Nevi, Premalignant, Nonmelanoma & Melanoma Skin Tumors PDF

DERMATOLOGY (IM) NOTE: This is purely based Topic: Nevi, Premalignant, Nonmelanoma & Melanoma Skin Tumors...

DERMATOLOGY (IM) NOTE: This is purely based Topic: Nevi, Premalignant, Nonmelanoma & Melanoma Skin Tumors on the PPT + lecture notes Lecture by: Dr. Del Rio FITZ PATRICK SKIN TYPE Junctional Compound Intradermal Lecture Discussion: Stages of Nevi Junctional Nevi – it is the youngest of the 3 types; they are hyperpigmented, flat (macules), and may have a fried-egg appearance (darker center than the periphery) Compound Nevi - some of the junctional nevi become elevated (papule) as we grow older therefore becoming a compound nevi Intradermal Nevi – some of our nevi, during our middle age (40s or 50s), become an intradermal nevi  dome shaped papules with or without hairs Incidence & Prevalence:  Not stable, grows, going through changes of maturation, and even of senescence  Maximum number of nevi is present between the ages 20 and 25, and the average number is 40 — flatten and fade, disappear completely by age 90  Nevi begin as small, flat pigmented macules o Junctional  Compound  Intradermal Junctional Compound Intradermal Lecture Discussion: Histologic Differences of Nevi Questions:  What is the Average number of nevi in a person’s body? 40 Junctional Nevi – the nests of melanocytes are purely in the epidermis  Do our moles change? Yes Compound Nevi – as the nevus mature, some of the nevus cells will migrate towards the upper dermis, but there are still nevus cells in the epidermis  TYPES OF CELLULAR NEVI mixed dermal & epidermal cells Intradermal Nevi – the nevus cells are all in the dermis  Appear in the first years of life and increase in prevalence and number of lesions over the following 2-3 decades, after which there is a steady Junctional Nevus: decline  Smooth, hairless, light to dark brown macule  Females have more nevi than males, and whites more than blacks  May have the characteristic target or fried egg appearance  Sun exposure appears to increase the number of moles in the exposed  Sites: palms, soles, scrotum skin  May be present at birth, but usually appear between 3-18 y/o  Less common in covered areas such as the buttocks, except in the dysplastic nevus syndrome  Adolescence and adulthood — become compound or intradermal  Women have more nevi on the legs, and men on the trunk Compound Nevus:  Blacks have more nevi than whites on the palms, soles, conjunctivae and nail beds  Both junctional and intradermal  Nevus cells extend into the dermis  Plantar nevi > palmar nevi  Mucous membrane and nail bed nevi unusual in all patients  Later, nevus cells become separated from the epidermis by a band of connective tissue — Intradermal Nevus Intradermal Nevus:  Found in middle-aged persons  Dome-shaped, sessile, warty or smooth papules, flesh-colored, brown to black, and with or without hairs #GrindNation Page 1 of 11 Strength in knowledge  DERMATOLOGY (IM) Topic: Nevi, Premalignant, Nonmelanoma & Melanoma Skin Tumors Lecture by: Dr. Del Rio Summary Table of Types of Nevi:  Pathogenesis: immunologically induced rejection of melanin or of a Junctional Compound Intradermal melanoma beginning in the nevus Smooth, hairless, Dome-shaped  Treatment: not indicated —regress spontaneously with time Lesions light to dark Papule, darker papule with or brown macule without hair EPITHELIOID & SPINDLE CELL NEVUS Epidermal &  Benign Juvenile Melanoma, Spitz Nevus Nevus cells Epidermal Dermal Dermal  Smooth-surfaced, raised, round, slightly scaly, firm papule with a Signs of Malignant Degeneration: distinctive pink, brownish red or  Recent enlargement purplish red color, 3-10 mm in  Irregular or scalloped border diameter  Asymmetry  Occur during the first two decades of life  Changes or variegation in color (red, white or blue)  Site: face (cheek), legs (pigmented type)  Surface changes (scaling, erosion, oozing,  Preponderance in females  Crusting, ulceration, or bleeding)  May occur as clustered papules in children and adults  Palpable thickening  A variant of compound nevus  Pain or tenderness  Histologic: nevus cells are pleomorphic, mostly spindle-shaped, or less  Signs of inflammation often polygonal, giant cells may be seen  Satellite pigmentation  “ugly duckling sign”: a nevi that does not share the same Treatment: characteristics as the majority  biopsy  Excision biopsy  Nevi with small dark dots that do not lie entirely within the lesion, but produce a small extension beyond the border Question:  Perifollicular hypopigmentation giving a notched appearance  A 3-month old female consulted because of the  New pigmented nevus in a patient > 35 y/o lesion which is present at birth. What is your  Hutchinson’ sign: pigmentation over the nail fold diagnosis? Giant Hairy Nevus Signs of Benignancy: GIANT PIGMENTED NEVUS  Diameter ≤ 3 mm  Giant Hairy Nevus, Bathing Trunk Nevus  Perfectly uniform pigmentation  large, > 20 cm in diameter, darkly pigmented hairy patch in which  Flaccid epidermis smaller, darker patches are interspersed or present as small satellite  Smooth, uniform border lesions  Unchanging size and color  Skin may be thickened and verrucous  Site: trunk (upper and lower back), usually dermatomal Treatment:  Present at birth and grow proportionally to the site of the body on Indications for removal and biopsy: which they are located  Signs of malignant transformation  Incidence of developing into melanoma is 3-7%  Cosmetic  40% of melanoma in children occur in large congenital nevi  Located in areas of irritation  Axial lesions associated with neurocutaneous melanocytosis  poor  Nevi on the hairy scalp, oral or vaginal mucous membrane prognosis because of hydrocephalus and leptomeningeal melanoma  An acquired longitudinal pigmented band in an adult involving only  Histologically: nevus cells in the lower 2/3 of the dermis, occ. one nail extending into the subcutis  Conjunctival nevi in the palpebral or formiceal  Conjunctiva, extension into the cornea or canalicular obstruction Treatment:  Tarsal pigmentation  Total surgical excision and resurfacing with autografts  Dermabrasion, curettage and laser ablation BALLOON CELL NEVUS  A pigmented nevus, from 1-5 mm, indistinguishable from the ordinary SMALL & MEDIUM-SIZED CONGENITAL NEVOCYTIC NEVUS pigmented or nonpigmented nevus, usually occurring on the head,  Small congenital nevocytic nevi: F  Inverse psoriasis  Chronic slowly progressive  Stages: Treatment: o Patch  Plaque  Tumor  Mohs’ microsurgery Plaque stage  stage where there is LN involvement  CO2 laser  Once tumors develop or lymph node involvement occurs, prognosis is  Monitor CEA levels for disease response guarded or may be fatal PAGET’S DISEASE OF THE BREAST Early Patch/Plaque Stage:  Macules or slightly infiltrated patches or plaques 1-5 cm in diameter  Unilateral, sharply defined eczema  Lesions may have an atrophic surface or mottled dyspigmentation and caused by epidermal metastases from telangiectasia underlying ductal adenocarcinoma of the  May be generalized or begin localized to one area, then spread breast  Sites: lower abdomen, buttocks, and upper thighs and breast  Begins as an erythematous crusted or keratotic, circumscribed pruritic patch Plaque Stage:  Later become infiltrated and ulcerated  Lesions are more infiltrated and may resemble psoriasis or a subacute  Nipple may be retracted dermatitis  Palms and soles may be involved with hyperkeratotic, psoriasiform, Lecture Discussion: and fissuring plaques Sometimes you will not be able to palpate a breast mass because the cancer is  Infiltration becomes more marked and leads to discoid patches or under the nipple. You will be able to detect it through mammogram or breast extensive plaques, which may eventually coalesce but with normal ultrasound skin interspersed Patient’s with paget’s disease of the breast are usually old patients  More advanced, painful superficial ulcerations may occur with o Differential Diagnosis is breast eczema  it responds to treatment enlarged, nontender, firm, and freely movable lymph nodes with corticosteroids, antihistamines. It usually affects both breasts, and no retraction of the nipple and patients are younger Tumor Stage:  Large nodules on infiltrated plaques and on apparently healthy skin Summary of Differences:  Nodules break down and form deep oval ulcers with bases covered Paget’s Disease Breast Eczema with a necrotic grayish substance and rolled edges Unilateral Often bilateral  Sites: trunk, anywhere on the skin, mouth and upper respiratory tract (+) Nipple retraction (-) Nipple retraction Older age Younger age Erythrodermic Type: Breast mass present and may not be  Generalized exfoliative process with universal redness No breast mass palpable  Hair is scanty, nails dystrophic, palms and soles hyperkeratotic and at Unresponsive to steroids Improve with steroids times, may have generalized hyperpigmentation Histopathology:  Presence of Paget cells: large, round, clear-staining cells with large nuclei, appearing singly or in small nests between the squamous cells  Frequent mitoses present #GrindNation Page 5 of 11 Strength in knowledge  DERMATOLOGY (IM) Topic: Nevi, Premalignant, Nonmelanoma & Melanoma Skin Tumors Lecture by: Dr. Del Rio Treatment:  Topical corticosteroids  Topical nitrogen mustard  Topical carmustine  Ultraviolet therapy  Radiation treatment  Biologic response modifiers: interferon  Retinoids  Systemic chemotherapy Erythrodermic Mycosis Fungoides  Generalized exfoliative process with universal redness  Hair is scanty, nails dystrophic, palms and soles hyperkeratotic and at times, may Lecture Discussion: have generalized hyperpigmentation Patch stage  erythematous scaly patches, ill defined. After a few months or years, it will become a plaque Plaque stage  within the patch there are plaques. Will later develop into a Lecture Discussion: tumor If you have a patient with exfoliative dermatitis  Tumor stage within the plaque, a tumor develops which ulcerates do a biopsy because it has multiple etiologies Erythrodermic MF  some patients originally have generalized erythroderma (psoriasis, drug allergy, lymphoma, mycosis from the onset fungoides)  if we know its etiology, we can treat it accordingly Natural History:  Chronic, slowly progressive disorder Sezary Syndrome  Begins as flat patches (Patch stage) which may or may not be  The leukemic phase of mycosis fungoides histologically diagnostic of MF (premycotic)  Triad:  Pruritus present 1. Generalized erythroderma  Over time, the lesions may become infiltrated plaques (Plaque stage) 2. Superficial lymphadenopathy  Tumors may eventually appear (Tumor stage) 3. Atypical cells (Sezary cells) in the  Some patients may present with or progress to erythroderma circulating blood  Eventually, noncutaneous involvement is detected  LN > peripheral blood > visceral organ  Patients with MF may progress to Sezary  Affects elderly patients and has a long evolution syndrome but usually patients are  Once tumors develop or LN involvement occurs, the prognosis is erythrodermic from the onset guarded and may be fatal  Superficial lymphadenopathy in the cervical, axillary and inguinal areas Evaluation & Staging:  Leukocytosis > 30,000/mm3 T1: 10% IB: T2N0M0 peripheral blood, skin and lymph nodes T3: tumors IIA: T1-2N1M0 T4: erythroderma IIB: T3N0-1M0 Treatment: N0: (-) IIIA: T4N0M0  Methotrexate N1: palpable but not MF IIIB: T4N1M0  Photophoresis N2: not palpable but MF pathologically IVA: T1-4N2-3M0  Interferon alfa N3: palpable and MF IVB: T1-4,N0-3M1 MO and BO: (-) viscera and blood inv.  Retinoids M1 and B1: (+)  Chlorambucil and prednisone  Fludarabine Staging Work-up:  Complete history and P.E. Questions:  Careful palpation of LN and mapping of skin lesions  What is the most important risk factor in the development of skin cancer? Sun exposure  even if you have very dark skin but if you are  CBC with assays for Sezary cells constantly sun exposed, there is a high chance of development of  Renal and liver function tests, LDH cancer  Chest x-ray  What type of cancer is Marjolin’s ulcer? Squamous cell cancer  Skin and lymph node biopsy  Marjolin’s ulcer is a type of ulcer of squamous cell cancer  CT scan which arises from an old scar (ex. Thermal & Electrical burns)  Of all the squamous cell cancer, marjolin’s ulcer has the highest risk of metastasis  What is the most common site of basal cell cancer? Nose  What is the most common type of melanoma? Superficially spreading #GrindNation Page 6 of 11 Strength in knowledge  DERMATOLOGY (IM) Topic: Nevi, Premalignant, Nonmelanoma & Melanoma Skin Tumors Lecture by: Dr. Del Rio  Advanced lesions, the surface may be cauliflowerlike, composed of densely packed, filamentous projections, between which are clefts Picture on Left: filled with viscid, purulent, malodorous exudate This is a melanoma of the nail bed. There is  On the lower lip, SCC often develops on actinic cheilitis destruction of nail already Hutchinson’s  History of smoking in lips sign – black or hyperpigmented vertical line  Lower lip SCC > upper lip  M>F SKIN CANCER Etiology:  The most common worldwide malignancy  Ultraviolet light  2 main categories:  Thermal injury to the skin 1. Nonmelanoma Skin Cancer (NMSC)  Chemicals such as polycyclic aromatic hydrocarbons, arsenic, paraffin,  Basal cell cancer (BCC) creosote, anthracene, tobacco smoke tars and chromates  Squamous cell cancer (SCC)  Chronic radiation dermatitis from x-radiation or radium 2. Melanoma Skin Cancer (MSC)  HPV esp. types 16, 18, 30, 33  Marjolin’s ulcer: cancers that arise in chronic, ulcers, sinuses and scras  NMSC > MSC most commonly from burns  NMSC – much easier to treat and have better long term prognosis  Certain dermatoses, such as porokeratosis of Mibelli, nevus because of its tendency to remain confined to their primary site sebaceous, and lichen sclerosus et atrophicus Histopathology: NONMELANOMA SKIN CANCER Squamous Cell Cancer  The greater the differentiation, the less the invasive tendency, thereby  Most common skin malignancy among Asian Indian and African the better prognosis Americans Borders Classification:  Second most common skin cancer among Hispanics and Chinese Japanese  Grade 1 – most cells are well-diffrentiated  Risk factors:  Grade IV – undifferentiated or anaplastic o Sun exposure – lifetime exposure is more significant o Chronic scarring – old scars can produce marjolin’s ulcer Metastases: o Areas of chronic inflammation  0.5 – 5.2%  Reginal lymph nodes  Local recurrence and metastasis are related to: 1. Treatment modality 2. Prior treatment 3. Location 4. Size 5. Depth 6. Histologic differentiation 7. Histologic evidence of desmoplastic features 8. Histologic evidence of perineural involvement 9. Precipitating factors other than UV light 10. Host immunosuppression Additional Information from Old Trans:  Scars (37.9%) > lip (13.7%) > external ear (8.8%)  Occurs in the skin and mucous membranes  Risk of metastasis rises for lesions larger than 2 cm, thicker than 4mm  Often begins at the site of actinic keratosis on sunexposed areas such and lip lesions thicker than 8 mm as the face and back of hands  Face: BCC > SCC Treatment:  Hands: SCC > BCC  Moh’s surgical technique  The lesion may be superficial, discrete and hard, and arises from an  Radiation therapy indurated, rounded, elevated base: dull red and contains  Retinoids, electrochemotherapy, photodynamic therapy, beta telangiectases carotene, interferons and intratumoral chemotherapy  May begin as small, erythematous, infiltrated, hard, scaly plaques on  Metastatic disease: cisplatin and doxorubicin or bleomycin skin that has been damaged by xrays, scars, or chronic ulcers   PREVENTION: sunscreens becomes larger, deeply nodular and ulcerated  On early stage, tumor is localized, elevated and freely movable  Later it gradually becomes more diffuse, depressed and fixed  invades underlying tissue #GrindNation Page 7 of 11 Strength in knowledge  DERMATOLOGY (IM) Topic: Nevi, Premalignant, Nonmelanoma & Melanoma Skin Tumors Lecture by: Dr. Del Rio Basal Cell Cancer Fibroepithelioma of Pinkus  Most common skin cancer in whites (65-75%)  Premalignant fibroepithelial tumor  Second most common after SCC in people of color (POC) (20-30%)  Elevated, skin-colored, sessile lesion on the lower trunk, lumbosacral  Rarely metastasize but can result in significant disfigurement area, groin and thigh and may be as large as 7 cm  Linked to UV light exposure  Superficial and resembles a fibroma or papilloma  Present in sun-exposed skin especially the face (90% on the head and  May overlie breast carcinomas neck in POC) Cystic Basal Cell Epithelioma  Dome shaped, blue-gray cystic nodules clinically similar to eccrine and apocrine hidrocystoma  4-8% of all BCCs Morphea-like Epithelioma  Waxy sclerotic plaques in the head and neck with absence of a rolled edge, ulceration and crusting  Telangiectasia is prominent  Resistant to radiation and electrocautery  2% of all BCCs Cicatricial BCC or “Field Fire Epithelioma”  A tumor composed of one or few small, waxy, semitransluscent  Resembles localized scleroderma that presents a cictricial surface with nodules forming around a central depression that may or may not be nests of active lesions that are usually ulcerated ulcerated.  Fine waxy border or threadlike raised edge and telangiectasia present  Crusted and bleeding  Occurs amost exclusively on the cheeks  The edge of the larger lesions has a characteristic rolled border  May be seen on the forehead  Telangiectases course through the lesion  Bleeding on slight injury is common Treatment:  Rarely metastasize  Excision: Moh’s icrosurgery or ionizing radiation therapy  Most frequently found on the face (85% are found in the head and neck) and esp. on the nose (25-30%) Rodent Ulcer/Jacob’s Ulcer  Deep ulcer that burrows into the subcutaneous tissue, cartilage and Types: bone with the floor of the ulcer covered by viscid necrotic material  Nodular or classic BCC (50-54% of BCC)  A neglected BCC which has formed an ulceration  Pigmented BCC  Cystic Basal cell Epithelioma Course:  Morphea-like Epithelioma  BCC runs a chronic course, during which new nodules develop, crusts  Cicatricial BCC form and fall off, and the ulceration enlarges  Rodent ulcer  As a rule, there is a tendency for the lesions to bleed without pain or  Superficial BCC other symptoms  Fibroepithelioma of Pinkus  Some lesions tend to heal spontaneously and form scar tissue as they  Keloidal BCC extend  Configurate, somewhat serpiginous patches  Aberrant BCC  85% on the head and neck esp. the nose (25-30%) forehead, ears, periocular areas and cheeks Superficial BCC  Upper trunk  Dry, psoriasiform, scaly lesions on the trunk and limbs that have little tendency to invade or ulcerate, and enlarge only very slowly Metastasis:  May grow to 10-15cm without ulceration  0.0028-0.55%  Erythematous plaques with a threadlike raised border, telangiectasia  Rare because the cancer is highly dependent on the connective tissue and atrophy stroma in which they lie  History of arsenic ingestion over a long period  Almost always due to incomplete excision or neglect  Seen in younger patients  Regional lymph nodes > lung > bone > skin > liver > pleura  9-11% of BCCs  Fewer than 20% survive 1 year and less than 105 will live past 5 years after metastasis Pigmented BCC  Has all features of the basal type, with brown or black pigmentation, usually on the trunk  More frequent in dark-complected persons  Caused by arsenic ingestion  6% of BCCs #GrindNation Page 8 of 11 Strength in knowledge  DERMATOLOGY (IM) Topic: Nevi, Premalignant, Nonmelanoma & Melanoma Skin Tumors Lecture by: Dr. Del Rio Epidemiology:  Nonmelanoma skin cancers constitute one third of all cancers diagnosed in the US and BCC account for more than 75%  Causes of BCC: 1. Excessive sunlight exposure 2. Chemical cocarcinogens 3. Genetic determinants Treatment:  Excision – lesions > 5-7mm  Moh’s microsurgery  Electrosurgery  Curettage  Ionizing radiation therapy  Topcial 5-FU  Cryosurgery  Laser therapy  90% of skin cancers is preventable Prophylaxis:  Regular self-examination of the skin  Sun avoidance  Know your ABCDE  Sunscreens  Avoid sun exposure  Use a daily broad-spectrum sunscreen MALIGNANT MELANOMA  6mm nail fold or bed  Hutchinson’s sign: black discoloration of the proximal nail fold at the  Occurs in most light skinned people end of a pigmented streak (melanonycjoa striata) may signal inv. Of  The lowest incidence is found among Asians nail matrix  The incidence is low until after puberty  Sign of malignancy in nail matrix Metastases to epitrochlear and  In children, melanomas occur at least half of the time from preexisting axillary nodes normal skin, where the clues to diagnosis are the same as adults, but there is often delayed recognition because of its overall low incidence Differential Diagnosis:  Hematoma (if there is trauma), sometimes you see elevation if there is Etiologic Factors: trauma, if you are not sure do nail BIOPSY (nail bed)-partial punch  Light complexion biopsy or partial ungiectomy  Light eyes (ex. blue-eyed)  Blond or red hair Nodular Melanoma  Occurrence of blistering sunburns in childhood  Pigmented papule or nodule of varying size  Heavy freckling  Arise without an apparent radial growth phase  Tendency to tan poorly and sunburn easily  No radial growth, only vertical growth  Chronically sun-exposed  15% of all melanomas  Sun-exposed areas of the head, neck and trunk Melanoma Types:  May grow much larger and become papillary fungoid or ulcerated  Lentigo maligna  Bleeding is usually a late sign  Superficially spreading melanoma – most common  Acral-lentigoius melanoma  Nodular melanoma Metastasis:  In the beginning, metastasis is manifested by pigmented nodules Lentigo maligna appearing around the site of the excision  Begins as a tan macule that extends peripherally, with gradual uneven  Regional lymphadenopathy may be the first sign darkening irregular edge and color variegation, due to areas of  Later, metastases occur via the blood stream regression  The chief site for metastatic melanoma is the skin, but all other organs  Gradually enlarges are at risk.  After a radial growth period 5-20 years, downwards vertically growing  CNS metastasis is the most common cause of death melanoma  Usually develops within it ) Lentigo maligna melanoma) Staging System: CLARK LEVEL  Palpable nodule within the original macule is the best evience of  Clark level I (pTis): melanoma in situ malignant transformation  Clark level II (pTI): tumors 0.75 mm or < in thickness but invades the  5% of all melanomas papillary dermis  Clark level III (pT2): >0.75 mm thick but not >1.5mm thick and/or Superficially spreading melanoma tumors that invade to the papillary reticular dermal interface  70% of all melanomas  Clark level IV (pT3): >1.5mm thick but 4mm thick and /or tumors that invade the subQ  Upper back for both sexes and shin for women are the commonest tissue and or satellites within 2 cm of the primary tumor sites  Tendency to multicoloration with a notched border Prognosis:  Horizontal or lateral growth into the adjoining epidermis continues for  Overall survival rate is 80% for early diagnosis 1-5 years, before invasion into the dermis –shorter radial growth  (+) regional LN disease: 30-35%  Faster growth than the Lentigo Melanoma  Distant metastases: 5- year survival rate is 10%  Spontaneous regression has been reported  3 Most common skin CA: o BCC (basal cell carcinoma) o SCC (squamous cell carcinoma) o Melanoma  Fastest rate of metastasis – Melanoma  Least rate of metastasis – Basal cell carcinoma #GrindNation Page 10 of 11 Strength in knowledge  DERMATOLOGY (IM) Topic: Nevi, Premalignant, Nonmelanoma & Melanoma Skin Tumors Lecture by: Dr. Del Rio Factors that determine prognosis:  Presence of tumor infiltrating lymphocytes o Better prognosis  Mitotic rate o The higher the mitotic rate, the lower the prognosis  Ulceration  Location (hair bearing limbs better prognosis than lesions on the trunk, head, neck and palm or sole)  Sex (F>M)  Female better prognosis  Age  Extremes of ages (poor prognosis)  Younger age the better prognosis  Presence of leukoderma at distal sites o Leukoderma is (+) immunologically mediated response to melanin o Paradoxical effect: can indicate metastasis but it has better prognosis because the immune system is already attacking malignant cells  Regression (poorer prognosis) Treatment:  Early diagnosis and excision remain the hope for cure of melanoma (better prognosis) Immunotherapy  Perfusion chemotherapy – extremity melanoma  Interferon alfa 2b  Radiation therapy- for CNS metastasis  Prevention is the best treatment esp. for high risk! References:  PPT  Lecture Notes #GrindNation Page 11 of 11 Strength in knowledge