Malignant Skin Tumours Flashcards
Basal cell carcinoma subtypes
Noduloulcerative (typical)
Pigmented variant
Superficial variant
Sclerosing (morpheaform) variant
Noduloulcerative BCC description
skin-coloured papule/nodule with rolled, translucent (“pearly”) telangiectatic border, and depressed/eroded/ulcerated centre
Pigmented variant BCC clinical presentation
■ flecks of pigment in translucent lesion with surface telangiectasia
■ may mimic malignant melanoma
Superficial variant BCC clinical presentation
■ flat, tan to red-brown plaque, often with scaly, pearly border and fine telangiectasia at margin
■ least aggressive subtype
Sclerosing (morpheaform) variant BCC clinical presentation
■ flesh/yellowish-coloured, shiny papule/plaque with indistinct borders, indurated
BCC pathophysiology
• malgnant proliferation of basal keratinocytes of the epidermis
■ low grade cutaneous malignancy, locally aggressive (primarily tangential growth), rarely metastatic
■ usually due to UVB light exposure, therefore >80% on face
■ may also occur in previous scars, radiation, trauma, arsenic exposure, or genetic predisposition (Gorlin syndrome)
BCC epidemiology
- most common malignancy in humans
- 75% of all malignant skin tumours >40 yr, increased prevalence in the elderly
- M>F, skin phototypes I and II, chronic cumulative sun exposure, ionizing radiation, immunosuppression, arsenic exposure
BCC ddx
- benign: sebaceous hyperplasia, intradermal melanocytic nevus, dermatofibroma
- malignant: nodular malignant melanoma, SCC
BCC management
- imiquimod 5% cream (Aldara®) or cryotherapy is indicated for superficial BCCs on the trunk
- fluorouracil and photodynamic therapy can also be used for superficial BCC shave excision + electrodessication and curettage for most types of BCCs, not including morpheaform
- Mohs surgery: microscopically controlled, minimally invasive, stepwise excision for lesions on the face or in areas that are difficult to reconstruct
- radiotherapy used in advanced cases of BCC where surgical intervention is not an option
- vismodegib is approved for metastatic BCC
- life-long follow-up every 6 mo-1 yr
- 95% cure rate if lesion <2 cm in diameter or if treated early
Workup/investigations of BCC and other non malignant skin cancers
- History: duration, growth rate, family/ personal Hx of skin cancer, prior therapy to the lesion
- Physical: location, size, whether circumscribed tethering to deep structures, full skin exam, lymph node exam
- Biopsy: if shallow lesion, can do shave biopsy; otherwise punch or excisional biopsy may be more appropriate
Surgical margins for non melanoma skin cancers
- Smaller lesions: electrodessication and curettage with 2-3 mm margin of normal skin
- Deep infiltrative lesions: surgical excision with 3-5 mm margins beyond visible and palpable tumour border which may require skin graft or flap; or Mohs surgery, which conserves tissue and does not require margin control
SCC clinical presentation
- indurated, pink/red/skin-coloured papule/plaque/nodule with surface scale/crust ± ulceration
- more rapid enlargement than BCC
- exophytic (grows outward), may present as a cutaneous horn
- sites: face, ears, scalp, forearms, dorsum of hands
SCC pathophysiology
- malignant neoplasm of keratinocytes (primarily vertical growth)
- predisposing factors include: UV radiation, PUVA, ionizing radiation therapy/exposure, chemical carcinogens (such as arsenic, tar, and nitrogen mustards), HPV 16, 18, immunosuppression
- may occur in previous scar (SCC more commonly than BCC)
SCC epidemiology
- second most common type of cutaneous neoplasm
- primarily on sun-exposed skin in the elderly, M>F, skin phototypes I and II, chronic sun exposure
- in organ transplant recipients SCC is most common cutaneous malignancy, with increased mortality as compared to non immunocompromised population
SCC differential diagnosis
- benign: nummular eczema, psoriasis, irritated seborrheic keratosis
- malignant: keratoacanthoma, Bowen’s disease, BCC
SCC management
- surgical excision with primary closure, skin flaps or grafting
- Mohs surgery
- lifelong follow-up (more aggressive treatment than BCC)
SCC prognosis
- good prognostic factors: early treatment, negative margins, and small size of lesion
- SCCs that arise from AK metastasize less frequently (~1%) than other SCCs arising de novo in old burns (2-5% of cases)
- overall control is 75% over 5 yr, 5-10% metastasize
- metastasis rates are higher if diameter >2 cm, depth >4 mm, recurrent, involvement of bone/muscle/ nerve, location on scalp/ears/nose/lips, immunosuppressed, caused by arsenic ingestion, or tumour arose from scar/chronic ulcer/burn/genital tract/sinus tract
Bowen’s disease (SCC in situ) clinical presentation
- sharply demarcated erythematous patch/thin plaque with scale and/or crusting
- often 1-3 cm in diameter and found on the skin and mucous membranes
- evolves to SCC in 10-20% of cutaneous lesions and >20% of mucosal lesions
Bowen’s disease (SCC in situ) management
- same as for BCC
- biopsy required for diagnosis
- topical 5-fluorouracil (Efudex®) or imiquimod (Aldara®) used if extensive and as a tool to identify margins of poorly defined tumours
- cryosurgery
- shave excision with electrodessication and curettage
Keratocanthoma clinical presentation
- rapidly growing, firm, dome-shaped, erythematous or skin-coloured nodule with central keratin-filled crater, resembling an erupting volcano
- may spontaneously regress within a year, leaving a scar
- sites: sun-exposed skin
Keratocanthoma pathophysiology
- epithelial neoplasm with atypical keratinocytes in epidermis
- low grade variant of SCC
Keratocanthoma etiology
• HPV, UV radiation, chemical carcinogens (tar, mineral oil)
Keratocanthoma epidemiology
• >50 yr, rare <20 yr
Keratocanthoma differential diagnosis
- treat as SCC until proven otherwise
* hypertrophic solar keratosis, verruca vulgaris
Keratocanthoma management
• surgical excision or saucerization (shave biopsy) followed by electrodesiccation of the base, treated similarly to SCC
Malignant melanoma clinical presentation
- malignant characteristics of a mole: “ABCDE” mnemonic
* sites: skin, mucous membranes, eyes, CNS
Malignant melanoma clinical subtypes of malignant melanoma
- lentigo maligna
- lentigo maligna melanoma (15% of all melanomas)
- superficial spreading melanoma (60-70% of all melanomas)
- nodular melanoma (30% of all melanomas)
- acral lentiginous melanoma (5% of all melanomas)
Malignant melanoma pathophysiology
• malignant neoplasm of pigment-forming cells (melanocytes and nevus cells)
Malignant melanoma epidemiology
- incidence: 1/75 (Canada) 1/50 (US)
- risk factors: numerous moles, fair skin, red hair, positive personal/family history, 1 large congenital nevus (>20 cm), familial dysplastic nevus syndrome, any dysplastic nevi, immunosuppression, > 50 common nevi, and sun exposure with sunburns, tanning beds
- most common sites: back (M), calves (F)
- worse prognosis if: male, on scalp, hands, feet, late lesion, no pre-existing nevus present
Malignant melanoma ddx
- benign: nevi, solar lentigo, seborrheic keratosis
* malignant: pigmented BCC
Malignant melanoma management
- excisional biopsy preferable, otherwise incisional biopsy
- remove full depth of dermis and extend beyond edges of lesion only after histologic diagnosis beware of lesions that regress – tumour is usually deeper than anticipated
- high dose IFN for stage II (regional), chemotherapy (cis-platinum, BCG) and high dose IFN for stage III (distant) disease
- newer chemotherapeutic, gene therapies, and vaccines starting to be used in metastatic melanoma
- radiotherapy may be used as adjunctive treatment
Does this patient have a mole or melanoma? abcde checklist
ABCDE checklist
Asymmetry
Border (irregula and/or indistinct)
Colour (varied)
Diameter (increasing or >6 mm)
Enlargement, elevation, evolution (i.e. change n colour, size, or shape)
Sensitivity 92% (CI 82-96%)
Specificity 100% (CI 54-100%)
Risk factors for melanoma
no SPF is a SIN
Sun exposure
Pigment traits (blue eyes, fair/red hair, pale complexion)
Freckling
Skin reaction to sunlight (increased incidence of sunburn)
Immunosuppressive states (e.g. renal transplantation)
Nevi (dysplastic nevi; increased number of benign melanocytic nevi)
When to conduct node dissection for lesions in melanoma
> 1 mm thick
OR <1 mm and ulcerated
OR >1 mitoses/mm2 (Stage IB or higher melanoma patients should be offered a sentinel lymph node biopsy)
• Assess sentinel node at time of wide excision
Melanoma staging
T1 < 1 mm
Stage I T1a (a = no ulceration)-T2a
5 year survival 90%
T2 1.01-2mm
Stage II T2b-T4b (b= ulceration)
5 year survival 70%
T3 2.01-4mm
Stage III any nodes
5 year survival 45%
T4 > 4 mm
Stage IV any mets
5 year survival 10%
Lentigo maligna clinical description
■ malignant melanoma in situ (normal and malignant melanocytes confined to the epidermis)
■ 2-6 cm, tan brown/black uniformly flat macule or patch with irregular borders
■ lesion grows radially and produces complex colours
■ often seen in the elderly
■ 10% evolve to lentigo maligna melanoma
Lentigo maligna melanoma clinical description
■ malignant melanocytes invading into the dermis
■ associated with pre-existing solar lentigo, not pre-existing nevi
■ flat, brown, stain-like, gradually enlarging with loss of skin surface markings
■ with time, colour changes from uniform brown to dark brown with black and blue
■ found on all skin surfaces, especially those often exposed to sun, such as the face and hands
Superficial spreading melanoma clinical description
■ atypical melanocytes initially spread laterally in epidermis then invade the dermis
■ irregular, indurated, enlarging plaques with red/white/blue discolouration, focal papules or nodules
■ ulcerate and bleed with growth
Nodular melanoma clinical description
■ atypical melanocytes that initially grow vertically with little lateral spread
■ uniformly ulcerated, blue black, and sharply delineated plaque or nodule
■ rapidly fatal
■ may be pink or have no colour at all, this is called an amelanotic melanoma
■ “EFG” elevated, firm, growing
Acral lentiginous melanoma clinical description
■ ill-defined dark brown, blue-black macule
■ palmar, plantar, subungual skin
■ melanomas on mucous membranes have poor prognosis
Cutaneous T-Cell Lymphoma clinical presentation
• Mycosis fungoides (limited superficial type)
■ characterized by erythematous patches/plaques/nodules/tumours, which may be pruritic and poikilodermic (atrophy telangiectasia, hyperpigmentation, hypopigmentation)
■ common sites include: trunk, buttocks, proximal limbs
■ mildly symptomatic, usually excellent prognosis for early disease
• Sézary syndrome (widespread systemic type)
■ rare variant characterized by erythroderma, lymphadenopathy, WBC >20 x 109/L with Sézary cells
■ associated with intense pruritus, alopecia, palmoplantar hyperkeratosis, and systemic symptoms (fatgue, fever)
■ often fatal
Cutaneous T-Cell Lymphoma pathophysiology
• clonal proliferation of skin-homing CD4 T-cells
Cutaneous T-Cell Lymphoma epidemiology
• >50 yr old, M:F 2:1
Cutaneous T-Cell Lymphoma ddx
• tinea corporis, nummular dermatitis, psoriasis DLE, Bowen’s disease
Cutaneous T-Cell Lymphoma investigations
- skin biopsy (histology, “lymphocyte antigen cell” markers, TcR gene arrangement)
- blood smear looking for Sézary cells or flow cytometry (e.g. CD4:CD8 >10 is Sézary)
- imaging (for systemic involvement)
Cutaneous T-Cell Lymphoma management
• Mycosis fungoides
■ depends on stage of disease
■ topical steroids and/or PUVA, narrow band UVB (NBUVB, 311-313mm)
• Sézary syndrome ■ oral retinoids and IFN ■ extra-corporeal photopheresis ■ may need radiotherapy for total skin electron beam radiation ■ may maintain on UV therapy ■ other chemotherapy agents
