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Dermatology Notes

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Dermatology Contents

Melanocytic Lesions Melanocytic Naevi:Melanocytes which fail to mature or migrate in utero Congenital: 1% of children have small naevi (rare giant 'bathing trunk' naevi - high risk of malignancy; Mongolian blue spot - due to melanocytes in dermis, benign) Acquired: develops after birth (usually <25 years old) o Junctional - macular o Compound - 'warty' o Intradermal - smooth + dome shaped o Halo naevus - undergoing regression, benign o Blue naevus - melanocytes in dermis, usually benign, often extremities

Sinister features:
- 50% of melanomas arise from naevi
- Changes in size
- Irregular shape
- Irregular colour
- >1cm diameter
- Itch
- Bleeding/ulceration

Malignant Melanoma:Types: o Superficial spreading (common, usually legs in women + trunk in men) o Nodular (poor prognosis, may be amelanotic) o Lentigo maligna melanoma (usually on face in elderly, arise within lentigo maligna) o Acral (palms or soles, can occur in Asian or Afro-Caribbean)

Treatment:
- Excision: optimum excision margin unknown, generally 1cm for every 1mm depth invasion
- Chemotherapy or immunotherapy of limited use Prognosis:
- Depends on depth of invasion, or Breslow thickness (depth in mm from granular cell layer)
- 5YSR: depth<1.5mm (90%), 1.5-3mm (60%), >3mm (40%)

Nonmelanoma Cancers and Benign Tumours Benign Tumours of Epidermis + Appendages Squamous cell papilloma
- Common tumour, arises from keratinocytes
- May resemble viral wart clinically
- Excision, or curettage with cautery to base is treatment of choice + histology should be checked Seborrhoeic keratosis (basal cell papilloma, seborrhoeic wart)
- Common benign epidermal tumour, unrelated to sebaceous glands
- Cause: usually unexplained. Multiple lesions may be inherited (autosomal dominant), occasionally follows inflammatory dermatosis
- Presentation: usually arise after age 50 (but flat inconspicuous lesions often visible earlier). Often multiple but may be single. Lesions more common face + trunk. Distinctive 'stuck-on' appearance; may be flat, raised or pedunculated; colour varies from yellow to dark brown and surface may have greasy scaling + scattered keratin plugs ('currant bun' appearance). Lesions may multiply with age but remain benign
- DD: pigmented naevus, malignant melanoma, basal cell carcinoma (BCC), AfroCaribbeans may have dermatosis papulosa nigra
- Ix: biopsy needed only in rare dubious cases. Histology is diagnostic - lesions lies above general level of surrounding epidermis + consists of proliferating basal cells +
horn cysts
- Treatment: can safely be left alone. Ugly/easily traumatised ones can be removed with curette under local (also provides histology), or by cryotherapy Skin tags (acrochordon)
- Common benign outgrowths of skin. Affect mainly middle-aged + elderly
- Cause: unknown. Trait is sometimes familial. Most common in obese women. Rare associations = tuberous sclerosis, acanthosis nigricans, acromegaly, diabetes
- Presentation: occur around neck + within flexures. Look unsightly + may catch on clothing/jewellery. Soft, skin-coloured or pigmented pedunculated papules
- DD: rarely confused with small melanocytic naevi
- Treatment: small lesions snipped off with fine scissors, frozen with liquid nitrogen or destroyed with hyfrecator without local anaesthetic. No way of preventing new ones. Linear epidermal naevus
- These lesions are an example of cutaneous mosaicism and so tend to follow Blashko's lines

Epidermoid and Pilar cysts
- Common. Occur on scalp, face, behind ears, trunk

MiliaOften have a central punctum which secretes foul-smelling material when ruptured Histologically, the lining of the cyst resembles normal epidermis (epidermoid) or outer root sheath of the hair follicle (pilar) Occasionally, an adjacent foreign body reaction is noted Treatment: excision, or excision followed by expression of contents + removal of cyst wall Small subepidermal keratin cysts Common on the face in all age groups Appear as white millet seed-like papules of 0.5-2mm diameter. Occasionally seen in sight of previous subepidermal blister (e.g. in epidermolysis bullosa or porphyria cutanea tarda) Contents of milia can be picked out with sterile needle without local anaesthesia

Chondrodermatitis nodularis helicis (painful nodule of the ear, ear corn)
- Strictly, not a neoplasm, but a chronic inflammation
- Painful nodule develops on helix (or antehelix) of ear, most often in men
- Looks like small corn, tender and prevents sleep
- Histologically, thickened epidermis overlies inflamed cartilage
- Treatment: wedge-resection under anaesthetic successful if cryotherapy or Intralesional triamcinolone (steroid) injection fails

Premalignant Tumours of Epidermis + Appendages Keratoacanthoma
- Some argue that this rapidly growing tumour should be classified as benign, but some do transform into squamous cell carcinoma
- Cause: photosensitising chemicals (e.g. tar, mineral oils) act as cocarcinogens with UVR. They may also follow therapeutic immunosuppression
- Clinical features: mainly occur on exposed skin in fair individuals. 2/3 on face, most of the rest on the arms. Lesion starts as a pink papule that rapidly enlarges (may reach 1cm in 1-2months). After 5-6weeks, centre of the nodule forms either a keratinous plug or a crater. If left, lesion often resolves spontaneously (6-12months) but leaves an ugly, depressed scar
- DD: need to distinguish from squamous cell carcinoma (which grow more slowly and usually lack symmetry)
- Histology: not possible to tell keratoacanthoma from squamous cell carcinoma histologically unless architecture of whole lesion assessed, including its base. Typical lesion is symmetrical + composed of proliferating fronds of epidermis which retain well-differentiated squamous appearance, with production of much 'glassy' keratin. Centre of the cup-shaped mass is filled with keratin
- Treatment: excision or curettage + cautery both effective. Occasionally, further curetting may be needed but this should be performed only once (if still ineffective, lesion must be excised) Intraepidermal carcinoma (Bowen's disease)
- Usually single, slowly expanding pink scaly plaques, take years to reach diameter of a few cm
- Border is sharply defined, with reniform (kidney-shaped) projections + notches
- ~3% progress to invasive squamous cell carcinoma. The presence of several may be clue to previous exposure to carcinogens
- DD: psoriasis, discoid eczema, superficial basal cell carcinoma, Paget's disease
- Treatment:

o o o o o o

Lesions unaffected by local steroids Small lesions left under observation in frail/elderly pts. Cryotherapy or curettage for small lesions on a site where healing is good (e.g. face or trunk) Excision is an alternative Photodynamic therapy useful for large lesions on poor healing site (e.g. lower legs of elderly) Topical 5-FU or imiquimod helpful for multiple lesions

Actinic Keratosis
- Discrete, rough-surfaced lesions appear on sun-damaged skin. Only a few turn into squamous cell carcinoma
- Cause: cumulative effects of sun exposure. Those with fair skin living near equator are most at risk and invariably develop these 'sun warts'. High melanin is protective.
- Presentation: affect middle-aged + elderly in temporate climates + young people in tropics. Pink or grey rough scaling macules or papules (usually <1cm)
- Complications: transition to squamous cell carcinoma (rare). Should be suspected if lesion enlarges, ulcerates or bleeds. Cutaneous horn = hard keratotic protrusion based on an actinic keratosis, squamous cell papilloma or viral wart
- DD: seborrhoeic wart, viral wart, keratoacanthoma, intraepidermal carcinoma or squamous cell carcinoma
- Ix: biopsy if concern over malignant change
- Histology: alternating zones of hyper + para-keratosis overlie thickened or atrophic epidermis. Normal maturation pattern of epidermis lost + occasional pleomorphic keratinocytes seen. Solar elastosis seen in sup dermis
- Treatment: o Freezing with liquid nitrogen or carbon dioxide snow o Curettage best for large lesions + cutaneous horns o 5-FU cream for multiple lesions (inc subclinical). Cream applied once/twice daily until marked inflammatory response in treated area (takes 3 weeks). Application then stopped. Healing then rapid occurs. Discomfort from treatment alleviated with short-term topical steroids. o 3% sodium diclofenac (new on the market) o Phototherapy (using aminolaevulinic acid then blue light) is effective but requires specialised facilities o Lesions that do not respond should be regarded with suspicion and biopsied

Malignant Epidermal Tumours Basal Cell Carcinoma
- Most common form of skin Ca. Most commonly found on faces of middleaged/elderly pts. Lesions invade locally but never metastasise
- Cause: prolonged sun exposure so most common in white people living near the equator. May also occur in scars caused by x-rays, vaccination or trauma. Photosensitising pitch, tar and oils can act as cocarcinogens with UVR. Previous treatment with arsenic predisposes to multiple BCCs many years later. Multiple BCCs are found in 'Naevoid BCC' syndrome (Gorlin's) - autosomal dominant
- Presentation: o Nodulo-ulcerative - most common type. Early lesion is small glistening translucent skin-coloured papule that slowly enlarges. Central necrosis leaves an ulcer with an adherent crust + rolled pearly edge. Fine telangectatic vessels run across tumour surface. Without treatment, lesions may reach 12cm in 5-10yrs

Cystic - lesion is at first like the nodular type, but later cystic changes predominate and the nodule becomes tense and more translucent, with marked telangectasia o Cicatricial (morphoeic) - slowly expanding yellow or white waxy plaques with ill-defined edge. Ulceration + crusting, followed by fibrosis, are common and the lesion may look like an enlarging scar o Superficial (multicentric) - These arise most often on the trunk. Several lesions may be present, each expanding slowly as a pink or brown scaly plaque with a fine 'whipcord' edge. Can grow >10cm in diameter o Pigmented - pigment may be present in all types of BCC causing all or part of the tumour to be brown or have specks of brown or black within it Clinical course: slow but relentless growth destroys local tissue. Untreated, a BCC can invade underlying cartilage or bone or damage important structures (e.g. tear ducts) Histology: small, darkly blue staining basal cells grow in well-defined aggregates which invade the dermis. Outer layer of cells is arranged in a palisade. Numerous mitoses and apoptotic bodies are seen. In the cicatricial type, the islands of tumour are surrounded by fibrous tissue DD: o Nodular BCC - intradermal melanocytic naevus, a SCC, a giant molluscum contagiusum or a keratoacanthoma o Pigmented BCC - seborrhoeic wart, MM o Cicatricial BCC - morphea, scar o Superficial BCC - IEC, psoriasis, discoid eczema Treatment: tailored to size + site of BCC, age and general health of pt. 5-year cure rate for all types of BCC is >95% but regular f/u needed to detect local recurrences when they are small + remediable o Excision + 0.5cm surrounding normal skin for discrete nodular/cystic BCCs in pts <60 o Moh's micrographic surgery for cicatricial tumours (ill-defined edges), lesions near vital structures, large (>1cm) tumours, cosmetically important sites (nose, inner canthus, nasolabial folds). Includes histological checks in all planes of tissue excised during operation o Radiotherapy is seldom used for biopsy-proven lesions in pts <70 but helpful when surgery contraindicated o Cryotherapy, curettage + cautery and photodynamic therapy useful for superficial lesions o Palliative treatment with curettage + cautery may be preferable to aggressive in elderly pts in poor health o-Squamous Cell Carcinoma
- Common tumour in which malignant keratinocytes show variable capacity to form keratin
- Cause: o Skin damage by long-term UVR, XR, infrared o Carcinogens (e.g. pitch, tar, mineral oils, inorganic arsenic) o Rare genetic disorders with defective DNA repair mechanisms (xeroderma pigmentosum) lead to multiple SCC + BCCs and to MM o DNA of HPV can be integrated into nuclear DNA of keratinocytes and cause malignant transformation o Immunosuppression predisposes
- Clinical presentation: o Tumours may arise as thickenings in an actinic keratosis

De novo, as small scaling nodules Rapidly growing anaplastic lesions may start as ulcers with a granulating base + an indurated edge o Common on lower lip + in mouth. Tumours arising on area of previous XR/thermal injury, chronic draining sinuses/ulcers/inflammation are most likely to metastasise. Tumours arising on non-exposed sites (perineum, sole of foot) have lesser malignant potential but may metastasise. Tumours arising in sunexposed areas and in actinic keratosis seldom metastasize. Metastatic potential increases with tumour diameter and depth of invasion, poor differentiation, perineural involvement, immunosuppressed pts Histology: keratinocytes disrupt dermo-epidermal junction and proliferate into dermis. Malignant cells usually retain capacity to produce keratin (often produce hyperkeratotic surface) Treatment: o Diagnosis confirmed with biopsy then tumour excised with 0.5cm border of normal skin o Moh's micrographic surgery useful for high-risk tumours o Radiotherapy effective but should be reserved for frail + elderly o oMalignant Melanoma
- Incidence: incidence in white people in UK and USA doubling every 10yrs. ~10 per 100,000 with females affected more than males. Higher incidence in people living near equator (+ female preponderance lost). Highest incidence (40 per 100,000/year) seen in White people living in Australia. Rare before puberty. Rare in black people +
Asians (palms, soles or mucous membranes if it does occur)
- Cause: o Genetic - most common in white people with blond/red hair, many freckles and a fair skin that tans poorly. 10-15% of melanomas are familial (2 or more 1st degree relatives affected). Molecular defects in tumour suppressor genes/oncogenes linked to these (e.g. CDKN2A). May affect several members of a single family in association with atypical (dysplastic) naevi o Sunlight - incidence + mortality | with |latitude. Tumours most often occur on exposed skin o Pre-existing melanocytic naevi - risk highest in those with atypical naevi, congenital naevi or many banal melanocytic naevi. Pre-existing naevus seen histologically in 30% of MMs
- Clinical features: 80% preceded by superficial or radial growth phase shown clinically as expansion of irregularly pigmented macule or plaque. Most are multicoloured (brown, black, blue, pink) with irregular margins with reniform projections + notches. Malignant cells at first confined to epidermis + uppermost dermis but eventually invade more deeply + may metastasise. 4 main types: o Lentigo Maligna Melanoma - occurs on exposed skin of the elderly. Irregularly pigmented, irregularly shaped macule (lentigo maligna) may have been enlarging slowly for years as an in situ melanoma before an invasive nodule appears o Superficial Spreading Melanoma - most common type in Caucasians. Radial growth phase shows varied colours and is often palpable. A nodule coming up within such a plaque signifies deep dermal invasion + poor prognosis o Acral Lentiginous Melanoma - occurs on palms and soles. Most common in Asian people. Invasive phase signalled by a nodule coming up within irregularly pigmented macule o Nodular Melanoma - appears as pigmented nodule with no preceding in situ phase. Most rapidly growing + aggressive type Melanomas can also be described by colour, site and degree of spread:

Totally amelanotic melanomas - rare and occur especially on soles of feet. Flecks of pigment can usually be seen with a lens o Subungual melanomas - painless areas of pigmentation expanding under the nail and onto the nail fold o Metastatic melanoma - has spread to surrounding skin, lymph nodes or other organs. Can rarely be cured at this stage
- Staging: staged by TNM classification and AJCC in USA (pg 271)
- Histology: Lentigo Maligna (numerousLentigo Maligna Melanoma (dermal atypical melanocytes, many in Often invasion occurs, with a breach of the groups, seen along basal layer years BM region. In situ changes seen in extending downwards in walls of adjacent epidermis) hair follicles) Superficial Spreading MelanomaSuperficial Spreading Melanoma in situ (large epithelioid 6 months (dermal nodule may be composed of melanoma cells permeate
- 2 years epithelioid cells, spindle cells or epidermis) naevus-like cells. In situ changes seen in adjacent epidermis) Acral Lentiginous Melanoma inAcral Lentiginous Melanoma Situ (atypical melanocytes seen in 6 months (melanoma cells invade the dermis. In base of epidermis + permeating
- 2 years situ changes seen in adjacent mid epidermis) epidermis) No in situ phase Nodular Melanoma (No in situ phase. Tumour comprises epithelioid, spindle, naevoid cells and no in situ melanoma in adjacent epidermis) oMicrostaging: histology used to assess prognosis. Breslow's method is to measure (with an ocular micrometer), the vertical distance from the granular cell layer to the deepest part of the tumour. Clark's method is to assess the depth of penetration of the melanoma in relation to different layers of the dermis
- DD: o Melanocytic naevus o Seborrhoeic keratosis o Pigmented actinic keratosis o Pigmented BCC o Sclerosing haemangioma o Subungual/peri-ungual haematoma (history of trauma) o Talon noir - pigmented petechial area on heel following minor trauma from illfitting shoes o Amelanotic melanoma most often confused with pyogenic granuloma or SCC
- Prognosis: Indicator Significance Depth of primary tumour Breslow
<0.75mm 5YSR 95%

0.76 - 1.5mm 5YSR 85%

1.51 - 4mm 5YSR 65%
>4mm 5YSR 45%
Sex Females do better than males Age Prognosis worsens after age 50 Site Prognosis poorer if trunk, upper arms, neck + scalp Ulceration Poorer prognosis Clinical Stage Prognosis worsens with advancing stage

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