Skin Neoplasia pathology - Zaloga Flashcards
1
Q
freckles aka ephelides
A
- light brown macules (1-2mm)
- response of melanocytes to UV exposure
- melanocyte count normal, but INCREASED melanin production**
2
Q
Lentigo
A
- hyperplasia of melanocytes in basal layer** –> hyper pigmented
- larger tan/brown macules or patches (5-10mm)
- cause: maybe due to FGR3 mutation in sebborheic keratosis
- associated with Peutz-Jeghers syndrome
- HMB45 is stain for proliferating melanocytes
- p63 is + keratinocyte marker
3
Q
acquired melanocytic nevus aka mole
A
- benign –> usually not malignant (dysplastic if malignant)
- activating mutations in BRAF and NRAS (proliferation)**
- collection of melanocytes –> pigmented lesion
- orderly growth**, well defined, good borders
- can be macule or papule
- little mitotic activity
4
Q
normal nevus growth
A
- maturation - basal orientation of melanocytes
- junctional - nests at dermal/epidermal junction (rete ridges)
- compound - proliferation of melanocytes into dermis
- dermal - melanocytes only in dermis
- neurotization - melanocytes become wavy, resemble neurons
5
Q
dysplastic nevi
A
- markers for melanoma risk, majority don’t reach malignancy
- larger nevi and variegation; fibrosis around rete ridges
- dysplastic nevus syndrome (>50% develop melanoma)
- cause: mutations in CDKN2A gene (p16,INK4a) and CDK4 (cell cycle regulation), TERT (telomerase activity increased) along with activating mutations of BRAF and NRAS genes (promote growth)**
- lentiginous compound nevus grows migrates into epidermis instead**
6
Q
melanoma
A
- dysplastic nevus that reach basement membrane and invade tissues (aggressive, irregular borders, atypical)
- not orderly growth, >10mm
- risk factors: UV, sunburn, light skin
- determine stage by depth (Breslow test)**
- cause: mutations in CDKN2A and CDK4, RAS/BRAF, PI3K and AKT (survival), and telomerase –> increase melanocyte proliferation/survival**
- acquiring mutations for invasion of tissues
- better prognosis with fewer mitoses, increased lymphocytes, no metastasis
- radial growth –> no invasion –> lentigo maligna/melanoma in situ
- vertical growth –> invasion/metastasis
7
Q
seborrheic keratosis
A
- benign, epidermal tumor
- cause: activating FGFR3 mutations
- associated with GI carcinomas**, sun exposure, and Leser-Trelat sign
- keratin filled cysts (horn cysts)**
8
Q
epithelial/epidermal/epidermoid/ follicular inclusion cyst (wen)
A
- epithelial lined cyst containing keratin expanding into epidermis
- intradermal or subcu invagination
9
Q
acanthosis nigrans
A
- thickened, hyper pigmented skin
- 80% benign –> due to diabetes and obesity**
- malignant –> due to GI adenocarcinomas
- cause: increased FGFR3 –> receptor upregulated –> thickening of epidermis (acanthosis)
10
Q
actinic keratoses
A
- sun damaged skin
- precursor to squamous cell carcinoma of skin
- cause: SCC and dysplasia (atypia)
- cutaneous horn from hyperkeratosis of corneum**
- parakeratosis
11
Q
squamous cell carcinoma (SCC)
A
- 2nd most common tumor due to sun exposure
- invasive/malignant if dysplastic cells reach basement membrane
- cutaneous SCC less aggressive than mucosal SCC**
- cause: DNA damage by UV light (TP53 tumor suppressor gene)**, immunosuppression (susceptible to HPV), ulcers, osteomyelitis, tobacco, chronic inflammation
- also mutations that increase RAS and decrease Notch signaling
12
Q
basal cell carcinoma (BCC)
A
- most common invasive cancer, aggressive
- nodular lesion in sun exposed areas
- rare metastasize, cured by excision (invade basal membrane if not treated)
- NBCCs aka Gorlin syndrome –> multiple BCCs –> due to PTCH (tumor suppressor) loss of function mutation **
- cause: mutations that activate Sonic Hedgehog path**
- associated with dilated blood vessels and medulloblastomas
13
Q
dermis tumor - benign fibrous histiocytoma (aka dermatofibroma)
A
- bening dermal neoplasms
- usually women legs
- tan/brown papules, spindle shaped cells
- occurs mid dermis**
- fibroblasts surround collagen bundles**
14
Q
dermis tumor - dermatofibrosarcoma protuberans
A
- malignant**
- aggressive, can recur, rarely metastasize
- more proliferation and dysplasia of fibroblasts**
- cause: mutations of collagen genes (COL1A1) and PDGFB (drives tumor growth)
- fibroblasts arranged in pinwheel (storiform) or honeycomb pattern**
- deep dermis or subcu tissue**
15
Q
adnexal (appendage) tumors
A
- tumors of sweat/sebaceous gland and hair follicles
- most are benign (except apocrine tumor malignancy)
16
Q
eccrine poroma
A
-tumors of palms and soles with numerous sweat glands
17
Q
cylindroma
A
- ductal (apocrine or eccrine) differentiation
- on forehead or scalp
- inactivating mutations in CYLD (tumor suppressor)**
- islands of cells resembling basaloid cells
- jigsawy puzzle**
18
Q
trichoepithelioma
A
- follicular tumor on malar area of face
- mutations in CYLD**
- basaloid cells resemble hair follicles**
19
Q
syringomas
A
- eccrine differentiation
- papules on lower eyelids
20
Q
pilomatricomas
A
- follicular differentiation; hair like differentiation
- activating mutations in CTNNB1 encoding beta catenin**
- Wnt signaling through beta catenin –> regulate hair growth
- keratin being formed
21
Q
sebaceous adenomas and Muir-Torre syndrome
A
- proliferation of sebocytes
- form lipids for hair waterproofing**
- associated with colon, GU, and skin cancer**
- sebaceous carcinoma –> meibomian glands of eyelid
22
Q
apocrine carcinoma
A
- tumors of apocrine glands in axilla and scalp
- apocrine carcinoma –> ductal differentiation and decapitation secretions**
23
Q
skin cellular migrants - mycosis fungoides (cutaneous T cell lymphoma, CTCL)
A
- tumor due to migration of T cells to skin
- lymphoma of CD4 T cells on skin when when cutaneous lymphocyte antigen is present –> cause ulcerations, erythema, and eczema-like patches**
- antigen presented to clonal population –> make the T cells epidermatrophic (settle and proliferate in skin)
- can develop Sezary syndrome if entering circulation –> malignant T cells with erythema
- pautrier micro abscess and cerebriform contour due to Sezary-Lutzer cells
