dermatopathology part 2 Flashcards
seborrheic keratosis
most common benign tumor in older individuals
begin as light brown flat macules
later they develop a velvety or waxy to finely verrucous surface
color may vary from pale brown with pink tones to dark brown or black
typically have an appearance of being stuck on the skin surface and crumble with scraping
the sign of leser trelat is the association of multiple eruptive seborrheic keratoses with internal malignancy
biopsy if suspicious for melanoma
dermatosis papulos nigra
brown to black, smooth dome shaped papules
can be numerous
most often seen on african americans
sub type of seborrheic keratosis
no treatment necessary (can be treated with electrodessication)
treatment with liquid nitrogen can cause hypopigmentation
Seborrheic keratosis histology
exophytic
show sheets of small basaloid cells
frequently pigmented
exuberant keratin production at surface
small keratin filled cysts known as horn cysts
loose laemellar “shredded wheat” or “onion skin” keratin
acanthosis nigricans
hyperpigmentation is first
hyperplasia of stratum spinosum makes skin thick and velvety
usually found in folds of the neck, axilla, and groin
80% are benign type; usually occurs in childhood or puberty; may be associated with endocrine abnormalities (example: DM)
malignant type occurs in middle aged and older, associated with visceral malignancy
may be early indication underlying disorder
epidermal (inclusion) cyst
a top 10 benign lesion
inflamed vs “quiet”
common on the head and/or neck in children
histologic: cyst wall resmebles normal epidermis filled with strands of keratin
if inflammed may be surgically excised.
actinic keratosis
earliest identifiable lesion that can develop in squamous cell carcinoma (SCC)
up to 60% of SCCs develop from actinic keratoses
one prospective study estimated that one AK/1000/year transform into SCC, while other studies predict that from 5-20% of all untreated AKs will progress to SCC
Risk factors: years of sun exposure, fair skin, immunosuppression
studies have shown that a patients with 10 or more AKs has a 10-15% risk of developing SCC
actinic keratosis gross descption
palpation is key to early diagnosis
initially may be hard to see but will have areas of rough or gritty skin
discrete, scaly, feels like “broken glass” surface lesion
devleop into poorly demarcated, slightly erythematous papule or plaque with adherent scale
commonly found on sun exposed areas: face, scalp, ears, posterior neck, forearms and legs
actinic keratosis histology
parakeratosis (retained nuclei) in stratum corneum
hyperplasia and cytologic atypia of basal layer cells
solar elastosis in superficial dermis
actinic keratosis treatment and other factors
no definitive way to dsitinguish between an AK and SCC without biosy use lcinical judgement for management
treatment of choice for isolated lesions is cryotherapy (liquid nitrogen)
5 fluorouracil is effective topical tx. for supperficial AK’s with major side effect of intense inflammation
other treatment options: excision electrodissection and curettage, CO2 laser, and imiquimod, photodynamic therapy
actinic keratosis treatment side effects and other things
if you use crytotherapy, it is normal for the patient to get mild blistering and then a scab that leads to the lesion falling off
however, if the patient returns for a follow up in 2-3 months and the lesion is now ulcerated or thickened compared to before, a biopsy is warranted to r/o SCC; recurrence is normal but thickened and tender lesions have a greater risk for progression to cancer
5FU often used when multiple lesions appear on face, neck and scalp; daily BID 2-4 weeks
imiquimod immune response modifier BID-TID 4-16 weeks
Non melanoma skin cancer
most common cancer in the US about equal to all other cancers combined
80 are basal cell carcinomas (BCC) and 20% are squamous cell carcinomas (SCC)
after developing an initial BCC or SCC, patients have approximately a 50% chance of devleoping another NMSC
Squamous cell carcinoma presentation and risk factors
may present as a variety of primary morphologies with or without associated symptoms
arises in the epithelium and is common in the middle aged and elderly populations
risk factors: male, elderly, UV and ionizing radiation, fairskin, arsenic, HPV, sites with chronic infection, thermal burn scars, and immunosuppression but UVB and UVA most important
common on the scalp, dorsal upper extremities, and ears
SCC in situ
can present with scaly pink patch or a thin keratotic papule
bowen disease
subtype characterized by a sharply demarcated pink plaque and can arise on non sun exposed skin
erythroplasia of queyrat
bowen disease of the galns penis, which manifests as one or more velvety red plaques
squamous cell ca in situ histology
no invasion thorugh absement membrane of dermoepidermal junction
atypical nuclei (enlarged and hyperchromatic) involved all levels of the epidermis
squamous cell ca histology
invade basement membrane
variable differentiation: orderly lobules of polygonal cells, areas of keratinization (well differentiated). anaplastic cells, necrosis, no organized keratin production (poorly differentiated).
invasive SCC
raised, firm pink to flesh colored keratotic papule or plaque arising on sun exposed skin
surface changes may include scaling, ulceration, crusting, or the presence of a cutaneous horn
subtype include oral and verrucous (resemble large warts)
metastases to regional lymph nodes <5% generally by deeply invasive tumors
diagnosis of SCC
definitive diagnosis of MNSC requires a biopsy (shave, punch, incisinona, or excisional)
must reach at least the depth of the mid dermis to allow for a determination of the presence or absence of invasive disease
lymph node biosy or FNA should be performed in regional lymphadenopaty is present
PET scanning, ultrasoundgudied FNA, and sentinel lymph node biosy all appear to offer a good chance of detecting subclinical nodal metastaasis in high risk pts.
metastasis for squamous cell carcinoa is in the range of 2-6% but can be much higher with high risk lesions
5 years survival rate of patients with nodal metastasis is as high as 73% with aggressive treatment
treatment of SCC
surgical removal
4 mm margin of normal tissue is recommended for lower risk lesions < 2 cm
> 2 cm, invasive to fat and in high risk locations a 6 mm margin is recommended
MOHs micrographic surgery
electrodesiccation and curettage (ED&C)- not usually recommended because can’t assess margins
may need adjuvant radiaton and chemotherapy
Keratoacanthoma clinical and shape
benign epithelial tumor that may progress to SCC vs. well differentiated SCC (controversial)
appear suddenly on actinically damaged skin, grow rapidly and spontaneously regress after a few months
red to flesh colored dome-shaped papule with a central crater filled with keratinous plug
pathologist have trouble differentiating the two
treat the same as SCC
keratoacathoma histology
large red glassy squamoid cells
cellular atypia and mitoses uncommon
neutrophil microabscesses common
eosinophils and lymphocytes are common in surrounding infiltrate
keratoacanthoma concerns
8% recurrence rate
may transform into SCC
may occur with SCC
may be well diffrentiated SCC
basal cell carcinoma
most common malignancy
annual incidence in US is about 1 million cases
estimated lifetime risk of BCC in the white population is 33-39% in men and 23-28 in women
pluripotential cells in the basal layer of the epidermis or follicular structures
slow growing and rarely metatstizes
can cause local destruction and disfigurement if negelected or inadequately treated
prognosis is excellent with proper therapy
BCC risk factors
UV radiation, x ray, arsenic immunosuppression, a number of hereditary syndromes and prior history of NMSC
often present with a non healing lesion that bleeds
commonly found on the face, ears, scalp, neck, or upper trunk
subtypes include nodular, superficial, and morpheaform, other rare subtypes
BCC superfical
second most common subtype (30%)
trunk is most common site
slightly scaly papule or plaque
light red color
atrophic center with fine translucent micropapules on rim
BCC nodular
most common
face is most common site
waxy papules with central depression
pearly appearance
erosion, ulceration or crusting
bleeding with minor trauma
rolled (raised) border
translucency
telangiectasias over the surface
Diagnosis of BCC
biopsy is requried to confirm the diagnosis and to identify the histologic subtype
shave or punch biosy is usually performed
if small the entire lesion may be removed but not exceeding clinical margins.
BCC histology
variable morphology
commonly ensts of basaloid cells which palisade at the border of the nest
nests in firbmyxoid stroma
most tumor nests /nodules attach to the undersurface of the epidermis
stroma separates from tumor nodules, separation artifact
TX of BCC
surgical method
radiatiion therapy
imiquimod
5FU
Mohs surgery
removal of tumor and a thin rim of normal appearing skin around the defect
specimen is sectioned and labeled
frozen section technique allows for an examination of tissue while the patient is in the office
if margins are not clear further excision will be done and normal tissue will be spared
best long term cure rates of any treatment modality
HIstory
very important toknow
