Benign And Malignant Neoplasms Of Skin Flashcards
Acquired melanocytic nevi dx:
Dysplastic nevus- histological or clinical atypical features, multiple lesions markers for increased risk of melanoma
Melanoma- atypical features, ABCD’s (E=evolving)
Seborrheic keratosis- surface is rougher or scaly, origin of these tumors is the keratinocytes not the melanocytes, idiopathic ‘liver spots/barnacles of life’, increase in incidence with age and sun exposure, genetic predisposition, any location but increased in sun exposed ones
Types of melanocytic nevi
Junctional- flat, small dark brown macule, often first stage of moles in children and young adults
Compound MN- epidermis and dermis nests (some are raised and some are colored)
Dermal MN- nests are all in dermis (skin colored and raised dome shape)
Lentigo is much lighter than nevi
Seborrheic keratosis exam
Well defined tan to brown papules
Keratosis, rough, warty or sometimes smooth (variations of color and texture)
Stuck on appearance- they can ‘pick it off’ with their fingernail underneath it (no melanocytic nevus can do this)
No therapy needed unless irritated or infected
White horn cysts that keratinocytes are making in the middle of dark brown area
Smooth things reflect light back to you, spaces in skin called verrucis where light gets trapped to make it appear dark brown- not pigment induced
Variations in distributions
Benign proliferation of keratinocytes due to infection:
Clinical exam
Dx:
Verruca- HPV infecting the basal cells causes hyperproliferation of virally infected keratinocytes
Well defined skin colored papules, keratotic surface, hands, plantar, genital, other locations
Lasts months to years
Dx: seborrheic keratosis, squamous cell carcinoma
Mucosal verruca are more filliform or cauliflower shaped
Verruca therapy
Physical or chemical destruction of epidermis- cryotherapy (liquid N2), salicyclic or trichloracetic acid, podophylin, laser (CO2 vs vascular)
Immune therapy- interferon, imiquimod cream
Occlusion
Observation
Benign proliferation of dermal fibroblasts
Dermatofibromas- smooth and raised, FIRM papules, skin colored/pink/red brown
Post traumatic vs. idiopathic
Dx: melanocytic nevi- can look like it, but nothing feels like a dermatofibroma
Hypertrophic scars and keloids- difference is if they are contained to the borders of scar or not*, increased collagen production, well defined, firm, smooth plaques or nodules, skin colored or hyperpigmented
Benign dermal vascular proliferation
Cherry Angioma- very common, small proliferation of capillaries in papillary dermis. Bright red to violaceous(more venous components), dome shaped papule that is smooth (all in dermis), strongly genetic, more numerous with advancing age, trunk>extremities
Dx: melanoma, melanocytic nevus
Hemangiomas- larger vessels in dermis and subcutaneous, present at birth or within 1st month of life, variable size, 3 phases of growth: proliferative/growth, stable, involution phases
Often disappear by 10yo
Benign derma neural proliferation
Neurofibroma- skin colored, soft/compressible (in comparison to dermatofibrosis), if have many lesions with cafe-au-lait spots consider Neurofibromatosis
Basal cell carcinoma appearance and Dx:
Treatment
Translucent, pearly, telangiectatic
Often shiny, skin colored, sometimes brown patch, papules or plaque
Begins to ulcerated centrally with a rolled border
Dx: amelanotic melanoma, dermal nevus
Excision vs. curretage and electrodesiccation
Mosh micro graphic surgery
Radiation
Immunomodulators- imiquimod cream
Malignant epidermal keratinocyte proliferation
Precursor
Therapy
Squamous cell carcinoma- two types
Sun induced- low propensity for metastasis. Narrow excision.
Non-Sun induced- high propensity for metastasis, occur in scars, radiation burns, genitalia, recta or mucosal area. Must be widely excised, radiation.
SCC is ill or well defined, persistent, solitary, scaling/keratotic papules/plaques/nodules
Actinic keratosis- erythematous scaling macule, sun exposed areas. Cryotherapy, topical chemo (5-FU), topical cytokine stimulator (imiquimod)
Malignant melanocytes proliferation
Types
Melanoma- growth of malignant cell is often very slow (can stay in epidermis for a long time)
Irregular pigment, border/shape, surface, size
Early excision with surgical margins based on histologic thickness (Breslow’s thickness) of lesion
Slow spreading lentigo maligna melanoma- can be present for a decade
Superficial spreading melanoma- has all clinical signs, but would not last for 10 years without killing patient
Nodular melanoma- early erosive features, persistent black borders still
Plantar melanoma- local spread and satellite macules
Amelanotic vulvar melanoma
Malignant dermal lymphocyte proliferation
Mycosis fungoides- cutaneous T cell lymphoma
T cells normally reside in skin around dermal capillaries
Monoclonal proliferation allows invasion of lymphs into epidermis (epidermotropism) and subsequently throughout dermis and subcutaneous tissue without spongiosis/edema
Lose homing of cells and can spread anywhere
Patch stage- chronic and asymptomatic in early stages, well defined scaling red patches
Plaque and early tumor stage reqs chemo
