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SKIN TUMOURS

SKIN TUMOURS. PROF.K.S.RAVISHANKAR M.S,F.I.C.S SHREE BALAJI MEDICAL COLLEGE. ANATOMY OF SKIN. SKIN TUMOURS SITES. CLASSIFICATION OF SKIN TUMOURS. BENIGN EPIDERMAL SEBORRHIC KERATOSIS PAPILLOMA TRICHILEMMAL TUMOUR SEBACEOUS ADENOMA SEBACEOUS EPITHELIOMA

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SKIN TUMOURS

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  1. SKIN TUMOURS PROF.K.S.RAVISHANKAR M.S,F.I.C.S SHREE BALAJI MEDICAL COLLEGE

  2. ANATOMY OF SKIN

  3. SKIN TUMOURS SITES

  4. CLASSIFICATION OF SKIN TUMOURS • BENIGN EPIDERMAL • SEBORRHIC KERATOSIS • PAPILLOMA • TRICHILEMMAL TUMOUR • SEBACEOUS ADENOMA • SEBACEOUS EPITHELIOMA • HYDROCYSTOMA,SYRINGOMA,SPIRADENOMA DERMAL -NEUROFIBROMA • DERMATOFIBROMA

  5. CLASSIFICATION OF SKIN TUMOURS • MALIGNANT TUMOURS • SQUAMOUS CELL CARCINOMA • BASAL CELL CARCINOMA • MALIGNANT MELANOMA • MALIGNANT SKIN ADNEXAL TUMOUR • SECONDARIES IN SKIN (eg. sister joseph nodule)

  6. SKIN ADNEXAL TUMOURS • Tumours arising from accessory skin structures like sebaceous glands , sweat glands , hair follicles • CLASSIFICATION • ECCRINE GLAND TUMOURS • Syringoma , Hidradenoma,Syringo cystadenoma • HAIR TUMOURS • Trichoepithelioma,Tricholemmoma

  7. PRE MALIGNANT LESIONS • Actinic Keratosis- 5-20% will develop Squamous/basal cell ca • Actinic Cheilitis • Paget’s disease of nipple • Xeroderma pigmentosa • Chronic Radiation Keratosis • Bowen’s Disease • Bowenoid Papulosis • Leukoplakia / Erythroplakia • Dysplastic Melanocytic Nevi (DMN)

  8. BCC AND SCC Risk factors:- • ACTINIC LIGHT:- 90% OF TUMORS OCCURSINSUN EXPOSED AREAS. • ARSENIC:- EXPOSURE PREDISPOSE TO DEVELOPMENT OF BOWENS DISEASE,MULTIPLE SCC AND BCC. • IRRADIATION:-FOR BENIGN CONDITIONS • COAL TAR EXPOSURE • IMMUNOSUPPRESSION:-POST TRANSPLANT

  9. CHRONIC INFLAMMATION AND TRAUMA:- CHRONIC OSTEOMYELITIS, FISTULAS,THERMAL OR ELECTRICAL BURNS. • ATROPHIC SKIN LESIONS:-DISCOID LUPUS. • VACCINATION SCARS.

  10. HEREDITARY FACTORS • XERODERMA PIGMENTOSA:-AUTOSOMMAL RECESSIVE. • BASAL CELL NEVUS SYNDROME:AUTOSOMALDOMINANT. INFECTIVE FACTOR;- • HUMAN PAPPILOMA VIRUS TYPES 5 AND 8:- VERRUCUS • SCC OF GENITALS:-HPV 16&18 • PERIUNGUAL SCC.

  11. Actinic keratosis Xeroderma pigmentosa Bowen’s disease of penis Leukoplakia

  12. BASAL CELL CARCINOMA • Most common skin cancer arising from the basal layer of epidermis and its appendages • Low metastatic potiential • Locally invasive, aggressive, and destructive to skin and bone.

  13. ETIOLOGY OF BCC • Sun exposure is the most important environmental cause of BCC. • Ionizing radiation causes mutation of tumor suppressor genes • UV B light: 280-320nm, UV A light 320-400nm • Amount of UV B exposure during childhood and adolescence is directly proportional to risk for BCC

  14. Clinical presentation Distribution of BCC: • 70% on face • 25% on trunk • 5% on penis, vulva, or perianal skin Clinical subtypes (4) • Nodular- most common • Superficial- small buds of tumour masses • Pigmented- resembles naevus or melanoma • Morpheaform- aggressive behavior, worst prognosis

  15. PIGMENTED NODULAR SUPERFICIAL MORPHEA FORM

  16. DIAGNOSIS Initial evaluation involves • Assessment of location • Punch or excisional biopsy • Staging

  17. SQUAMOUS CELL CA

  18. SQUAMOUS CELL CA TYPES • Bowen’s disease • SCCA in situ • Full thickness dysplasia • Bowenoid SCCA • Looks like bowen’s • Invades through BM • Adenoid SCCA • Nodular ulcerative lesion • Often periauricular • Generic SCCA • Most common • Highest rate of metastasis • Verrucous SCCA • Verruciform lesions • Invades by blunt, pseudopod-like growth • Spindle SCCA • Indistinct clinically

  19. CLINICAL FEATURES • An ulcerative or ulceroproliferative lesion • Raised and everted edge • Indurated, bloody discharge from lesion + • Regional lymph nodes commonly involved • Variants- marjolin’s ulcer and verrucous carcinoma

  20. Histology of SCC • Malignant whorls of squamous cells with epithelial or keratin pearls are characteristic. • Broder’s classification: • I-Well differentiated:75% keratin pearls • II-Moderately differentiated: 50% keratin pearls. • III- Poorly differentiated: 25% keratin pearls • IV- < 25% keratin pearls

  21. DIAGNOSIS • Although the diagnosis of SCC is often strongly suspected based on clinical findings, a skin biopsy is required for definitive diagnosis. • A shave biopsy, punch biopsy, incisional biopsy, or excisional biopsy, wedge biopsy may be used. • All skin biopsy samples obtained to diagnose SCC must reach at least the depth of the mid dermis to allow for determination of the presence or absence of invasive disease.

  22. STAGING • TX - Primary tumor cannot be assessed • T0 - No evidence of primary tumor • Tis - Carcinoma in situ • T1 - Tumor less than 2 cm in greatest diameter • T2 - Tumor 2-5 cm in greatest diameter • T3 - Tumor greater than 5 cm in greatest diameter • T4 - Tumor with deep invasion into cartilage, muscle, or bone.

  23. Regional lymph nodes[N] • NX Regional lymph nodes cannot be assessed • NO No regional lymph node metastasis • N1 Regional lymph node metastasis, DISTANT METASTASIS[M] • MX Presence of distant mets cannot be assessed • M0 No distant metastasis • M1 Distant metastasis

  24. MANAGEMENT • ACTINIC KERATOSIS:-LIQUID NITROGEN , ELECTRICAL CURETTAGE. • BCC:-TRADITIONAL SURGICAL RESECTIONS, MOH’ S MICROGRAPHIC SURG INDICATIONS FOR MOH’S SURG:- • LOCATED IN REGIONS WHERE HIGH RISK FOR TUMOR RECURRENCE AREAS, • DIAMETER >1CM ON FACE, • PERINEURAL INVASION, • MORHEFORM,SCLEROTIC AND INFILTRATIVE TYPE BCC.

  25. ELECTRO CURETTAGE, CRYOSURGERY, RADIOTHERAPHY, EXTENSIVE RESCTION AND RECONSTRUCTION: -AMPUTATION IN CERTAIN CASES • CHEMOTHERAPHY:- NO ADJUVANT ROLE,MAY BE OFUSE NMETASTATIC SKIN LESIONS

  26. MOH’S SURGERY SUPERFICIAL BRACHYTERAPY

  27. FOLLOW UP • Low-risk tumors are usually cured with appropriate surgical therapy; recurrence may occur. • Thus, patients with a history of SCC should be evaluated with a complete skin examination every 6-12 months. • Patients with high-risk tumors require skin and lymph node examinations at 3- to 6-month intervals for at least 2 years after diagnosis.

  28. Marjolin’s ulcer • Well differentiated squamous cell ca that occurs in chronic scars like burn scar, scar of venous ulcer • No lymphatics in scar tissue hence no spread to regional lymph nodes. • Scar contains no nerves, hence painless. • Wide excision or amputation for larger lesions • Radiotherapy contraindicated for fear of transformation into poorly differentiated sq cell ca.

  29. Verrucous cancer • Dry, exophytic,warty growth • No lymph node spread • No blood spread • Surgery is the treatment of choice- wide excision • Examples: • Giant Condyloma Acuminatum (Buschke-Lowenstein tumour)- in genitalia • Carcinoma cuniculatum-( Verrucous ca of feet) • Oral florid verrucous ca

  30. Melanoma - Outline • General statistics and development • Risk factors and patient assessement • Pathology and prognosis • Work-up and staging • Surgical treatment • Lymph node controversy/sentinel node • Adjuvant therapy

  31. Melanoma - Statistics • Mortality increase 2nd only to lung • 5th most prevalent, incidence 7%/year increase • 5% skin cancer, 75% skin cancer death • Men common sites- front and back of trunk • Women common sites- lower leg • Mostly arise from benign naevus or adjacent area

  32. Development of Nevi • Junctional nevi • nests along dermal-epidermal junction • Compound nevi • “invade” dermis, first as nests then cords and single cells • Dermal nevi • junctional component lost only in papillary and reticular dermis Histologically, nevi are classified generally as having atypical cells, as in dysplastic nevi, or normal cytology, as in the common nevus.

  33. Junctional Nevi

  34. Compound Nevi

  35. Dermal Nevi

  36. Dysplastic Nevi

  37. Types of Melanoma • Acral lentiginous • Amelanotic melanoma • Superfical spreading melanoma • Lentigo maligna melanoma • Nodular melanoma

  38. Superficial spreading • Most common, 70% of all melanomas • 4th to 5th decade • Clinically variable pigmentation,irregular borders, biphasic growth • Histologically-asymmetry, poor circumscription and lack of maturation

  39. Superficial spreading

  40. Lentigo maligna • 20% of cutaneous melanomas • Most benign form of melanoma • Longest radial growth phase >15 yrs • Occurs in Hutchinson’s freckle • Elderly sun exposed areas • Clinical dark, irregular ink spot

  41. Lentigo maligna

  42. Nodular melanoma • 12% of all melanomas • Most malignant type • Aggressive vertical growth phase • Sun-exposed and nonexposed areas • Usual presentation- darkly pigmented raised nodule

  43. Nodular melanoma

  44. Acral lentiginous melanoma • Occurs in palms,soles and subungual areas • Worse prognosis than superficial spreading • Pigment spread to the proximal or lateral nail folds is termed the Hutchinson sign, which is a hallmark for acral lentiginous melanoma.

  45. AMELANOTIC MELANOMA • Appear pink but close inspection reveals pigmentation • Lack of pigmentation causes delay in diagnosis. • Worst prognosis of all melanomas

  46. Melanoma 70% of melanomas occur on a pre existing nevus. 30% of melanomas occur de-novo

  47. When to suspect malignant transformation in a mole? • Asymmetrical outline--- A • Border irregularity-------B • Colour change------------C • Diameter>6mm-----------D • Elevation------------------E

  48. Diagnosis • Excision biopsy of suspected lesions mainstay of diagnosis • Performed with 1-2mm margin and has to be full thickness to ascertain the following: • Tumor thickness (Breslow depth) • Presence of ulceration • Anatomic level of invasion (Clark level) • Presence of mitoses • Presence of regression • Lymphatic/vessel invasion or vascular involvement • Host response (tumor-infiltrating lymphocytes)

  49. LYMPHATIC SPREAD:-SINGLE REGIONAL LYMPHNODES[N1], • MULTIPLE NODES{2-3 NODES}[N2A] • SATELLITE NODULE AND INTRANSIT NODULES WITHOUT NODES • MORE THAN FOUR NODES WITH INTRANSIT[N3].

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