Skin Pathology

Infections
1. Viral
  1. – HPV: warts/verrucae, Genital warts
  2. – Herpes zoster/simplex
  3. –HIV: Transient, itchy eruption
2. Bacterial
  1. Abscesses, Furuncle/Boil (single hair follicle), Carbuncle (several contiguous hair follicles)
  2. Mycobacteria: TB of skin, Leprosy
  3. Impetigo: S. aureus in kids; Streptococcus in older, ‘scrum pox’
  4. Cellulitis: Swollen, hot, red, painful, S. pyogenes
3. Fungal
  1. Superficial: Tinea: ringworm, athletes foot; Candida: thrush
  2. Deeper: Tropical, immunosuppressed
4. Protozoan
  1. Rare in temperate climate Leishmaniasis: sandflies; amoebiasis, trypanosomiasis
Non-Infectious Inflammation
1. Lichen Planus
  1. Puritic, purple, polygonal, planar papules and plaques Destruction of keratinocytes ,1% pop, middle age Lymphohistiocytic infiltrate at dermo-epidermal junction; band like distribution • Lymphocytic attack of basal layer – Bullaeformation • Postinflammatory hypo/hyperpigmentation
2. Psoriasis
  1. Common (1-2% pop) inflammatory condition, genetics • Elbows, knees, scalp, mean onset 25y Well-demarcated, pink-salmon plaque, silvery scale Scraping off the scale reveals bleeding points Microscopically – ↑Epidermal cell turnover – Downward elongation of rete ridges, thinned epidermis – Dilated vessels, polymorphs, sterile pustules
3. Urticaria
  1. Reaction Pattern of Hives and Wheals Oedema of dermis: -> erythematous and/or oedematous papule (Papule: small elevated skin lesion < 5-10 mm), Clinically: itching and swelling Examples: nettles rash, hives Histology: inflammation, separation of collagen bundles, eosinophils, mast cells, histamine, IgE
Eczema/Dermatitis
1. ‘Bubble up / Boil over’ Reaction pattern rather than disease. Common, 10% pop (40% at some point in life) Signs: – Red (erythematous) skin – Tiny vesicles develop Surface develops scales-> cracking, bleeding -> discomfort – Skin becomes tender; secondary infection Variation – Cause: contact, site Effects: Barrier damage Water loss, entry of allergens Treatment: – Topical creams, steroids
  1. Underlying pathological processes – Swelling within epidermis Separation of keratinocytes by fluid accumulation (spongiosis). Hyperkeratosis: ↑ thickness of stratum corneum Parakeratosis: retention of nuclei in SC: scales Inflammation: oedema
Blistering (Bullous) Disorders
1. Pemphigus
  1. Rare auto-immune blistering disorder • Middle-aged (40-60y) • Fatal if untreated – Serum electrolyte loss, infection • Intra-epidermal blister – Location varies with type • Circulating auto-antibodies (IgG) directed at components of intercellular bridges w/in epidermis – epidermisfallsapart – loose keratinocytes
2. Dermatitis herpetiformis
  1. Young adults (20-40y), rare – Knees, elbows • Blister at dermo-epidermal junction – Very pruritic: rarely see intact blister • Associated with coeliac disease • Granular IgA deposit on BM
3. Bullous Pemphigoid
  1. Elderly, > 60 yr, 0.7/100,000 • Self- limiting • Blister at dermo-epidermal junction • Circulating auto-antibodies (IgG) on BM – Immunofluorescence • Antigen-antibody complex – Degranulation of mast cells, eosinophils
Epidermal Cell Conditions
1. Malignant Epidermal Neoplasms
  1. SCC (#2)
    1. Keratoacanthoma
      1. Variant of SCC • Clinically benign and regresses • Crater-like symmetrical architecture – Keratin debris • Most common site is face – Sun damaged skin
    2. Arises from keratinocytes of upper layers of epidermis • Common- 15% skin malignancies • Locally invasive, metastasise late • Elderly, face, hands, M>F – Chronic sun exposure, in situ lesions – Chemicals eg tar, oil, ionising-irradiation • Grossly – Roughened keratotic areas, papules, nodules, ulcers or horns • Histologically – Disorganised keratinocytes, malignant cytology • T reatment – Surgical excision, more resistant to radiotherapy than BCC
  2. BCC (#1)
    1. • Arises from basal keratinocytes of epidermis • Common,70% skin malignancies • Slow growing, locally very invasive, rarely metastasise • Face, elderly, pale skin – Chronic sun exposure • Grossly – Ulcerated irregular lesion, raised pearly border (Rodent ulcer) – Prominent, dilated blood vessels (telangectasia) • Histological – Clumps of cells surrounded by rim of cells with nuclei line up like a picket fence (palisading). • Treatment – Local excision +/- radiotherapy
2. Benign Epidermal Neoplasms
  1. Skin tags
    1. – Fibroepithelial polyp, friction -Pedunculated, benign
  2. Squamous cell papilloma
    1. -HPV -Verrucae/warts
  3. Seborrhoeic wart / keratosis
    1. Keratosis = excess keratin] • Basal cell papilloma (benign) • Proliferation of cells that resemble basal cells • Common in elderly, trunk – extremities, head, neck • Rarely become malignant • Keratin-filled plugs, cysts • Exophytic, coin-like plaques – ‘stuck-on’ appearance – Dark, greasy-looking irregular
3. Pre-Malignant Epidermal Neoplasms
  1. Squamous cell carcinoma is preceded by series of progressive dysplastic changes – chronic exposure to sunlight – hyperkeratosis – > Actinic (sun-related) keratosis • > 1 cm, tan-brown / red, rough (sandpaper) • Hyperplasia of basal cells • Solar elastosis (blue-grey elastic fibres)
Melanocytes
1. Freckles (Ephilides)
  1. • Focal area of increased melanocyte activity • Common, children, lightly pigmented individuals • Fade and darken according to sun exposure
2. Lentigo
  1. • Common, localised, benign hyperplasia of melanocytes • Skin, mucous membranes • Small, oval, tan-brown patches • Do not darken in response to sunlight
3. Melanocytic Naevi ‘Moles’
  1. Malignant Melanoma
    1. Tumour composed of malignant melanocytes – More correctly ‘melanocarcinoma’ – Skin, (retina, leptomeninges) • Usually pigmented macules, papules or nodules – Visible from early stages – Sun exposed surfaces • Excision prior to dermal invasion = cure • Aetiology – **UV light • episodic, acute exposure with burning, fair skin – Gene mutations • CDNK2A (TSG)germline, familial melanomas • BRAF / NRAS (oncogenes), somatic
      1. Can arise from any melanocyte – Expect from benign naevi: larger numbers cells • Post mitotic – Classes of naevi with active junctional component – De novo • Prognosis – Depends on thickness (Breslow) – Completely excised non-ulcerated melanoma < 1 mm ~ 100% cure • Clinical course – Metastatic spread, early in development – Skin, brain, GI – Excise primary lesion
    2. Lentigomaligna (15%) Elderly, face
    3. Superficial spreading**(50%) • Flat, female, leg
    4. Acrallentiginous (10%) •Palms / soles of feet, most common non- Caucasian type
    5. Nodular (25%) • Pigmented nodule, may ulcerate, male, trunk

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Skin Pathology

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	Created by Sara Hojabri about 7 years ago