Inflammatory skin pathology and skin tumours Flashcards
Eczema/Dermatitis stages
Clinically 3 stages:
- Acute dermatitis = Skin red, weeping serous exudate +/- small vesicles
- Subacute dermatitis = Skin is red, less exudate, itchier, crusting
- Chronic dermatitis = Skin thick and leathery, secondary to scratching
Eczema/Dermatitis histology
- Spongiosis = = intercellular oedema within epidermis
- Chronic inflammation – predominantly superficial dermis
Atopic eczema
- Usually starts in childhood, Often FH and associated with asthma and allergic rhinitis
- Type 1 hypersensitivity reaction to allergen
Contact irritant dermatitis
- Direct injury to skin by irritant; affects anyone in contact with irritants e.g. acid, detergent
Contact allergic dermatitis
- Affects those with hypersensitivity to irritant; combines with epidermal proteins to become immunogenic; e.g. nickel, dyes, rubber
Dermatitis of unknown aetiology
- Seborrheic dermatitis – affects areas rich in sebaceous glands – scalp, forehead, upper chest
- Nummular dermatitis – coin shaped lesions
Psoriasis definition
- 1-2% of population
- Well defined, red oval plaques on extensor surfaces (knees, elbows, sacrum)
- Fine silvery scale
- Auspitz sign = small bleeding points after removal of scale layers
o+/- pitting nails. +/- sero-negative arthritis - Cancer – increased risk of non-melanoma skin cancer
Psoriasis histology
- Psoriasiform hyperplasia
- Regular elongated club shaped rete ridges
- Thinning of epidermis over dermal papillae
- Collection of neutrophils in scale – Munro micro-abscesses
Psoriasis aetiology
- Genetic – FH: multiple loci e.g. PSORS gene in MHC of Chromosome 6p2
- Environmental – infection, stress, trauma, drugs
DLE =
- Discoid lupus erythematosus – skin only
SLE =
- Systemic–visceral disease
- Butterfly rash on cheeks and nose
Lupus Erythematosus
- Red scaly patches on sun-exposed areas, scalp involvement
- Autoimmune disorder primarily affecting connective tissue
- Histology:
Thin atrophic epidermis with thickened basement membrane
Dermatomyositis
Symptoms:
- Peri-ocular oedema and erythema (Heliotropic rash)
- Erythema in photosensitive distribution
- Myositis – proximal muscle weakness - can check for CK
- 25% associated with underlying visceral cancer
Bullous pemphigoid
- Formation of fluid filled blisters
- Sub-epidermal
- Ends in D = deep
- Autoantibodies to glycoprotein in basement membrane. Destruction causes blister formation which do not rupture
- Elderly
- Can be localised or extensive disease
Dermatitis Herpetiformis
- Small intensely itchy blisters on extensor surfaces
- Often young patients - associated with coeliac disease
- IgA deposition in dermal papillae on immunofluorescence
- Histology – neutrophil micro-abscesses in dermal papillae – sub-epidermal bulla
Basal Cell Carcinoma
- Commonest malignant tumour of skin
- Aetiology = sun exposure, radiotherapy, Gorlin’s syndrome
Clinically: - Early – nodule
- Late – rodent ulcer
- Morphoeic BCC = ill-defined and infiltrative
- Histology - islands of basaloid cells
Squamous cell carcinoma aetiology
- UV irradiation
- Radiotherapy
- Hydrocarbon exposure
- Chronic scars/ulcers (SCC arises with these)
- Immunosuppressed – renal transplant patients at increased risk
- Drugs – e.g. BRAF inhibitors for melanoma
Squamous cell carcinoma features
- Clinically - nodule with ulcerated crusted surface
- Histology - invasive islands wit trabeculae of squamous cells with cytological atypia
Acitinic Keratosis
- Pre-malignant disease of SCC
- Dysplasia to squamous epithelium
- Very common on chronic sun exposed sites
- Scaly lesion with erythematous base
Melanocyte tumours
- Melanocytes derive from neural crest
- Function – produce melanin which is transferred to epidermal cells to protect the nucleus from UV radiation
- Give rise to naevi/moles (benign) and melanoma (malignant)
Naevi/moles
- Local benign collections of melanocytes
Several types: - Superficial – congenital or acquired
- Deep – blue naevi (Mongolian spot)
Atypical mole syndrome
- Families with increased incidence of melanoma
- Multiple clinically atypical moles
- Histologically atypical/ dysplastic
- Increased risk of developing melanoma
Melanoma risk factors
- Sun exposure – especially short intermittent severe exposure
- Race – celtic with red hair, blue eyes, fair skin who tan poorly most at risk.
- Family history – atypical mole syndrome
- Giant congenital naevi
Lentigo Maligna Melanoma
- Face, elderly people, slow growing, flat, pigmented patch
- Proliferation of atypical melanocytes along basal layer of epidermis
- Skin also shows signs of chronic sun damage
- Late in disease, melanocytes may invade dermis which can metastasise
Acral Lentiginous Melanoma
- Palms and soles; commonest form in afro-Caribbean people
- Forms enlarging pigmented patch
- No marked sun damage
Superficial spreading melanoma
- Commonest type of melanoma in UK
- Early – flat macule
- Late – black/blue nodule
- Histology – proliferation of atypical melanocytes which invade epidermis and dermis
- Genetics – often BRAF mutations targets for anticancer agents.
Nodular melanoma
- Starts as pigmented nodule +/- ulceration
- Poor prognosis
- Histology – invasive atypical melanocytes invade dermis to produce nodules of tumour cells
Prognosis of melanoma
- Most important factor = Breslow thickness
- Measure on microscope from granular layer of epidermis to base of tumour
- Back, arms, neck, scalp = poorer prognosis
- Sentinel node - first to be drained and tested
Treatment of melanoma
- Surgery – excise primary and lymph nodes if sentinel node is +ve
- BRAF inhibitors – 60% of melanomas have B-RAF gene mutations
Breslow thickness thresholds
Breslow thickness (mm) 5yr survival % <1 91-95 1-2 75-90 2-4 60-75 >4 45-60