Cutaneous Onoclogy Flashcards
Name two genetic conditions that may pre-dispose youth cutaneous cancer.
basal cell nevus syndrome (loss of tumor suppression)
xeroderma pigmentosum (impaired DNA repair)
note the immune system plays a major role in promoting/ controlling cancer
Describe conditions on the spectrum of malnocytic lesions.
common nevi (junctional, compound, dermal), small and medium congenital nevi and dysplastic nevi, melanoma
What are the clinical features of benign melanocytic nevi?
groups of melanocytes in the skin,
distribution and number related to genetics
number of nevi associated with melanoma risk
3 types junctional, compound and dermal
born with few, gain more from late childhood to mid 30’s; should be oval to round and well-circumscribed
Compare and contrast junctional, compound and dermal nevi.
junctional: flat dark mark (1st/2nd decade)
compound: occur at the junction at the dermis, appear lighter and raised
dermal are within the dermis and are domed pink papules
What are the treatments for common nevi?
reassurance that it is not cancerous, discuss photo protection, excise (if changing or atypical, repeatedly traumatized or cosmetic)
What are the clinical presentation of congenital nevi?
present at birth
small, medium or large
frequently cobbled and develop coarse hair
giant congenital nevi have an increased risk of melanoma
What is the clinical presentation of dysplastic nevi?
nevi with atypical cells and abnormal nevus architecture, variegated tan, brown or pink, irregular shape, indistinct borders and frequently >5mm that continue to develop throughout life not normally apparent until puberty, common on trunk; excision is warranted in giant nevi or with serverely displastic nevi
Describe the prevalence and risk factors of melanoma.
malignant proliferation of melanocytes accounts for 75% of cancer deaths although it it not the most common kind
risk factors include:
numerous, large, dysplastic nevi, history of melanoma, tanning, sunburn, higher SE, genie DNA repair defects and immunosuppression
Describe the development of melanoma.
⅓ arise from nevi, ⅔ arise de novo, melanocytes lose their normal growth regulation and grow out radially then grow enter a vertical growth phase (most important marker is Breslow depth
What doe the ABCDE of melanoma stand for?
asymmetry, borders, color, diameter and evolving
What are the 4 subtypes of melanoma?
superficial spreading(60-70%, long radial growth phase), nodular (15-30%, shortest radial growth phase, fastest growing), lentigo maligna (5-15%), older adults, longest radial growth phase, flat asymmetric color variation, common on the face) a and acral lentiginous (5-10% common with darker skin types, palmar, plantar or subugual location)
What is a Hutchinson sign?
blacken patch that spreads to the proximal nail fold
What is the standard treatment for melanoma?
wide excision with appropriate margins, setinal lymph node biopsy for melanomas (1-4 mm depth), close follow-up with skin exams and lymph node surveillance
What is the single greatest predictor of survival of melanoma prognosis?
Breslow depth, lymph node or distant metastases make the disease more difficult to treat
What are often difficult to differentiate from melanoma?
dysplatic nevi
What is an epidermoid cyst?
trapped epidermal cells caused by injury to the skin or blocked hair follicle which becomes a pocket of macerated keratin.
What is the clinical presentation of an epidermoid cyst?
domed nodule (compressible and mobile subcutaneous mass attached to epidermis), foul-smelling, ricotta cheese like keratin may be expressed, rupture may lead to inflammation but true infection is rare
What is the treatment for a epidermoid cyst?
intralesional steroids or oral antibiotics if inflamed, if excised, must excise entire cyst if recurrently inflamed (do not excise when actively inflamed)
What is a seborrheic keratosis/ clinical presentation?
benign overgrowth of the epidermis which is common is 40s or 50s which can be flesh-colored, tan, brown or black most common to appear no the trunk (grow on top of skin)
note: pseudohorn cysts grow with pearls of keratin
How are seborrheic keratosis treated?
inflamed lesions can be scrapped up (curettage) or frozen off cyrotherapy and reassurance
What is actinic keratosis/ clinical presentation?
sun-induced, pre-cancerous lesions of the epidermis where DNA damage causes dysregulation of the cell cycle and differentiation. presents as pink to red sandpapery papules (better felt than seen) on sun-exposed areas
Are actinic keratosis dangerous?
only 1-2% convert to squamous cell carcinoma, but be suspicious is lesion: persists after treatment, rapidly grows, becomes indurated or ulcerated/mucosal
Squamous cell carcinoma is the second most common skin cancer and is 3x more likely than BCC to affect people who are _____. SCC affects which areas?
immunocompromised; affects sites lined with squamous epithelium (skin, mouth, esophagus, penis, anal mucosa with high risk for metastasis with lips, ears, perianal/genital regions and hand)
What might cause pathogenesis of SCC?
DNA disruption (UV or HPV, chemical carcinogens), chronic inflammation (ulcers or burns) or may progress from actinic keratosis
