Benign: 1. Viral warts: some times misdiagnosed on the face & the hands of elderly & it is one of the few tumors in human without doubt caused by a virus 2. Seborrheic keratosis (basal cell papilloma, seborrheic wart): this is common benign epidermal tumor unrelated to sebaceous glands Causes: usually unexplained but: - multiple lesions may be inherited (autosomal dominant) - occasionally follow an inflammatory dermatosis - very rarely the sudden eruption of hundreds of itchy lesions is associated with an internal neoplasm (leser-Trelat sign)
Presentation: seborrheic K. usually arise after the age of 50 yrs, but flat in conspicuous lesions are Often visible earlier they are often multiple but may be single lesions are most common on the face & trunk the sexes are equally affected Physical signs: -a distinctive "stuck-on" appearance -may be flat, raised or pedunculated -color varies from yellow to dark brown -surface may have greasy scaling & scattered keratin plugs (current-bun appearance) Clinical course: Lesion may multiple with age but remain benign Differential diagnosis: 1. Pigmented cellular naevus 2. pigmented basal cell carcinoma 3. Most importantly malignant melanoma Investigation: -biopsy is needed rarely Treatment: -seborrheic K. can be left safely -ugly or easily traumatized ones can remove with a curette under local anesthesia, or by cryotherapy
Seb.keratosis
4. Skin tags (acrochordon): these common benign out growths of skin affect mainly the middle aged & elderly. Cause: -this is unknown but the trait is sometimes familial -skin tags are most common in obese woman -rarely associated with tuberous sclerosis acanthosis nigricans or acromegaly & diabetes Presentation & clinical course: skin tags occur around the neck & within the major flexures the look unsightly & may catch on clothing & jewellery They are soft skin-colored or pigmented pedunculated papules Differential diagnosis: tags are rarely confused with small melanocytic naevi Treatment: -small lesion can be snipped off with fine scissors -freezing with liquid nitrogen *there is no way of preventing new ones from developing 5. linear epidermal naevus: these lesions follow the lines of blaschko & are an example of cutaneous mosaicism 6. melanocytic naevi: the term naevus refers to a lesion often present at birth, which has a local excess of one or more normal constituents of the skin, melanocytic naevi (moles) are localized benign proliferation of melanocytes, there classification based on the site of aggregation of naevus cells, so the classification of melanocytic naevus -congenital melanocytic naeviLinear Epid N
Skin tag-aquired melanocytic naevi: -junctional naevus -compound naevus -intradermal neavus -spitz naevus -blue naevus -atypical melanocytic naevus Causes & evolution: -the cause is unknown -the genetic factor is likely in many families, working together with excessive sun exposure during childhood -with the exception of congenital melanocytic naevi most appear in early childhood often with sharp increase in numbers during adolescence -further crops may appear during pregnancy, estrogen therapy or rarely after cytotoxic chemotherapy & immunosuppression but new lesions come up less often after the age of 20 yrs -melanocytic naevi of childhood are usually of the junctional type, with proliferating melanocytes in clumps at the dermoepidermal junction, later the melanocytes round off & drop in to the dermis -a compound naevus has both dermal & junctional components, with maturation the junctional component disappears so that the melanocytes in an intradermal naevus are all in the dermis
Presentation: -Congenital melanocytic naevi: these are present at birth or appear in the neonatal period & are seldom less than 1cm in diameter, their color varies from brown to blue-black with maturity some become protuberant & hairy, with cerebriform surface, such lesions can be disfiguring (bathing trunk naevi) Such lesions carryon an increased risk of malignant transformation -junctional melanocytic naevi: these are roughly circular macules, their color ranges from mid to dark brown & may vary even within a single lesion, most naevi of the palms, soles & genitals are of this type -compound melanocytic naevi: these are domed pigmented nodule of up to 1cm in diameter they may be light to dark brown but their color is more even than that of junctional naevi most are smooth, but larger ones may be cerebriform -intradermal melanocytic naevi: these look like pigmented compound naevi but are less pigmented & often skin colored Differential diagnosis of melanocytic naevi: -malignant melanoma -seborrhoeic keratosis -lentigines -ephelides (frecklels)
Cong.melanocytic n.
Junctional M NCompound MN
Complication: -inflammation (pain & swelling) due to trauma, infection or F.B reaction after hair shaving -depigmented halo -malignant changes: this is extremely rare except in congenital melanocytic naevi, it should be considered if the following changes occur in the melanocytic naevus : 1. Itch 2. Enlargement 3. Increase or decrease pigmentation 4. Alterd shape 5. Alterd contour 6. Inflamation 7. Ulceration 8. Bleeding Treatment: -excision is needed when: 1.anaevus is unsightly 2.malignancy is suspected or is a known risk e.g. in a large congenital melanocytic naevus 3. anaevus is repeatedly inflamed or traumatizedPremalignant tumors: 1. Keratoacanthoma: rapidly growing tumor, very few transform into sequamous cell carcinoma Cause: photosensitizing chemicals such as tar & mineral oils can act as carcinogens with UV radiation; they may also follow therapeutic immunosuppersion Clinical features: they occur mainly in the exposed skin of fair individuals, mainly on the face & the rest on the arms start as pink papule rapidly enlarge it may reach a diameter of 1cm in month or two, after 5-6 weeks the center of the nodule forms either a keratinous plug or a crater, if left the lesion resolve spontaneously over 6-12 months but leaves an ugly depressed scar Differential diagnosis: sequamous cell carcinoma is the main DDX Treatment: excision or curettage & cautry are both effective 2. Intraepidermal carcinoma (Bowen's disease): is an intraepidermal SCC that probably arise from adenxal epithelium & invades the adjacent epidermis, it may ultimately become invasive. Clinical features: May found on any part of the body as an erythematous, slightly scaly & crusted, non infiltrated patch, from few millimeters to many centimeters in
keratoacanthoma
diameter, as the lesion enlarge spontaneous cicatrisation may develop in portions of the lesions, when intra epithelial growth becomes invasive the lesion may appear ulcerated & fungating. Etiology: -Bowen's disease affects mostly older white men in whom the lesions occur primarily on sun exposed surface -most patients with Bowen's disease have chronic sun damage -chronic arsenism produce BD in non exposed sites -high risk HPV types (HPV16-,-18,-31 &35) have been implicated in lesions involving periungual & genital regions Differential diagnosis: -psoriasis -discoid eczema -superficial basal cell carcinoma -Paget disease in the perianal region Treatment: -topical treatment (cryotherapy, topical 5-FU, imiquimod 5% cream) -simple excision of small lesions -Moh's microsurgery for large lesions 3. Actinic Keratoses (Solar Keratosess): these are discrete rough-surfaced lesions crop on sun damaged skin. They are premalignant, although only a few turn into a sequamous cell CaBowens disease
Cause: -the effects of sun exposure are cumulative -those with fair complexion living near the equator one most at risk & invariably develop these lesions. -melanin protects & actinic keratoses are not seen in black skin -albinos are especially prone to develop them Presentation: -they affect the middle aged & elderly in temperate climates, but younger people in tropics -the pink or rough gray scaling macules or papules seldom exceed 1cm in diameter Complication: -transition into a sequamous cell Ca should be suspected if lesions enlarge, ulcerate or bleed -a cutaneous horn is a hard kratotic protrusion based on an actinic keratoses, sequamous cell Ca or viral wart Differential diagnosis: -seborrhoeic keratoses -viral wart -keratoacanthoma -intraepidermal Ca -sequamous cell Ca Investigation: Biopsy is needed
Actinic keratosis
Treatment: Since some percentage of actinic keratoses may progress to SCC, so their treatment is indicated *Cryotherapy with liquid nitrogen is most effective & practical when there are a limited number of lesions *for extensive broad, or numerous lesions, topical chemotherapy is recommended, the two agents most commonly used: 5FU cream, 0.5-5% or Imiquimod 5% cream Malignant epidermal tumors: 1.Basal cell carcinoma (rodent ulcer): is the most common cancer it's crops up most commonly on the faces of middle aged or elderly lesions invade locally but never or rarely metastasize . Cause: -prolonged sun exposure is the main factor, so these tumors more common in white people living near the equator -intermediate intense sun exposure as identified by sun burns -they may also occur in scars caused by x-rays, vaccination or trauma -photosensitivity pitch, tar & oils can act as carcinogens with ultraviolet radiation-previous treatment with arsenic, once present in many "tonics" predispose to multiple BCC -multiple BCC are found in the naevoid BCC syndrome (Gorlin's syndrome) where they may be associated with palmoplanter pits, jaw cysts & abnormalities of the skull, vertebrae & ribs, the syndrome inherited as an autosomal dominant trait & genetic abnormality lies on chromosome 9q Presentation of BCC: 1. nodulo-ulcerative: this is the most common type an early lesion is a small glistening translucent skin colored papule that slowly enlarges, central necrosis although not always leaves an ulcer with an adherent crust & rolled pearly edge, fine telangiectatic vessels often run across the tumour's surface, without treatment such lesion may reach 1-2cm in diameter in 5-10 years, most common site face, but any part of the body may be involved. 2. Cystic BCC: these dom-shaped, blue-gray cystic nodules are clinically Similar to eccrine & apocrine hydrocystomas in the beginning very similar to nodular BCC but later cystic changes predominant & the nodule becomes tense & more translucent, with marked telangiectasia 3. cicatricial (morphoeic) BCC: this type of BCC present as white sclerotic-plaque, 95% of these BCC occur on the head & neck, ulceration, & rolled border & crusting are usually absent, telangiectasia may be present the lesion may look like an enlarging scar.
BCC
4. superficial (multicentric) BCC: these arise most often on the trunk, several lesions may be present, each expanding slowly as pink or brown scaly plaque with fine edges, such lesions can grow to more than 10cm in diameter, it may be misdiagnosed as psoriasis or eczema & have little tendency to ulcerate or invade, & may show atrophy or scaring occasionally, it is the most common pattern seen in patients with HIV infection & BCC 5. Pigmented BCC: this variety has all the features of nodular BCC in addition to brown or black pigmentation is present, this the most common type of BCC in dark complexioned persons such as Latin Americans, Hispanics, or Asians 6. Fibroepithelioma of pinkus: the tumor is usually an elevated skin colored, sessile lesion on the lower trunk, the lumbosacral area, groin or thigh & may be as large as 7cm the lesion is superficial & resemble fibroma or papilloma 7. Polypoid BCC: these tumors present as exophytic nodules of the head & neck Clinical course: -BCC run a chronic course as the lesion slowly enlarge & tend to become ulcerative, as a rule there is tendency for the lesions to bleed without pain or other symptoms
Pigmented BCC
Cystic BCC-UN treated but relentless growth destroys tissue locally & may invade underlying cartilage or bone-at least half of deaths that occur from BCC result from direct extension into a vital structures rather than metastasisEtiology:-it appears that BCC arise from immature pleuripotential cells associated with hair follicleDifferential diagnosis:Small BCC & small SCC is an intellectual exercise-nodular BCC may be confused with (intradermal melanocytic naevus, SCC, molloscum contagiosum –gaint one-, keratoacanthoma)-pigmented BCC should be distinguished from (seborrhoeic keratosis & malignant melanoma)-cicatricial BCC may mimic morphea, or scar -superficial BCC may be confused with intraepidermal Ca, with psoriasis or nummular eczema Treatment:-each lesion of BCC must be thoroughly evaluated individually-age, sex of the patient as well as the size, site & type of lesion are important factors to be considered
-a biopsy should be performed in all cases of suspected BCC -aim of treatment is permanent cure with the best cosmetic results, because the most common location of BCC is the face -treatment of BCC is usually surgical but some forms of BCC amenable to medical treatment -topical therapy: appears to be effective in treating superficial BCC -topical 5FU & imiquimod commonly used - Photodynamic therapy may be used -in general, excision with 0.5cm of surrounding normal skin is the treatment of choice of discrete nodular & cystic BCC -Moh's micrographic surgical technique is indicated in tumors >1cm tumors & for those on cosmetically important sites such as the nose Sequamous cell carcinoma-SCC-: is the 2nd most common form of skin cancer, most cases of SCC of the skin are induced by UVR (ultraviolet radiation)
Causes: -these tumors arise in skin damaged by long term UVR & also by X-rays & infrared rays -other carcinogens include pitch, tar, mineral oils & inorganic arsenic -certain rare genetic disorders with defective DNA repair mechanisms such as xeroderma pigmentosum lead to multiple SCC & BCC & to malignant melanoma -human papilloma viruses (HPV-16, -18, -31, & -35 primarily) play a role in SCCs that develop on the genitalia & periungually - A chronic ulcer, hideradenitis suppurativa, prior X ray-radiation exposure, PUVA treatment, recessive dystrophic epidermolysis bullosa, lesions of discoid lupus & erosive lichen planus are all risk factors for the development of SCC Clinical presentation & course: -tumors may arise as thickenings in actinic keratoses or denovo as small scaling nodules -rapidly growing a neaplastic lesion may start as ulcer with granulating base & an indurate edge - SCC is common on the lower lip & in the mouth -tumors arising in areas of previous x-radiation or thermal injury, chronic draining sinuses, chronic ulcers, chronic inflammation or Bowen's disease are most likely to metastasize
SCC
SCC
-tumors arising in non-exposed sites such as perineum & sole of foot & on the ear & lip have a lesser malignant potential but may metastasize -SCCs arising in sun-exposed areas & in the actinic keratoses seldom metastasize -tumors more than 2cm in diameter are twice as likely to recur & metastasize compared with smaller tumors -metastatic potential is greater in patient with tumor more than 4mm in depth or invading the subcutaneous tissue, in poorly differentiated tumors, in tumors with perineural involvement & in those arising in immunosuppressed Differential diagnosis: -keratoacanthoma -hyperkeratotic actinic keratoses Treatment:- after the Dx has been confirmed by biopsy, the tumor should be excised with a 0.5cm border of normal skin -Moh's micrographic surgery is useful for high risk tumors -radiotherapy is effective but should be reserved for the frail & the elderly