Pathology-Dermatopathology Flashcards
(32 cards)
What would you expect to see clinically and histologically in a junctional nevus?
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Where would you expect to find melanocyte nests in a section from a raised nevus?
In the dermis. A nevus with melanocytes at the dermoepidermal junction and in the dermis are compound nevi.
What happens to the deeper melanocytes in a benign compound nevus?
They maturate and shrink.
*What would you expect to see clinically from this patient?
*Dysplastic nevi because there is asymmetry in the nests in the histological section.
Why are dysplastic nevi more concerning than junctional nevi?
The nests have cytologic atypia with hyperchromatic nuclei.
What characteristics are typical of melanoma?
*Radial growth along dermoepidermal junction, pagitoid spread, hyperchromatic cells, mitotic figures, no maturation and red nuclei.
A patient presents to your office with a waxy, dark lesion that looks like it was just stuck onto the skin. What might the biopsy of this look like?
*Keratin horn cysts are hallmarks of Seborrheic Keratosis
What did Elizabeth have on her shoulder?
Fibroepithelial Polyp (skin tag)
What is the precursor for squamous cell carcinoma?
*Actinic Keratosis. Cytologic atypia, hyperplasia of basal cells and hyperkeratosis.
A patient presents with nodular growth on his forehead with crusting. What might his biopsy look like?
Invasive squamous cell carcinoma. Note downward growth and nests invading into dermis.
A patient presents with pearly papules and prominent telangiectasia. What might this patient have and what might the biopsy look like?
Basal cell carcinoma. Note basophilic cells with hyperchromatic nuclei lining up in their clusters separated by clefts.
A middle-aged female patient presents with a non-encapsulated raised nodule on her legs. Histological staining shows entrapped collagen. What might this patient have?
Dermatofibroma. Look for fibroblasts surrounding collagen bundles and spindle cell proliferation.
A patient presents with a flesh-colored firm nodule with a storiform appearance. What might this patient have?
Dermatofibrosarcoma Protuberans. Note spindle cell proliferation as if spokes of bicycle wheel were extending outwards.
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Uticaria. Note perivascular infiltration and edema evident by spaces between collagen bundles.
A patient is allergic to laundry detergent and comes to see you looking like this. What does he have?
Acute Contact Dermatitis
How do the blisters of pemphigus folaceus, vulgaris and bullous pemphagoid differ?
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What would you see in clinic and histologically in pemphigus vulgaris?
Note eroded plaques, blistering with rounded keratinocytes due to acantholysis and “row of tombstones”.
What determines where blisters form in bullous diseases?
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What would you see in a clinic and histologically in bullous pemphigoid?
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A patient took aspirin and comes to your clinic with wheals that you say will go away in a few hours. What other triggers could cause this condition?
IgE antigens, opiates, antibiotics, curare, contrast dye and uncontrolled complement activation.
A patient presents to your clinic with red, papulovesicular oozing and crusted lesions that are developing into scaling plaques. What might this patient have and how would a biopsy differ in early stages vs. late stages?
Eczema.
Why might someone who regularly uses a tanning bed be less susceptible to a contact dermatitis condition?
In contact dermatitis, Langerhans cells come into contact with the antigen and activate CD4 cells which release cytokines and cause eczema. UV light is injurious to Langerhans cells.
How does eczema from contact dermatitis differ from eczema from a medication?
Contact dermatitis will have inflammatory cells in the superficial dermal layer. Medication related eczema will have eosinophils around deep dermal vessels.
A patient presents to your clinic with blisters. He says they started in his mouth and progressed to his face, scalp, axilla, groin and trunk. You observe the blisters and note Nikolsky’s sign. What is your diagnosis?
Pemphigus vulgaris. It normally starts in the mouth. Blisters begin in the deep supra basal epidermis due to IgG autoantibodies against dsg1 and dsg3.
