Cutaneous Oncology Flashcards
basal cell nevus syndrome
auto dom
inactivation of tumor suppressor genes
basal cell cancers at young age
*photoprotection
benign melanocyte nevi (moles)
epi: # peaks in 3rd decade
patho: nevi originate from melanoblasts
-junctional nevus=epiderm
-cmpd=epiderm+derm
-dermal=derm
migrate from epiderm to derm as they mature
clin: sym, oval/round
- junctional: uniform, brown macule
- cmpd: exophytic, lighter brown
- dermal: more exophytic, lighter in color
treat: excise if inflamed, photo protection, discuss surveillance
congenital nevi
epi: present at birth, darken over time, giant ones at risk for melanoma
patho: melanocytes penetrate deeper, surround hair follicles, bl vessels, other adnexal structures
clin: developed cobbled surface over time, coarse hair growth
treat: excision, monitor, biopsy if focal changes
dysplastic nevi
epi: evident at puberty and develop over life, fair skinned
path unknown
clin: tan, brown, pink macule often surrounds papular center 5-12mm (larger than common nevi) irregular shape indistinct borders trunk common site
histo: range of atypia
treat: observation if mild
excise if moderate to severe
malignant melanoma
epi: 75% of skin cancer
patho: evolve from melanocytes at dermoepidermal junction, radial growth phase that enlarges sum, vertical growth phase
- breslow depth (deepest pt of invasion) is impt prognostic factor
clin: ABCDE
* skin, liver, and lung involvement are most common
treat: excise w/ large margins
lymph nodes biopsy/excision
chemo
regular skin and lymph node exam
melanoma risk factors
numerous nevi large nevi dysplastic nevi history moderate freckling UV, tanning sunburns higher SES genetic DNA repair defects immunosupp
amelanotic melonoma
pink variant of malig melanomas
epidermoid cysts
epi: after pub
patho: plugging of afire of a hair follicle, epidermal implantation (like scar)
* not sebaceous
clin: compressible, mobile subcutaneous mass, attached to epidermis, min surface change, ricotta cheese inside (stinky keratin)
treat: observe, intralesional steriod injection, oral antibiotics, excision
seborrheic ketatoses
epi: 4th or 5th decade onset
patho: genetic prediposition
clin: flesh, tan, brown, black, variegated
“stuck on”
rough, warty, waxy, ketatotic surface
pseudohorn cysts are classic (small white foci)
treat: observation, curettage, cryotherapy
actinic keratoses (AKs)
epi: majority remain stable, 1-2% covert to sq. cell carcinoma
- risk factors: intense, intermittent, frequent sun; fair skin; male; old; history
patho: UV induces mut –> aberrant growth
clin: rough, scaly papules and lesions, tender
- malig: persist after treat, rapid growth and induration, ulcerated mucosal lesions
squamous cell carcinoma (SCC)
epi: 2nd most common skin cancer, immunocompromised
“in situ”= limited to epidermis
patho: UV damage, HPV incr. risk, chronic inflam
clin: erythematous, indurated base, thick SCALE, may become nodular or ulcerated,
- in situ: sharply demarcated, scaly, thin, erythematous plaque
basal call carcinoma (BCC)
epi: most common cancer, immunocompetent
patho: UV damage to cells of basal layer
clin:
- nodular: 50-80%, translucent/pearly, telangiectasias, rolled border, friable
- superficial: 15%, trunk and extrem, erythematous thin plaque w/ overlying scale, slow growing
- morpheaform: 5%, depressed, atrophic, scar like, hypo pigmented, indistinct margins –> Mohs
indications for Mohs
recurrent BCC and SCC high risk sites (periocular, nasal, prenatal, auricular) aggressive tumor morphology perineural invasion tumor >2cm
