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SKIN
HISTOLOGY AND FUNCTION
THREE LAYERS : EPIDERMISBASEMENT MEMBRANE DERMIS
EPIDERMIS : COMPOSED OF KERATINOCYTESNO MATRIXDEEP BASAL LAYER MITOTICALLY ACTIVESPINOUS LAYER – MATURE –HYALINHORNY LAYER – AGED CELLS –SHEDTRANSIT TIME: 40 TO 56 DAYSKERAINS 5 & 14
MELANOCYTES ORIGIN FROM NEURA CREST1:35MELANIN – TYROSINE & CYSTEINEMELANOSOME – TO KERATINOCYTESDENSITY OF MELANOCYTES CONSTANTMELANIN 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 FACTORSFAIR COMPLEXIONRADIOATION EXPOSURESUN BURNSIMMUNO SURESSION
PATHOLOGYARISE FROM BASAL LAYER OF EPIDERMISPILOSEBACEOUS ADENEXA
TYPES:a) NODULARb) SUPERFICIALc) MICRONODULARd) INFILTRATING e) SCLEROSINGINFILTRATING AND SCLEROSING TYPES MOST AGGRESSIVE 10 %
CLINICAL FEATURES
PEARLY, TRANSLUCENT MASSRAISED BORDERSULCERATEERYTHMATOUS PATCHES, SCALYSCARING, (DD.PSORIASIS, EZEMA)ISLANDS OF TUMOUR EXTENDING SURROUNDING
DIAGNOSISBIOPSY – SHAVE , PUNCH, INCISION, EXCISION
TREATMENTELECTRO DESICCATION CURETTAGENODULAR TYPE LESS THAN 2 cmSUPERFICIAL ANY SIZE90 – 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 BCCARISE FROM KERATINOCYTES EPIDERMISARISE FROM ACTINIC KERATOSIS, LEUKOPLAKIA, RADIATION DERMATITIS, SCARS, CHRONIC ULCER, BOWEN DISEASE – INSITUSKIN PATCHES, NODULE – CENTRAL INFLAMATIONINDURATION, NECROSIS – OOZINGMETASTASES – DIRECT INFILTARTION, LYMPHATICHAEMATOGENOUS
AUSTRALIA: HIGH UV EXPOSURERACE : WHITE COMPLEXIONSEX : MALE / FEMALE 2:1AGE : ABOVE 60 years
RISK FACTORS: IONIZING RADIATION, ARSENIC etc
DIFFERENTIAL DIAGNOSISACTINIC KERATOSISBCCMELANOMAKERATOACANTHOMAPYODERMA GANGRENOSUMWARTS
INVESTIGATIONSCT, MRI, DEPTH OF INVASIONBIOPSY : PUNCH, SHAVE, INCISIONAL, EXCISIONAL
HISTOLOGYNEST OF EPIDERMAL CELLS – MIXTURE OF NORMAL AND ANAPLASTIC CELLSWELL DIFFERENTIATED – EPITHELIAL PEARL‐ CONCENTRIC LAYERS OFSQUAMOUS CELLS WITH CENTRAL KERANTINIZATIONPOORLY DIFFERENTIATED LACKS HORN PEARLSSPECIAL STAINS : S100 NEGATIVE FOR SCC
POSITIVE FOR MELANOMA
STAGING – TNMPRIMARY TUMOURTx – PRIMARY TUMOUR CANNOT BE ASSESSEDTo – NO EVDIENCE OF PRIMARY TUMOURT1 ‐ TUMOUR 2 cmT2 – TUMOUR 2‐4 cmT3 – TUMOUR LARGER THAN 4 cmT4 – TUMOUR INVADES DEEPER STRUCTURES
REGIONAL NODESNX – NODES CANNOT BE ASSESSEDN0 – NO NODESN1 – SINGLE IPSILATERAL NODE – 3 cm N2 – a) SINGLE
b) MULTIPLEc) BILATERAL
METASTASISMX ‐ DISTANT METASTASIS CANNOT BE ASSESSED M0 – NO DISTANT METASTASISM1 – 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 TREATMENTCURETTAGE AND ELECTROSURGERYREPEATED SEVERAL TIMESNO SPECIMEN AVAILABLE FOR HPE96 % CURE
CRYOSURGERYLIQUID NITROGENCURE 97 %
EXCISIONLOCAL EXCISION – HPE – 92 % CURE4 mm MARGIN – RECURRENCE 5 ‐8 %WELL DIFFERENTIATED LESIONS
MOH’S MICROGRAPHIC SURGERY
LESIONS ARE REMOVED IN STAGESHORIZONTAL FROZEN SECTIONING – PERIPHERAL AND DEEP MARGINS
CURE RATE SCC 96 % IN 5 YEARSFOR RECURRENT SCC 90 % CURE RATETISSUE SPARING – DISFIGUREMENT IN DISTINCT MARGIN, GENITALPENILE SHAFTLOCAL ANAESTHESIA, SAY CASE OF SURGERY COST EFFECTIVEMOH’S SURGERY NOT USEFUL IN INVASIVE LESIONSSENTINEL NODE BIOPSY
LASER SURGERYRADIATION THERAPYOLDER PATIENT, NO HPE
PREVENTIONSPF – SUN PROTECTING FACTORCLOTHING SUNSCREEN’S – SPR 30↑ZINC OXIDE, TITANIUM OXIDEAPPLIED EVERY 30 MINTS DURING EXPOSURE
MALIGNANT MELANOMAMALIGNANT TRANFORMATION OF MELANOCYTES MELANOCYTES DERIVED FROM NEURAL CRESTSKIN, GIT, BRAIN – ADULTSWHITE POPULATION HIGHESTASIAN’S LOWEST
ETIOLOGY
FAMILY HISTORYPOSITIVE IN 5 – 10 %
PERSONAL
BLUE EYES, FAIRSUN BURNFRECKLINGNEVI ‐ DYSPLASTICIMMUNOSUPPRESSIVE STATE
SUN EXPOSURE
HIGH U‐V RADIATIONLOW LATITUDEBLISTERING SUN BURNSDYSPLASTIC NEVI OVER A TIME MELANOMA
CLINICAL PRESENTATION
ABCDEA ‐ ASYMMETRYB ‐ BORDER IRREGULARC ‐ COLOUR VARIATIOND ‐ DIAMETER > 6 cmE ‐ ELEVATED SURFACE
ITCHING, BLEED, ULCERATION, SATELITE LESIONS
BIOPSY: EXCISION / INCISION, 2 mm MARGINFULL THICKNESS SKIN
SAPPEY : LYMPHATIC DRAINAGE DEPEND ONANATOMICAL LOCATIONLYMPHATIC OVER LAP
HISTOLOGICAL CLASSIFICATION
GROWTH PATTERN
SUPERFICIAL SPREADING
70 % OF MELANOMACELLS AT DERMS – EPIDERAL JUNCTIONMIGRATE TO S.GRANULOSUM & CORNEUMPAPPILARY DERMISFROM DYSPLATIC NEVUSFLAT, ELEVATED LATTER2 cm DIAMETER, VARIGATED COLOURS
NODULAR MELANOMAEXTENSIVE VERTICAL GROWTH INTO DERMIS THAN RADIAL
15‐30 %BLUE BLACKOCCUR WITHOUT PRE EXISTING LESION
LENTIGO MALGNA MELANOMA
4 – 10 % MELANOMASPINDLE SHAPE HYPERCHROMATIC CELLSEPIDERMIS ATROPHICSIZE 3 cms, FLAT, FRECKLE, FACE, NECKARISE IN HUTCHINSON’S FRECKLE (LENTIGO MALIGNA)
ACRAL LENTIGINOUS MELANOMA
2‐8% IN WHITE30 – 60% IN DARK SKINNED PEOPLEDERMO EPIODERMAL JUNCTION – INVASION PAPILLAR DERMISPALMS, SOLES , FLAT IRREGULAR BORDERS ULCERATIONS
DESMOPLASTIC MELANOMA
1% RAREPERI NEURAL INVASIONHIGHER LOCAL RECURRENCELOWER REGIONAL METASTASIS
CLASSIFICATION AND STAGING
BRESLOW’STHICKNESS 0.75 mm or LESSTHICKNESS 0.75 – 1.5 mmTHICKNESS 1.5 – 4 mmTHICKNESS > 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 MELANOMATOXICRELAPSE REDUCED
GM‐CSF (GRANULOCYTE STIMULATING FACTOR)
STIMULATES IMMUNE SYSTEMNOT TOXIC AND OVER ALL SURVIVAL ↑STAGE III & IVPALLIATION ONLY
CYTOKINE AND VACCINE THERAPY
TUMOUR SPECIFIC TARGETS – ONCOGENE
CDK4, TRP‐2, MART‐1AUTOLOGOUS (ALLOGENIC)
CHEMOTHERAPY
TEMOZOLOMIDEDACARBAZINE
SURGICAL TREATMENT
STAGE – O :0.5 % TO 1.5 % cm MARGIN EXCISION IN‐SITU/OBSERVATION
STAGE – I : T₁ LESION1 TO 2 cms MARGINSENTINEL NODE BIOPSYCLOSURE – PRIMARY, SKIN GRAFTING
STAGE II
2 cms MARGIN – NO ADVANTAGE IN 4 – 6 cms MARGINSLYMPH ADENCTOMYSENTINEL NODE BIOPSY IN NO NODES CLINICALLYHYPERTHERMIC ARTERIAL LIMB PERFUSION – MELPHALANADJUVANT THERPAY
STAGE III
2 cm MARGINREGIONAL LYMPHADENOCTOMY
STAGE IVREFRACTORYCONSIDER FOR CLINICAL TRIALSDTC , BCNURADIATION
THANK YOU