SKIN HISTOLOGY AND FUNCTION

SKIN HISTOLOGY AND FUNCTION

THREE LAYERS : EPIDERMIS BASEMENT MEMBRANE DERMIS EPIDERMIS : COMPOSED OF KERATINOCYTES NO MATRIX DEEP BASAL LAYER MITOTICALLY ACTIVE SPINOUS LAYER MATURE HYALIN HORNY LAYER AGED CELLS SHED TRANSIT TIME: 40 TO 56 DAYS KERAINS 5 & 14 MELANOCYTES ORIGIN FROM NEURA CREST 1:35 MELANIN TYROSINE & CYSTEINE MELANOSOME TO KERATINOCYTES DENSITY OF MELANOCYTES CONSTANT MELANIN PRODUCTION INFLUENCED BY MSH, ACTH, UV RAYS etc

BASEMENT MEMBRANE ZONE ANCHOR EPIDERMIS TO DERMIS BY PROTEIN STRUCTURES DERMIS : 70% OF WEIGHT COLLAGEN TYPE I TENSILE STRENGTH ELASTIC FIBRES GROUND SUBSTANCE POLYSACCHARIDE, POLYPEPTIDES FIBROBLASTS THROUGHOUT DERMIS PROTEIN MATRIX NET WORK OF BLOOD VESSELS PAPILLARY DERMIS GLOMUS BODIES: TORTUOUS A V SHUNTS REGULATES BODY TEMPERATURE SENSORY NERVE ENDINGS RECEPTORS, PACINIAN, MEISSNER, RUFFINI FREE NERVE ENDINGS MERKEL S CELLS, HAIR FOLLICLE ADENEXCAL : SWEAT GLANDS PALMS, SOLE, AXILLA APPOCRINE GLANDS AXILLA, PERINEUM SCENT

MALIGNANT TUMOURS EPIDEMIOLOGY EXPOSURE TO UV RADIATION CHEMICAL CARCINOGEN TAR, ARSENIC, NITROGEN MUSTARD HPV SQUAMOUS CELL CA RADIATION DERMATITIS CHRONIC IRRITATION MARJOLIN S ULCER etc IMMUNO SUPPRESSION HIV BASAL CELL CARCINOMA SLOW GROWING RARELY METASTASIS LOCALLY DESTRUCTIVE SITES FACE, SCALP, NOSE, CHEEK

PRE DISPOSING FACTORS FAIR COMPLEXION RADIOATION EXPOSURE SUN BURNS IMMUNO SURESSION PATHOLOGY ARISE FROM BASAL LAYER OF EPIDERMIS PILOSEBACEOUS ADENEXA TYPES: a) NODULAR b) SUPERFICIAL c) MICRONODULAR d) INFILTRATING e) SCLEROSING INFILTRATING AND SCLEROSING TYPES MOST AGGRESSIVE 10 %

CLINICAL FEATURES PEARLY, TRANSLUCENT MASS RAISED BORDERS ULCERATE ERYTHMATOUS PATCHES, SCALY SCARING, (DD.PSORIASIS, EZEMA) ISLANDS OF TUMOUR EXTENDING SURROUNDING DIAGNOSIS BIOPSY SHAVE, PUNCH, INCISION, EXCISION TREATMENT ELECTRO DESICCATION CURETTAGE NODULAR TYPE LESS THAN 2 cm SUPERFICIAL ANY SIZE 90 98 % CURE RATE

CRYOTHERAPY: LESION 2 cm Scarring, HYPOPIGMENTATION NO HISTELOGICAL CONFIRMATION USED ONLY LESS AGGRESSIVE LESIONS NOT USED IN PERI ORAL, ORBITAL AREAS SURGICAL EXCISION CURE RATE 90 % MARGIN 2 5 mm DEPEND ON SIZE MOH S MICROGRAPHIC SURGERY PERI ORAL AREA 99 % PRIMARY 96 % RECURRENT NASAL ALA LESIONS

SQUAMOUS CELL CARCINOMA MORE COMMON THAN BCC ARISE FROM KERATINOCYTES EPIDERMIS ARISE FROM ACTINIC KERATOSIS, LEUKOPLAKIA, RADIATION DERMATITIS, SCARS, CHRONIC ULCER, BOWEN DISEASE INSITU SKIN PATCHES, NODULE CENTRAL INFLAMATION INDURATION, NECROSIS OOZING METASTASES DIRECT INFILTARTION, LYMPHATIC HAEMATOGENOUS AUSTRALIA: HIGH UV EXPOSURE RACE : WHITE COMPLEXION SEX : MALE / FEMALE 2:1 AGE : ABOVE 60 years RISK FACTORS: IONIZING RADIATION, ARSENIC etc

DIFFERENTIAL DIAGNOSIS ACTINIC KERATOSIS BCC MELANOMA KERATOACANTHOMA PYODERMA GANGRENOSUM WARTS INVESTIGATIONS CT, MRI, DEPTH OF INVASION BIOPSY : PUNCH, SHAVE, INCISIONAL, EXCISIONAL HISTOLOGY NEST OF EPIDERMAL CELLS MIXTURE OF NORMAL AND ANAPLASTIC CELLS WELL DIFFERENTIATED EPITHELIAL PEARL CONCENTRIC LAYERS OF SQUAMOUS CELLS WITH CENTRAL KERANTINIZATION POORLY DIFFERENTIATED LACKS HORN PEARLS SPECIAL STAINS : S100 NEGATIVE FOR SCC POSITIVE FOR MELANOMA

STAGING TNM PRIMARY TUMOUR Tx PRIMARY TUMOUR CANNOT BE ASSESSED To NO EVDIENCE OF PRIMARY TUMOUR T 1 TUMOUR 2 cm T 2 TUMOUR 2 4 cm T3 TUMOUR LARGER THAN 4 cm T4 TUMOUR INVADES DEEPER STRUCTURES REGIONAL NODES N X NODES CANNOT BE ASSESSED N0 NO NODES N1 SINGLE IPSILATERAL NODE 3 cm N2 a) SINGLE b) MULTIPLE c) BILATERAL METASTASIS M X DISTANT METASTASIS CANNOT BE ASSESSED M0 NO DISTANT METASTASIS M1 DISTANT METASTASIS PRESENT

TREATMENT : DRUG THERAPY ACTINIC KERATOSIS 5 FLUORORACIL TOPICAL DICLOFENAC GEL BIOPSY CONFIRMATION SCC/BCC IMIQUIMOD 5 % CREAM SUPERFICIAL IMMUNE MODIFIER THROUGH LESIONS ONLY INTERFERON, CYTOKINES PHOTODYNAMIC THERPAY (PDT) PHOTOSENSITIZING DRUGS LIGHT ACTIVATES OXYGEN, FREE RADICALS DESTROY, TARGETED TISSUE. ALA AMINOLEVULINIC ACID SKIN TUMOURS ACTIVE PROTOPORPHYRIN IX ACTINIC KERATOSIS, FACIAL LESION 90 %

SURGICAL TREATMENT CURETTAGE AND ELECTROSURGERY REPEATED SEVERAL TIMES NO SPECIMEN AVAILABLE FOR HPE 96 % CURE CRYOSURGERY LIQUID NITROGEN CURE 97 % EXCISION LOCAL EXCISION HPE 92 % CURE 4 mm MARGIN RECURRENCE 5 8 % WELL DIFFERENTIATED LESIONS MOH S MICROGRAPHIC SURGERY LESIONS ARE REMOVED IN STAGES HORIZONTAL FROZEN SECTIONING PERIPHERAL AND DEEP MARGINS

CURE RATE SCC 96 % IN 5 YEARS FOR RECURRENT SCC 90 % CURE RATE TISSUE SPARING DISFIGUREMENT IN DISTINCT MARGIN, GENITAL PENILE SHAFT LOCAL ANAESTHESIA, SAY CASE OF SURGERY COST EFFECTIVE MOH S SURGERY NOT USEFUL IN INVASIVE LESIONS SENTINEL NODE BIOPSY LASER SURGERY RADIATION THERAPY OLDER PATIENT, NO HPE PREVENTION SPF SUN PROTECTING FACTOR CLOTHING SUNSCREEN S SPR 30 ZINC OXIDE, TITANIUM OXIDE APPLIED EVERY 30 MINTS DURING EXPOSURE

MALIGNANT MELANOMA MALIGNANT TRANFORMATION OF MELANOCYTES MELANOCYTES DERIVED FROM NEURAL CREST SKIN, GIT, BRAIN ADULTS WHITE POPULATION HIGHEST ASIAN S LOWEST ETIOLOGY FAMILY HISTORY POSITIVE IN 5 10 % PERSONAL BLUE EYES, FAIR SUN BURN FRECKLING NEVI DYSPLASTIC IMMUNOSUPPRESSIVE STATE

SUN EXPOSURE HIGH U V RADIATION LOW LATITUDE BLISTERING SUN BURNS DYSPLASTIC NEVI OVER A TIME MELANOMA CLINICAL PRESENTATION ABCDE A ASYMMETRY B BORDER IRREGULAR C COLOUR VARIATION D DIAMETER > 6 cm E ELEVATED SURFACE ITCHING, BLEED, ULCERATION, SATELITE LESIONS BIOPSY: EXCISION / INCISION, 2 mm MARGIN FULL THICKNESS SKIN

SAPPEY : LYMPHATIC DRAINAGE DEPEND ON ANATOMICAL LOCATION LYMPHATIC OVER LAP HISTOLOGICAL CLASSIFICATION GROWTH PATTERN SUPERFICIAL SPREADING 70 % OF MELANOMA CELLS AT DERMS EPIDERAL JUNCTION MIGRATE TO S.GRANULOSUM & CORNEUM PAPPILARY DERMIS FROM DYSPLATIC NEVUS FLAT, ELEVATED LATTER 2 cm DIAMETER, VARIGATED COLOURS NODULAR MELANOMA EXTENSIVE VERTICAL GROWTH INTO DERMIS THAN RADIAL

15 30 % BLUE BLACK OCCUR WITHOUT PRE EXISTING LESION LENTIGO MALGNA MELANOMA 4 10 % MELANOMA SPINDLE SHAPE HYPERCHROMATIC CELLS EPIDERMIS ATROPHIC SIZE 3 cms, FLAT, FRECKLE, FACE, NECK ARISE IN HUTCHINSON S FRECKLE (LENTIGO MALIGNA) ACRAL LENTIGINOUS MELANOMA 2 8% IN WHITE 30 60% IN DARK SKINNED PEOPLE DERMO EPIODERMAL JUNCTION INVASION PAPILLAR DERMIS PALMS, SOLES, FLAT IRREGULAR BORDERS ULCERATIONS

DESMOPLASTIC MELANOMA 1% RARE PERI NEURAL INVASION HIGHER LOCAL RECURRENCE LOWER REGIONAL METASTASIS CLASSIFICATION AND STAGING BRESLOW S THICKNESS 0.75 mm or LESS THICKNESS 0.75 1.5 mm THICKNESS 1.5 4 mm THICKNESS > 4 mm

CLARK LEVEL I INVOLVES EPIDERMIS ONLY IN SITU LEVEL II INVADES PAPILLARY DERMIS ONLY LEVEL II INVADES PAPILLART & INTERFACE LEVEL IV INVADER RETICULAR DERMIS NOT SUB CUTANEOUS TISSUE LEVEL V INVADES INTO SUB CUTAEOUS TISSUE TNM STAGING T X PRIMARY TUMOUR CANNOT BE ASSESSED

T0 NO EVIDENCE TUMOUR T15 IN SITU INVOLVES ONLY EPIDERMIS T1 1 mm LESS THICKNESS T2 1 1.2 mm LESS THICKNESS T3 2 4 mm LESS THICKNESS T4 > 4 mm, INVADES SUB CUTANEOUS TISSUE SATELLITE TUMOURS WITHIN 2 cm a) TUMOUR > 4 mm b) WITHOUT ULCERATION c) ULERATION REGIONAL NODES NX CANNOT BE ASSESSED N0 NO REGIONAL NODE METS

N1 ONE NODE N2 2 3 NODES N3 4 OR MORE DISTANT METASTASIS MX DISTANT METASTASIS CANNOT BE ASSESSED M0 NO DISTANT METS M1 DISTANT METASTASIS a) SUB CUTANEOUS TISSUE, NODES b) METASTASIS TO LUNG c) METASTASIS TO OTHER ORGANS

MEDICAL MANAGEMENT INTERFERON (α 2BIFN) STAGE III MELANOMA TOXIC RELAPSE REDUCED GM CSF (GRANULOCYTE STIMULATING FACTOR) STIMULATES IMMUNE SYSTEM NOT TOXIC AND OVER ALL SURVIVAL STAGE III & IV PALLIATION ONLY CYTOKINE AND VACCINE THERAPY TUMOUR SPECIFIC TARGETS ONCOGENE

CDK4, TRP 2, MART 1 AUTOLOGOUS (ALLOGENIC) CHEMOTHERAPY TEMOZOLOMIDE DACARBAZINE SURGICAL TREATMENT STAGE O : 0.5 % TO 1.5 % cm MARGIN EXCISION IN SITU/OBSERVATION STAGE I : T₁ LESION 1 TO 2 cms MARGIN SENTINEL NODE BIOPSY CLOSURE PRIMARY, SKIN GRAFTING

STAGE II 2 cms MARGIN NO ADVANTAGE IN 4 6 cms MARGINS LYMPH ADENCTOMY SENTINEL NODE BIOPSY IN NO NODES CLINICALLY HYPERTHERMIC ARTERIAL LIMB PERFUSION MELPHALAN ADJUVANT THERPAY STAGE III 2 cm MARGIN REGIONAL LYMPHADENOCTOMY STAGE IV REFRACTORY CONSIDER FOR CLINICAL TRIALS DTC, BCNU RADIATION

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