Growths, neoplasms, and cancers of the skin

In this video, we will be differentiating between harmless growths and benign and malignant neoplasms of the skin.

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ADDITIONAL TAGS
Angioma
AKA cherry angioma
Presents as red papule
Acrochordons (skin tags)
Fleshy growths of skin, with blood supply, can be skin colored or brown
Common in armpit, groin, eyes, and neck
Seborrheic keratosis
Benign superficial growth
Epi: common after 30 yo, all skin except soles/palms, often more than one
Don’t go away but are harmless
Often dark and pigmented, but can be tan or hypopigmented, esp on darker skin
Characteristic “stuck on” appearance, waxy or oily
Lipoma
Benign tumor of fat tissue
Epidermal inclusion cyst
AKA EIC, epidermoid cyst, sebaceous cyst
Benign cyst usually found on skin, made of thin layer of squamous epithelium
Caused by implantation of epidermis into dermis, often from trauma → debris like dead skin, oil then collect within cyst → can produce
Pilar cyst
Dermatofibroma
Keloid
Solar lentigo
AKA sun spot, age spot, liver spot
Basal cell carcinoma
Epi: most common skin cancer, common in head/neck
Often presents as pearly pink papules… can vary (see morphologies)
Risk factors: sun exposure, fair skin, xeroderma pigmentosum
Diagnose with shave biopsy before excision
Originate from keratinocytes, basal layer → UV light damages DNA
Notable UV-induced mutation: PTCH (tumor suppressor gene)
Various morphologies:
Nodular - pearly papule/nodule, often telangiectasias. Often on head and neck.
Superficial - pink/translucent color, often telangiectasias in patch or thin plaque
Can also be pigmented (resembles melanoma), ulcerated, or any combination
Treat: curette and desiccation, cryosurgery, excise surgery, MMS
Non surgical alternative: imiquimod/5-FU creams, radiation
Actinic keratosis
Scaly plaques, often on forehead/face, rough/gritty texture on touch
Premalignant, sometimes progress to PCC
Risk factors: fair skin, age, genetics/fam hx, immunosuppression, sun exposed surfaces
When on the lip = actinic cheilosis
Squamous cell carcinoma
More prevalent in fair skin exposed to sun
Higher mortality than BCC, lower than melanoma
Rate of metastasis to lymph nodes = 5%
Originates in keratinocytes
Notable UV-induced mutation: p53 (tumor suppressor gene)
Risk factors: sun exposure, fair skin, xeroderma pigmentosum, arsenic poisoning
Morphologies: scales, pink/red/skin-colored, papule/plaque/nodule, exophytic/indurated, horn, friable, puritic
SCC in situ → Bowen’s dz
Congenital nevi
AKA congenital melanocytic nevus, congenital mole
Melanocytic nevus found starting at birth
Often dome shaped, especially on the face
Sometimes mammillated, sometimes increased hair density/coarseness
Acquired nevi
AKA acquired mole
Melanocytic growth acquired after birth
Usually appears before age 20, more commonly in sun exposed areas
Over time, nevi change from brown macules and papules to pink/skin colored papules while diameter stays constant
Dysplastic nevus syndrome
AKA atypical mole syndrome (AMS), familial atypical multiple mole-melanoma (FAMMM) syndrome), B-K mole syndrome
Disorder characterized by unusual nevi and increased risk of or multiple inherited melanomas
nevi, usually appearing near puberty but continues into older age
Melanoma
AKA malignant melanoma
Cancer that develops from pigment-containing melanocytes most commonly in the epidermis but also in the mouth, intestines, or eye
Usually present asymptomatically -- appear as pigmented papules, plaques, or nodules
Any or all of the ABCDEs… patients often report change
May also crust, bleed, erode
Can develop from preexisting nevus or de novo, usually in sun exposed areas
Originates in melanocytes
Etiology: exposure to UVB (and/or UVA) radiation from prolonged/cumulative sun exposure; can also be sporadic
Epi: affects all ages, lifetime risk has increased over time
Risk factors: immunosuppression, personal/fam hx, UV exposure, tanning booth use, fair skin/hair/eyes, old age, many acquired nevi
CDKN2A, CDK4, p53, BRCA2 are notable genes involved
Prognostic factor: Breslow depth (thickness, to deepest part of tumor) is most important
High cure rates when detected early
Subtypes
Superficial: spreads horizontally rather than down; most common type
Lentigo maligna: primarily slow horizontal spread, occurs on sun damaged skin and in elderly
Nodular: rapid vertical growth → poor prognosis
Acral lentiginous: common in darker skin, so diagnosis often delayed
Amelanotic: variable appearance, often confused with other conditions, so difficult to diagnose
Treatment: surgical excision (+/- biopsy), ipilimumab (anti-CTLA-4 to stimulate immune rxn to melanoma), BRAF inhibitors (vemurafenib, dabrafenib), follow up/sun protection for life

• Category

  Familial Malignant Melanoma