Derm Flashcards
vitiligo
chronic depigmenting condition from complete loss of epidermal melanocytes
Autoantibody against melanin concentrating hormone receptor 1
association for vitiligo
pernicious anemia and Hashimoto thyroiditis
may be autoimmune
locations for vitiligo
predilection for acral areas (fingers, limbs, ears)
orifices (mouth, eyes, nose, anus)
description of vitiligo rash
asymptomatic white macules with sharp borders that gradually enlarge
hair will also lose pigment
treatment of vitiligo
topical steroids, calcineurin inhibitors (tacrolimus) and light therapy
histology of vitiligo
giant melanosome in depigmented areas
ephelis
freckle
basal layer hyperpigmentaiton
darken with sun exposure
no risk of malignancy
lentigo
hyperpigmentation of cells just above the basement membrane
do not darken with sun exposure
histology of lentigo
age or liver spot
rete ridges are elongated and appear club-shaped or tortuous
increased melanocytes in basal layer
melanophages appear in upper dermis
melanocytic nevi
tan to brown
uniformly pigmented
well defined, rounded borders
histology of melanocytic nevi
well nested at dermal-epidermal junction
melanocytes mature as they descend in dermis
no deep mitoses
no deep pigment in melanocytic nests
histology of junctional melanocytic nevus
nests at dermal-epidermal junction
restricted to the tips and sides of rete
compond melanocytic nevus
more raised and dome shaped than junctional nvus
histology of compound melanocytic nevus
intraepidermal nevus cell nests and nests and cords in underlying dermis (mature and become smaller)
dermal melanocytic nervus histology
epidermal nests are completely lost
spitz nevus characteristics
composed of spindle and/or epithelioid cells
sharply defined laterally
symmetry from left to right
clefts separating nests from keratinocytes
clinical characteristics of spitz nevus
common in children
deep red color, may be confused with hemangiomas
dyskeratotic melanocytes (Kamino bodies)
eosinophilic bodies along dermal-epidermal junction
histology of spitz nevus
nests of melanocytes within the epidermis
nests separated from epidermis by clefts
dysplastic melanocytic nevus characteristics
commonly large, oval, and multiple
irregular pigment common
fading border or fied egg appearance
histology of dysplastic melanocytic nevus
usually compound, concentric papillary dermal fibrosis
horizontally oriented nests with bridging of adjacent rete
at the tips and sides of rete
hyperchromatic, enlarged nuclei
melanoma characteristics
malignancy of pigment producing cells (derived from neural crest)
found in skin, eyes, GI tract, letpomeninges, oral and genital mucosa
number one cause of skin cancer deaths worldwide
melanoma
determination of tumor stage
vertical phase
can lead to metastasis to lymph nodes, brain, GI, bone, liver and lungs
common mets in melanoma
brain (third after lung and breast cancer)
risk factors for melanoma
changing mole (number 1) atypical nevi, numerous large congenital nevi previous melanoma or nonmelanoma sun sensitivity xeroderma pigmentosum fair skin and history of blistering sunburns
management of suspicious lesions
asymmetry border irregularity color variation diameter evolving
biopsy lesion
full thickness skin extending into subcutaneous fat with 2mm lateral margins
excision, punch or incisional if large
radial growth phase
horizontal spread within the epidermis and superficial dermis
lack ability to metastasize
vertical growth phase
invade downward into deeper dermal layers as a mass
metastatic potential
cells do not mature
superficial spreading melanoma
most common melanoma
radial growth phase of uncertain length before vertical growth phase develops
may show multiple shades-red, tan, brown, blue, black, gray and white
typical location of superficial spreading mel
back of men and lower legs of women
histological superficial spreading mel
buckshot scatter of atypical melanocytes
not symmetrical
deep mitoses
typically fails to mature from top to bottom
lentigo maligna
slow growing lesion
long radial growth phase
tan-brown macule that graudally enlarges, devlops darker, asymmetric foci
location for lentigo maligna
face of old men
histological features of lentigo maligna
junctional growth of atypical melanocytes
poorly nested and confluent melanocytes at dermal-epidermal junction
adnexa extension
lentigo maligna melanoma
lentigo maligna with vertical growth phase
acral lentiginous melanoma
least common
most common melanoma in AA and Asians
palms, soles, beneath nail plate
Hutchinson’s sign
sign of malignant melanoma on fingernail
nodular melanoma histology
vertical growth phase
no apparent radial growth
mitoses are frequent and often atypical
breslow measurement
actual measurement from skin surface
clark measurement
number of layers of skin that the tumor has penetrated
most closely correlates with survival statistics
sentinel node biopsy
radioactive tracer and gamma probe
for intermediate tumors (1-4mm) or high risk thin tumors
helpful in staging
seborrheic keratosis
most common benign tumor in older individuals
looks like melanoma
begin as light brown, flat macules-then become velvety or waxy
sign of Leser-Trelat
multiple eruptive SK with internal malignancy
dermatosis papulosa nigra
brown to black, smooth, dome shaped papules
subtype of SK in AA
liquid nitrogen can cause hypopigmentation
histology of SK
sheets of small, basaloid cells
exuberant keratin production
horn cells and loose lamellar keratin
horn cysts
keratin filled cysts
acanthosis nigricans
hyperpigmentation and hyperplasia of stratum spinosum
found in folds of neck, axilla, groin
acanthosis benign type
associated with endocrine abnormalities (DM)
malignant acanthosis
middle aged and older
associated with visceral malignancy
epidermal inclusion cyst
common on head or neck of children
may be excised if inflammed
cyst wall resembles normal epidermis, filled with strands of keratin
actinic keratoses
can develop into SCC
palpation-rough or gritty skin, feels like broken glass
slightly erythematous papule or plaque with adherent scale
locations of actinic keratoses
face, scalp, ears, posterior neck, forearms and legs
histology of actinic keratoses
parakeratosis (retained nuclei) in stratum corneum
hyperplasia and cytologic atypia of basal cells
solar elastosis in superficial dermis
treatment of actinic keratoses
isolated-cryotherapy
5FU (causes intense inflammation)
excision, electrodissection, curettage, CO2 laser, Imiquimod, photodynamic therapy
side effect of cryotherapy
mild blistering and then scab
if ulcerated or thickened-rule out SCC
most common cancer in the US
nonmelanoma skin cancer
80% BCC
20% SCC
SCC
arises in epithelium and is common in middle aged and elderly
risk factors for SCC
male, elderly, UV and ionizing radiation, fair skin, arsenic, HPV, burn scars and immunosuppression
MOST IMPORTANT IS DNA DAMAGE FROM UV LIGHT-UVB#1
common locations for SCC
scalp, dorsal upper extremities, ears
Bowen disease
sharply demarcated pink plaque and can arise on non-sun exposed skin
SCC in situ
erythroplasia of Queyrat
Bowen disease of glans penis
manifests ad one or more velvety red plaques
SCC in situ
Bowen histology
no invasion through basement membrane of dermoepidermal junction
atypical nuclei involve all layers of epidermis
SCC histology
invade basement membrane
lobules of polygonal cells, area of keratinization in well differentiated
anaplastic, necrosis, no keratin organization in poorly differentiated
intercellular bridges
SCC
invasive SCC
raised, firm, pink to flesh colored keratotic papule
metastases to regional lymph nodes
surface changes include scaling, ulceration, crusting or presence of cutaneous horn
diagnosis of SCC
requires biopsy (shave, punch, incisional, or excisional)
lymph node biopsy or FNA if lymphadenopathy is present
PET, ultrasound guided FNA and sentinel to determine nodal mets
treatment of SCC
surgical removal (less margin than melanoma) ED and C not recommended
keratoacanthoma
benign epithelial tumor that may progress to SCC
look alike
appear suddenly on actinically damaged skin and regress
red to flesh colored dome-shaped papule with central keratinous plug
histology of keratoacanthoma
large, red, glassy squamoid cells
mitoses uncommon
neutrophil microabscesses common
eosinophils and lymphocytes are common in surrounding infiltrate
BCC
most common
pluripotential cells in basal layer of epidermis and follicular structures
can cause local destruction and disfigurement
BCC risk factors
UV radiation, xray, arsenic, immunosuppression
common presentation of BCC
non-healing lesion that bleeds
common location BCC
face, ears, scalp, neck, upper trunk
nodular BCC
most common type
face most common site
waxy with central depression
telangiectasias over surface
superficial BCC
trunk most common site
atrophic center with fine translucent micropapules on rim
light red color
diagnosis of BCC
biopsy to confirm
shave or punch
histology of BCC
basaloid cells which palisade at border of nest
nests in fibromyxoid stroma
separation artifact-stroma separates from tumor nodules
treatment of BCC
currettage, excision with margin examination Mohs micrographic surgery radiotherapy radiation Imiquimod 5FU
Mohs surgery
removal of tumor and thin rim
frozen section allows examination of tissue while patient is in office
best long term cure rates of any treatment modality
acanthosis
diffuse epidermal hyperplasia
dyskeratosis
premature keratinization within cells below stratum granulosum
hydropic swelling
intracellualr edema of keratinocytes
seen in viral infections
hypergraunulosis
hyperplasia of granulosum due to intense rubbing
hyperkeratosis
thickening of straum corneum due to qualitative abnormality of keratin
lentiginous
linear pattern of melanocyte proliferation within the epidermal basal cell layer
papillomatosis
surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae
parakeratosis
keratinization with retained nuclei in stratum corneum
normal in mucous membranes
spongiosis
intercellular edema of epidermis
dermatofibroma
benign fibrous histiocytoma
very common benign lesion that occurs on lower legs
display dimple sign
fibrous reaction to some past trauma to skin
histology of dermatofibroma
proliferations of fibroblasts with collagen
whirling fibroblasts with collagen bundles
overlying hyperkeratosis and hyperpigmentation-reddish brown color
dermatofibrosarcoma protuberans histology
primary fibrosarcoma of skin
extends from dermis into subcutaneous fat in honeycomb pattern
fibroblasts in pinwheel pattern
mycosis fungiodes
T cell lymphoma that presents in skin and may evolve into generalized lymphoma
stages of mycosis fungiodes
patch-scaly, red-brown
plaque-raised, indurated, irregular, red, scaly
nodule-fungating, red-brown
histology of mycosis fungiodes
T helper cells form bands in superficial dermis
invade epidermis as single cells or small clustures (Pautrier microabscesses)
urticaria pigmentosa
usually children
round to oval, red-brown papules and plaques, pruritic and may blister, appear shortly after birth
systemic mastocytosis
usually adults
skin lesions similar to urticaria pigmentosa plus multi-organ mast cell infiltration
organ involvement in systemic mastocytosis
bone marrow, liver, spleen, lymph nodes