Dermatology 5th year, 1st lecture (Dr. Mohammad Yousif)
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Dermatology 5th year, 1st lecture (Dr. Mohammad Yousif)

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The lecture has been given on Dec. 12th, 2010 by Dr. Mohammad Yousif.

The lecture has been given on Dec. 12th, 2010 by Dr. Mohammad Yousif.

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Dermatology 5th year, 1st lecture (Dr. Mohammad Yousif) Presentation Transcript

  • 1. Epidermal Tumors
  • 2. Tumors of the surface epidermis
    C) Carcinomas
    B) Precancerous (in situ)
    A) Benign
    Paget’s dis.
    20%
    • Seborrheickeratosis
    • 3. Keratoacanthoma
    • 4. Epidermal nevi
    • 5. Cutaneous cysts
    • 6. Warty dyskeratoma
    • 7. Clear cell acanthoma
    • 8. Solar keratosis
    Precancerous leukoplakia
    Oral florid papillomatosis
    • Bowen’s dis.
    • 9. Erythroplasia of Queyrat (Bowen’s dis. of glans penis)
    10%
    6-17%
    5-11%
    SCC
    30%
  • 10. Seborrheic keratosis
    One or more sharply defined, light brown to black, slightly raised lesions (as if stuck on surface) with soft velvety or finely verrucous surface. It occurs on trunk, face or extremities.
    Treatment
    1. Removal with a small sharp curette.
    2. Freezing.
    3. TCA.
    4. Cauterization.
  • 11.
  • 12.
  • 13.
  • 14. Seborrheic Keratosis (Cont’d)
    Keratoacanthoma (KA): rapidly growing, self healing, epidermal tumor that has a striking resemblance, both clinically & histologically to SCC.
    • Solitary KA: firm, skin-colored to pink, dome-shaped nodule with a horn filled crater in its center. It usually involutes spontaneously in less than 6 ms with slightly depressed scar.
  • Seborrheic Keratosis (Cont’d)
    • Multiple KAs:
    • 15. Multiple self-healing epitheliomas (Ferguson-Smith).
    • 16. Eruptive keratoacanthoma (Crzybowzki).
  • 17. Treatment of KA
    • Excision biopsy to exclude SCC.
    • 18. Curettage and cauterization of small lesions.
    • 19. 5-fluorouracil intralesionally.
    • 20. Radiotherapy.
    • 21. Multiple KAs: methotrexate or oral retinoids.
  • Epidermal nevi
    They are circumscribed hamartomatous lesions composed only of keratinocytes. They present usually at birth or shortly later.
    I) Localized type“Nevus Unius Lateris”
    II) Systematized type“Ichthyosis hystrix”
  • 22. Epidermal nevi
    • Epidermal nevus is a general term referring to birthmarks which originate from skin structures
    • 23. “Nevus verrucous” is keratinocytes
    • 24. “Nevus sebaceous” from sebaceous glands
    • 25. “Nevus comedomicus” from hair follicles
    • 26. “Nevus syringocystadenoma” from sweat glands
  • 27.
  • 28. Cutaneous cysts
    Epidermal cysts(the most common type)
    • Spontaneously.
    • 29. Traumatic implantation of epidermis into the dermis.
    • 30. The wall of the cyst is composed of true epidermis, i.e. squamous, granular & horn cells. The cyst is filled with horny material arranged in laminated layers.
  • 31.
  • 32. Milia
    • Primarymilia: arise spontaneously on face.
    • 33. Secondarymilia: arise
    • 34. In association with many dermatoses, e.g. BP, DEB, PCT, LSA.
    • 35. After trauma, e.g. dermabrasion.
  • Steatocystoma multiplex
    Sites
    • Sternal region, axillae and scrotal area.
  • 36.
  • 37. Actinic keratosis (AK) “Solar keratosis”
    • Most common premalignant skin lesion in elderly persons (≥40 yrs), fair complexion, with excessive sun exposure, > in men.
    • 38. Sun-exposed areas as face, dorsa of hands & bald portions of the scalp in men.
    • 39. Multiple erythematous, ill-defined macules or papules, often covered by adherent scales with little or no infiltration. Marked hyperkeratosis may be seen.
  • 40.
  • 41. Actinic keratosis (Cont’d)
    • SCC may develop in one or more of the lesions of AK in about 20% of the patients, usually after a long latent period, e.g. 10 years.
    • 42. SCC arising in AK or de-novo in sun-damaged skin very rarely metastasize (0.5%), but in actinic cheilitis, the incidence is 11%.
  • Actinic keratosis (Cont’d)
    Histopathology
    • SCC in situ.
    • 43. Morphologically,anaplastic cells are present. However, biologically, the lesions are still benign. Invasion into the dermis, if present at all, is limited to the most superficial portion.
  • Actinic keratosis (Cont’d)
    Treatment
    • Sun avoidance.
    • 44. Electrodessication & curettage.
    • 45. Cryosurgery with liquid nitrogen.
    • 46. Topical chemotherapy: 5-fluorouracil, 0.1-5% (5-FU) – Efudex cream®.
    • 47. Chemical peel with TCA 35%.
    • 48. Retinoids: oral or topical.
    Radiotherapy is contraindicated.
  • 49. Leukoplakia
    White patch or plaque on the mucosa that can’t be rubbed-off.
    Types:
    • Homogeneous leukoplakia: low malignant potential.
    • 50. Verrucousleukoplakia.
    • 51. Speckled leukoplakia: white nodules on an erythematous background. Increased risk of malignant change.
    • 52. Smokers keratosis.
    • 53. Oral hairy leukoplakia.
    All cases of leukoplakia should be examinedhistologically.
  • 54. Leukoplakia (Cont’d)
    Etiology
    • Chemical irritation, tobacco smoking.
    • 55. Mechanical irritation through dental stumps.
    • 56. HPV: HPV-11 & HPV-16.
    • 57. Candidal infection.
    • 58. Syphilis (usually on the dorsum of the tongue).
  • Leukoplakia (Cont’d)
    • The overall transformation rates of leukoplakia to SCC range from 6-17%.
    • 59. The site is important:leukoplakias on the buccal mucosa are usually benign, whereas leukoplakias of the floor of the mouth have higher transformation rates.
  • Leukoplakia (Cont’d)
    80%
    • Benign
    In situ anaplasia (precancerous leukoplakia)
    • 17%
    20%
    • 3%
    Infiltrating SCC
  • 60. Bowen’s disease
    • On exposed skin (predisposed by chronic exposure to sun).
    • 61. Unexposed skin (caused by the ingestion of arsenic).
    • 62. On lesions of EV (caused by HPV-5).
    • 63. On lesions of porokeratosis.
    • 64. No etiological factors.
    5
  • 65. Bowen’s disease (Cont’d)
    • Slowly enlarging erythematous patch of sharp but irregular outline, showing little or no infiltration.
    • 66. In 5-11% of cases of Bowen’s disease, SCC develops.
  • 67. Squamous cell carcinoma (SCC)
    • Malignant tumor of epidermal keratinocytes with an average metastatic rate of 2-3% of all patients.
  • Squamous cell carcinoma (SCC)
    Etiology
    I) Extrinsic factors:
    • Ultraviolet radiation: the major factor for the development of non-melanoma skin cancer (NMSC). PUVA therapy also increases the risk for development of SCC.
    • 68. Exposure to carcinogenic cpds, e.g. coal, arsenic, tobacco.
    • 69. Ionizing radiations from X-rays.
    • 70. HPVs, e.g. HPV-16 (cervical & penile SCCs), HPV-5 & -8 (oncogenic in EV) & HPV-6 & -11 (verrucous carcinoma of anogenital areas).
  • SCC – Etiology (Cont’d)
    II) Intrinsic factors (Cont’d)
    • Genodermatoses: e.g. xeroderma pig., albinism, porokeratosis & dysk. congenita have a high incidence of SCC & other cut. malignancies.
    • 71. Immunosuppression: 2ry to immunosuppressive drugs, HIV inf., lymphomas or organ transplants.
  • SCC (Cont’d)
    Clinically
    • Solitary, firm, slowly enlarging nodule with indurated base.
    • 72. Shallow ulcer with raised everted edge, indurated base.
    • 73. Verrucous or fungoid lesions.
    Histopathology
    • The more malignant the tumor, the greater is the number of atypical squamous cells & the less the number of differentiated cells (horn pearls).
  • SCC (Cont’d)
    Grading system
    • Grade 1 (less malignant): more than 75% of the cells are differentiated, i.e. several horn pearls with relatively slight atypicality.
    • 74. Grade 2, more than 50%.
    • 75. Grade 3, more than 25%.
    • 76. Grade 4, less than 25% are differentiated (more malignant).
    The degree of atypicality of the tumor cells & the depth of penetration are important factors in grading.
  • 77. Treatment
    • Local destruction:
    • 78. Curettage & electrodessication.
    • 79. Cryosurgery.
    • 80. CO2 laser ablation.
    • 81. Intralesional & topical 5-fluorouracil.
    • 82. Radiotherapy.
    • 83. Excisional: with a safety margin.
  • Paget’s disease of the breast
    • Exclusively in women.
    • 84. Age: 55 years.
    • 85. It occurs unilaterally on the areola & nipple as a sharply defined, slightly infiltrated area of erythema showing scaling, oozing & crusting. Ulceration or retraction of the nipple may be found.
    • 86. It is commonly associated with intraductal carcinoma of the breast.
  • Paget’s disease of the breast (Cont’d)
    Origin of Paget cells
    • The glandular origin was supported by immuno-histochemical studies, e.g. carcinoembryogenic antigen is found in Paget cells which is found also in normal apocrine & eccrine glands but not in keratinocytes or melanocytes.
    Treatment
    • Modified radical mastectomy.
  • 87. Extramammary Paget’s disease
    • Occurs commonly in the anogenital region, e.g. vulva, perianal area, scrotum or axillae, i.e. areas in which apocrine glands occur.
    • 88. In 20% of cases, it is 2ry to extension of an adenocarcinoma, either of the rectum to the perianal region, of the cervix to the vulva, or of the urinary bladder to the urethra & glans penis.
  • Extramammary Paget’s disease (Cont’d)
    Clinically
    • There is slowly enlarging, erythematous patch with oozing & crusting, with sharp but irregular border & in contrast to mammary type, itching is common.
    Treatment
    • Surgical excision.
  • Tumors of epidermal appendages
    Trichoepithelioma
    • Multiple:
    • 89. Autosomal dominant.
    • 90. Numerous, rounded, skin-colored, firm nodules located mainly in the nasolabial folds, forehead & upper lip.
    • 91. Solitary: non-hereditary.
  • 92. Tumors of epidermal appendages (Cont’d)
    Nevus sebaceous of Jadassohn (Organoid nevus)
    • At or soon after birth, solitary, linear or round yellow-brown, hairless, slightly elevated plaque usually located on the scalp or face.
    • 93. In puberty, verrucous or nodular.
    • 94. Later in life, some lesions may develop various types of appendage tumors, e.g. syringocystadenoma papilliferum, BCC.
    3
    Stages
  • 95. Three phases of N. sebaceus
    Tumor phase
    Adults usually
    Exact % unknown
    Probably <5%
    Infant phase
    Flat, smooth
    Decreased hair
    Pubertal phase
    Grows when oil glands expand – papular
    Orange peel surface
  • 96.
  • 97.
  • 98. Syringoma
    • An adenoma of intraepidermal eccrine ducts.
    • 99. More in females.
    • 100. In lower lids, cheeks, axillae, abdomen and vulva.
    • 101. Small, skin-colored or slightly yellow, soft papules.
    • 102. Eruptive hidradenoma or syringoma: the lesions arise in large numbers in successive crops on the anterior trunk of young persons.
  • 103.
  • 104. Basal cell carcinoma “BCC”
    • BCC is the most common malignancy in humans.
    • 105. Although rarely metastatic, it is capable of significant local destruction & disfigurement.
  • BCC (Cont’d)
    Predisposing factors
    • UV light.
    • 106. Chronic intake of inorganic arsenic.
    • 107. Predisposing skin conditions: dermatofibromas, nevus sebaceous of Jahadsson, burn scars.
    • 108. Predisposing syndromes: nevoid basal cell carcinoma syndrome, Basex syndrome, Rombo’s syndrome & xeroderma pigmentosum.
    • 109. Immunsuppression & X-ray irradiations.
    However, BCC may arise without apparent cause.
  • 110. BCC (Cont’d)
    Clinical features
    • It occurs almost exclusively on hair-bearing skin, especially on the face.
    Clinical types
    • Nodulo-ulcerative.
    • 111. Pigmented.
    • 112. Superficial.
    • 113. Morphea-like.
    • 114. Fibroepithelioma of Pinkus.
  • BCC (Cont’d)
    Histologically: 2 types of BCC are known
    • Undifferentiated (solid) BCC: composed of basaloid cells. The peripheral cell layer of tumor masses show a palisade arrangement of nuclei.
    • 115. Differentiated: either toward hair structure (keratotic BCC), toward glandular structures (adenoid BCC) or toward sebaceous structures.
  • BCC (Cont’d)
    Treatment
    • Excision: with safety margin ½ inch for small tumors.
    • 116. Radiotherapy.
    • 117. Curettage & electrosurgery.
    • 118. Cryosurgery.
    • 119. Mohs micrographic surgery (MMS).
    • 120. Cytotoxic agents: e.g. 5-fluorouracil topically.
    • 121. Intralesional injection of -2b interferon (IntronA®).
    • 122. Photodynamic therapy.