Skin Neoplasms And Eruptions Flashcards
Epidermal neoplasms
Verrucae (warts)
Actinic keratosis
Squamous cell carcinoma
Basal cell carcinoma
Verruca Vulgaris
HPV associated
Papillomatosis- surface with peaks and valleys
A lot of extra keratin in warts (hyperkeratosis), dozens of layers of normal skin= scaly, white clinical appearance
Thickening of epidermis (epidermal hyperplasia)
Hypergranulosis and koilocytes (haloes around nuclei)
Actinic (solar) keratosis
‘Pre-cancer’ induced by UV light, fair skin, chronically photo-exposed skin, may progress to squamous cell carcinoma
Rough, scaly pink spots
Early- atypia limited to epidermal layers that has not progressed up, nuclei are big, crowded, dark.
Later- large basal and spinous cells, parakeratosis (retained nuclei in s. corneum), inflammatory cells seen in dermis, basal cells have divided and sent their progeny to superficial layers.
Squamous cell carcinoma
Flat, scaly well defined
In situ- limited to epidermis (why its flat), when the squamous cell in situ invades, it sends islands into dermis, which lifts whole epidermis up= elevated nodule
Chronic inflammation can also be a risk factor next to radiation and UV damage. Xeroderma pigmentosum also a RF.
Rarely metastatic
Histo- in situ: every epidermal layer reveals abnormal cells that are large, multinucleated, abnormal mitotic figures.
Histo- invades down pink islands into dermis making keratin. Islands with central whorled keratin “pearls” and surrounding abnormal epidermal cells with tons of cytoplasm, scattered nuclei
Basal cell carcinoma
Most common type of skin cancer, pearly translucent papule with prominent blood vessels, metastasis is extremely rare.
Histo- no keratin, so will be smooth in clinic, one nodule of blue cells budding the epidermis within the dermis causing a retraction artifact (between tumor and dermis). Cells at periphery of nodule line up, mimic get basal cells, elongated with a lot of nuclei with little cytoplasm= peripheral palisading
Malignant melanoma
Originate from melanocytes
In situ- ‘radial growth’, single and grouped large, atypical melanocytes with abundant cytoplasm in all layers of epidermis. ‘Nests’ have variability in nuclei size.
Invasive into dermis- vertical growth (most important prognostic factor) now nodular clinical presentation, sheets of melanocytes fill papillary dermis, melanin deposits can be seen to give nodule its dark color
Metastasizes via lymphatics to regional lymph nodes and by blood to brain, lung, liver, bone.
Not a well defined border, abnormal asymmetry
Spongiotic dermatitis- histology
Types
Stages
Lymphocytes in dermis surrounding BVs eventually go into epidermis, spongiosis (edema of epidermis- white space between keratinocytes and pushes them apart)
Allergic contact dermatitis- type IV hypersensitivity
Irritant contact dermatitis- toxic
Atopic dermatitis- multifactorial (filaggrin mutation)
Seborrheic dermatitis- idiopathic, yeast
Histologic stages- acute, subacute, chronic (can tell difference by histology)
Atopic dermatitis
Chronic with periods of remission and exacerbation
Associated with atopic diathesis- asthma and hay fever
Develops before age of 5 and clears by adolescence
Pruritus (itch) is primary symptom
Multifactorial- genetics, skin barrier dysfunction, impaired immune response, environment
*one of many clinical faces of spongiotic dermatitis
Acute spongiotic dermatitis histology
Severe spongiosis with vesicle, lymphocyte exocytosis (entry epidermis- usually only inflammatory cell in epidermis are the LH cells )
Subacute dermatitis
Less spongiosis, parakeratosis, epidermal hyperplasia, lymphocytes: get a crust/scaling
Chronic dermatitis
No spongiosis, marked epidermal hyperplasia- reflected as hyperpigmented, elevated lesion on skin
Psoriasis
Flaky, red rash usually on extensor surfaces, pits in fingernails, other places, can have joint pain
Regular epidermal hyperplasia- can draw a perfect line below ridges*
Diffuse parakeratosis (scaling), dilated vessels (Ausptiz sign) with lymphocytes around them (erythema)- so scaly, they pick it off and bleed because they take the scale and a few extra layers of epidermis with it to expose dilated vessels underneath
Loss of granular layer
Exocytosis of neutrophils* (dermatitis has lymphocytes)
Acanthosis (thick epidermis)- elevated lesion
T cell mediated
Usually affects knees, elbows, scalp, umbilicus, gluteal cleft
Associated with metabolic syndromes- overweight, diabetes, high blood pressure, high cholesterol
Pemphigus Vulgaris
Good portion of epidermis is lifted away from dermis to reveal a space- causes erosion
Normal basal cells lining dermal papilla
Suprabasilar cleft* leaving a tombstoning of basal cells
Biopsy normal skin adjacent to lesion for immunofluorescence- antibodies bind desmosome and cause disruption of bridges between one keratinocyte to another- desmoglein* spans from inside to outside of keratinocyte. Reveals deposition around epidermal cells in a ‘chicken wire’ pattern
Acquired autoimmune mediated blistering
Affects oral mucosa, skin of scalp, face, trunk
Intraepidermal blisters
