Dermatology

A chronic, immune-mediated papulosquamous disease in which IL-17/23-driven T-cell inflammation accelerates keratinocyte turnover. The exam picture is well-demarcated salmon-pink plaques with silvery scale on extensor surfaces; the discriminators against eczema are sharp demarcation, extensor (not flexural) distribution and the Auspitz sign.

A chronic, relapsing, intensely itchy inflammatory skin disease driven by skin-barrier (filaggrin) dysfunction and Th2 inflammation, part of the atopic march (asthma, allergic rhinitis). Itch is the cardinal symptom; the distribution is FLEXURAL in children — the mirror image of psoriasis.

An eczematous reaction to an external agent. Two mechanisms: IRRITANT contact dermatitis (non-immune direct toxicity — the commonest, e.g. soaps, water, detergents) and ALLERGIC contact dermatitis (a type IV delayed hypersensitivity to a sensitiser, e.g. nickel, fragrances, chromate, hair-dye PPD). The distribution mirroring an exposure is the clue.

A chronic inflammatory disease of the pilosebaceous unit driven by four factors: follicular hyperkeratinisation, androgen-driven sebum excess, Cutibacterium acnes colonisation, and inflammation. The presence of COMEDONES is what separates it from rosacea.

A chronic, relapsing inflammatory facial dermatosis with vascular hyperreactivity. Subtypes: erythematotelangiectatic, papulopustular, phymatous, and ocular. Central-face distribution with papulopustules but NO comedones is the discriminator from acne.

A chronic T-cell-mediated inflammatory disorder of skin and mucous membranes. Remember the six Ps: Purple, Pruritic, Polygonal, Planar (flat-topped) Papules and Plaques. Wickham striae and flexor-wrist distribution are the giveaways.

Superficial dermal swelling (weals/hives) from mast-cell histamine release, sometimes with deeper angioedema. Acute (=6 weeks; spontaneous or inducible). The hallmark is that each individual weal is fleeting and leaves no mark.

An acute, self-limiting papulosquamous eruption (probably HHV-6/7 reactivation) of young adults. A herald patch precedes a fir-tree distribution of oval scaly patches on the trunk. The job is to recognise it, reassure, and exclude secondary syphilis.

A superficial, highly contagious bacterial skin infection, usually Staphylococcus aureus. Non-bullous (the common form) shows golden honey-coloured crusts around the mouth/nose; bullous impetigo (toxin-mediated) shows flaccid blisters. Common in children.

Inflammation of the hair follicle, most often a superficial bacterial infection (Staphylococcus aureus). Each pustule is centred on a hair — the discriminator from acne (no comedones) and from a boil (deeper). "Hot-tub" folliculitis is a Pseudomonas variant after whirlpool/spa exposure.

An acute bacterial infection of the deep dermis and subcutaneous tissue, usually Streptococcus pyogenes or Staphylococcus aureus. Classically a unilateral, hot, tender, spreading erythema of the lower leg. Erysipelas is the more superficial, sharply-demarcated variant. The key job is to spot the spreading infection that needs urgent surgery — necrotising fasciitis.

Dermatophyte (ringworm) infection of keratinised tissue: tinea corporis (body), cruris (groin), pedis (athletes foot), capitis (scalp), unguium/onychomycosis (nail). The exam picture is an asymmetrical annular plaque with a raised scaly ACTIVE EDGE and central clearing — KOH/scrape confirms it.

A common superficial yeast (Malassezia) overgrowth producing fine scaly macules of altered pigment on the upper trunk. The pigment change (hypo- or hyperpigmented, more visible after sun exposure) and fine branny scale are the giveaways. Not contagious.

Candida albicans overgrowth in warm, moist flexures (intertrigo) — submammary, groin, axillae, abdominal folds, and between digits. Beefy-red plaques with characteristic SATELLITE papules/pustules, often with predisposing diabetes, obesity, occlusion or antibiotics.

Benign epidermal proliferations caused by human papillomavirus. Common warts (firm hyperkeratotic papules on hands), plantar warts/verrucae (inward-growing, painful on pressure), and plane warts (flat). Most are self-limiting and resolve over months to a couple of years, especially in children.

An intensely itchy infestation by the Sarcoptes scabiei mite, which burrows in the stratum corneum. Severe itch worse at night, burrows in the finger web-spaces, and affected household contacts are the triad. Crusted (Norwegian) scabies is a hyperinfestation in the immunosuppressed/elderly.

Infestation of the scalp hair by the head louse, spread by head-to-head contact, common in school-age children. Live lice confirm active infestation; nits (egg cases) alone may be old. Itch is from sensitisation and may be absent early.

A common, self-limiting poxvirus infection producing pearly, dome-shaped, umbilicated papules. Usually in children (skin contact) or as a sexually transmitted lesion in adults. Reassurance is the mainstay — it self-resolves over months.

A spectrum of severe, usually drug-induced, mucocutaneous reactions with keratinocyte apoptosis and skin detachment. SJS (30%), overlap in between. A dermatological emergency with significant mortality — the key is to stop the culprit drug and transfer to a burns/ICU setting.

A life-threatening, rapidly progressive bacterial infection tracking along the fascial planes, causing tissue necrosis. Type 1 is polymicrobial (diabetics, post-surgical — includes Fournier gangrene of the perineum); type 2 is Group A Streptococcus. The hallmark is pain out of proportion to the skin appearance, with systemic toxicity. It is a SURGICAL emergency.

A toxin-mediated blistering disease of YOUNG CHILDREN: Staphylococcus aureus exfoliative toxins (A/B) cleave desmoglein-1, splitting the superficial epidermis. Diffuse tender erythema then superficial peeling, but — unlike SJS/TEN — the MUCOSAE ARE SPARED. The Staph focus is often elsewhere (conjunctivitis, umbilicus, nose).

Erythema affecting >90% of the body surface — a dermatological emergency regardless of cause, because the inflamed skin loses its barrier functions (fluid, heat, protein). Causes: pre-existing dermatoses (psoriasis, eczema), drug reactions, cutaneous lymphoma (Sézary syndrome), and idiopathic.

The commonest skin cancer — a slow-growing, locally invasive malignancy of basal keratinocytes that virtually never metastasises. The classic nodular BCC is a pearly papule with a rolled telangiectatic edge and central ulceration ("rodent ulcer") on sun-exposed skin of older adults.

A malignancy of epidermal keratinocytes that, unlike BCC, CAN metastasise. Arises on sun-damaged skin (and from actinic keratoses/Bowen disease) or in immunosuppressed patients (transplant recipients). A rapidly growing, keratotic, tender or ulcerated nodule that needs the suspected-cancer pathway.

A malignancy of melanocytes with the potential for early metastasis — the skin cancer that kills. Recognised by the ABCDE rule and the "ugly duckling" sign. Prognosis is driven by BRESLOW THICKNESS (depth of invasion), which is why early excision matters so much.

Squamous cell carcinoma in situ — full-thickness epidermal dysplasia that has not yet breached the basement membrane. A slowly enlarging, well-demarcated, erythematous SCALY plaque, classically on the lower legs of older women. A small proportion progress to invasive SCC.

A pre-malignant patch of keratinocyte dysplasia from cumulative sun damage. Rough, scaly macules/papules on chronically sun-exposed skin — often better felt than seen (sandpaper texture). A small proportion progress to invasive SCC, so thick/changing lesions are treated and reviewed.

A rapidly growing, dome-shaped nodule with a central keratin-filled crater that classically arises over weeks and may then spontaneously regress. Because it is histologically and clinically hard to separate from well-differentiated SCC, it is generally treated as an SCC — excised, not watched.

A benign proliferation of melanocytes (a "mole"). Junctional (flat, at the dermo-epidermal junction), compound (raised, both layers), and intradermal (dome-shaped, skin-coloured, older lesions). The whole point of the card is telling a benign naevus from melanoma using symmetry, uniformity and stability.

A common benign cyst lined by epidermis and filled with keratin. A mobile, dome-shaped dermal nodule with a central PUNCTUM, classically discharging foul cheesy keratin if squeezed. Often mislabelled "sebaceous cyst". Only needs treatment if symptomatic, inflamed or infected.

A common benign fibrous dermal nodule, often on the legs of women, frequently following minor trauma or an insect bite. The diagnostic test is the DIMPLE (Fitzpatrick) sign — lateral pinching causes the lesion to dimple inward.

A very common benign warty plaque of older adults with a characteristic "stuck-on" appearance, as if it could be flicked off. Sharply demarcated with a greasy/verrucous surface and horn cysts. The job is to distinguish it confidently from melanoma and pigmented BCC.

A benign tumour of mature fat — the commonest soft-tissue tumour. A soft, mobile, painless subcutaneous lump that "slips" under the fingers. Reassurance is usually all that is needed.

The commonest benign tumour of infancy — a proliferation of vascular endothelium ("strawberry naevus"). Typically appears in the first weeks of life, proliferates for months, then spontaneously involutes over years. Most need only reassurance; a minority need treatment for complications.

A common benign reactive overgrowth of capillaries (lobular capillary haemangioma) — neither pyogenic nor a granuloma. A rapidly growing, friable, bright-red nodule that BLEEDS profusely with minor trauma, often after a minor injury, in pregnancy, or on the fingers/lips. (One of the lesions Raahat met in the exam.)

A common chronic, relapsing inflammatory dermatitis of the sebaceous-rich areas (scalp, face, central chest), driven by an inflammatory response to commensal Malassezia yeast. Infantile form = cradle cap. Florid or sudden severe disease is a flag for HIV/Parkinson disease.

A chronic, relapsing inflammatory disease of follicular occlusion in apocrine-gland-bearing flexures (axillae, groin, inframammary, perianal). Recurrent painful nodules and abscesses that rupture, discharge and form sinus tracts and scars. Strongly associated with smoking and obesity.

An acquired autoimmune disorder in which melanocytes are destroyed, producing well-demarcated patches of complete DEPIGMENTATION (stark white). Non-segmental (symmetrical, commonest, associated with other autoimmune disease) and segmental (unilateral, dermatomal, younger). The discriminator from pityriasis versicolor is the absence of scale and the total pigment loss.

A reactive inflammation of subcutaneous fat (septal panniculitis) presenting as crops of tender, red, raised nodules, classically on the SHINS. It is a marker — the task is to find the underlying cause (infection, sarcoidosis, IBD, drugs, pregnancy) because the rash itself is self-limiting.

An acute, usually self-limiting, immune-mediated reaction characterised by TARGET lesions, most often triggered by herpes simplex virus (and Mycoplasma in children) rather than drugs. The key job is to separate this generally benign condition from SJS/TEN.

Symmetrical, velvety, hyperpigmented thickening of flexural skin (neck, axillae, groin). Almost always a sign of INSULIN RESISTANCE (obesity, type 2 diabetes, PCOS); a sudden, extensive or atypical-site onset in a thin adult is the paraneoplastic red flag for an internal (classically gastric) adenocarcinoma.

A net-like (reticulated), mottled, purplish discolouration of the skin from sluggish/obstructed dermal microcirculation. Benign physiological cutis marmorata (cold-induced, reversible) versus a pathological persistent pattern pointing to vasculopathy — the antiphospholipid syndrome being the high-yield association.

Non-blanching skin discolouration from extravasated blood: petechiae (1 cm). The two questions are: is it PALPABLE (vasculitis) or flat (thrombocytopenia/clotting), and is the child/adult systemically unwell (meningococcal sepsis is the emergency).

A chronic leg ulcer from sustained venous hypertension (valvular incompetence). Shallow, exudative ulcers in the GAITER area (medial malleolus), surrounded by the signs of venous disease. The decisive step before treatment is measuring the ankle-brachial pressure index (ABPI) to make compression safe.

A leg/foot ulcer from inadequate arterial supply (peripheral arterial disease). PUNCHED-OUT, painful ulcers at the distal points and pressure areas (toes, heel, lateral malleolus), with a cold, pulseless, hairless limb. Compression is contraindicated — these need revascularisation.

A PAINLESS ulcer at a weight-bearing pressure point, caused by the loss of protective sensation (peripheral neuropathy — most often diabetic). Repeated unnoticed trauma over a bony prominence (metatarsal heads, heel) breaks the skin, often with surrounding callus. Part of the diabetic foot, managed by offloading.

Localised damage to skin and underlying tissue from sustained pressure (and shear) over a bony prominence — sacrum, heels, ischial tuberosities, greater trochanter. Largely PREVENTABLE; managed by relieving pressure, optimising the patient, and graded by depth (Category/Grade 1–4).

Tissue injury from heat, chemicals, electricity or radiation. The acute management (fluid resuscitation by the Parkland formula, airway, analgesia) is covered on the Acute Care page; this card is the DERMATOLOGICAL view — assessing depth and surface area, and knowing the referral thresholds.

An autoimmune SUBepidermal blistering disease of the ELDERLY: IgG autoantibodies against hemidesmosomal antigens (BP180/BP230) split the skin below the epidermis, producing TENSE, intact blisters. Because the split is deep, the roof is thick — blisters are tense and Nikolsky NEGATIVE. Mucosal involvement is uncommon.

An autoimmune INTRA-epidermal blistering disease: IgG autoantibodies against desmoglein-3 break the bonds between keratinocytes (acantholysis), so the split is high within the epidermis. The thin roof means blisters are FLACCID and rupture into painful EROSIONS, with a POSITIVE Nikolsky sign. Mucosal involvement is early and prominent, often the presenting feature.

A rare, painful, ulcerating neutrophilic dermatosis — NOT an infection despite the name. A rapidly enlarging ulcer with a characteristic violaceous, undermined, overhanging border, classically on the legs. Strongly associated with IBD, inflammatory arthritis and haematological disease, and it Koebnerises — so debriding/operating on it makes it worse.

Reactivation of latent varicella-zoster virus (from prior chickenpox) in a single sensory dorsal-root/cranial ganglion, producing a painful vesicular rash in ONE dermatome that does not cross the midline. Key exam points are early antivirals, the ophthalmic (Hutchinson sign) and otic (Ramsay Hunt) danger zones, and post-herpetic neuralgia.

A dermatological EMERGENCY: widespread herpes simplex virus infection superimposed on eczema (or another barrier-defective dermatosis). A rapidly spreading eruption of MONOMORPHIC punched-out erosions in an unwell, febrile patient — needs prompt systemic aciclovir, and ophthalmology if near the eyes.

An intensely itchy, chronic, blistering eruption that is the cutaneous expression of COELIAC disease (gluten-sensitive enteropathy), mediated by IgA antibodies. Symmetrical grouped vesicles/papules on the extensor surfaces; the key links are the gluten enteropathy and the response to a gluten-free diet (and dapsone).