Skin Patho Day 3 Flashcards
Seborrheic Keratoses
Due to mutations in FGF receptor 3
Middle aged/elderly get these
Brown/tan/waxy papules, benign
Trunk/face
- Leser-Trelat:* sudden onset of many macules lead to cancer
- Histology:* hyperkeratotic, papillomatous epidermis; horn/pseudocysts
Actinic Keratosis
Sign of preneoplasia; 0.1-10% turn malignant
Middle aged/elderly
Result sun damage
Red/tan/brown macules with sand paper scale
Histology: hyperchromatic cells, parakeratosis (retained nuceli in corneum), dermis–solar elastosis
Squamous Cell Carcinoma
Common neoplasm in elderly
UV radiation, chronic ulcers, burn scars, HPV, radiation, arsenic, immunosupression all triggers
Red scaly plaque or nodular if invasive
Invasive 5%, metastasis 2-4%
Makes up 20% of skin cancers
Histology: wind blown appearance (polarity completely gone), keratin pearls
Keratocanthoma
Form of SCC with nodule and central plug
Grows 2-10 weeks in sun exposed skin of elder
Worse/more in immunosuppressed
Treat with surgery
Histology: well differentiated epitehlium with central pit
Basal Cell Carcinoma
Most common human cancer; secondary to UV radiation (due to dysreg. of sonic hedgehog pathway or PTCH)
RARELY metastasizes
Pink pearl papules with blood vessels
Histology: more bluish color because from basal layer; nodular cells and nests of keratinocytes in dermis
Melanocytic Tumors (“nevi”)
CATEGORY–Either present at birth or acquired from sun exposure causing growth down into dermis
- Junctional (epidermis), Compound (epidermis and dermis), Intradermal (dermis)
- Round to oval cells that grow in nests
- Acquired ones are often pink/tan/brown and uniformly pigmented macules and papules
Includes dysplastic nevi and melanoma
Dysplastic Nevi
More significant than regular nevi
Increase in dyplastic nevi causes an increase in cancer (or can change to melanoma)
- Dysplastic nevus sx:* 80+ dysplastic nevi; familial due to autosomal dominant CDKN2A 9p 21-11 mutation
- Histology:* NEVER intradermal; can be enlarged cell nests with abnormal fusing
Replacing normal basal cell layer is called “lentiginous hyperplasia”
Melanoma
Disease of adulthood, more common in whites (back in men, legs in women)
–multifactoral (TONS of risk factors); can have precursor melanoma; CDKN2A or BRAF mutations
A=Asymmetry
B=Borders uneven
C=Color uneven
D=Diameter >6mm
E=Change in color/size
Early treatment is surgery
Biopsy sentinal lymph node also possible
Histology of Melanoma
Asymmetric population melanocytes as single cells/clusters throughout epidermis
Tons of cytoplasm (pleomorphic nuclei, eosinophilic)
What is the difference between radial growth and vertical growth in melanoma?
RADIAL GROWTH–> in epidermis only
VERTICAL GROWTH–> down into dermis
Breslow thickness tells depth of invasion
What are the different types of melanoma?
Superficial spreading type: most common; back and extremities
Nodular type: no radial growth phase so bad prognosis (trunk and legs)
Lentigo maligna type: sun damaged; head and neck
Acral lentiginous type: palm, sole, nail; most common in African Americans; older females
Mycosis Fungoids
T cell lymphoma, most common
Late adulthood in males/blacks commonly
Red or pink scaly patches
- Path phase–patches on lower trunk, buttocks
- Plaque phase–annular well-demarcated lesions purple and scaly
- Tumor phase–red, shiny, tense surface with ulceration
Usually chronic progression
Sezary Syndrome
Blood involvement T Cell lymphoma with erythroderma (skin red and scaly); survival 1-3 years
Lymphoma histology
Lymphocytes that have colonized epidermis
Large cells with irregular nuclei-Sezary/mycosis cells (“brain” look)
CD4+ cells
Impetigo
Superficial bacterial infection
Highly infectious; childhood; S. aureus or S. pyogenes
*small vesicles –> rupture –> thick yellow crust (honey colored)
Histology: neutrophillic infiltrate; cocci in gram stain
