair follicles, giving retained perifollicular pigmentation.
Thus, pale or depigmented skin with small darker follicular dots creates the “salt-and-pepper” appearance. It is most obvious on the scalp, upper back, chest and sometimes face, particularly in darker skin.
Viva answer:
“It represents vitiligo-like depigmentation from melanocyte injury, with relative sparing of follicular melanocytes because the follicular microenvironment is relatively protected. Retained perifollicular pigment against depigmented skin produces the salt-and-pepper pattern.”
It is a manifestation of cutaneous systemic sclerosis, not necessarily coexistent vitiligo. Rheumatology, 2-Volume Set, 2022, systemic sclerosis section.
Why is it spared
Reading File
Finding Sources
Searching PubMed
systemic sclerosis pigmentation melanocytes perifollicular
Searching the Web
systemic sclerosis salt pepper pigmentation why perifollicular sparing melanocytes mechanism
Perifollicular pigment is spared because the area around a hair follicle has a richer capillary network, which may provide relative warmth and better local perfusion. This is thought to protect melanocyte function and preserve melanogenesis despite surrounding scleroderma-associated melanocyte injury.
Also, the hair follicle is a recognised niche containing melanocyte stem cells, so it may retain or replenish pigment more effectively than the surrounding interfollicular epidermis.
So the proposed mechanism is:
SSc causes surrounding depigmentation, while relatively well-perfused follicular skin retains pigment, producing dark dots around hair follicles on a pale background.
For a viva, say “The exact mechanism is not fully established, but relative perifollicular vascular protection and preservation of the follicular melanocyte reservoir are the leading explanations.” A published clinical discussion similarly proposes a richer perifollicular capillary network and local warming as the explanation for retained melanogenesis (case discussion).
This is a shared conversation. Sign in to Orris to start your own chat.