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DR2.1,DR3.1-3,DR4.1 | Papulosquamous & Pigmentary Disorders — Graded Quiz
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A 48-year-old bus driver presents with thickened, scaly plaques over both elbows, knees, and the sacral region for 8 years. The plaques are well-demarcated, erythematous, and covered with silvery scale. He mentions that his fingernails have small pits and a brownish 'oil drop' discolouration under the free edge. He also reports morning stiffness and swelling in the distal interphalangeal joints of both hands for 6 months. Which of the following BEST describes the significance of the joint findings in this patient?
Correct. Psoriatic arthritis complicates ~30% of psoriasis cases. DIP joint involvement with nail changes (pitting, oil-drop sign) is a classic pattern. Recognising joint disease is critical because it requires DMARDs (e.g. methotrexate — which conveniently treats both skin and joints) or biologics targeting joint inflammation, and alters prognosis and monitoring.
Psoriatic arthritis occurs in ~30% of psoriasis patients; DIP joint involvement (often with associated nail disease — pitting, onycholysis, oil-drop sign) is one of its classic patterns. Psoriatic arthritis changes management to include DMARDs (methotrexate, sulfasalazine) or biologics targeting joint disease in addition to skin; dermatology and rheumatology co-management is required.
Incorrect. DIP joint involvement with nail changes (pitting, oil-drop sign) in a patient with chronic plaque psoriasis is psoriatic arthritis until proven otherwise. This changes management significantly — DMARDs and/or biologics targeting joint destruction are added; dermatology-rheumatology co-management is required. Psoriatic arthritis can present with axial, DIP, oligoarticular, polyarticular, or arthritis mutilans patterns.
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A 55-year-old woman with long-standing chronic plaque psoriasis (BSA 40%, PASI 24) has failed two courses of methotrexate (hepatotoxicity) and one course of cyclosporine (hypertension). She is obese and has type 2 diabetes. Her dermatologist proposes acitretin. Which statement about acitretin in this clinical scenario is MOST accurate?
Correct. Acitretin is an oral retinoid — effective for severe plaque psoriasis, particularly when methotrexate and cyclosporine have failed. In post-menopausal women the teratogenicity concern is eliminated, making it an acceptable option. Key monitoring: fasting lipids (LDL/TG can rise, particularly important with pre-existing diabetes and obesity) and LFTs.
Acitretin is an oral retinoid (second-generation, less teratogenic than etretinate but still teratogenic); effective in plaque, pustular, and erythrodermic psoriasis. Major concerns: teratogenicity (contraindicated in women of childbearing age; contraception required for 2 years after stopping), dyslipidaemia (LDL↑, TG↑ — important monitoring in diabetics), mucocutaneous dryness, hepatotoxicity (monitor LFTs). Post-menopausal women are not exempt from lipid monitoring.
Incorrect. Acitretin is an oral retinoid, not an antihistamine. It is effective in severe psoriasis (plaque, pustular, erythrodermic). Key concerns are teratogenicity (critical in women of childbearing age; post-menopausal safer), dyslipidaemia (LDL and triglycerides must be monitored — important in this diabetic patient), and mucocutaneous dryness. Diabetes alone is not a contraindication, but lipid monitoring is mandatory.
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A 26-year-old man presents with multiple flat-topped, violaceous, intensely pruritic papules on both wrists and the lower back, present for 10 weeks. Wood's lamp shows no accentuation. Biopsy of one papule is reported as: 'band-like lymphocytic infiltrate hugging the basal layer with vacuolar degeneration of basal keratinocytes and scattered colloid bodies.' Which diagnosis does this histology CONFIRM?
Correct. The described histology — band-like lymphocytic infiltrate at the DEJ with vacuolar basal degeneration and colloid (Civatte) bodies — is the classic lichenoid tissue reaction of lichen planus. The 'saw-tooth' rete ridges pattern may also be noted. This histology confirms the clinical impression of flat-topped violaceous papules on the wrists.
The histological hallmarks of lichen planus are: (1) band-like (lichenoid) T-cell infiltrate at the dermoepidermal junction; (2) vacuolar degeneration (liquefactive necrosis) of basal keratinocytes; (3) civatte/colloid bodies (necrotic keratinocytes); and (4) 'saw-tooth' rete ridges. These reflect the CD8+ T-cell attack on basal keratinocytes at the DEJ — the pathological basis of the lichenoid tissue reaction.
Incorrect. The histological triad of: band-like lymphocytic infiltrate at the DEJ + vacuolar degeneration of basal keratinocytes + colloid bodies = lichenoid tissue reaction = lichen planus. Psoriasis shows regular epidermal hyperplasia, thinned suprapapillary plates, Munro microabscesses, and no colloid bodies. DLE shows focal basal degeneration + perivascular/periappendageal infiltrate + mucin. Pityriasis rosea shows focal parakeratosis and mild perivascular infiltrate.
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A 16-year-old girl presents with a single, well-defined, hypopigmented patch (4 × 3 cm) over the right cheek present for 1 year. Sensation within the patch is reduced on fine-touch testing. There is no scaling. Slit-skin smear is negative. A thickened great auricular nerve is palpable on the right side. Wood's lamp shows slight (but not brilliant) accentuation. What is the most likely diagnosis?
Correct. The diagnostic triad is (1) hypopigmented patch with impaired sensation + (2) palpable nerve thickening (great auricular) + (3) negative slit-skin smear = paucibacillary (TT/BT) leprosy. This is the leprosy differential always sought when examining pale patches. Wood's lamp does not show brilliant accentuation (contrast with vitiligo, which shows chalk-white fluorescence).
The triad of a hypopigmented (not depigmented) patch + reduced sensation within the patch + thickened peripheral nerve (great auricular nerve) clinches tuberculoid/borderline tuberculoid leprosy. The slit-skin smear is negative in paucibacillary leprosy (by WHO definition, ≤5 lesions, smear-negative). Wood's lamp does NOT show brilliant accentuation (contrast with vitiligo). Nerve thickening is absent in all other diagnoses here.
Incorrect. Reduced sensation within the patch and a palpable thickened nerve are the critical discriminators that rule out vitiligo (normal sensation), pityriasis alba (no nerve involvement, no hypoaesthesia), and discoid eczema (eczematous, pruritic, not hypopigmented with nerve thickening). The combination of hypoaesthetic hypopigmented patch + nerve thickening = leprosy until proven otherwise.
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A dermatology registrar is conducting a Grattage test on a 34-year-old patient with suspected chronic plaque psoriasis. After gently scraping the plaque with the edge of a glass slide, the test reveals: Step 1 — thin silvery scales dislodge easily in flakes. Step 2 — a smooth, shiny, semi-transparent surface is exposed. Step 3 — further gentle scraping produces multiple pinpoint bleeding points. The registrar correctly interprets all three endpoints. Which SINGLE pathological mechanism BEST explains why the pinpoint bleeding appears at Step 3?
Correct. The pathological basis of Auspitz sign is: psoriatic epidermis has a markedly thinned suprapapillary plate (last membrane) overlying elongated, dilated capillary loops in the dermal papillae. When the last membrane is removed by scraping, these capillaries are directly exposed and bleed at multiple points — the 'pinpoint' pattern mirrors the arrangement of the papillary capillaries.
In psoriasis the suprapapillary epidermis is markedly thinned (the last membrane, ~2 cells thick) overlying elongated, dilated, tortuous capillary loops in the dermal papillae (angiopathy driven by VEGF from activated keratinocytes/T-cells). Removing the last membrane with the glass slide exposes these dilated capillaries, which bleed on minimal trauma — producing the characteristic pinpoint Auspitz sign (named after Heinrich Auspitz).
Incorrect. The pinpoint bleeding of Auspitz sign reflects the unique psoriatic vascular architecture — elongated, dilated papillary capillaries lying just beneath a markedly thinned suprapapillary epidermis. When this thin membrane is removed, the capillaries bleed at multiple punctate points. Acantholysis (blistering) is the mechanism in pemphigus; vessels are not present in parakeratotic scale; Koebner phenomenon is a delayed isomorphic response, not an immediate bleeding mechanism.
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A 62-year-old man presents to casualty with generalised redness, scaling, and exfoliation involving approximately 92% of his body surface area, accompanied by chills, high fever, and oedema. His wife reports he had chronic plaque psoriasis and was self-medicating with oral prednisolone (20 mg/day) which he stopped abruptly 2 weeks ago. What is the MOST LIKELY precipitant of this presentation, and which IMMEDIATE management step is HIGHEST priority?
Correct. Systemic steroid withdrawal is the classic and most dangerous precipitant of erythrodermic psoriasis (or generalised pustular psoriasis). With >90% BSA involvement, complications are hypothermia, high-output cardiac failure, fluid/electrolyte/protein loss, and secondary sepsis. Immediate priorities are IV fluid resuscitation, temperature regulation, and urgent specialist referral — NOT restarting steroids.
Abrupt withdrawal of systemic corticosteroids in psoriasis is the classic precipitant of erythroderma (>90% BSA) or generalised pustular psoriasis. Erythroderma carries mortality from hypothermia, high-output cardiac failure, fluid and protein loss, and secondary infection. Management priorities: haemodynamic stabilisation (IV fluids, electrolytes, albumin), thermoregulation (warming blankets), treat secondary infection, urgent dermatology referral; do NOT re-prescribe systemic steroids. This is why systemic steroids are absolutely contraindicated in psoriasis.
Incorrect. This is erythrodermic psoriasis precipitated by systemic steroid withdrawal — the very reason steroids are absolutely contraindicated in psoriasis. The correct immediate management is haemodynamic stabilisation (IV fluids for fluid/electrolyte loss), thermoregulation, treatment of secondary infection, and urgent dermatology referral. Restarting steroids is contraindicated. TEN from steroids is possible but does not explain the psoriasis history and steroid-withdrawal timeline.
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A 41-year-old woman presents with lichen planus limited to the oral mucosa — bilateral white reticulate streaks on the buccal mucosa, asymptomatic. Skin examination is normal. Which management strategy is MOST appropriate for asymptomatic oral lichen planus?
Correct. Asymptomatic reticular oral lichen planus does not require active treatment. Regular follow-up (every 6–12 months) is indicated to monitor for erosive change and for the small risk of oral malignant transformation (SCC). Systemic or aggressive therapy is not justified for asymptomatic reticular disease.
Asymptomatic reticular oral lichen planus requires no active treatment but does require monitoring because oral LP carries a small (0.3–3%) risk of malignant transformation to squamous cell carcinoma — higher for erosive oral LP. Systemic steroids are reserved for symptomatic, erosive oral LP or widespread skin disease. Topical corticosteroids or topical tacrolimus are first-line for symptomatic oral LP.
Incorrect. Asymptomatic reticular oral LP (white streaks, no burning or ulceration) does not warrant systemic corticosteroids, surgery, or antifungals. It is not candidiasis. The appropriate approach is watchful monitoring with regular oral reviews, patient education about symptoms to report, and counselling about the small malignant transformation risk. Treatment is escalated only when symptoms (burning, erosions) develop.
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A 33-year-old man has had depigmented patches on both hands and feet for 5 years. He is referred for NBUVB phototherapy. Which type of vitiligo, based on pattern and clinical assessment, responds BEST to NBUVB phototherapy, and in which situation is surgical repigmentation preferred?
Correct. NBUVB is most effective for non-segmental (generalised) vitiligo; it stimulates residual follicular melanocytes via perilesional repigmentation. Stable segmental vitiligo is the ideal surgical indication — it does not progress, responds incompletely to NBUVB, and shows excellent durable repigmentation with grafting (punch, split-skin, or MKTP).
NBUVB phototherapy is the standard for widespread (non-segmental/generalised) vitiligo — it stimulates residual follicular melanocytes to repigment. Acrofacial and lip vitiligo respond poorly (few follicular melanocytes). Stable segmental vitiligo (stopped spreading for ≥1 year) is the optimal surgical candidate (punch grafting, split-skin grafting, melanocyte-keratinocyte transplantation) because segmental disease does not recur after grafting, whereas generalised non-segmental disease may repigment grafted areas only to redepigment later.
Incorrect. NBUVB is the preferred modality for widespread non-segmental vitiligo; segmental vitiligo (which is stable) responds better to surgical repigmentation because it does not spontaneously progress, leaving clear graft margins, and does not redepigment post-graft as frequently as non-segmental disease.
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A 29-year-old bank clerk presents with new-onset lichen planus on both forearms following a new medication started 6 weeks ago for a systemic condition. She was started on hydroxychloroquine for systemic lupus erythematosus. The dermatologist suspects a lichenoid drug reaction. Which statement BEST distinguishes lichenoid drug eruption from idiopathic lichen planus that would guide management?
Correct. Histological clues of lichenoid drug reaction: eosinophils in the infiltrate and parakeratosis (uncommon in idiopathic LP). Clinical clue: photo-exposed distribution. Management: ideally stop the culprit drug after liaison with the prescribing specialist — lesions typically resolve over weeks to months. Hydroxychloroquine is a well-recognised cause.
Lichenoid drug eruptions mimic lichen planus clinically but show eosinophils and parakeratosis on histology (idiopathic LP has neither). Common culprits include hydroxychloroquine, gold salts, penicillamine, beta-blockers, ACE inhibitors, NSAIDs, and thiazide diuretics. Management: if possible, withdraw the offending drug (coordination with the prescribing specialist). Resolution follows drug withdrawal over weeks-months. If withdrawal is not feasible, treat symptomatically as for LP.
Incorrect. Lichenoid drug eruptions CAN be distinguished from idiopathic LP by histology (eosinophils, parakeratosis) and temporal relationship to drug initiation. The correct management is to evaluate whether the causative drug can be safely stopped in coordination with the prescribing specialty. These eruptions are not fungal and are not restricted to the oral mucosa.
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A 52-year-old man with psoriasis vulgaris is counselled about his disease. He asks whether his children are at risk. Which statement BEST represents the current understanding of the genetics of psoriasis for patient counselling?
Correct. Psoriasis is polygenic — HLA-Cw6 (PSORS1) is the strongest single locus but accounts for only a fraction of heritability. Empirical recurrence risks (~15–25% with one affected parent, ~50–65% with both affected) are the clinically useful counselling figures. The incomplete concordance in MZ twins (~70%) confirms environmental triggers are also required.
Psoriasis has a complex polygenic inheritance — the strongest genetic association is with HLA-Cw6 (PSORS1 locus on chromosome 6p21). Risk to offspring: ~15–25% if one parent affected; ~50–65% if both parents affected; ~70% concordance in monozygotic twins (indicating significant environmental component). This counselling point is important for doctor-patient communication about prognosis and family planning.
Incorrect. Psoriasis is polygenic, not monogenic autosomal dominant or recessive. The HLA-Cw6 allele is the strongest susceptibility marker (PSORS1). Empirical risks for offspring are approximately 15–25% with one affected parent and 50–65% with two affected parents — not the 50% of a simple Mendelian dominant. The incomplete twin concordance confirms environmental triggers contribute.
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