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Benign and Malignant Skin Leisions

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  • the epidermis,
    the basement membrane zone, the dermis and the subcutaneous
    layer
  • The innermost layer of the epidermis consists of a single row of columnar cells called basal cells. Basal cells divide to form keratinocytes (prickle cells), which comprise the spinous layer. The cells of the spinous layer are connected to each other by intercellular bridges or spines, which appear histologically as lines between cells. The keratinocytes synthesize insoluble protein, which remains in the cell and eventually becomes a major component of the outer layer (the stratum corneum). The cells continue to flatten, and their cytoplasm appears granular (stratum granulosum); they finally die as they reach the surface to form the stratum corneum.
  • The epidermis is a stratified epithelium of ectodermal origin
    that arises from dividing basal keratinocytes. The downward
    projections of the epidermis into the dermis are called the
    ‘rete ridges’. The lower epidermal cells (basal layer) produce
    a variety of keratin filaments and desmosomal proteins (e.g.
    desmoglein and desmoplakin), which make up the ‘cytoskeleton’.
    This confers strength to the epidermis and prevents it
    shedding off. Higher up in the granular layer, complex lipids
    are secreted by the keratinocytes and these form into intercellular
    lipid bilayers, which act as a semipermeable skin
    barrier. The upper cells (stratum corneum) lose their nuclei
    and become surrounded by a tough impermeable ‘envelope’
    of various proteins (loricrin, involucrin, filaggrin and keratin).
    Changes in lipid metabolism and protein expression in the
    outer layers allow normal shedding of keratinocytes.
    Keratinocytes can secrete a variety of cytokines (e.g.
    interleukins, gamma-interferon, tumour necrosis factor alpha)
    in response to tissue injury or in certain skin diseases. These
    play a role in specific immune function, cutaneous inflammation
    and tissue repair. There is a further layer of protection
    against microbial invasion called the innate immune system
    of the skin. This comprises neutrophils and macrophages as
    well as keratinocyte-produced antimicrobial peptides (called
    β-defensins and cathelicidins). Expression of these peptides
    is both constitutive and induced by skin inflammation and
    they are active against bacterial, viral and fungal pathogens.
    There is evidence to suggest a deficiency of these peptides
    may account for the susceptibility of patients with atopic
    eczema to skin infection.
  • The innermost layer of the epidermis consists of a single row of columnar cells called basal cells. Basal cells divide to form keratinocytes (prickle cells), which comprise the spinous layer. The cells of the spinous layer are connected to each other by intercellular bridges or spines, which appear histologically as lines between cells. The keratinocytes synthesize insoluble protein, which remains in the cell and eventually becomes a major component of the outer layer (the stratum corneum). The cells continue to flatten, and their cytoplasm appears granular (stratum granulosum); they finally die as they reach the surface to form the stratum corneum.
  • Other cells in the epidermis
    Melanocytes are found in the basal layer and secrete the
    pigment melanin. These protect against UV irradiation. Racial
    differences are due to variation in melanin production, not
    melanocyte numbers.
    Merkel cells are also found in the basal layer and originate
    either from neural crest or epidermal keratinocytes. They are
    numerous on finger tips and in the oral cavity and play a role
    in sensation.
    Langerhans’ cells are dendritic cells found in the suprabasal
    layer. They derive from the bone marrow and as they
    express the cytokine CCR6, they are guided to normal skin,
    which contains a CCR6 agonist called macrophage inflammatory
    protein 3α. Langerhans’ cells endocytose extracellular
    antigens in the skin and then migrate to local lymph nodes
    for T-cell presentation and thus act as antigen-presenting
    cells.
  • The dermis is of mesodermal origin and contains blood
    and lymphatic vessels, nerves, muscle, appendages
    (e.g. sweat glands, sebaceous glands and hair follicles)
    and a variety of immune cells such as mast cells and lymphocytes.
    It is a matrix of collagen and elastin in a ground
    substance.
    The dermis is divided into two layers: the thin upper layer, called the papillary layer, is composed of thin, haphazardly arranged collagen fibers; the thicker lower layer, called the reticular layer, extends from the base of the papillary layer to the subcutaneous tissue and is composed of thick collagen fibers that are arranged parallel to the surface of the skin. Histiocytes are wandering macrophages that accumulate hemosiderin, melanin, and debris created by inflammation. Mast cells, located primarily about blood vessels, manufacture and release histamine and heparin.
  • is a term used to describe the seborrheic keratoses of the face seen more commonly in African-Americans.
    1 to 2 mm, dark brown keratotic papules concentrated around the eyes and upper cheeks, with an incidence of 30-35% in African-Americans
  • Treatment may be indicated for symptomatic lesions.
    Lesions may be removed when they are symptomatic and this usually occurs when they are located in an area of friction and frequent trauma.
    Removal is often requested for cosmetic reasons.
  • Level II

Transcript

  • 1. Skin Tumors Seyed Morteza Mahmoodi
  • 2. Skin • Weight - 16% TBW • Surf. Area - 2sq.m • Thickness - 0.5-4mm • Layers -Epidermis - Basement membrane -Dermis - Subcutaneous Layer
  • 3. Composition of skin
  • 4. Epidermis o Thickness - 0.07-12 mm o Stratified sq. epithelium o Different layers Stratum corneum (Stratum lucidum) Stratum granulosum Stratum spinosum Stratum basale
  • 5. Cells of the Epidermis  Melanocytes  basal layer protect against UV irradiation  Racial differences are due to variation in melanin production, not melanocyte numbers  Merkel cells sensation  Langerhans’ cells  Dendritic cells  Antigen-presenting cells
  • 6. Dermis  Thickness - 0.6-3mm  2 layers papillary reticular  Skin appendages  Blood vessels  Nerve endings  Cells: Mast cells and Histiocytes
  • 7. Benign Tumors  Seborrheic Keratosis  Melanocytic neavi  Dermatofibroma  Keratoacanthoma  Pilar cyst  Epidermal cyst  Skin tags  Syringoma  Others
  • 8. Seborrheic Keratosis  One of the most common benign tumors of the skin  Often confused with malignancies  Seborrheic keratoses unusual before age 30  Most people develop at least one seborrheic keratosis in their lifetime  Seborrheic keratoses are cosmetically bothersome, but may also be subject to irritation and traumatization,
  • 9. Seborrheic Keratosis
  • 10. Clinical Findings  Typically multiple  Most often seen on the trunk  The size and surface appearance of the lesions vary considerably  Most are 2 mm to 2.0 cm, although larger lesions are common  Lesions may be flat or raised  The surface may be smooth, velvety, or verrucous.
  • 11. Color and structure  The color of lesions is extremely variable,  Lesions tend to be sharply demarcated, oval, and often oriented along skin cleavage lines  Most have a “stuck-on” appearance and waxy texture. The surface tends to crumble when picked.  Raised or pedunculated seborrheic keratoses may be indistinguishable from skin tags and compound melanocytic nevi.
  • 12. Irritated seborrheic keratosis  When inflamed, SKs become slightly swollen and develop an irregular, red flare in the surrounding skin.  Itching and erythema can then appear spontaneously in other SKs that have not been manipulated and in areas without SKs.  With continued inflammation, the SK loses most of its normal characteristics and becomes a bright red, oozing mass with a friable surface that itches intensely and resembles an advanced melanoma or a pyogenic granuloma.
  • 13. Seborrheic keratosis vs. Melanoma  SKs can show many of the features of a malignant melanoma, including an irregular border and variable pigmentation.  The key differential diagnostic features are the surface characteristics.  Melanomas have a smooth surface that varies in elevation and in color, density, and shade.  SKs preserve a uniform appearance over their entire surface.  Many SKs occur in sun-exposed areas.
  • 14. Clinical variants Dermatosis papulosa nigra Stucco keratoses
  • 15. Treatment  Cryosurgery is effective for flat to minimally raised lesions  Thicker lesions are best removed by cautery and curettage under local anesthesia.  Hypopigmentation or hyperpigmentation are possible side effects  Residual scarring is minimal. Applying gentle pressure to the surrounding skin often provides enough tension to allow for easy curettage of lesions.
  • 16. Benign Tumors  Seborrheic Keratosis  Melanocytic neavi  Dermatofibroma  Keratoacanthoma  Pilar cyst  Epidermal cyst  Coetaneous tags  Syringoma
  • 17. Moles  Moles (melanocytic naevi) as they are due to a proliferation of melanocytes  Moles may be flat or protruding. They vary in colour from pink to dark brown or black.  The number of moles a person has depends on genetic factors and on sun exposure.  Melanocytic naevi may be present at birth (congenital) but more usually begin to grow during childhood although new ones can appear at any age, sometimes in crops
  • 18. Variants  Junctional naevi  compound naevi  Intradermal naevi  Cellular naevi.  Blue naevi  Moles may darken following sun exposure or during pregnancy.  During adulthood they often lose their pigmentation, and they may even disappear in old age.
  • 19. Risk of melanoma  Malignant melanoma sometimes develops within congenital melanocytic naevi.  The risk in a small or medium-sized mole is under 1%  Melanoma is more likely in the giant naevi (perhaps about 5% over a lifetime) especially in those that lie across the spine; the cancer can start in the skin or within the central nervous system. It is then very difficult to detect and treat.
  • 20. Removal of moles  Although most moles are harmless and can be safely left alone, moles may be treated under the following conditions:  Possible malignancy: a mole that has bled, has an unusual shape, is growing rapidly or changing colour.  Nuisance moles: a mole that is irritated by clothing, comb or razor.  Cosmetic reasons: the mole is unsightly.
  • 21. Removal  Shave biopsy  scalpel or by electrosurgery. The wound heals to leave a flat white mark, but sometimes the colour remains the same as the original mole.  Excision biopsy  if the mole is a flat one or melanoma is suspected
  • 22. Benign Tumors  Seborrheic Keratosis  Melanocytic neavi  Dermatofibroma  Keratoacanthoma  Pilar cyst  Epidermal cyst  Coetaneous tags  Syringoma
  • 23. Dermatofibroma  Dermatofibroma is a common, benign, dermal papule.  The etiology is unknown.  Pontaneous benign neoplastic process Vs. reactive hyperplasia in response to injury or bite  These lesions occur more often in women  Most are asymptomatic, but itching and tenderness may occur occasionally
  • 24. Clinical findings  Dermatofibromas discrete firm dermal papules, 3- 7 mm in diameter.  Most are dome shaped  Dermatofibromas typically flesh colored to pink with a poorly defined rim of tan to brown pigmentation  Larger ( >3cm) lesions can be worrisome and may require a biopsy for definitive diagnosis  Dermatofibromas should be stable in size, appearance, and color.  If they are not, they should be biopsied to confirm their benign nature.
  • 25. Dermatofibroma Palpation  The lesion is fixed within the skin, but movable over the underlying subcutaneous fat. On palpation, the lesion feels like a firm button. Pinching a dome-shaped dermatofibroma between two fingers causes the lesion to retract and dimple below the level of surrounding skin. Pigmented variant  Rarely, lesions may be blue to black in color as a result of hemosiderin deposition, which may resemble melanoma. The surface may be smooth and shiny to scaly or excoriated. Location/Region  Although dermatofibromas may arise on any cutaneous surface, most are found randomly distributed on the extremities. Lesions are usually solitary, however, multiple lesions are not uncommon. Rarely, dermatofibromas occur on the palms or the soles. Dermatofibromas should be stable in size, appearance, and color
  • 26. Treatment  Dermatofibromas are benign skin tumors that do not require treatment unless they are symptomatic, repeatedly traumatized, or cosmetically bothersome.  Surgical excision with primary closure is the treatment of choice for symptomatic lesions.  If incompletely excised, the patient should be warned of possible recurrence.
  • 27. Benign Tumors  Seborrheic Keratosis  Melanocytic neavi  Dermatofibroma  Pilar cyst  Keratoacanthoma  Epidermal cyst  Coetaneous tags  Syringoma  Others
  • 28. Pilar Cyst  A pilar cyst is a firm, subcutaneous, keratin-filled cyst originating from the outer root sheath of the hair follicle.  Roughly 90% of pilar cysts are found on the scalp, with the remaining 10% occurring on the face, neck, back, and scrotum.  The epithelium of the outer root sheath undergoes a different form of keratinization than cutaneous epithelium.
  • 29. Clinical findings  The surface is smooth and dome-shaped.  Pilar cysts may be difficult to distinguish from epidermal cysts clinically, except by location.  Both present as a firm, subcutaneous nodules ranging from 0.5 to 5.0 cm.  No central punctum is seen over a pilar cyst, as is found over an epidermal cyst.  When dissected, a pilar cyst possesses a tough, white-gray wall that is more resistant to tearing than the wall of an epidermal cyst.  The pilar cyst wall separates easily and cleanly from the surrounding dermis.  If a pilar cyst ruptures, the area becomes inflamed, red, and tender and boggy on palpation.
  • 30. Clinical findings  Pilar cysts almost always develop after puberty.  The tendency to develop pilar cysts often has an autosomal dominant inheritance.  Pilar cysts are multiple in 70% of patients who have them.  Pilar cysts persist indefinitely and slowly grow to a stable size unless they rupture.  Pilar cysts rupture less frequently than epidermal cysts, presumably because the pilar cyst possesses a thicker wall.  Rupture usually results from an external trauma.  A brisk foreign body inflammatory reaction follows and can be quite painful and resembles a furuncle.
  • 31. Clinical findings pilar cyst  Large cysts may be cosmetically objectionable.  Some cysts are so large and tender, they may interfere with wearing hats and helmets.  Acute inflammation after rupture is often misdiagnosed as infection.  Antibiotics are of little value in such cases.  Incision and drainage under local anesthesia improve comfort and limit scarring.  Elective excision before rupture prevents
  • 32. Treatment  Pilar cysts are easily removed with excision under local anesthesia.  An incision is made over the cyst, exposing the cyst’s glossy white external surface.  The cyst wall is freed easily from the surrounding connective tissue by blunt dissection.  At this stage, smaller cysts may be expressed intact up through the incision by steady, firm pressure on each side of the incision.  The incised cyst wall is clamped, and through a combination of gentle traction and pressure on each side of the incision, the now smaller, partially emptied cyst is delivered through the incision.  Larger cysts, which cannot be expressed in this manner, should be incised and their contents removed by curettage.  Sutures may be needed to close the incision site.
  • 33. Benign Tumors  Seborrheic Keratosis  Melanocytic neavi  Dermatofibroma  Pilar cyst  Keratoacanthoma  Epidermal cyst  Cutaneous tags  Syringoma  Others
  • 34. Keratoacanthoma Description  Keratoacanthoma is a rapidly growing crateriform nodule with a distinctive clinical appearance that is best regarded as a low-grade squamous cell carcinoma. The peak incidence of keratoacanthoma is between ages 50 and 70. This tumor is rare before 40 years of age. Caucasians with fair complexions are most often affected. Epidemiology  Chemical exposure and human papillomavirus have been implicated as a cause in animal models, although their role in humans is controversial. Historically, keratoacanthomas have been regarded as benign regressing lesions, however, they should be thought of as variants of squamous cell carcinoma and treated as s
  • 35. Clinical findings common features  A keratoacanthoma is a characteristic solitary flesh-colored to red, crateriform nodule, usually 0.5 to 2.0 cm in diameter.  The lesion erupts rapidly and is often quite tender.  A central keratotic plug or depression conceals a deep keratinous cavity.  This plug or depression gives the nodule its characteristic volcano-like shape.  The nodule is firm in texture, tender to palpation and pressure.  Keratoacanthoma nearly always appears on sun- damaged skin.  Typical locations include the face, neck, dorsal hands and sun exposed extremities.  It occurs on the legs more often in women.
  • 36. Keratoacanthoma Clinical findings :
  • 37. Growth phases ka  Three growth phases are described:  1. Proliferative phase: a solitary papule appears suddenly and then rapidly grows to its maximum size over 2 to 4 weeks.  2. Mature phase: the lesion is stable in size and appearance for weeks to months; it may appear crateriform if the core has been partially removed.  3. Resolving phase: the base becomes indurated, the central core is expelled, and the base resorbs, leaving a pitted scar. This phase may last several months.
  • 38. Treatment Topical 5-FU Mechanical debridement Cryotherapy Curettege & Electrodesiccation Dermabrasion Surgical excision
  • 39. Ka Treatment  It is best to presume a diagnosis of squamous cell carcinoma pending biopsy results and clinical follow-up.  An excisional biopsy or shave removal should be performed.  It is important to biopsy deep enough to evaluate the dermis for possible invasion.  Treatment options include complete excision with margins and electrodesiccation and curettage.  Any of these options are curative in the vast majority of cases.
  • 40. Benign Tumors  Seborrheic Keratosis  Melanocytic neavi  Dermatofibroma  Keratoacanthoma  Pilar cyst  Epidermal cyst  Skin tags  Syringoma  Others
  • 41. Epidermal Cyst  Description  An epidermal cyst is a firm, subcutaneous, keratin-filled cyst originating from true epidermis, most often from the hair follicle infundibulum.  Epidermal cysts are common, usually solitary, and arise spontaneously.  They occur most commonly on the trunk, postauricular fold and on the posterior neck.
  • 42. Potential to rupture  Cysts frequently develop in areas of friction.  Most epidermal cysts arise from the squamous epithelium of the hair follicle.  Unlike pilar cysts, the epidermal cyst wall is fairly delicate and thus prone to rupture.  Rupture is followed by foreign body reaction to keratin extruded into the dermis and acute inflammation.  Such lesions appear to be infected. However, cultures are usually sterile.
  • 43. Typical findings/characteristic findings  Epidermal cysts are firm, dome-shaped, pale yellow, cystic nodules ranging in size from 0.5 to 5.0 cm in size.  Cysts are somewhat mobile but are tethered to the overlying skin through a small punctum that often appears as a comedo.  This punctum represents the follicle from which the cyst developed.  These cysts may be flat or flush to the surface of the skin or elevated well above the surface. In either case, they are easily palpable.
  • 44. Excision  Epidermal cysts that have not previously ruptured can be excised easily and completely under local anesthesia. Epidermal cysts on the face may rupture and lead to scarring.  Cosmetic considerations of elective surgical excision must be weighed against scar formation resulting from rupture.  Such lesions are far more difficult to remove once they have ruptured.  Recurrent epidermal cysts that have previously ruptured and scarred are best excised along with the surrounding scar once the inflammation has subsided.  Asymptomatic epidermal cysts occurring elsewhere do not require treatment.
  • 45. Benign Tumors  Seborrheic Keratosis  Melanocytic neavi  Dermatofibroma  Keratoacanthoma  Pilar cyst  Epidermal cyst  Skin tags  Syringoma  Others
  • 46. Skin Tags  Description  Skin tags or achrocordons, are common, benign, fleshy papules occurring in the skin folds.  They are uncommon before age 30 and common thereafter.  Skin tags are more common in overweight persons. Roughly 25% of adults have at least one skin tag.  The majority of patients with skin tags have only a few such lesions.  There may be a familial tendency toward multiple skin tags.  Undisturbed lesions are usually asymptomatic.  Skin tags may become irritated by friction, jewelry or clothing.  They may become tender and may bleed, when traumatized, twisted, torn, or thrombosed.
  • 47. Clinical findings  Skin tags are skin-colored or slightly pigmented, 1 to 5 mm pedunculated papules.  They are typically not difficult to diagnose.  They may be flat or filiform, although most are soft, fleshy, and pedunculated on a thin stalk.  The axillae are the most common location to find skin tags.  Skin tags also occur on the neck, eyelids, as well as in other intertriginous areas such as the inframammary and inguinal creases.  The overwhelming majority of skin tags are benign and have no internal disease association.
  • 48. Treatment  Asymptomatic skin tags do not require treatment.  Patients often request removal for bleeding, tenderness or for cosmetic reasons.  Skin tags are best treated by scissor excision with or without local anesthesia.  Electrocautery and cryosurgery can also be used.  Many dermatologists feel that histologic confirmation is usually not necessary, but submission of all skin tags for histologic review is a topic of debate
  • 49. Benign Tumors  Seborrheic Keratosis  Melanocytic neavi  Dermatofibroma  Keratoacanthoma  Pilar cyst  Epidermal cyst  Skin tags  Syringoma  Others
  • 50. Syringoma Description  Syringomas are the most common tumor of the intraepidermal eccrine sweat glands.  These appendage tumors develop after puberty and increase in number throughout young adulthood.  Lesions are asymptomatic, stable in size and appearance, and persistent.  The autosomal dominant inheritance of multiple syringomas is well established.  Syringomas occur with increased frequency in individuals with Down syndrome or trisomy 21.
  • 51. Clinical Findings  Syringomas are small, skin-colored to yellow, 1- to 2-mm papules.  They are most commonly found on the lower eyelids.  They also occur on the malar cheeks, axillae, upper chest, abdomen, umbilicus, and vulva.  Papules are usually symmetrically distributed and asymptomatic.  Syringomas persist indefinitely and remain small.  They have no potential for malignancy.  They may resemble flat warts or sebaceous hyperplasia.  Facial lesions are of cosmetic concern, and most patients request removal of larger lesions.  The patient may be concerned that the lesions are cancerous.  Women seeking evaluation of vulvar lesions may
  • 52. Treatment  Syringomas may be removed for cosmetic purposes.  Electrodesiccation and curettage, laser surgery, and trichloroacetic acid may be used with variable success.  Sharp dissection or scissor excision of lesions is easily performed under local anesthesia.  All of these procedures can lead to scarring, so care and precision are warranted.  In some patients, syringomas are too numerous to remove all lesions completely.
  • 53. Benign Tumors  Seborrheic Keratosis  Melanocytic neavi  Dermatofibroma  Keratoacanthoma  Pilar cyst  Epidermal cyst  Coetaneous tags  Syringoma  Others
  • 54. Pyogenic granuloma  Pyogenic granulomas are a benign overgrowth of blood vessels. They present as rapidly growing pinkish red nodules which are friable and readily bleed. They may follow trauma and are often found on the fingers and lips. They are best excised to exclude an amelanotic malignant melanoma.
  • 55. Cherry angioma  Campbell de Morgan spots  These are benign angiokeratomas that appear as tiny pinpoint red papules, especially on the trunk, and increase with age. No treatment is required.
  • 56. Swellings arising from the skin Benign Tumors  Benign Papillomata  Sebaceous cyst  Strawberry nevus  Histiocytoma
  • 57. Premalignant Lesion Leukoplakia Actinic Keratosis Radiation Keratosis Tar Keratosis Arsenical Keratosis Bowens disease  Erythroplakia of Queyrat Pagets disease
  • 58. Leucoplakia  Etiology : Smoking, Syphilis, Sepsis, Sharp edge of the tooth, Spirits, Spices --- the 6 S  Incidence: Occurs in 40 – 70 yrs of age with male dominance
  • 59. Histopathology  Gross feature: White hyperkeratotic patch in the mucosa  Histology : hyperkeratosis over a thickened acanthotic but orderly mucosal epithelium.
  • 60. Leukoplakia  White plaques  Etiology * age = 40-70 yrs * sex = males * habits = tobacco ,alcohol ,use of chronic irritants * inf. = HPV-16 * others = ill fitting dentures
  • 61.  Clinical findings :
  • 62. Actinic or solar keratosis  Etiology : Sun exposure (U.V) and hydrocarbons contact  Incidence : in persons past middle life  Prognosis : SCC may develop
  • 63. Actinic Keratosis Etiology • Synonyms - solar keratosis, senile keratosis • Age = >40 • Sex = male • Occupation = outdoor works • Race = fair skinned, blue eyes • Genetics = xeroderma pigmentosum
  • 64. Histopathology  Gross feature: White hyperkeratotic patch in the mucosa  Histology : hyperkeratosis over a thickened acanthotic but orderly mucosal epithelium.
  • 65. Histopathology  Gross feature: Lesions are less than 1 cm in diameter; are tan brown, red or skin colored; and have a rough, sandpaper like consistency.  Multiple lesions on the face and the backs of hands  Histology : Building up of excess keratin, cytological atypia and associated basal cell hyperplasia
  • 66.  Clinical findings:
  • 67. Prevention  recreational exposure  Sunscreen & protective clothing
  • 68. Radio dermatitis  Early: erythema, which goes onto desquamation and pigmentation  Late: atrophy, irregular hyperpigmentation and telangectasis and hair loss.  SCC may eventually develop
  • 69. Radiation Keratosis Etiology : Exposure to ionizing radiation
  • 70. Clinical findings
  • 71. Arsenical Keratosis  Clinical findings:
  • 72. Tar Keratosis Synonym : Tar wart Etiology : exposure to polycyclic aromatic hydrocarbons
  • 73. Clinical findings :
  • 74. Bowen Disease  A.k.a. carcinoma in situ and squamous intraepidermoid neoplasia.  Etiology : Involve predominantly skin unexposed to the sun (i.e., protected). Role of HPV 16.  Incidence : Involves the genital region of both men and women above the age of 35  Prognosis : May transform into SCC
  • 75. Histopathology  Gross feature : Solitary, thickened, gray- white, opaque plaque with shallow ulceration and crusting  Histology : the epidermis shows proliferation with numerous mitoses, some atypical.
  • 76. Bowen’s disease Clinical findings:
  • 77. Erythroplasia of Queyrat  Etiology : Role of HPV 16  Incidence : Men, usually above age of 25yrs  Prognosis : Has a potential to develop into invasive carcinoma
  • 78. Histopathology  Gross feature : Appears on the glans penis and prepuce as single or multiple shiny red, velvety plaques.  It may at times produce a discharge and become painful.
  • 79. Erythroplasia of Queyrat  Bowen’s disease of the penis  Clinical features :
  • 80. Management  Excision biopsy  Curettage  Electrodessicatio n  Cryotherapy  Protection  5 fluorouracil cream  Dermabrasion  CO2 laser vaporization.  Photodynamic therapy (for Bowen Disease)
  • 81. Cutaneous Horn Synonym – cornu cutaneum Clinical finding :
  • 82. Paget’s Disease Clinical findings:
  • 83. Carcinomas  Basal cell carcinoma  SCC  Malignant melanoma (nodular)
  • 84. BASAL CELL CARCINOMA BCC  Definition and etiology:  Basal cell carcinoma is a malignant neoplasm arising from the basal cells of the epidermis  Most basal cell carcinomas are caused by sunlight-induced damage to the skin.
  • 85. BCC
  • 86. Clinical features:BCC  Basal cell carcinoma is the most frequent malignancy in the United States,  with more than 750,000 new cases reported annually. Although basal cell carcinoma almost never metastasizes, its malignant nature is emphasized by the local destruction that it can cause. As with other sun-induced neoplasms of the skin, fair-complected  individuals and those with a lot of sunlight exposure are most likely to develop basal cell carcinoma.
  • 87. Clinical features BCC  Clinically, there are four major types of basal cell carcinomas: nodular,  superficial, morpheaform, and pigmented.  Rarer types include cystic and keratotic carcinoma and fibroepithelioma of Pinkus.  They are, of course, found most commonly on sun-exposed skin.  Nodular basal cell carcinomas, the most common type, appears  as a pearly semitranslucent papule or nodule that has a depressed center,  telangiectasia, and rolled waxy border. Crusting and ulceration frequently occur.  The most common location is on the face, particularly the nose. Superficial basal cell carcinomas look quite different.  They are red, slightly scaling, slightly crusted, well-demarcated  eczematous-appearing patches that most commonly occur on the trunk.  Infiltrative or morpheaform basal cell carcinoma appears as an atrophic, whitish, scarlike eroded or crusted plaque.  Pigmented basal cell carcinoma is a shiny brown, blue, or black papule or nodule.
  • 88. DD BCC The differential diagnosis  of basal cell carcinoma depends on the type.  For nodular basal cell carcinoma, the differential diagnosis includes ;  Sebaceous hyperplasia, fibrous papule of the nose, nonpigmented nevus, and squamous cell  carcinoma. Dermatitis, psoriasis, and Bowen’s disease (squamous cell carcinoma in  situ) appear similar to superficial basal cell
  • 89. DD BCC  Seborrhoeic keratosis,pigmented nevus, and, most important, malignant melanoma must be ruled out in the case of pigmented basal cell carcinoma.  For crusted nonhealing scarlike lesions, the differential diagnosis is mainly between basal cell and squamous cell carcinoma.  A skin biopsy, either shave, punch, or excision, should be accomplished to confirm the diagnosis of basal cell carcinoma.  The tumor is composed of a thickened epidermis with invasive buds and lobules of basaloid cells.
  • 90. BCC Treatment:  Curettage and electrodesiccation of the lesion or excision are the most common surgical modalities used to treat basal cell carcinoma.  Because of the locally destructive nature and potential for recurrence of the disease, treatment should be done by an experienced clinician who can individualize the therapeutic modality  based on location of the lesion, histopathologic type, size of the basal cell carcinoma, and its primary or recurrent status.  Less commonly used treatments are radiation therapy, cryosurgery, and topical chemotherapy.  A specialized surgical technique, Mohs’ surgery, is indicated for recurrent basal cell carcinoma and for primary tumors with a high risk of recurrence.
  • 91. Basal cell carcinoma  Synonyms: basal cell epithelioma, basalioma,rodent ulcer  A malignancy arising from the epidermal basal cells.
  • 92. Etiology and Pathogenesis  Genetics: chromosome 9q22.3 (PTCH)  Sunlight  Ionizing radiation: 10 Gy  Carcinogens: tar, oils and arsenic  Chronic skin damage: scars of trauma and vaccination  Other factors : immunosuppression
  • 93. Epidemiology  Incidence 40- 80/10000. U.S 500,000/ year  Age =>60 years  Gender = > men  Race= less in dark skinned  Occupation= outdoor exposure  Geography = high altitudes,equator
  • 94. Clinical findings  Majority in the face  Line connecting the corners of the mouth to the bottom of the ears  Lower part of the face, scalp and upper part of the trunk
  • 95. Initial basal cell carcinoma  Tiny ,indurated pearly area  crusted or scabbed area  Rolled edge  Cheek and nose
  • 96. Nodular basal cell carcinoma  Nodular  Pearly or waxy border  Prominent telangiectases  Central dell or ulceration D.D: intradermal melanocytic nevus, squamous cell carcinoma, giant
  • 97. Ulcerated basal cell carcinoma  Synonyms:Ulcus rodens,rodent ulcer  Large ,destructive  Ragged border  Nasolabial fold,medial canthus and about the ear  Crusts and granulation tissues D.D: factitial ulcers
  • 98. Pigemented basal cell carcinoma  Blacks,Hispanics, Native Americans, Orientals  Papular or nodular  Slate-blue to black D.D:melanocytic nevus, blue nevus, malignant melanoma, vascular lesions(angiokerato
  • 99. Cicatricial basal cell carcinoma  Synonym; morpheaform basal cell carcinoma  Yellow and white waxy plaques  Ill defined edge  Enlarging scar  Nose, forehead  Mimic keloid  Clinically aggressive
  • 100. Cystic basal cell carcinoma  Soft translucent papule  Marked telangiectasia  eyes D.D hidrocystoma, adnexal tumors
  • 101. Superficial basal cell carcinoma  Synonyms: multicentric, pagetoid, eczematoid  Superficial,multiple  Pink or brown scaly plaque  Whip cord edge  >10cm  Tumor buds
  • 102. Fibroepithelioma,Metatypical, BCC in scars  Fibroepithelioma= soft pink flesh coloured or pale coloured nodules on the trunk  Metatypical= cannot differentiate b/w BCC and SCC under the microscope  BCC in scars= ulcer not a telangiectatic nodule. Recurrent BCC and a scar
  • 103. Metastatic BCC  0.0028 to 0.1%  Metatypical BCC  Large ulcerated basal cell carcinomas in the mid face  Elderly  immunocompromised
  • 104. histopathology
  • 105. Histopathology
  • 106. Therapy  size  Location  Subtype
  • 107.  Excision  Micrographic surgery  Cyrotherapy  Curettage and electrodesiccation  Radiation therapy
  • 108. Course and prognosis  Slow relentless growth destroys tissue locally  Untreated invades bone, cartilage  Usually 95% cure rate
  • 109. SQUAMOUS CELL CARCINOMA  Definition and etiology:  Squamous cell carcinoma is a malignant neoplasm of keratinocytes that is locally  invasive and has the potential to metastasize.  Ultraviolet radiation, x-rays, papillomavirus infection, and chemical carcinogens such as soot and arsenic cause squamous cell carcinoma.
  • 110. Clinical features SCC  Squamous cell carcinoma is the second most common skin cancer in the United States, with more than 100,000 new cases diagnosed annually.  As with other sunlight-induced skin cancers, the frequency of squamous cell carcinoma is increased in those who are fair complected or engage in many outdoor activities.  The history of a bleeding growth or ulcer should arouse suspicion of squamous cell carcinoma.  Squamous cell carcinoma most often arises in sun-damaged skin.  It also develops on the mucous membranes and in areas of chronic injury such as burn scars, chronic radiodermatitic lesions, chronic draining sinuses, and areas of erosive discoid lupus erythematosus.
  • 111. SCC  The examination reveals a hard papule or nodule that is erythematous to flesh- colored, smooth, scaling, and crusted.  Squamous cell carcinoma in situ(Bowen’s disease) has a different appearance, being a well-demarcated, slightly scaling, slightly crusted, eczematous-appearing patch.
  • 112. DD SCC  The differential diagnosis of squamous cell carcinoma includes  keratoacanthoma, hypertrophic actinic keratosis, wart, basal cell carcinoma, and seborrheic keratosis. Any lesion that is crusted or ulcerated should be suspected of being squamous cell carcinoma, and biopsy must be done.  This reveals a hyperkeratotic thickened epidermis containing atypical keratinocytes that invade the dermis.
  • 113. Treatment SCC Squamous cell carcinoma should be totally excised.  Follow-up to monitor for local recurrence as well as metastases is required.  The squamous cell carcinomas most likely to metastasize are those that are large or histologically poorly differentiated, have deep invasion, or occur in damaged skin or the mucous membranes of the lips, glans penis, and vulva.  Metastasis is generally to the regional lymph nodes, and careful attention should be given to examining them for lymphadenopathy.
  • 114. Squamous cell carcinoma  Primary cutaneous SCC is a malignant neoplasm of keratinising epidermal cells
  • 115. Epidemiology  30-60/100000  Basal: squamous =5:1 to 10:1  Age=>40 years  Sex= men  Occupation= outdoor workers  Genetics = xeroderma pigmentosum  Geography= equator or high altitudes
  • 116. Etiology and pathogenesis  Irradiation: UV,PUVA,Heat  Chronic degenerative and inflammatory process  Chemical carcinogenesis:petroleum, tobacco  Oncogenic Viruses: HPV  Genetic disorders: xeroderma pigmentosum, Ferguson-Smith  Immunosuppression  Personal habits: alcohol and tobacco
  • 117. Clinical findings  indistinct clinical picture  Hard exophytic,inflamed nodule  vermiottes  Ulcerated and necrotic  more destructive  Metastases Unfavourable signs: rapid growth,induration, bleeding
  • 118. Histopathology
  • 119. Histopathology
  • 120. Differential Dx:  Adnexal tumors  Amelanotic malignant melanoma  Seborrheic keratosis  Nodular,indurated, ulcerated lesion
  • 121. Course  Sun exposed and actinic keratoses =less metastases  >2cm  >4mm depth  Poorly differentiated  immunosuppresed }}More likely toMore likely to metastasizemetastasize
  • 122. Prognosis  Location  Size  Thickness  Degree of differentiation  5 year survival <20-25% if regional nodes are involved
  • 123. Therapy  Excision  Cyrotherapy  Curettage and electrodesiccation  Radiation Therapy  Sentinal lymph node dissection
  • 124. Marjolin’s ulcer  A squamous cell carcinoma which develops in a chronic scar such as along standing ulcer or osteomyelitis sinus.  Slow growth – relatively avascular  Painless  Absence of secondary deposits in regional lymph nodes
  • 125. Extent of the tumor Prognosis Management Malignant Melanoma
  • 126. Level I Clark Level V Level IV Level III Level II
  • 127. Breslow 0.75 mm 0.76-1.5 mm 1.51-3.0 mm >3.0 mm
  • 128. Skin grafts STSG epidermis + part of dermis FTSG whole thickness of the skin excised
  • 129. SGT