Skin Tumors PDF

BENIGN, PREMALIGNANT & MALIGNANT EPITHELIAL TUMORS OF SKIN DR MUHAMMAD ABRAR BARAKZAI MBBS, MPhil (Histopath), FCPS (Histopath),  LEARNING OBJECTIVES 1. Discuss the classification of tumors of the skin. 2. Describe the pathogenesis, diagnostic features and natural history of relevant...

BENIGN, PREMALIGNANT & MALIGNANT EPITHELIAL TUMORS OF SKIN DR MUHAMMAD ABRAR BARAKZAI MBBS, MPhil (Histopath), FCPS (Histopath),  LEARNING OBJECTIVES 1. Discuss the classification of tumors of the skin. 2. Describe the pathogenesis, diagnostic features and natural history of relevant tumors of the skin.  BENIGN EPITHELIAL LESIONS Benign epithelial neoplasms are common and probably arise from stem cells residing in the epidermis and hair follicles. Biologically insignificant, although they may cause significant psychological discomfort for the affected individual. These tumors grow to a limited size and generally do not undergo malignant transformation. Seborrheic Keratosis Fibroepithelial polyp Acanthosis Nigricans Actinic keratosis SEBORRHEIC KERATOSIS Occur most frequently in middle-aged or older individuals In people of color, multiple small lesions on the face are termed dermatosis papulosa nigra. Characteristically appear as round, flat, coin- like, waxy plaques that vary in diameter from millimeters to several centimeters, dark brown and have a velvety to granular Surface. Very common Doesn’t turn malignant. Fast growing , itchy , bleeds Trunk, extremities, head, and neck Well demarcated round –oval waxy appearance , velvety surface.  PATHOGENESIS. Activating mutations in the fibroblast growth factor receptor- 3 (FGFR3) gene which possesses a tyrosine kinase activity that stimulates Ras and the PI3K/AKT pathways. May occur explosively in large numbers, as part of a paraneoplastic syndrome (Leser-Trélat sign), produced by tumor cells, of the GI tract adenocarcinoma  MORPHOLOGY Histologically, these neoplasms are exophytic and sharply demarcated from the adjacent epidermis composed of sheets of small cells resemble basal cells of the normal epidermis. Basaloid cells. Variable melanin pigmentation is present within these basaloid cells (brown coloration) Exuberant keratin production (hyperkeratosis) occurs at surface, and small keratin-filled cysts (horn cysts) and invaginations of keratin into the main mass (invagination cysts). When seborrheic keratoses become irritated and inflamed, they develop whirling foci of squamous differentiation. Basaloid cells , Hyperkeratosis Horn cysts Invagination cysts DERMATOSIS PAPULOSE NIGRA :- Popular in dark skin. Old pt Sun exposure. DD :- Verruca Plana = warts Acquired melanocytic nevi Pigmented BCC  LESER –TRELAT SIGN:- Explosive onset. Multiple seborrheic keratosis. Paraneoplastic syndrome of Adenocarcinoma of GI. Produced by the release of epidermal growth factors by tumors. Cytokines. DERMATOFIBROMA :- Benign Tumor of fibrohistiocytes. Females more Firm button like nodule, 5-10mm in size, skin coloured, tan or brown. Asymptomatic Dimple sign PYOGENIC GRANULOMA : Vascular tumor. Origin = Capillaries. Cause= From minor trauma. On Hands Feet Hips. Round pedunculated or sessile smooth surface bright red. Bleed easily. Increased in Pregnancy and children. Drug induced. Treatment :- electrocautery + Curettage  EPIDERMOID CYST : Epidermal inclusion sebaceous cyst. Cyst containing keratin and break down products. Cysts are lined by stratified squamous epithelium. In the dermis. Face neck shoulder back. On pressing/rupture, creamy paste like malodorous material comes out. Treatment : surgical Excision.  ACANTHOSIS NIGRICANS It is marked by thickened, hyperpigmented skin with a “velvet-like” texture. Seen in flexural areas (axillae, skin folds of the neck, groin, and anogenital regions). Divided into two types, the benign type, which constitutes about 80% of all cases, develops gradually and usually occurs in childhood or during puberty. The most common association are with obesity and diabetes. The malignant type refers to lesions arising in middle-aged and older individuals in association with underlying cancers, (GI adenocarcinomas).  MORPHOLOGY The epidermis and underlying enlarged dermal papillae undulate sharply to form numerous repeating peaks and valleys Variable hyperplasia may be seen, along with hyperkeratosis and slight basal cell layer.  FIBROEPITHELIAL POLYP It has many names (squamous papilloma, skin tag). It is generally detected as an incidental finding in middle-aged and older individuals. On the neck, trunk, face, as a soft, flesh-colored, bag-like tumor often attached to the surrounding skin by a slender stalk. Micro :- Histologically these tumors consist of fibrovascular cores covered by benign squamous epithelium. Fibroepithelial polyps are usually insignificant, but can occasionally be associated with diabetes, obesity, and intestinal polyposis.  PREMALIGNANT EPIDERMAL TUMORS = ACTINIC KERATOSIS Epidermal malignancy is arsenicals may induce similar typically preceded by lesions. progressively worsening dysplastic changes, which are analogous to the precursor Premalignant condition. lesions that give rise to Seen in skin type 1 & 2 & 3. Squamous Cell Carcinoma. Prolonged and repeated sun In the skin, these precursor exposure. lesions are called actinic Males keratoses; these usually occur in sun-damaged skin and Caucasian people. exhibit hyperkeratosis. Light skin. They occur with particularly Exposure to : Arsenic, Industrial high incidence in lightly hydrocarbons, Radiations ( esp pigmented individuals. UVB) Exposure to ionizing radiation, industrial hydrocarbons and Out of 1000 cases only 1 case can develop to SCC. ACTINIC KERATOSIS = SOLAR KERATOSIS Actinic keratoses are usually less than 1 cm in diameter; are tan- brown, red, or skin-colored; and have a rough, sandpaper-like consistency. Some lesions may produce so much keratin that a “cutaneous horn” develops. Such horns may become so prominent that they actually resemble the horns of animals. Sun-exposed sites (face, arms, dorsum of hands) are most frequently affected. The lips may also develop similar lesions (termed actinic cheilitis). Size most common Sclerosing Pigmented -> common in KSA. RISK FACTORS :- HPV 16,18,33,35 (Anogenital warts) Sun exposure Skin type Immunosuppression Defects in DNA repair ( Xeroderma pigmentosum) Arsenic Genetic disorders ( Gorlin’s syndrome, autosomal dominant disorder by mutations in genes on chromosome 9) ( Multiple BCC seen in Xeroderma pigmentosum and Gorlin’s syndrome) Seborhheic keratosis Basaloid cells , Hyperkeratosis Horn cysts Invagination cysts Dermatofibroma Dimple sign on macro Epidermoid cyst Cyst containing keratin and break down products lined by stratified squamous epithelium Actinic Keratosis Peaks and Valley Hyperkeratosis Fibroepithelial Polyp fibrovascular cores covered by benign squamous epithelium. Actinic keratosis Hyperkeratosis Cytologic atypia Hyperplasia of basal cells or Atrophy Intercellular bridges are present, Elastosis Parakeratosis BCC Palisading arrangement of the peripheral cells. Mitosis Basaloid cells Polymorphic Retraction of the stroma Seborrheic keratosis + Adenocarcinoma of GI Leser –Trelat sign Acanthosis Nigricans Child = obesity and diabetes. Adult =cancers, (GI adenocarcinomas). Fibroepithelial polyp diabetes, obesity, and intestinal polyposis. BCC Gorlin's syndrome immunosuppression xeroderma pigmentosum. QUESTIONS…..