Summative Revision Notes
These notes summarise the seven Morning Rounds in the Dermatology series. They are written for rapid pre-exam revision, not first-time learning. Each section is self-contained. Read the debrief panels in the quizzes for the full clinical reasoning; use these notes to consolidate what you already know.
| Disorder | Split Level | Acantholysis | Antigen | DIF Pattern | Nikolsky |
|---|---|---|---|---|---|
| Pemphigus vulgaris | Suprabasal | Yes | Dsg3 (± Dsg1) | Intercellular IgG (chicken-wire) | Positive |
| Pemphigus foliaceus | Subcorneal | Yes | Dsg1 only | Intercellular IgG | Positive |
| Bullous pemphigoid | Subepidermal | No | BP180 + BP230 | Linear IgG + C3 at BMZ | Negative |
| Dermatitis herpetiformis | Subepidermal | No | eTG (TG3) | Granular IgA at papillary tips | Negative |
| SSSS | Subcorneal | Yes | Dsg1 (exfoliatin) | N/A (not autoimmune) | Positive |
| TEN | Subepidermal | No | Drug-induced | N/A | Positive |
Desmoglein compensation theory: Dsg3 is abundant in mucosa; Dsg1 dominates in superficial skin. Anti-Dsg1 alone (PF, SSSS) spares mucosa because Dsg3 compensates. Anti-Dsg3 (PV) always involves mucosa.
SSSS vs TEN: SSSS = subcorneal, no mucosa, no scarring, sterile blister fluid, children. TEN = full-thickness necrosis, mucosa invariably involved, significant mortality (SCORTEN). Frozen section of blister roof distinguishes them emergently.
Dermatitis herpetiformis: associated with coeliac disease in virtually 100%. Gluten-free diet is definitive treatment. Dapsone for rapid symptom control. Check G6PD before dapsone.
Auspitz sign: stepwise scraping reveals candle grease → Bulkley membrane → pinpoint bleeding (dilated papillary capillaries). Histology: parakeratosis, Munro microabscesses, suprapapillary thinning. Nail changes in frequency order: pitting > onycholysis > subungual hyperkeratosis > oil-drop sign. Koebner positive.
4 Ps: Pruritic, Purple, Polygonal, Papules. Wickham striae = focal hypergranulosis. Histology: saw-tooth rete ridges, band-like lymphocytic infiltrate at DEJ, Civatte bodies, hypergranulosis. Oral LP erosive type = potentially premalignant. Associated with hepatitis C. Koebner positive. Heals with post-inflammatory hyperpigmentation.
Herald patch precedes generalised eruption by 1–2 weeks. Secondary lesions follow Langer lines → Christmas tree pattern on back. Collarette scaling from inner edge. Spares face, palms, soles. Self-limiting 6–8 weeks. HHV-6/7 association. Trap: secondary syphilis mimics PR but involves palms and soles — always check VDRL in sexually active adults.
Age-based distribution: infantile (<2 yr) = face + extensors; childhood (2–12 yr) = flexures (antecubital, popliteal); adult = flexural + hand eczema. Elevated IgE. Atopic triad: AD + asthma + allergic rhinitis. Dennie-Morgan lines; Hertoghe sign. Filaggrin (FLG) gene mutation = barrier defect. Treatment: emollients first; topical calcineurin inhibitors (tacrolimus) safe on face.
Allergic CD: Type IV hypersensitivity, requires sensitisation (10–14 days minimum), patch test positive, can spread beyond contact area. Most common allergen: nickel. Irritant CD: non-immunological, first exposure, strictly confined, patch test negative. India-specific: Parthenium dermatitis (Congress grass, airborne), bindi dermatitis (PTBP resin).
Koebner: Psoriasis, LP, Vitiligo Dapsone: check G6PD always RF does NOT follow skin strep
| Nerve | Deformity / Deficit |
|---|---|
| Ulnar (most common overall) | Claw hand — ring & little fingers; medial 1.5 finger sensory loss |
| Common peroneal | Foot drop; steppage gait |
| Posterior tibial | Plantar anaesthesia; trophic ulcers |
| Radial cutaneous | Sensory loss, dorsum of hand |
| Facial | Lagophthalmos → exposure keratitis → blindness |
| Greater auricular | Thickened, visible nerve at neck |
| Type 1 (Reversal) | Type 2 (ENL) | |
|---|---|---|
| Leprosy types | BT, BB, BL only | LL and BL only |
| Hypersensitivity | Type IV (cell-mediated) | Type III (immune complex) |
| Skin | Existing lesions inflamed/oedematous | New tender erythematous nodules |
| Nerve | Sudden nerve function impairment | Less prominent |
| Systemic | Absent | Fever, iritis, orchitis, nephritis |
| Treatment | Prednisolone | Thalidomide (DOC); steroids if contraindicated |
PB (≤5 lesions): Rifampicin 600 mg monthly + Dapsone 100 mg daily — 6 months. MB (>5 lesions): Rifampicin 600 mg monthly + Clofazimine 300 mg monthly and 50 mg daily + Dapsone 100 mg daily — 12 months. Rifampicin = only bactericidal drug. Clofazimine: reddish-brown pigmentation + ichthyosis. MDT is continued through reactions.
Pure neuritic leprosy: more common in India Lepromin = NOT diagnostic; tests CMI only Elimination ≠ eradication
Pathognomonic lesion: burrow (linear track of female Sarcoptes scabiei in stratum corneum). Nocturnal pruritus. Treatment: permethrin 5% cream, neck to toes, 8–12 hours, repeat at 1 week. Treat all contacts simultaneously. Norwegian scabies: immunocompromised, millions of mites, minimal itch, highly contagious — oral ivermectin required. Post-scabietic nodules = hypersensitivity, not re-infection.
Cause: Malassezia furfur. KOH: spaghetti and meatballs (short hyphae + round spores). Wood lamp: golden-yellow. Hypopigmentation due to azelaic acid inhibiting tyrosinase. Pigment change persists months after treatment — warn patients.
Bullous: Staph aureus phage group II, localised exfoliatin cleaving Dsg1, flaccid bullae, sterile. Non-bullous: Staph or Strep pyogenes, honey-coloured crusts. Critical distinction: non-bullous impetigo (Strep) can cause PSGN. Skin strep does NOT cause rheumatic fever. Treatment: topical mupirocin for localised disease.
Ramsay Hunt syndrome: VZV in geniculate ganglion → ear vesicles + ipsilateral facial palsy + sensorineural hearing loss. Worse prognosis than Bell palsy. Hutchinson sign: vesicles on nasal tip (nasociliary branch, V1) → risk of ophthalmic zoster and corneal damage → urgent ophthalmology. PHN = most common complication; early antivirals reduce risk.
Endothrix (T. tonsurans): spores inside shaft, black dot, no Wood lamp fluorescence. Most common in India and USA. Ectothrix (Microsporum): spores outside shaft, green fluorescence. Oral antifungal mandatory (topical cannot penetrate shaft). Kerion: boggy mass, do not incise. Favus (T. schoenleinii): scutula, mousy odour, permanent scarring alopecia.
Erythrasma: coral-red Wood lamp Corynebacterium minutissimum → porphyrins
| Vitiligo | Albinism (OCA1) | |
|---|---|---|
| Melanocytes | Absent (destroyed) | Present, non-functional |
| Mechanism | Autoimmune destruction | Tyrosinase deficiency |
| Wood lamp | Chalk-white fluorescence | Not useful |
| Eye signs | None | Nystagmus, photophobia, reduced VA |
| Main risk | Autoimmune associations | SCC in sun-exposed skin |
| Treatment | NB-UVB; topical tacrolimus | Photoprotection; skin surveillance |
Leukotrichia (white hairs in vitiligo) = poor prognosis for repigmentation. Repigmentation begins perifollicularly. Vitiligo autoimmune associations: thyroid, DM type 1, Addison, pernicious anaemia, alopecia areata.
Epidermal type: Wood lamp accentuates (better treatment response). Dermal type: not accentuated (harder to treat). Kligman formula (hydroquinone + tretinoin + mild steroid) = most effective single regimen. Prolonged hydroquinone → exogenous ochronosis. Sunscreen mandatory and lifelong. Oral tranexamic acid for resistant cases.
Freckles (ephelides): normal melanocyte count, increased melanin per cell, fade in winter, childhood onset, MC1R gene. Lentigines: increased melanocyte count, do not fade in winter. Lentigo maligna: slow-growing irregular macule on sun-damaged skin = premalignant (in situ lentigo maligna melanoma).
NF-1: ≥6 CALMs (>15 mm adults), Lisch nodules (iris hamartomas, pathognomonic), axillary freckling (Crowe sign). Chr 17, neurofibromin. CALMs: smooth coast of California borders. McCune-Albright: irregular coast of Maine borders + polyostotic fibrous dysplasia + precocious puberty. NF-2: chr 22, bilateral acoustic neuromas, fewer CALMs, no Lisch nodules.
Scrape base of fresh vesicle; stain Giemsa. Positive in: HSV (multinucleate giant cells with nuclear moulding), VZV (same), Pemphigus vulgaris (acantholytic cells, no nuclear moulding). Negative in: bullous pemphigoid, DH, impetigo. Does not distinguish HSV-1 from HSV-2 or from VZV.
| Condition | Fluorescence Colour | Organism / Mechanism |
|---|---|---|
| Erythrasma | Coral-red | Corynebacterium minutissimum — porphyrins |
| Tinea versicolor | Golden-yellow | Malassezia furfur |
| Microsporum tinea capitis | Bright green | Ectothrix |
| Pseudomonas infection | Yellow-green | Pyocyanin |
| Vitiligo | Chalk-white (enhanced) | Absent melanin |
| Tuberous sclerosis (ash-leaf) | White (enhanced) | Hypomelanosis |
| Trichophyton tinea capitis | No fluorescence | Endothrix |
| Dermal melasma | Not accentuated | Deep pigment |
Patch test: Type IV CMI, 48 h occlusion + read at 48 and 96 h, gold standard for ACD, most common positive allergen = nickel. Prick test: Type I IgE-mediated, read at 15–20 min, for atopy/food allergy. Patch test: not during systemic steroids; not on active eczema.
PAS: fungi in tissue sections (magenta — cell wall polysaccharides). KOH mount: dissolves keratin, direct microscopy of hyphae/spores. GMS (Grocott): fungi in tissue (black, more sensitive than PAS). India ink: Cryptococcus in CSF (clear capsular halo). ZN stain: acid-fast mycobacteria.
Melanoma: irregular pigment network, blue-white veil, regression structures. BCC: arborising telangiectasia, blue-grey ovoid nests, leaf-like areas. Seborrhoeic keratosis: comedone-like openings, milia-like cysts, brain-like fissures. Scabies: jet with contrail sign (mite body at burrow tip). Dermatofibroma: central white patch + peripheral pigment network.
Recurs at exact same site on re-exposure. Violaceous plaque → resolves with residual hyperpigmentation. Common sites: genitalia, lips, perianal. Most common cause: cotrimoxazole. Others: NSAIDs, metronidazole, tetracyclines, paracetamol. Mechanism: CD8+ T cells resident at prior FDE sites.
Onset 2–8 weeks after drug start (long latency is the clue). Morbilliform rash + facial oedema + fever + lymphadenopathy + eosinophilia + organ involvement (liver most common) + HHV-6 reactivation. Aromatic AEDs cross-react: phenytoin, carbamazepine, phenobarbitone — never substitute one for another. Other causes: allopurinol, sulphonamides, dapsone, minocycline. Mortality ~10%.
SJS <10% BSA; SJS/TEN overlap 10–30%; TEN >30% BSA. Both require mucosal involvement. Most common cause worldwide: allopurinol (HLA-B*58:01 in Han Chinese/Thai). Other causes: sulphonamides, aromatic AEDs, oxicam NSAIDs, nevirapine. Stop the drug immediately = single most important step. SCORTEN predicts mortality. Management: ICU/burns unit, cyclosporine or IVIG as adjuncts.
Phototoxic: non-immunological, first exposure, sun-exposed only, any person. Drugs: doxycycline, fluoroquinolones, amiodarone, thiazides, NSAIDs. Photoallergic: Type IV, sensitisation required, can spread beyond sun-exposed areas. Drugs: sulphonamides, phenothiazines, sunscreens (PABA), griseofulvin.
| Drug | Pigmentation | Extra |
|---|---|---|
| Amiodarone | Slate-grey, sun-exposed | Phototoxic + lipofuscin; corneal deposits; thyroid dysfunction |
| Minocycline | Blue-grey (skin, teeth, sclerae, bone) | Can be permanent |
| Clofazimine | Reddish-brown, diffuse | Ichthyosis; reversible slowly |
| Bleomycin | Flagellate hyperpigmentation (linear streaks) | Along scratch lines; post-chemotherapy |
| Busulfan | Diffuse Addisonian-like | MSH-like effect |
| Hydroxychloroquine | Blue-grey | Corneal deposits + retinopathy (monitor annually) |
| Silver (argyria) | Permanent grey-blue, sun-exposed | No treatment available |
| Gold (chrysiasis) | Blue-grey, sun-exposed | Permanent |
FDE: same site = pathognomonic DRESS: 2-8 weeks, eosinophilia TEN: stop drug first Allopurinol + HLA-B*58:01
For clinical reasoning practice, return to the seven Morning Rounds quizzes linked in the series index.