Flashcards in Skin Deck (352)
Xanthogranuloma: Constituent cells.
Touton giant cells.
Neutrophils, eosinophils, lymphocytes.
Xanthogranuloma: Immunohistochemical distinction from Langerhans' cell histiocytosis.
Langerhans' cells express CD1a, S100, and langerin.
Reticulohistiocytosis: Clinical forms.
Localized: Limited to skin.
Systemic: Involves skin, heart, bone, joints, lymph nodes.
Systemic reticulohistiocytosis: Associations (3).
Reticulohistiocytoma: Morphology of defining cell.
Epithelioid histiocyte with abundant, pale-pink, glassy cytoplasm.
Granuloma annulare: Typical anatomic sites.
Dorsa of hands and feet, knees, ankles, elbows.
Granuloma annulare: Distribution of histiocytes.
Palisaded, interstitial, or a combination of both.
Granuloma annulare: Histological distinction from rheumatoid nodule.
- Necrobiosis is more eosinophilic and sometimes fibrinoid; no mucin.
- Subcutaneous location.
Granuloma annulare in children.
May be subcutaneous and hence difficult to distinguish from rheumatoid nodule.
Rheumatoid nodule: Anatomic sites (2).
PIP joints, MCP joints.
Necrobiosis lipoidica: Classic anatomic site.
Necrobiosis lipoidica: Appearance of necrobiosis.
Basophilic degeneration of collagen.
Necrobiosis lipoidica: Relevance to diabetes (2).
Occurs in less than 1% of diabetics.
Occurs at a later age in diabetics than in non-diabetics.
A. Clinical association.
B. Typical anatomic location.
B. Periorbital skin.
Necrobiotic xanthogranuloma: Histology (3).
Foam cells, Touton giant cells, lymphocytes.
Intervening zones of necrobiosis.
Lymphoid follicles sometimes.
A. Site of lesions.
B. Clinical significance.
A. Central face.
B. Increased risk of pulmonary sarcoidosis.
Löfgren's syndrome: Clinical triad.
Hilar adenopathy, acute polyarthritis, erythema nodosum.
A variant presentation of sarcoidosis.
Sarcoidosis: Appearance of granulomas.
Noncaseating; minimal peripheral lymphocytic infiltrate.
Sarcoidosis: Appearance of panniculitis.
Lobular pattern; noncaseating granulomas.
Foreign substances that can cause sarcoidal granulomas (3).
Inflammatory infiltrate of leprosy:
B. Foam cells; few lymphocytes.
C. Foam cells and epithelioid histiocytes in poorly formed granulomas; many lymphocytes.
Leprosy: Where to find organisms.
Abundant in lepromatous leprosy; few in tuberculoid leprosy.
Found in histiocytes, nerves, arrectores pilorum.
Histologically resembles a histiocytoma but is full of acid-fast bacilli.
Lupus vulgaris: Etiologies (2).
Hematogenous spread to skin from reactivated pulmonary focus of TB.
Lymphatic spread to skin from cervical lymph nodes.
A. Anatomic site.
B. Clinical course.
A. Central face.
B. Peripheral extension with atrophy and occasional ulceration.
Lupus vulgaris: Histology (3).
Tuberculoid granulomas with little or no caseation.
In older lesions, fibrosis replaces granulomas.
Epidermis may be atrophic, ulcerated, or hyperplastic.
Lupus vulgaris: Demonstration of bacilli.
Special stains rarely help.
PCR is better.
Lupus vulgaris: Complication.
Development of SCC or BCC.
Deep mycoses: Typical histology.
Pseudoepitheliomatous hyperplasia with extensive dermal suppurative and granulomatous inflammation.