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

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Presentation on theme: "PROF.K.S.RAVISHANKAR M.S,F.I.C.S SHREE BALAJI MEDICAL COLLEGE"— Presentation transcript:

1 PROF.K.S.RAVISHANKAR M.S,F.I.C.S SHREE BALAJI MEDICAL COLLEGE
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 OCCURS IN SUN 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 INFECTIVE FACTOR;-
XERODERMA PIGMENTOSA:-AUTOSOMMAL RECESSIVE. BASAL CELL NEVUS SYNDROME:AUTOSOMAL DOMINANT. INFECTIVE FACTOR;- HUMAN PAPPILOMA VIRUS TYPES 5 AND 8:- VERRUCUS SCC OF GENITALS:-HPV 16&18 PERIUNGUAL SCC.

11 Xeroderma pigmentosa Actinic keratosis 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: nm, UV A light nm 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 Bowenoid SCCA Adenoid SCCA
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 N Regional lymph node metastasis, DISTANT METASTASIS[M] MX Presence of distant mets cannot be assessed M No distant metastasis M 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 EXTENSIVE RESCTION AND RECONSTRUCTION: -AMPUTATION IN CERTAIN CASES
ELECTRO CURETTAGE, CRYOSURGERY, RADIOTHERAPHY, EXTENSIVE RESCTION AND RECONSTRUCTION: -AMPUTATION IN CERTAIN CASES CHEMOTHERAPHY:- NO ADJUVANT ROLE,MAY BE OF USE N METASTATIC SKIN LESIONS

26

27 MOH’S SURGERY SUPERFICIAL BRACHYTERAPY

28 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.

29 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.

30 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

31 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

32 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

33 Development of Nevi Junctional nevi Compound nevi Dermal 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.

34 Junctional Nevi

35 Compound Nevi

36 Dermal Nevi

37 Dysplastic Nevi

38 Types of Melanoma Acral lentiginous Amelanotic melanoma
Superfical spreading melanoma Lentigo maligna melanoma Nodular melanoma

39 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

40 Superficial spreading

41 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

42 Lentigo maligna

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

44 Nodular melanoma

45 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.

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

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

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

49 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)

50 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].

51 DISTANT METASTASES:- METS TO SKIN SUBCUTANEOUS TISSUE[DISTANT NODES]{M1A} {M1B} METS TO LUNG {M1C} ANY VISCERAL METS WITH RAISED LDH

52 SENTINEL LYMPH NODE BIOPSY
Sentinel lymph node biopsy (SLNB) is indicated for pathologic staging of the regional nodal basin for primary tumors greater than or equal to 1 mm depth and when certain high-risk histologic features (eg, ulceration, extensive regression) are present in thinner melanomas < 1mm)

53 STAGING-CLARKE’S AND BRESLOW

54 Staging-Clark Level I - in situ at basement membrane
Level II - through basement membrane into papillary dermis Level III - spread to papillary/reticular interface Level IV - spread to reticular dermis Level V - sub-cutaneous invasion

55 Staging-Breslow <0.76 mm - thin 0.76 - 1.49 - intermediate
>4.00 mm - thick Latest Breslow classification <1mm- Thin melanomas 1-4mm- Intermediate thickness melanomas >4mm- Thick melanomas

56 AJCC Staging

57 Work-up Labs and imaging CXR , CT chest and LFT H&N CT neck routine
If stage III(regional) or IV (distant) - CT head, chest, abdomen, pelvis Hpe: S-100 and homatropine methylbromide (HMB45) stains are positive in melanoma.

58 Surgical Treatment Treatment of Primary (WLE)
Current recommendations for margins of excision are as follows: Lesions <1 mm in thickness - 1 cm margin Lesions 1-2 mm in thickness - 2 cm margin Lesions >2mm in thickness – 3 cm margin All depths to underlying muscle fascia

59 Management of lymph nodes
SLN biopsy Node dissection Isolated limb perfusion

60 Adjuant chemotherapy Metastatic disease Cytotoxic drugs Interferon BCG
Bleomycin, Oncovin, Lomustin Dacarbazin Tamoxifen interleukin

61 Prognosis anatomic site, ulceration, gender, histologic type, nodal disease head and neck, trunk and acral regions worse prognosis women better prognosis than men Ulceration, angiogenesis and vascular invasion-poor prognosis

62 Prognosis Breslow (thickness in millimeters) strongest predictor
Depth of tumor invasion 5 yr survival (%) <0.5 mm 99 > 3 mm 30

63 Prognosis Clark level less predictive, thin melanomas useful(<1mm)
Tumor extent 5 yr Survival (%) I Tumor is confined to epidermis (in situ) 100 II Tumor extends beyond basal lamina into papillary dermis 85 III Tumor extends into papillary dermis and abuts onto, but does not invade, the reticular dermis 65 IV Tumor extends into reticular dermis 50 V Tumor extends into subcutaneous fat 15

64 Prognosis Survival according to regional lymph node involvement
5 yr survival (%) Negative nodes 75 (85% for negative SLN) 1 – 3 positive nodes 50 4 or more positive nodes 25

65 Prognosis Survival according to metastatic spread Stage Extent
5 yr survival (%) II Local recurrences within 3 cm of primary site 30 III Satellitosis <20 IV Distant metastases <10

66

67 NECROLYTIC MIGRATORY ERYHTEMA
ACANTHOSIS NIGRICANS

68 Thank You


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