4/21 Skin Review - Corbett Flashcards
skin structure
macro
- epidermis
- dermis
- subcutaneous tissue
skin histology
layers of keratinocytes
layers of keratinocytes: (deep to superficial)
- stratum basale [melanocytes at same level]
- stratum spinosum
- stratum granulosum
- stratum lucidum
- stratum corneum
layers of skin
definitions
- macule
- papule
- nodule
- plaque
- pustule
- vesicle/bulla
epidermal changes
summary
epidemal changes
hyperkeratosis
thickening of stratum corneum
assoc: psoriasis
epidemal changes
parakeratosis
flattened keratinocyte nuclei within stratum corneum
assoc: psoriasis
epidemal changes
hypergranulosis
thickened granular layer
assoc: luchen planus
epidemal changes
acanthosis
thickened squamous layer (thick skin)
assoc: acanthosis nigricans
epidemal changes
acantholysis
separation and rounding up of keratinocytes (loss of adhesions)
assoc: pemphigus vulgaris
epidemal changes
spongiosis
intracellular edema between keratinocytes
assoc: eczematous dermatitis (NOT urticaria)
seborrheic keratosis
who, where, association, mutation
appearance: buzzwords, key fts
- BENIGN epidermal tumors
- common: elderly
- spontaneous
- on trunk (also extremities, head, neck)
- Leser Trelat sign: sudden appearance of many lesions w paraneoplastic syndrome (GI cancers)
assoc with activating mutations in FGFR3 (fibroblast growth factor receptor 3)
buzzwords: velvety, stuck-on, coin-like lesons
- sharply demarcated, composed of sheets of small cells resembling basal cells of nl epidermix
key features:
- hi keratin production at surface (hyperkeratosis)
- small keratin-filled cysts (horn cysts) and invaginations of keratin into main mass (invagination cysts)
actinic keratosis
- high incidence in light pigmented individs with sun exposure
- many lesions show progressive dysplastic changes →→→ squamous cell carcinoma
- happens often enough to perform local eradication
- tx: curettage, freezing, or topical application of chemotx agents
scaly red/tan irreg plaques
hyperkeratosis, dysplasia
basal cell carcinoma
basics
appearance
NBCCS and mech
most common tumor on sun-exp sites in older people
primary cause: DNA damage induced by UV-B exposure
- immunosuppression
- genetic disorders of DNA repair
appearance: pearly, telangiectic nodules w peripheral palisading
NBCCS: nevoid basal cell carcinoma syndrome aka Gorlin syndrome
- auto dom
- devpt of multiple basal cell carcinomas before age 20 + other abnl
- assoc gene: PTCH (tumor suppressor) - receptor for sonic hedgehog
- mutation → unbridled SHH signaling
squamous cell carcinoma
second most common tumor on sun-exp sites in older ppl
cause: DNA damage induced by UV exp
* risk: immunosuppression, industrial carcinogents (tars, oils), chronic ulcers and draining osteomyelitis, old burn scars, ionizing rad, tobacco, betel nut chew
well differentiated keratin pearls??? pathognomonic!
deeply invasive, involve subcutis BUT rarely metastasize
MU
Marjolin’s ulcer
- chronic nonhealing wound w lots of infl and turnover
- malignancy develops over time
this SCC is VERY AGGRESSIVE
melanocytes
- derived from neural crest cells → ID w special staining
- ex. tyrosinase
- reside in basal layer (epidermal-dermal jx)
- 1 melanocyte has interaction w 30-40 keratinocytes to which it’s distributing melanosomes
vitiligo
why diff from albinism?
- unknown etiology, likely autoimmune-related
- involves antibodies to surface and cytoplasmic melanocyte antigens → loss of melanocytes from dermis
contrasts w albinism bc…
- albinism involves mutation of enzymes involved in production of melanin
- vitiligo is autoimmune destruction of melanocytes altogether
oculocutaneous albinism 1
auto recessive
absence of tyrosinase → inability to produce melanin
leads to high risk of skin cancer
vision problems
features:
- white hair
- white/pink skin
- blue eyes
- impaired vision
other types:
- type 1: no tyrosinase
- type 2: less tyrosinase than normal
- others: affect any step in production of melanin, packaging/export of granules, taking up into keratinocytes
ephelides
freckles
- multiple sm tan macules
- uniform pigmentation on sun-exp areas assoc w incr melanin production BUT no change in melanocyte number
melasma
linked to
features
unknown etiology
linked to:
- UV radiation → induces melanocyte proliferation, migration, melanogenesis
- estrogen (F >>> M)
- overexpression of c-kin → incr melanin prod
see incr melanin deposition in all layers of epidermis, potentially incr numbers of melanocytes
nevi (moles)
table
congenital melanocytic nevi
more a congenital malformation than a benign nevus
- small: < 2cm diameter
- medium: 2-20cm diameter
- giant: >20cm
- darkly pigmented, can be hairy
- 5-15% develop into melanoma → removal due to risk
possibly error in devpt of neural ectoderm
junctional nevus
compound nevus
progression of melanocytic nevi
dysplastic nevus
potentially direct precursors of melanoma
- multiple? incr risk for melanoma
- mech: activating mutations in NRAS and BRAF genes → incr CDK4 activation
dysplastic nevus syndrome
- auto dom disorder assoc w loss of function in CDKN2A (cyclic dep kinase inhibitor 2) - neg regulator of CDK4
- incr risk for multiple dysplastic nevi
- risk of melanoma over 50% by 60, leads to devpt of many melanomas at diff sites
melanoma
basics
risk factors
mutations (accumulation order)
deadliest skin cancer
- small lesions, rapidly progressive (compared to basal cell, squamous cell carcinomas)
- much more likely to metastasize
BRAF mutation → then loss of CDKI (CDKN2A, PTEN loss) → then tumor gains metastatic potential
greatest risk: UV exposure, sensitivity to UV radiation, family hx
melanoma path
identification
ABCDE: asymmetry, uneven borders, multicolored, large diameter (over .25in), evolving size/shape/color
stages of melanoma
types of melanoma
predictor/indicator of prognosis
benign nevus → dysplastic nevus → radial growth phase → vertical growth phase → metastatic melanoma
- superficial spreading
- lentigo maligna
- nodular - WORST bc early entry into vertical phase
- acral lentiginous
thickness of lesion is best predictor of pt prognosis
