1. Basal Cell Carcinoma

2.  Basal cell carcinoma (BCC) is a nonmelanocytic skin cancer (ie, an epithelial tumor) that arises from basal cells (ie, small, round cells found in the lower layer of the epidermis).  The prognosis for patients with BCC is excellent.  Waxy papules with central depression  Pearly appearance  Erosion or ulceration: Often central and pigmented  Bleeding: Especially when traumatized  Oozing or crusted areas: In large BCCs  Rolled (raised) border  Translucency  Telangiectases over the surface  Slow growing: 0.5 cm in 1-2 years  Black-blue or brown areas

4.  Nodular: Cystic, pigmented, keratotic; the most common type of BCC; usually presents as a round, pearly, flesh-colored papule with telangiectases.  Morpheaform: Appears as a white or yellow, waxy, sclerotic plaque that rarely ulcerates; is flat or slightly depressed, fibrotic, and firm.  Superficial: Seen mostly on the upper trunk or shoulders; appears clinically as an erythematous, well-circumscribed patch or plaque, often with a whitish scale.

17. Cutaneous Melanoma

18.  Melanoma is a malignancy of pigment-producing cells (melanocytes) located predominantly in the skin, but also found in the eyes, ears, GI tract, leptomeninges, and oral and genital mucous membranes.  Melanoma accounts for only 4% of all skin cancers.  A new or changing mole or blemish is the most common warning sign for melanoma.  Majority of cutaneous melanoma arises de novo (ie, on normal appearing skin and not in association with a precursor nevus.

19. ABCD Asymmetry. Irregular border. Irregular colour. Diameter over 1 cm.

20. Glasgow seven-point chek-list  Major features:  Change in size  Change in shape  Change in colour.  Minor features:  Diameter more than 5 mm  Inflammation  Oozing or bleeding.  Mild itch or altered sensation.  One major feature considered for removal.  Presence of additional minor features cilinical suspicion.

23.  Melanoma occurs most commonly on the trunk in white males and the lower legs and back in white females.  In African American, Hispanic, and Asian persons, the most common site is the plantar foot, followed by subungual, palmar, and mucosal sites.  Four major clinicopathologic (or histogenetic) subtypes of primary cutaneous melanoma have been identified. These include superficial spreading melanoma, nodular melanoma, lentigo maligna melanoma, and acral lentiginous melanoma.  Superficial spreading melanoma characteristics are as follows:  It accounts for nearly 70% of cutaneous melanoma and is the most common subtype in individuals aged 30-50 years.It is most common on the trunk in men and women and on the legs in women.

25.  Nodular melanoma characteristics are as follows:  This subtype occurs in 15-30% of patients.  It is seen most commonly on the legs and trunk in men and women.  Lentigo maligna :  It is typically located on the head, neck, and arms (chronically sun-damaged skin) of fair-skinned older individuals (average age 65 y).

29. Acral lentiginous melanoma : It is the most common subtype of melanoma in dark-skinned individuals.

33. ACTINIC KERATOSES

34.  Actinic keratoses (AKs) are cutaneous neoplasms consisting of proliferations of cytologically aberrant, epidermal keratinocytes that develop in response to prolonged exposure to ultraviolet radiation.  Actinic keratoses are clinically important lesions, not only because of their potential to develop into SCC, but because they are one of the strongest predictors that an individual may subsequently develop SCC or basal cell carcinoma (BCC) of the skin.  After acne vulgaris and dermatitis, AKs are the third most common reason for patients to see a dermatologist.

36.  Various risk factors have been identified for the expression of AKs, with the two major groups being individual susceptibility and cumulative ultraviolet radiation exposure.  One of the most important susceptibility risk factors is age, as all the epidemiologic studies indicate that AKs increase in prevalence with increasing age.  Other individual susceptibility risk factors include a phenotype of fair skin that easily burns and freckles.  Immunosuppression, as it is well known that organ transplant recipients are at increased risk of developing AKs and SCCs.  Genetic syndromes are at greater risk of developing AKs, namely albinism and xeroderma pigmentosum.  Cumulative exposure to ultraviolet radiation, including tanning beds, is the other major risk factor for developing AKs.

37.  Age at which a person received the greatest amount and intensity of exposure to ultraviolet radiation appears to be a risk factor, with such exposure in childhood apparently posing the greatest risk.  Ultraviolet radiation is responsible for the development of AK, and eventually SCC, in two ways: first, it causes mutations in cellular DNA that, when unrepaired, lead to unrestrained growth and tumor formation, and, second, it acts as an immunosuppressant to prevent tumor rejection.  Ultraviolet radiation–induced mutations in the tumor-suppressor gene p53 play a pivotal role in the initiation of AKs.

38.  Prevention  Limiting the amount and intensity of sun exposure, especially in childhood and adolescence, should prove effective in decreasing their prevalence.  Sunscreens.  There is some evidence that adhering to a diet low in fat may decrease the incidence of Aks.  Oral retinoids are effective in preventing NMSC and AKs, especially in high- risk patients such as organ transplant recipients and patients with xeroderma pigmentosum, but they are only effective as long as the patient is taking the medication.  Topical tretinoin has been advocated as prophylaxis of both AKs and NMSC in renal transplant recipients

39. Clinical Manifestations  The typical person who presents with AKs is an elderly, fair-skinned, light-eyed individual who has a history of significant sun exposure, who burned and freckled rather than tanned, and who has significant solar elastosis on examination.  AKs (80 percent) are typically found on chronically sun-exposed sites of the body, such as the head, neck, forearms, and dorsal hands.  Head, neck, forearms, and dorsal hands.  The typical AK lesion, sometimes called the erythematous AK, presents most commonly as a 2- to 6- mm erythematous, flat, rough or scaly papule. It is usually easier felt than seen.  AKs can vary in size, and sometimes reach up to several centimeters in diameter. They are most often found amongst a background of solar elastosis, with dyspigmentation, yellow discoloration, ephelides, telangiectases, and sagging skin being prominent.  Hypertrophic AK (HAK) presents as a thicker, scaly, skin-colored, gray or erythematous, rough papule or plaque It can be found on any chronically sun-exposed site on the body, but has a propensity for the dorsal hands and arms.

44.  Cutaneous horn, also known as cornu cutaneum, refers to a reaction pattern and not a particular lesion.  AK, SCC, seborrheic keratosis, filiform verruca vulgaris, trichilemmoma, keratoacanthoma, or BCC. The most common underlying lesion in elderly, fair- skinned persons is a HAK.

46.  Actinic cheilitis represents confluent AKs on the lips, most often the lower lip.  Persons with this condition present with red, scaly, chapped lips, and at times erosions or fissures may be present.  The vermilion border of the lip is often indistinct, and focal hyperkeratosis and leukoplakia may also be seen.  persistent dryness and cracking of the lips, and the diagnosis of actinic cheilitis should always be suspected in elderly patients with such complaints.  Persistent ulcerations or indurated areas on the lip require biopsy to ensure that SCC is not present.

52.  The pigmented AK presents as a flat, tan to brown-colored, scaly papule. Clinically, it is difficult to distinguish from a solar lentigo.  Diagnosis and Differential Diagnosis  The diagnosis of AK is accurately made by clinical examination in most instances when the examiner is familiar and skilled in making such diagnoses.  seborrheic and irritated seborrheic keratoses, verruca vulgaris, Bowen's disease, SCC, keratoacanthoma, basal cell carcinoma, discoid lupus erythematosus, psoriasis, and other variants of cheilitis.  pigmented AKs are difficult to distinguish from solar lentigos, spreading pigmented AKs from lentigo maligna or a large seborrheic keratosis.  Distinguish an AK from a SCC, induration, larger size, ulceration, bleeding, rapid growth, and recurrence or persistence after treatment should make the diagnosis of SCC more suspect.

59.  Prognosis and Treatment  An AK can persist, regress, or undergo malignant transformation to invasive SCC. The range of risk for progression of AK to SCC in the literature varies from <1 percent up to 20 percent.  60 percent of SCCs arose from a previous AK, while others have found that in 100 percent of histopathologically confirmed SCCs, an AK was found at the periphery or within the confines of the existing SCC.  The presence of AKs on an individual serves as a marker for chronic sun damage and identifies a high-risk group of people who are at risk for developing SCC, BCC, and, to a lesser extent, melanoma.  The estimate of metastases arising from actinically derived SCC has ranged from 1 to 2 percent up to 6 percent. The risk of metastases is much higher in actinically derived SCC of the lip, perhaps up to 20 percent.

60.  The most common treatment method for AKs in the United States is cryosurgery, with liquid nitrogen (-195.8°C [-320.4°F]) being the most common cryogen.  Cure rates of up to 98.8 percent have been reported when employing liquid nitrogen cryosurgery for the treatment of AKs.  Curettage, with or without electrosurgery, is another commonly used treatment for AKs.  Potential side effects include infection, scarring, and dyspigmentation  Another frequently employed treatment for AKs is the use of the topical chemotherapy agent 5-fluorouracil (5-FU).  FDA-approved method consists of twice-daily application of 5-FU to the entire affected region, typically for 2 to 4 weeks. Spot treatment of specific lesions is not recommended. . Treatment should be continued until the treated area demonstrates erythema, erosion, crusting, and necrosis, according to the treatment guidelines.

61.  Physicians who prescribe topical 5-FU should spend time with the patient educating him or her about the proper application and the expected outcomes.  Patients should expect discomfort, pruritus, and burning at the sites of application, as well as erythema, erosion, crusting, and ulceration.  It is ideal for compliant patients who have numerous AKs in a given region of the body, such as the face or arms. It is not very effective for treating hypertrophic AKs.  Recurrence of AKs following treatment with 5-FU is commonly reported in the literature, with recurrence rates of 25 to 75 percent.  Less-common treatments for AKs include dermabrasion, chemical peels, cryopeels, laser therapy, and photodynamic therapy (PDT). being seen with follow-up periods extending beyond 12 months.

63.  Persistent erythema, activation of herpes simplex infection, scarring, dyspigmentation, and bacterial infection are potential side effects. It is ideal for patients with severe photodamage and multiple AKs, who frequently require repeated treatments of their AKs.  Medium-depth chemical peels with Jessner's solution and 35% trichloroacetic acid have reported efficacy rates of 75 percent at 1-month follow-up in one study, with equal efficacy to topical 5-FU therapy at 12-month and 32-month follow-ups.  Prolonged erythema and activation of herpes simplex infection are potential side effects, and scarring and infection are rare in the hands of skilled clinicians.  This treatment modality is ideal for patients with diffuse solar damage and numerous AKs, but it is not effective for treating hypertrophic Aks.

64.  Laser therapy for the treatment and prophylaxis of AKs is a recently explored option. The carbon dioxide (CO 2 ) laser in preliminary, small series studies has been reported to be effective in clearing multiple facial AKs, with no recurrence reported at 6 to 24 months in one study.  Dyspigmentation, scarring, and infection are also potential complications.  PDT of AKs is another treatment modality that is gaining popularity in the treatment of AKs. Topical PDT was approved by the FDA in 1999. With PDT, topical 5-aminolevulinic acid (5-ALA) is applied directly to targeted AKs on the skin.  Uncommon treatments for AKs include excision, interferon, topical immune response modifiers, oral and topical retinoids, α-hydroxy acids, and salicylic acid.  Topical immune response modifiers, such as imiquimod, were recently investigated as potential treatment options for AKs.

65. Leukoplakia

66.  Leukoplakia is a fixed, predominantly white lesion of the mucosa, which cannot be clinically or histopathologically characterized as any other disease.  Leukoplakia is most often seen on the oral and anogenital mucosal surfaces.  Some lesions are benign and others will transform into cancer.  Like erythroplakia, leukoplakia should be considered a clinical diagnosis until a definitive histopathologic diagnosis has been determined following biopsy.  Alcohol and tobacco use, in addition to chronic trauma and infection.

67.  Clinical Manifestations  Leukoplakia associated with carcinogenesis typically occurs in an older male, in the fifth to seventh decades of life.  A history of long-standing tobacco use and/or alcohol abuse is not uncommon.  Premalignant or malignant leukoplakia lesions are most likely to be found on the floor of the mouth, lateral and ventral tongue, and soft palate.  Lesions in these sites are much less likely to be caused by trauma or infection, and they carry a higher risk of premalignancy and malignancy.  In fact, it has been estimated that leukoplakic lesions in these anatomic sites have an approximate 40 percent risk of being malignant or premalignant.  As a general group, oral leukoplakias carry a 5 to 25 percent risk of harboring some form of dysplasia or malignancy.

68.  Clinically, leukoplakia presents as an asymptomatic, asymmetric white plaque. It cannot be easily rubbed off.  It may have overlying roughness or a granular surface or it may be soft and smooth.  Some lesions that also have concomitant areas of redness are termed erythroleukoplakia.  This latter lesion carries a more ominous prognosis, because the risk of premalignancy or malignancy being present in the erythematous portion of the lesion is much greater.

73.  Diagnosis and Differential Diagnosis  In general, leukoplakia should be biopsied to determine the true histopathologic diagnosis.  As mentioned earlier, leukoplakia on the floor of the mouth, lateral and ventral tongue, and soft palate carry a much greater risk of being malignant or premalignant and thus should be carefully evaluated, biopsied, and probably removed completely regardless of the histopathologic diagnosis.  Other conditions that may present with oral or mucosal white plaques include oral white sponge nevus, lichen planus, candidiasis, syphilis, lichen sclerosus, leukoedema, smoker's keratosis, Darier's disease, and cheek bitin.

78.  Prognosis and Treatment  The prognosis for reactive leukoplakias is quite good. For all leukoplakias the risk of progression to malignant SCC is approximately 4 percent, and even higher in the high-risk anatomic sites.  Patients should be followed closely, at regular intervals, and reevaluated should the leukoplakia persist or recur following adequate intervention.  Treatment depends on the site. Lesions at low-risk sites, such as the buccal mucosa, hard palate, and gingival mucosa can be followed closely if the histopathologic features are benign or reactive.  Lesions on high-risk sites, such as the floor of the mouth, lateral and ventral tongue, and soft palate should be removed completely.  Surgical excision or Mohs micrographic surgery are treatment options.  Topical 5-FU, laser ablation, and cryosurgery. Patients should also be advised to discontinue tobacco use and alcohol consumption.