Eczema, psoriasis, skin cancers, infections, blistering disorders, and drug reactions — clinical features and management.
Common inflammatory skin condition affecting ~85% of adolescents and young adults. Caused by a combination of excess sebum production, follicular hyperkeratinisation, Cutibacterium acnes colonisation, and inflammation. Presents with comedones, papules, pustules, and in severe cases, nodules and cysts. Treatment is stepwise from topical retinoids/benzoyl peroxide to oral isotretinoin for severe/scarring disease.
Pre-malignant epidermal lesions caused by cumulative UV damage, commonly on sun-exposed skin of fair-skinned individuals. Approximately 5–10% may progress to squamous cell carcinoma over 10 years. Managed with cryotherapy, topical 5-FU, imiquimod, or photodynamic therapy per NICE CKS guidance.
Hair loss is classified as scarring (cicatricial) or non-scarring, and further by pattern and distribution. Non-scarring causes include androgenetic alopecia, telogen effluvium, and alopecia areata. Scarring causes include lichen planopilaris and discoid lupus. Diagnosis requires careful history, examination, and sometimes scalp biopsy. Early treatment is essential for scarring alopecias to prevent irreversible loss.
An autoimmune non-scarring alopecia characterised by well-circumscribed patches of hair loss with exclamation mark hairs. T-cell mediated attack on hair follicle bulb. Associated with other autoimmune conditions (thyroid, vitiligo). ~50% recover within 1 year. Severe forms include alopecia totalis (whole scalp) and universalis (whole body). Baricitinib (JAK inhibitor) is NICE-approved for severe disease.
Localised swelling of the deep dermis, subcutaneous, or submucosal tissue caused by increased vascular permeability. May accompany urticaria (histamine-mediated) or occur in isolation (often bradykinin-mediated). Hereditary angioedema (HAE) due to C1-esterase inhibitor deficiency is a rare but important cause requiring specific treatment with C1-INH concentrate or icatibant.
Chronic relapsing inflammatory skin condition representing the most common form of eczema. Part of the atopic triad with asthma and allergic rhinitis. Characterised by intensely pruritic, dry, erythematous skin in a flexural distribution. Pathogenesis involves filaggrin gene mutations causing epidermal barrier dysfunction and Th2-mediated immune dysregulation.
The most common skin cancer in the UK, arising from basal keratinocytes. Locally invasive but almost never metastasises. Strongly associated with cumulative UV exposure. Managed per NICE NG12 suspected cancer pathway with 2-week wait referral.
The most common autoimmune blistering disease, caused by IgG autoantibodies against BP180 and BP230 antigens at the dermal-epidermal junction. Presents with tense blisters on an erythematous or urticarial base in elderly patients. Managed with potent topical corticosteroids (clobetasol) or systemic immunosuppression.
An acute, spreading bacterial infection of the dermis and subcutaneous tissue, most commonly caused by beta-haemolytic streptococci and S. aureus. Presents with erythema, warmth, swelling, and pain, predominantly affecting the lower limbs. Managed with flucloxacillin 500 mg–1 g QDS. Eron classification guides severity and setting of treatment (NICE NG141).
Inflammatory skin reaction caused by direct contact with an external substance. Two main types: irritant contact dermatitis (ICD, ~80%) caused by direct chemical damage, and allergic contact dermatitis (ACD, ~20%) caused by a type IV delayed hypersensitivity reaction. Occupational dermatitis is the most common occupational skin disease.
An intensely pruritic blistering skin disease caused by IgA deposition at the dermal papillae, strongly associated with coeliac disease. Virtually all patients have underlying gluten-sensitive enteropathy on duodenal biopsy, even if asymptomatic. Managed with strict gluten-free diet and dapsone for symptom relief.
Adverse cutaneous reactions to medications, representing ~2% of all drug adverse effects. Range from mild morbilliform (exanthematous) rashes to life-threatening Stevens-Johnson syndrome/toxic epidermal necrolysis. The most common pattern is morbilliform eruption appearing 7–14 days after drug initiation. Identification and withdrawal of the causative drug is the cornerstone of management.
Common inflammatory skin condition characterised by pruritus, erythema, and dry skin. Encompasses atopic eczema (most common), contact dermatitis, discoid eczema, varicose eczema, and seborrhoeic dermatitis. Atopic eczema affects ~20% of children and ~5% of adults in the UK. Management follows a stepwise approach with emollients as the cornerstone.
An acute, self-limiting, immune-mediated condition characterised by typical target lesions predominantly on the extremities. Most commonly triggered by herpes simplex virus (HSV) infection (~90%). Distinct from Stevens-Johnson syndrome. Usually resolves within 2–4 weeks without treatment. Recurrent cases may benefit from prophylactic aciclovir.
The most common form of panniculitis (inflammation of subcutaneous fat), presenting as tender, red nodules on the anterior shins. Most frequently idiopathic or triggered by streptococcal infection, sarcoidosis, drugs (OCP, sulfonamides), or inflammatory bowel disease. Self-limiting over 3–6 weeks. Treatment is supportive with NSAIDs and leg elevation.
Common ectoparasitic infestation caused by Pediculus humanus capitis, predominantly affecting primary school-aged children. Transmitted by direct head-to-head contact. Diagnosis requires identification of live lice by wet combing (detection combing). Treated with dimeticone 4% lotion or physical removal by wet combing ('Bug Busting').
Reactivation of varicella-zoster virus (VZV) from dorsal root ganglia, causing a painful unilateral vesicular eruption in a dermatomal distribution. Lifetime risk ~30%. Complications include post-herpetic neuralgia (PHN) and herpes zoster ophthalmicus. Antiviral treatment (aciclovir or valaciclovir) within 72 hours of rash onset reduces severity. Shingrix vaccine now offered at age 65.
Excess melanin deposition in the skin, classified as epidermal (brown), dermal (grey-blue), or mixed. Common causes include post-inflammatory hyperpigmentation, melasma, and drug-induced pigmentation. Systemic causes such as Addison's disease and haemochromatosis must be excluded. Management targets the underlying cause with photoprotection as the cornerstone.
Chronic wounds of the lower leg persisting >2 weeks. Venous ulcers account for ~70%, arterial ~15%, and mixed ~10–15%. Venous ulcers are managed with compression bandaging (after excluding arterial disease with ABPI). NICE NG168 provides guidance. Estimated prevalence ~1% of UK adults, costing the NHS ~£1 billion/year.
A chronic inflammatory dermatosis characterised by pruritic, polygonal, purple, flat-topped papules (the '5 Ps'). Affects skin, mucous membranes, nails, and hair. T-cell mediated attack on basal keratinocytes. Associated with hepatitis C. Usually self-limiting over 1–2 years but oral disease may persist.
A chronic inflammatory skin condition predominantly affecting the anogenital region, causing white, atrophic patches with intense pruritus. Most common in postmenopausal women. Associated with ~4–5% risk of vulval SCC. First-line treatment is ultrapotent topical corticosteroids (clobetasol propionate 0.05%).
A serious autoimmune blistering disease caused by IgG antibodies against desmoglein 3 (±desmoglein 1), leading to intraepidermal acantholysis. Presents with painful oral erosions and flaccid skin blisters. Nikolsky sign positive. Untreated mortality historically >75%; now ~5–10% with immunosuppressive therapy.
Localised injuries to the skin and underlying tissue caused by sustained pressure, often over bony prominences. Classified into 4 stages (NPUAP/EPUAP). Major cause of morbidity in hospitalised and immobile patients. Prevention is paramount — using risk assessment tools (Waterlow score), regular repositioning, and pressure-relieving devices. NICE CG179 provides UK guidance.
Chronic immune-mediated inflammatory skin disease affecting ~2–3% of the UK population. Characterised by well-demarcated, erythematous plaques with silvery scale, typically on extensor surfaces and scalp. Driven by Th17/IL-23 pathway. Associated with psoriatic arthritis (up to 30%), cardiovascular disease, metabolic syndrome, and depression.
Chronic inflammatory arthritis associated with psoriasis, affecting up to 30% of psoriasis patients. Classified into five patterns by Moll & Wright: asymmetric oligoarthritis (most common), symmetric polyarthritis, DIP-predominant, spondylitis, and arthritis mutilans. Diagnosis is clinical using CASPAR criteria. Treatment follows a treat-to-target approach with DMARDs and biologics.
A highly contagious parasitic infestation caused by the mite Sarcoptes scabiei. Presents with intense pruritus (worse at night) and characteristic burrows in finger web spaces, wrists, and genitalia. Transmitted by prolonged skin-to-skin contact. Treated with permethrin 5% cream or oral ivermectin, with simultaneous treatment of close contacts.
Second most common skin cancer in the UK, arising from epidermal keratinocytes. Unlike BCC, SCC carries significant metastatic potential (2–5%). Strongly associated with cumulative UV exposure, immunosuppression, and pre-malignant lesions such as actinic keratoses and Bowen's disease.
A severe, immune-mediated mucocutaneous reaction characterised by widespread epidermal necrosis and mucosal erosions. SJS involves <10% BSA detachment; overlap SJS-TEN 10–30%; TEN >30%. Mortality: SJS ~5%, TEN ~25–30%. Most commonly drug-induced (allopurinol, anticonvulsants, antibiotics). Requires immediate drug withdrawal, supportive care in a burns unit, and consideration of ciclosporin.