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CUTANEOUS
MALIGNANCIES
⦁ DERMIS
⦁ 15 – 20 times thicker than epidermis
⦁ Collagen, elastic fiber, ground substance
⦁ Nerve, vessels, lymphatics
⦁ Fibroblast, mast cell, histiocytes, lymphocytes
⦁ Papillary layer
⦁ Reticular layer
⦁ EPIDERMIS
⦁ 5% of total skin
⦁ Thickest @ palms, soles, back and buttocks
⦁ 5 layers-SC,SG,SS,SB,SL
⦁ Keratinocytes, Melanocytes, Langerhans cells
CLASSIFICATION OF SKIN TUMOURS
⦁ Most common risk factors is exposure to ultraviolet (UV) light
⦁ BCC accounts for 75% of cases of NMSC
⦁ SCC accounts for the remaining majority of NMSC
CUTANEOUS SCC
• Second most common skin cancer
• Malignant tumour of keratinising cells of the epidermis or its appendages.
• ETIOLOGY
⦁ UVB radiation – chronic uv exosure
⦁ Sun light exposure
⦁ Increase in incidence in sunnier climates
⦁ Lower rates in darker skin types
⦁ Use of tanning devices is associated with 2.5-fold increase in SCC risk and 1.5-fold increase
in BCC risk
⦁ Phototherapy, utilized in the treatment of various skin diseases, is also associated with
increased risk of NMSC
⦁ Exposures to arsenic, organic hydrocarbon, ionizing radiation, and cigarette smoke have
been associated with increasing risk for SCC
⦁ Human papillomavirus(HPV) pathogenic for SCC
⦁ HPV prolong keratinocyte cell cycle, with degradation of p53
⦁ Impaired immunity, especially cell- mediated , is a well-established cause of SCC
⦁ Chronically immunosuppressed patients who undergone organ transplantation
⦁ Immunosuppressive drugs such as azathioprine, cyclosporine, and prednisone increase
the risk for SCC by 50%
• PREMALIGNANT CONDITIONS
• ACTINIC KERATOSIS
• BOWENS DISEASE
• LEUKOPLAKIA
• ERYTHROPLAKIA
• KERATO ACANTHOMA
• XERODERMA PIGMENTOSUM
• RADIATION DERMATITIS
 BOWENS DISEASE
 An early stage intraepidermal SCC – SCC insitu
 Common above 60 years
 Common at genitalia
 Typically presents as a gradually enlarging, well-demarcated erythematous plaque with
irregular border, crusted or scaling surface
⦁ Actinic keratosis
 Common above middle age and elderly
 Characterized by papule or plaque with
rough surface
 May develop cutaneous horn or become
malignant
 10-20% of lesions progress to SCC
• COMMON SITES
• Dorsum of hand, limbs, face, and skin of abdominal wall
• SCC can occur in external genitalia,
• mucocutaneous junction,
• oral cavity,
• respiratory system,
• oesophagus, gall- bladder,
• in urinary bladder as metaplasia from transitional cell lining.
EXAMINATION
• VARIANTS OF SCC:
• Marjolins ulcer – scc occurring in chronic scars with out lymph node spread – no
lymphatics in scar tissue
• Verrucous carcinoma
HISTOLOGY
• An invasive, epidermal keratinising tumour characterised by proliferation of atypical squamous cells
with ‘keratin pearls’
TREATMENT
⦁ Choice of treatment depends on:
⦁ Risk stratification of the tumor, patient preference or suitability, and availability of local
services
⦁ High-risk tumor have greater risk of recurrence and require more aggressive
treatment – multimodal treatment
TREATMENT
• Wide excision with 2cm clearance followed by SSG or Flap
reconstruction
• Gold standard surgery is Mohs Micrographic Surgery(MMS)
• Amputation with one joint above.
• For lymph nodes, block dissection of the regional lymph nodes is
done.
• Chemotherapy is given using methotrexate, vincristine, bleomycin.
• Field therapy using cryo-probe or topical fluorouracil or
electrodessication.
• Brachytherapy using radiation needles,moulds may be given.
• Radiotherapy is also useful in tumors which are not adherent to deeper
planes or cartilage as SCC is radiosensitive.
• Effective treatment modality for patients who are unable to undergo
surgery
• Efficacy is overall lower than with surgery
• Beneficial postoperatively for tumors with perineural invasion
• When complete margin excision is not possible
BASAL CELL CARCINOMA
• It is the commonest (70%) malignant skin tumour.
• It is more common in white-skinned people
• This tumour of low-grade malignancy
• there is no precursor skin lesion for BCCs
• It does not arise from mucosa
• Common in face above the line joining angle of mouth to ear lobule
• Onghren’s line
• EXAMINATION:
• starts as a small brownish-red painless nodule
with translucent colour and shiny surface
showing a network of capillaries.
• Tumor becomes ulcerated with a well defined
hard and raised edge with a beaded
appearance.
• There is a central scab; the margin gradually
spreads and infiltrates into the surrounding
tissues as well as deeper tissues even up to the
bone.
• This characteristic feature of eroding the
tissues, which come in contact with it, has given
it the name ‘rodent’.
• No lymphatic or blood spread – no distant mets
• TYPES:
• Nodular – most common
• Cystic/nodulocystic
• Ulcerative
• Multiple – syndromic
• Pigmented BCC – mimics Melanoma
• Basi-squamous – behaves like SCC
• Geographical/ field fire type BCC – widely spreading with active proliferating edge
• TREATMENT:
• Wide excision (1 cm clearance) with skin grafting/ primary suturing/ flap is the procedure
of choice – Mohs Micrographic Surgery is the gold standard
• Cryosurgery
• Laser treatment – for superficial BCC
• Radiosensitive tumor – RT if not amenable to surgery/ near vital structures - RT is not
given to BCC of ear and close to lacrimal canaliculi
• Excellent prognosis if completely removed
MMS
RISK FACTORS FOR RECURRENCE OF NMSC
SCC
• Tumour size greater than 2 cm
• Tumour thickness greater than 4 mm
• Moderate or poor histological
• differentiation
• Anatomic site over ear, lip, Genitalia
• Perineural invasion, Lympho-vascular
invasion
• Immunosuppressed patients
• Tumours arising from chronic scars or
ulcers
BCC
• Tumour size greater than 2cm
• Infiltrative, micronodular
• Histological subtype
• Perineural invasion
• Anatomic site over central face
MALIGNANT MELANOMA
• Arise from melanocytes in basal layer in the epidermis
• The worst prognosis and morbidity in all skin cancers
• Accounts for 4% of all skin cancers
• Responsible for > 77% of all skin cancer deaths
• Mostly arise from skin ( 95 % )
• Also found in the eyes, ears, GI tract, and mucous membranes
• Can also present as metastasis with unknown primary
PRECURSOR LESIONS
• Atypical or Dysplastic nevi
• Congenital nevi
• Acquired nevi
RISK FACTORS
MODIFIABLE
• Amount of UV exposure
• Severity of UV exposure
• Occupational exposure to coal tar,
arsenic or radium
• Immunosuppression
NON MODIFIABLE
• Very fair skin
• Higher no of nevi
• Nevi developed in adult hood
• Histologically
• dysplastic nevi
• Family history of melanoma
• Personal or family history of BCC or
SCC
SIGNS OF MELANOMA
• A changing mole
• Most common warning sign
• Pruritis
• most common early sign of melanoma is pruritis
• Bleeding and ulceration are late signs showing advanced disease
WARNING SIGNS (ABCDE)
• Asymmetry – one half does not match the other
• Border- Irregular/ poorly defined
• Colour - Variable. Tan brown/black. Red Blue, white
• Diameter - >6mm
• Evolving in color/size/ shape over time
TYPICAL PRESENTATION
• Non painful, firm itchy lesion, in sun exposed sites, with a recent change in
colour/ size, with ulcer formation often covered with a crust.
• Bleeding and sub acute infection is common.
• The regional lymph nodes are involved quite early. Nodes are hard to firm in
consistency
• Satellite nodules may be seen in the skin and subcutaneous tissue between the
primary tumor and the nearest regional lymph nodes.
TYPES
• Superficial spreading – 70% - trunk
and legs
• Nodular melanoma – worst prognosis
– common in legs and trunk
• Lentigo maligna – best prognosis –
head neck and arms
• Acral lentiginous – palm, soles, hand
and subuncal areas
• Amelanotic melanoma
HISTOPATHOLOGICAL CLASSIFICATION
• According to the histological invasion of tumor
• CLARK’S LEVELS
• BRESLOW’S THICKNESS
• CLARK’S CLASSIFICATION
• According to the depth of tumor invasion
• Level 1: Only in epidermis
• Level 2: Extension into papillary dermis
• Level 3: Filling of papillary dermis completely
• Level 4: Extension into reticular dermis Level
• 5: Extension into subcutaneous tissue
• BRESLOW CLASSIFICATION
• Based on the thickness of invasion – most
important prognostic indicator until nodal
spread
• Level 1: less than 0.76 mm thick
• Level 2: between 0.76– 1.50 mm
• Level 3: between 1.50 - 4.00 mm
• Level 4: exceed 4.00 mm in thickness
PROGNOSTIC FACTORS
Stage I : No metastasis (Local Disease)
Stage II : Nodal metastasis (Regional Disease)
Stage III : Distant Metastasis (Systemic Diasese
TREATMENT
• The treatment of choice of melanoma is wide
surgical excision with a negative margin
• Surgical treatment options includes:
• Biopsy
• Wide Local Exsicion
• Staging with Sentinel Lymph Node biopsy
• Therapeutic Lymph Node Dissection
• The only adjuvant therapy approved is high-dose Interferon alfa-2b administered
at a dose near the maximally tolerated dose, with 1 month of IV therapy
• Radiotherapy is only used as a palliative therapy for pain management
CONCLUSION
• The important principles in the management of cutaneous malignancies are
the same
• Clinicians must have a low threshold for biopsy of new or changing skin
lesions.
• The diagnosis is made by biopsy and histologic analysis.
• Surgical excision should be performed, with histologically negative margins.
• Further treatment and follow-up schedules will be determined by the specifc
diagnosis.

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Cutaneous malignancies and related disorders.pptx

  • 2. ⦁ DERMIS ⦁ 15 – 20 times thicker than epidermis ⦁ Collagen, elastic fiber, ground substance ⦁ Nerve, vessels, lymphatics ⦁ Fibroblast, mast cell, histiocytes, lymphocytes ⦁ Papillary layer ⦁ Reticular layer ⦁ EPIDERMIS ⦁ 5% of total skin ⦁ Thickest @ palms, soles, back and buttocks ⦁ 5 layers-SC,SG,SS,SB,SL ⦁ Keratinocytes, Melanocytes, Langerhans cells
  • 4. ⦁ Most common risk factors is exposure to ultraviolet (UV) light ⦁ BCC accounts for 75% of cases of NMSC ⦁ SCC accounts for the remaining majority of NMSC
  • 5. CUTANEOUS SCC • Second most common skin cancer • Malignant tumour of keratinising cells of the epidermis or its appendages. • ETIOLOGY
  • 6. ⦁ UVB radiation – chronic uv exosure ⦁ Sun light exposure ⦁ Increase in incidence in sunnier climates ⦁ Lower rates in darker skin types ⦁ Use of tanning devices is associated with 2.5-fold increase in SCC risk and 1.5-fold increase in BCC risk ⦁ Phototherapy, utilized in the treatment of various skin diseases, is also associated with increased risk of NMSC ⦁ Exposures to arsenic, organic hydrocarbon, ionizing radiation, and cigarette smoke have been associated with increasing risk for SCC
  • 7. ⦁ Human papillomavirus(HPV) pathogenic for SCC ⦁ HPV prolong keratinocyte cell cycle, with degradation of p53 ⦁ Impaired immunity, especially cell- mediated , is a well-established cause of SCC ⦁ Chronically immunosuppressed patients who undergone organ transplantation ⦁ Immunosuppressive drugs such as azathioprine, cyclosporine, and prednisone increase the risk for SCC by 50%
  • 8. • PREMALIGNANT CONDITIONS • ACTINIC KERATOSIS • BOWENS DISEASE • LEUKOPLAKIA • ERYTHROPLAKIA • KERATO ACANTHOMA • XERODERMA PIGMENTOSUM • RADIATION DERMATITIS
  • 9.  BOWENS DISEASE  An early stage intraepidermal SCC – SCC insitu  Common above 60 years  Common at genitalia  Typically presents as a gradually enlarging, well-demarcated erythematous plaque with irregular border, crusted or scaling surface
  • 10. ⦁ Actinic keratosis  Common above middle age and elderly  Characterized by papule or plaque with rough surface  May develop cutaneous horn or become malignant  10-20% of lesions progress to SCC
  • 11. • COMMON SITES • Dorsum of hand, limbs, face, and skin of abdominal wall • SCC can occur in external genitalia, • mucocutaneous junction, • oral cavity, • respiratory system, • oesophagus, gall- bladder, • in urinary bladder as metaplasia from transitional cell lining.
  • 13. • VARIANTS OF SCC: • Marjolins ulcer – scc occurring in chronic scars with out lymph node spread – no lymphatics in scar tissue • Verrucous carcinoma
  • 14. HISTOLOGY • An invasive, epidermal keratinising tumour characterised by proliferation of atypical squamous cells with ‘keratin pearls’
  • 15.
  • 16. TREATMENT ⦁ Choice of treatment depends on: ⦁ Risk stratification of the tumor, patient preference or suitability, and availability of local services ⦁ High-risk tumor have greater risk of recurrence and require more aggressive treatment – multimodal treatment
  • 17. TREATMENT • Wide excision with 2cm clearance followed by SSG or Flap reconstruction • Gold standard surgery is Mohs Micrographic Surgery(MMS) • Amputation with one joint above. • For lymph nodes, block dissection of the regional lymph nodes is done.
  • 18. • Chemotherapy is given using methotrexate, vincristine, bleomycin. • Field therapy using cryo-probe or topical fluorouracil or electrodessication. • Brachytherapy using radiation needles,moulds may be given.
  • 19. • Radiotherapy is also useful in tumors which are not adherent to deeper planes or cartilage as SCC is radiosensitive. • Effective treatment modality for patients who are unable to undergo surgery • Efficacy is overall lower than with surgery • Beneficial postoperatively for tumors with perineural invasion • When complete margin excision is not possible
  • 20. BASAL CELL CARCINOMA • It is the commonest (70%) malignant skin tumour. • It is more common in white-skinned people • This tumour of low-grade malignancy • there is no precursor skin lesion for BCCs • It does not arise from mucosa • Common in face above the line joining angle of mouth to ear lobule • Onghren’s line
  • 21. • EXAMINATION: • starts as a small brownish-red painless nodule with translucent colour and shiny surface showing a network of capillaries. • Tumor becomes ulcerated with a well defined hard and raised edge with a beaded appearance. • There is a central scab; the margin gradually spreads and infiltrates into the surrounding tissues as well as deeper tissues even up to the bone. • This characteristic feature of eroding the tissues, which come in contact with it, has given it the name ‘rodent’. • No lymphatic or blood spread – no distant mets
  • 22. • TYPES: • Nodular – most common • Cystic/nodulocystic • Ulcerative • Multiple – syndromic • Pigmented BCC – mimics Melanoma • Basi-squamous – behaves like SCC • Geographical/ field fire type BCC – widely spreading with active proliferating edge
  • 23. • TREATMENT: • Wide excision (1 cm clearance) with skin grafting/ primary suturing/ flap is the procedure of choice – Mohs Micrographic Surgery is the gold standard • Cryosurgery • Laser treatment – for superficial BCC • Radiosensitive tumor – RT if not amenable to surgery/ near vital structures - RT is not given to BCC of ear and close to lacrimal canaliculi • Excellent prognosis if completely removed
  • 24. MMS
  • 25. RISK FACTORS FOR RECURRENCE OF NMSC SCC • Tumour size greater than 2 cm • Tumour thickness greater than 4 mm • Moderate or poor histological • differentiation • Anatomic site over ear, lip, Genitalia • Perineural invasion, Lympho-vascular invasion • Immunosuppressed patients • Tumours arising from chronic scars or ulcers BCC • Tumour size greater than 2cm • Infiltrative, micronodular • Histological subtype • Perineural invasion • Anatomic site over central face
  • 27. • Arise from melanocytes in basal layer in the epidermis • The worst prognosis and morbidity in all skin cancers • Accounts for 4% of all skin cancers • Responsible for > 77% of all skin cancer deaths • Mostly arise from skin ( 95 % ) • Also found in the eyes, ears, GI tract, and mucous membranes • Can also present as metastasis with unknown primary
  • 28. PRECURSOR LESIONS • Atypical or Dysplastic nevi • Congenital nevi • Acquired nevi
  • 29. RISK FACTORS MODIFIABLE • Amount of UV exposure • Severity of UV exposure • Occupational exposure to coal tar, arsenic or radium • Immunosuppression NON MODIFIABLE • Very fair skin • Higher no of nevi • Nevi developed in adult hood • Histologically • dysplastic nevi • Family history of melanoma • Personal or family history of BCC or SCC
  • 30. SIGNS OF MELANOMA • A changing mole • Most common warning sign • Pruritis • most common early sign of melanoma is pruritis • Bleeding and ulceration are late signs showing advanced disease
  • 31. WARNING SIGNS (ABCDE) • Asymmetry – one half does not match the other • Border- Irregular/ poorly defined • Colour - Variable. Tan brown/black. Red Blue, white • Diameter - >6mm • Evolving in color/size/ shape over time
  • 32. TYPICAL PRESENTATION • Non painful, firm itchy lesion, in sun exposed sites, with a recent change in colour/ size, with ulcer formation often covered with a crust. • Bleeding and sub acute infection is common. • The regional lymph nodes are involved quite early. Nodes are hard to firm in consistency • Satellite nodules may be seen in the skin and subcutaneous tissue between the primary tumor and the nearest regional lymph nodes.
  • 33.
  • 34. TYPES • Superficial spreading – 70% - trunk and legs • Nodular melanoma – worst prognosis – common in legs and trunk • Lentigo maligna – best prognosis – head neck and arms • Acral lentiginous – palm, soles, hand and subuncal areas • Amelanotic melanoma
  • 35. HISTOPATHOLOGICAL CLASSIFICATION • According to the histological invasion of tumor • CLARK’S LEVELS • BRESLOW’S THICKNESS
  • 36. • CLARK’S CLASSIFICATION • According to the depth of tumor invasion • Level 1: Only in epidermis • Level 2: Extension into papillary dermis • Level 3: Filling of papillary dermis completely • Level 4: Extension into reticular dermis Level • 5: Extension into subcutaneous tissue
  • 37. • BRESLOW CLASSIFICATION • Based on the thickness of invasion – most important prognostic indicator until nodal spread • Level 1: less than 0.76 mm thick • Level 2: between 0.76– 1.50 mm • Level 3: between 1.50 - 4.00 mm • Level 4: exceed 4.00 mm in thickness
  • 38. PROGNOSTIC FACTORS Stage I : No metastasis (Local Disease) Stage II : Nodal metastasis (Regional Disease) Stage III : Distant Metastasis (Systemic Diasese
  • 39. TREATMENT • The treatment of choice of melanoma is wide surgical excision with a negative margin • Surgical treatment options includes: • Biopsy • Wide Local Exsicion • Staging with Sentinel Lymph Node biopsy • Therapeutic Lymph Node Dissection
  • 40.
  • 41. • The only adjuvant therapy approved is high-dose Interferon alfa-2b administered at a dose near the maximally tolerated dose, with 1 month of IV therapy • Radiotherapy is only used as a palliative therapy for pain management
  • 42. CONCLUSION • The important principles in the management of cutaneous malignancies are the same • Clinicians must have a low threshold for biopsy of new or changing skin lesions. • The diagnosis is made by biopsy and histologic analysis. • Surgical excision should be performed, with histologically negative margins. • Further treatment and follow-up schedules will be determined by the specifc diagnosis.