Neoplastic Study Guide Flashcards
Keratinocytes
held together via desmosomes (tight junctions)
Produce keratin
Keratinocytes
held together via desmosomes (tight junctions)
Produce keratin
Melanocytes
produce melanin
Langerhans cells
involved in immune response
- dendrocytes function similarly in the dermis
macule
flat lesion ≤ 5mm
patch
flat lesion > 5mm
papule
elevated lesion ≤ 5mm
plaque
elevated lesion >5mm
scale
dry, plate-like lesion
excoriation
traumatic break in the epidermis
lichenification
thickened, rough skin
pustule
discrete, pus-filled, raised lesion
vesicle
fluid filled, raised lesion ≤ 5mm
bulla
fluid filled, raised lesion > 5mm
wheal
itchy, elevated lesion with variable blanching and erythema; transient
onycholysis
separation of the nail plate from the nail bed
acanthosis
diffuse epidermal hyperplasia
dyskeratosis
abnormal premature kertinization
erosion
discontinuity of the skin with incomplete loss of the epidermis
ulceration
discontinuity of the skin with complete loss of the epidermis
exocytosis
infiltration of the epidermis by inflammatory cells
hydropic change
intracellular edema
spongiosis
intercellular edema
parakertosis
retention of nuclei in uppermost layers of the epidermis
ephelis
freckles - most common pigmented lesions of childhood
particularly common in light-skinned ppl
often appear after sure exposure
once present, fade and darken in a cyclic pattern during winter and summer
lentigo
aka age spots
small tan-brown macula’s or patches
do not darken upon exposure to sunlight
melanocytic nevi
aka moles, common benign neoplasms
acquired melanocytes nevi- most common type
tan-brown to black, uniform pigmented
well-defined round borders
nests of round melanocytes with uniform nuclei - inconspicuous nucleoli, little to no mitotic activity
grow in nests along the dermoepidermal junction (junctional nevus)
grow in the dermis and dermoepidermal junction - compound nevus
grow only in the dermis -intradermal nevus
at the deepest point in there dermis the cells become less rounded and start to grow in fascicles that resemble neural tissue- neurotization, implies maturation/growth of nevus cells
congenital nevus
present at birth or nearly infancy
no associated with sun exposure
have irregular borders
may be hair bearing
similar to acquired nevi on histology but grow along adnexal structure such as hair follicles
dysplastic nevus
grossly and histology abnormal
may give rise to melanoma
larger than benign nevi
irregular borders
variability in pigmentation
can e seen in both sun exposed and non sun exposed areas
nests of enlarged nevus cells that fuse along the dermoepidermal junction - individual nuclei are enlarged and hyper chromatic with irregular borders
melanoma
strongly linked to acquired mutations caused by UV radiation in sunlight
vast majority arise in skin- other sites include oral mucosa, angogential mucosa, esophagus, meninges, uvea of eye
mutations of melanoma
p16 and p14 lead to increased melancytic proliferation due to loss of cell cycle control
p16 mutation prevent RB from arresting cells in the G1 phase of the cell cycle leading to uncontrolled cell growth
p14 mutations enhance p53 activity leading to uncontrolled cell growth
Other melanoma mutation
BRAF mutations are seen in 40-50% of melanomas, ucontrolled cell proliferation
TERT promoter mutations turn on telomerase- prevent cell senescence
clinical warning signs of melanoma
A - asymmetry
B- irregular borders
C- color changes
D- increasing diameter
E- evolution over time
melanoma radial growth
horizontal spread within the epidermal and superficial dermis
melanoma vertical growth
tumor cells invade deeper into the dermis
Breslow depth - depth of invasion of melanoma measured from granular of epidermis to deepest point of invasion- measured mircroscopically , most important prognostic factor
histology of melanoma
individual cells are larger than those seen in benign nevi
Enlarged nuclei with irregular borde Characteristic prominent, cherry red nucleolus
Cells grow singly and in nests along the dermoepidermal junction (lentiginous
growth) and extend down into the dermis
There is no evidence of maturation/neurotization as malignant cells
extend into the dermis
favorable prognostic indicators (melanoma)
thinner Breslow depth, less mitotic activity, brisk tumor infiltrating lymphocyte response
poor prognostic indicators (melanoma)
ulceration, lymph node metastases (even with few cells)
Seborrheic keratosis
common in middle aged older individuals
o Arise spontaneously
o Activating mutations in FGFR3 are thought to drive growth
o Leser-Trelat sign – sudden appearance of large numbers of seborrheic keratoses
Paraneoplastic syndrome associated with GI malignancies
o Round, flat, waxy plaques
Often appear “stuck on”
o Sheets of small basal epithelial cells with exuberant keratin production
Pseudohorn cysts – invaginations of epithelium with abundant laminated
keratin
Actinic Keratosis
scaly erythematous lesion seen in sun damaged skin
Tan-brown, red, or flesh colored with a rough consistency
o Dysplastic cells are present in the lowermost layers of the epidermis
o Parakeratosis is seen in the superficial epidermis
o Associated solar elastosis
Thickened, blue-grey elastic fibers Result of sun damage
o May progress to squamous cell carcinoma
Squamous cell carcinoma (SCC) of the skin
related to DNA damage induced by exposure to UV light
Tumor incidence is proportional to the degree of lifetime sun exposure
o Other patients at particular risk for SCC: chronic immunosuppression, industrial
carcinogens, chronic ulcers, draining osteomyelitis, old burn scars, arsenic, ionizing
radiation, tobacco
o DNA damage caused by UV radiation (sun exposure) gives keratinocytes increased
susceptibility to infection with and transformation by oncogenic viruses such as human papillomavirus (HPV), particularly HPV types 16 and 18 o High incidence of TP53 mutations
p53 is not able to arrest the cells in G1 phase of the cell cycle for repair of DNA
damage or elimination via apoptosis
DNA damage induced by UV radiation is passed on to daughter cells
o SCC in situ – atypical cells are confined to the epidermis Grossly appear as sharply defined, red, scaly plaques
o Invasive SCC – lesions become nodular with variable keratin production May ulcerate
o Well differentiated tumors consist of atypical squamous cells with enlarged,
hyperchromatic nuclei
Large areas of keratinization
May be swirls of keratin – “keratin pearls”
o As tumors become more poorly differentiated the tumor cells become larger and more
irregularly shaped
Less and less keratinization may be present
Basal cell carcinoma
Slow growing tumors
o Rarely metastasize
o Nevoid basal cell carcinoma syndrome (aka Gorlin syndrome)
Germline mutations of PTCH gene
Uncontrolled cell growth and survival
o Pearly papules with prominent telangiectasias Advanced lesions may ulcerate
Superficial BCCs may present as an erythematous, scaly, plaque
o Tumor cells resemble normal basal cells of the epidermis
Polygonal with enlarged, hyperchromatic nuclei Grow in nests/clusters that can extend along the epidermal surface or deep
down into the dermis Cells at the periphery of the clusters show peripheral palisading Stromal clefting – stroma retracts from islands of tumor cells
Artifact of processing Fairly specific for BCC
dermatofibroma
aka benign fibrous histocytoma
firm tan brown papule
benign spindle cells
dermatofibrosarcoma protuberans (DFSP)
well differentiated fibrosarcoma of the skin
slow growing but locally agressive
characteristic translocation t(17:22)
firm nodule that my ulcerate
storiform patter of fibroblasts
mycosis fungoides
lymphoma of CD4 T cells that presents in the skin
patch, plaque and nodular stages
Sezary-Lutzner cell with characteristic hyperconvoluted/ceribriform nucleus
