Dermatopathology part 1 Flashcards
What is Vitiligo? What disease is it typically associated with?
Chronic depigmenting condition from complete loss of epidermal melanocytes
Associated with pernicious anemia and hasimoto’s thyroiditis.
How does vitaligo cause depigmentation
Autoantibody against melanin concentration hormone receptor 1 in serum.
Presents on the 2nd or 3rd decades.
Higher in africans.
Predilection of vitiligo
Acral areas and orifices.
Presents as asymptomatic white macules with sharp borders that gradually enlarge.
Hair will also lose pigments.
Can see the lesions better under a wood’s lamp.
TX of vitiligo
slowly progressive, but 10-20% experience spontaneous regression.
some benefit with topical steroids, calcineruin inhibitors, and light therapy
Freckle (Ephelis)
Basal layer hyperpigmentation
appear after sun exposure in lighhtly pigmented kids
darken with sun expsoure
no risk of malignancy
Lentigo (lentigines)
Small (<1.0 cm) circumscribed brown macular lesions.
Hyperpigmentation of cells just above the basement membrane
unlike ephelides, lentigines do not darken with sun exposure.
Lentigo histology
The rete ridges are elongated and appear club shaped or tortuous. Melanocytes are increased in the basal layer and melanophages appear in the upper dermis.
Melanocytic nevi Gross features
tan to brown.
uniformly pigmented
small (usually <6mm in greatest dimension)
flat to elevated
well defined, rounded borders.
melanocytic nevi histology
sharply defined
well nested at the dermal epidermal junction
melanocytes mature as they descend in dermis
no deep mitoses
no deep pigment in melanocytic nests
Melanocytic nevi progression of maturation
junctional > compound > intradermal
Junctional melanocytic neves
melanocytic nests at the dermal epidermal junction
nests restricted to the tips and sides of rete.
compound melanocytic nevus
more raised and dome shaped than junctional nevus
histologic features of junctional nevus (intraepidermal nevus cell nets) + nests and cords of nevus cell in underlying dermis
as cells invade the dermis they mature and become smaller.
Dermal melanocytic nevus histology
epidermal nests are lost completly
spitz nevus description of what it presents cellularly
composed of spindle and/or epitheliod cells
dyskeratotic melanocytes (kamino bodies): eosinophilic bodies along dermal epidermal junction
sharply defined laterally
line symmetry from left to right
celfts separating nets from keratinocytes
Sptiz nevus. Who get this and describe what it looks like
common in children
deep red color may be confused with hemangiomas
Kamino bodies
eosinophilic collections of dyskeratotic melanocytes
Spitz nevus location of the nests and caveats
netsts of melanocytes within the epidermis
nets are seperated from the epidermis by clefts
dysplastic (atypical) melanocytic nevus description
commonly large, oval, and multiple
irregular pigment common
fading boarder or fried egg appearance (central papule, surrounding macule)
dysplastic (atypical) melanocytic nevus Histologically
Histologic: usually compound, concentric papillary dermal fibrosis.
dysplastic (atypical) melanocytic nevus nets
horizontally orieted nests with bridging of adjacent rete
nets are at the tips and sides of rete
cytologic atypia: hyperchromatic, enlarged nuclei
Melanoma
1 cause of skin cancer deaths worldwide
malignancy of pigment producing cells (melanocytes which are derived from the neural crest)
develops de novo or from pre existing mole
found in the skin, eyes, GI tract, leptomeninges, oral and genital mucosa.\
4% of all skin cancers
Verticle phase of melanoma
determiens tumor stage and this phase can lead to metastasis to lymph nodes, brain, GI tract, bone, liver and lungs most commonly
Risk factors of melanoma
Changing mole
other things
ABCDE rule of skin lesions
assymetry, border irregularity, color variation, diameter > 6mm, evolving
radial growth phase
horizontal spread of melanoma cells within the epidermis and superficial dermis
tumor cells lack the ability to metastasize
verticle growth phase
tumor cells invade downward into deeper dermal layers as a mass
cells with metastatic potential emerge
invading cells do not mature as in melanocytic nevi
grossly, a nodule appears
superficial spreading
most common (50-75% of all melanomas)
25% from preexisting lesion
sun exposed skin, typically on backs of men and lower legs of women but any age
evolved lesions may show ultiple shades: red, tan, brown , blue, black, grey and white
superficial spreading: histologic features
buckshot scatter of atypical melanocytes within the epdiermis (pagetoid spread)
typically not symmetrical (R to L)
Typically fails to mature from top to bottom
deep mitoses may be present
cytologic atypia
Lentigo maligna 1 what gender typically gets it. Describe growth.
indolent, slow growing lesion
typically, face of old men
long radial growth phase, 10-50 years
starts as tan brown macule, gradually enlarges, develops darker, asymmetric foci
5% of intraepidermal lesions evolve to become clinically palpable, signaling dermal invasion and transformation into lentigo maligna melanoma.
Lentigo maligna 2 caused by, type of growth, and cell descrption
broad lesion on sun damaged skin
predominantely junctional growth of atypical melanocytes
cytologic atypia
Lentigo maligna 3 distinguishing features
distinguishing features: malignant melona in situ. poorly nested and confluent melanocytes at the dermal epidermal junction. adnexal extension. Heavily sun-damaged skin (severe dermis solar elastosis)
lentigo maligna melanoma
lentigo maligna with a vertical growth phase
acral lentiginous melanoma
least common, < 5% of all melanomas
most common melanoma in african americans adn asians
palms, soles, beneath the nail plate
hutchinson’s sign
nodular melanoma where on the body
15-30% of melanomas
anywhere on the body
can be amelanotic
Nodular melanoma histo
vertical growth phase melanoma
no apparent radial growth phase
dermal growth occurs in isolation or occasionally, in association with an epidermal component
mitoses are frequent and often atypical
Breslow measurement
actual measurement of tumor
most closely correlates with survival statistics
clark level
not based on measurement, but on the number of layers of skin that the tumor has penetrated
- epidermis
- papillary dermis, not yet to papillary reticular junction
- fills papillary dermis
- reticular dermis
- subcutaneous tissues
Sentinel node biopsy
lymphoscintigraphy radioactive tracer and a gamma probe is used
recommended for intermediate tumors (1 to 4 mm thickness) or high risk thin tumors
minimally invasive technique that has been shown to help accurately stage the regional nodal basin with a lower associated rate of complications and costs compared to ELND
subsequently full lymph dissection is performed if metastatic disease is present and adjuvant therapy like interferon alpha is administered
prognostic factors
tumor thickness
mitotic rate
ulceration
lymph node involvement
satellite lesions
distant metastases
age: older the wrose
gender: female have better prognosis
anatomic location: upper extremities better than head, neck, trunk, +/- lower extremities
