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76 Cards in this Set
- Front
- Back
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tender sunburn, no tan
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I
pure white |
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tender sunburn, light tan
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II
pure white |
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non-tender sunburn, dark tan
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III
white |
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no sunburn, dark tan
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IV, V, VI
beige, brown, black |
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used in tanning beds
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UVA
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does not penetrate glass
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UVB
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Commonly called moles
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COMMON MELANOCYTIC NEVUS
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Appear in early childhood
Reach a maximum in young adulthood [new pigmented area in middle age is of concern] Gradually involute and most disappear by age 60 Junctional: macular, brown, pigment is in the epidermis Compound: elevated, tan to brown color, pigment is epidermal and dermal Dermal nevus : flesh-colored as pigment is in the dermis, elevated |
COMMON MELANOCYTIC NEVUS
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Pigmented lesions present at birth, rare varieties become apparent within first 12 months of life
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CONGENITAL NEVUS
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Lifetime risk for development of melanoma:
Large CN: 6.3% (>1.5cm) 50% of melanomas that develop in large CN occur between ages 3-5 years Small CN: risk is low Management: Small CN (<1.5cm) Atypical appearing CN should be excised as soon as possible Large CN (>1.5cm) Any nevus this size should be excised before age 12, even if not obviously dysplastic Giant CN should be removed as soon as possible Prognosis: Melanoma that develops in a giant CN has a poor prognosis |
CONGENITAL NEVUS
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what is perhaps one of the most important signs of malignant melanoma
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enlargement
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3 parts
>50 in number non-sun areas histologically atypical |
DYSPLASTIC NEVUS SYNDROME
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Incidence:
Almost all patients with familial cutaneous melanoma 30-50% of patients with sporadic primary melanomas of the skin 5% of the general white population Arise in childhood, before puberty Increased numbers of moles (>50-100) in sun-exposed areas Moles also present in non-sun-exposed areas Autosomal dominant |
DYSPLASTIC NEVUS SYNDROME
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Essentially dysplastic nevus syndrome with 2 blood relatives with melanoma
May cluster with other malignancies such as pancreas cancer |
FAMILIAL ATYPICAL MOLE AND MALIGNANT MELANOMA (FAMMM)
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a general term that refers to a number of different (usually benign) pigmented lesions of the skin. Most birthmarks and moles are placed into the category
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NEVI
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Lifetime risk of developing melanoma:
General Population - 0.8% Dysplastic nevus syndrome - 18.0% FAMMM Syndrome - _____ |
100%
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Treatment:
Benign pigmented nevi – monitoring, excision if cosmetically undesired (shave/punch), laser Dysplastic nevi - Surgical excision (do not laser or freeze), careful monitoring by patient monthly and provider annually, avoid sunbathing, tanning booths, use sunscreen [monitor patient regularly, need to look at moles monthly, remove only - don't shave, punch, laser] FAMMM – _____________ |
same as dysplastic nevi but may be more aggressive at removing clinically
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what are these:
Presence of precursor lesions Family history of melanoma in 1st degree relative Phenotype: Blonde or red hair Blue or green eyes Lighter skin type Freckling tendency |
Predisposing Factors for Melanoma
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what are these:
History of blistering sunburns Increased sun exposure between 10 – 24 years of age Chronic, continuous sun exposure linked with lentigo maligna melanoma Intermittent, intense sun exposure linked with superficial spreading and nodular melanoma |
Predisposing Factors for Melanoma
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Synonymous with Sutton’s nevus or Leukoderma acquisitum centrifugum
Occur in 1% of the general population |
HALO NEVI
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Etiology: due to circulating cytotoxic antibodies
Associated with vitiligo vitiligo: or leukoderma is a chronic skin condition that causes loss of pigment, resulting in irregular pale patches of skin. Usually within the first three decades of life Can occur around primary melanoma |
HALO NEVI
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[bulk of growth is on horizontal plane]
Account for 70% of all melanomas Age: 30 - 50 years Median 37 years Gender: Slightly higher in females Only 2% occur in skin phototypes V and VI Evolves over a period of 1 - 5 years |
SUPERFICIAL SPREADING MELANOMA
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the most common form of cutaneous melanoma in Caucasians. The average age at diagnosis is in the fifth decade, and it tends to occur on sun-exposed skin, especially on the backs of males and lower limbs of females.
Often, this disease evolves from a precursor lesion, usually a dysplastic nevus. Otherwise it arises in previously normal skin. A prolonged radial growth phase, where the lesion remains thin, may eventually be followed by a vertical growth phase where the lesion becomes thick and nodular. As the risk of spread varies with the thickness, early SSM is more frequently cured than late nodular melanoma. |
SUPERFICIAL SPREADING MELANOMA
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[bulk of growth is on vertical plane]
Account for 16% of all melanomas Age: Median 50 years Evolves over 6 - 18 months Rarely associated with a nevus remnant |
NODULAR MELANOMA
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is the most aggressive form of melanoma. It grows in vertical direction from the outset and grows very fast (months).
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NODULAR MELANOMA
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The microscopic hallmarks are:
• Dome-shaped at low power • Epidermis thin or normal • Dermal nodule of melanocytes with a 'pushing' growth pattern • No "radial growth phase" ] |
NODULAR MELANOMA
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is a melanoma in situ: it consists of malignant cells but does not show invasive growth. It can remain in this non-invasive form for years. It is normally found in the elderly (peak incidence in the 9th decade), on skin areas with high levels of sun exposure (for example, face and forearms).
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LENTIGO MALIGNA
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Synonymous with Hutchinson’s nevus, Hutchinson’s freckle, melanoma in situ
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LENTIGO MALIGNA
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Flat, macular, intraepidermal neoplasm and the precursor or evolving lesion of Lentigo Maligna
Melanoma (LMM) Age: Median age is 65 Gender : Equal in males and females Older population with increased sun exposure |
LENTIGO MALIGNA
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[off label: wart medication, aldera is helpful]
Account for 5% of all melanomas Age: Seventh decade Gender: Equal in males and females Predominantly occur on the head and neck May take up to 20 years to evolve from a Lentigo Maligna |
LENTIGO MALIGNA MELANOMA
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varients:
subungal: nail bed volar: palms and soles] Prognosis: Survival rates for the volar type are less than 50% Subungual type has a 5year survival rate of 80% |
ACRAL LENTIGINOUS MELANOMA
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Account for 2 to 8% of all melanomas
Age: Median is 65 years Gender: Male:Female ratio 3:1 Race: the principal melanoma in American and African blacks Accounts for 50 - 70% of melanomas in Japanese Evolves over 2.5years |
ACRAL LENTIGINOUS MELANOMA
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Typical symptoms include:
• longitudinal tan, black, or brown streak on a finger or toe nail (melanonychia striata) • pigmentation of proximal nail fold • areas of dark pigmentation on palms of hands or soles of feet Any new area of pigmentation or an existing one that shows change should be checked by a dermatologist. If caught early this type of melanoma has a similar cure rate as the other types of superficial spreading melanoma.] |
ACRAL LENTIGINOUS MELANOMA
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which stage:
localized disease with no clinically palpable nodes Invasive Melanoma 83% of newly diagnosed melanomas Five year survival based on tumor thickness: <= 0.85mm - 99% 0.85-1.69mm - 94% 1.70-3.64mm - 78% [metastasize to >= 3.65mm - 42% |
stage I
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which stage:
palpable regional lymph nodes High Risk Melanoma 15% of newly diagnosed melanomas Five year survival rate is 30-40% |
stage II
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which stage:'
presence of distant metastasis Regional Metastasis 2% of newly diagnosed melanomas Median survival rate is six months |
stage III
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within 5cm of primary site
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local
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>5cm from primary site
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intransit metastases/regional nodes
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Skin, subcutaneous tissue and distant lymph nodes (42-57%)
Lungs (18-36%) Liver (14-20%) Brain (12-20%) Bone (11-17%) Small intestines (1-7%) |
distant metastases
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is a non-invasive diagnostic technique for the in vivo observation of pigmented skin lesions, allowing a better visualization of surface and subsurface structures. This diagnostic tool permits the recognition of morphologic structures not visible by the naked eye, thus opening a new dimension of the clinical morphologic features of pigmented skin lesions.
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dermoscopy
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precancerous lesion in mouth
Sharply defined, white, macular, slightly raised area, cannot be rubbed off, remains after irritant removed |
ORAL LEUKOPLAKIA
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Age:
40-70 years Gender: M:F - 2:1 Predisposing Factors: Tobacco Alcohol Human Papilloma Virus Types 11 and 16 Prognosis: 10% progress to malignancy Leukoplakia on the floor of the mouth more likely to progress to squamous cell carcinoma (SCC) |
ORAL LEUKOPLAKIA
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Result of therapy
Cancer (SCC) Acne (BCC) Vascular lesions (BCC) Psoriasis (BCC) |
RADIATION DERMATITIS
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Accidental or occupational exposure (SCC)
Total doses: 3000-6000 rad Atrophy Hyper and hypopigmentation Telangiectasias Squamous cell carcinoma may develop after years Multiple tumors that metastasize |
RADIATION DERMATITIS
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Single or multiple, discrete, dry, rough, adherent, scaly lesions on habitually sun-exposed skin
Age: Usually middle age Gender: More common in males Skin phototypes I, II, III Rare in IV Almost never in V or VI Outdoor workers, sportspersons and sunworshipers 1 SCC in an estimated 1000/year |
ACTINIC KERATOSIS
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also called solar keratosis, ) is a premalignant condition of thick, scaly, or crusty patches of skin. It is most common in fair-skinned people who are frequently exposed to the sun, because their pigment isn't very protective. It usually is accompanied by solar damage. Since some of these pre-cancers progress to squamous cell carcinoma, they should be treated.
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ACTINIC KERATOSIS
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When skin is exposed to the sun constantly, thick, scaly, or crusty bumps appear. The scaly or crusty part of the bump is dry and rough. The growths start out as flat scaly areas, and later grow into a tough, wart-like area.
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ACTINIC KERATOSIS
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site commonly ranges in between 2 to 6 millimeters, and can be dark or light, tan, pink, red, a combination of all these, or the same pigment of one's skin. It may appear on any sun-exposed area, such as the face, ears, neck, scalp, chest, back of hands, forearms, lips etc.]
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ACTINIC KERATOSIS
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Most common type of skin cancer
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BASAL CELL CARCINOMA
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Locally invasive, aggressive and destructive - but it does not metastasize
Does not have the capacity to metastasize Incidence: 500-1000 per 100,000 Age: Over 40 years Gender: Males > Females Predisposing factors: Phototypes I and II Prolonged sun exposure Previous therapy with X-rays Basal Cell Nevus Syndrome |
BASAL CELL CARCINOMA
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Treatment:
Excision with primary closure, skin flaps or grafts Cryosurgery, curettage and electrosurgery are options, but have higher recurrence rates Imiquimod (aldera) -causes inflammatory response For lesions in the danger zones (around eyes, in the ear canal, posterior auricular sulcus and in sclerosing BCC) Moh’s surgery is the best approach -more curative than regular surgery [pearly quality, often central clearing and/or umbilication, telangectasia, rolled border [pigmented- do punch biopsy] [often find behind ears from baseball cap use] [opposite: prevelence and mortality] |
BASAL CELL CARCINOMA
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The risk of developing is increased for individuals with a family history of the disease and with a high cumulative exposure to UV light via sunlight or, in the past, were exposed to carcinogenic chemicals, especially arsenic. Treatment is with surgery, topical chemotherapy, x-ray, cryosurgery or photodynamic therapy. It is rarely life-threatening but, if left untreated, can be disfiguring, cause bleeding and produce local destruction (eg., eye, ear, nose, lip). almost never spreads; but, if untreated, it may grow into surrounding areas and nearby tissues and bone]
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BASAL CELL CARCINOMA
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Malignant tumor of skin and mucous membranes
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SQUAMOUS CELL CARCINOMA
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can occur in pt who have been immunocompromised after an organ transplant
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SQUAMOUS CELL CARCINOMA
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Age:
Over 55 years Gender: Males>Females Phototypes I and II Phototypes IV - VI can develop SCC from numerous agents other than sunlight exposure Incidence: 12 per 100,000 white males 7 per 100,000 white females 1 per 100,000 African Americans |
SQUAMOUS CELL CARCINOMA
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Predisposing factors:
Human papillomavirus (types 16, 18, 31, 33 and 35) Immunosuppression PUVA Scars Chronic ulcers (of any etiology) Discoid Lupus Erythematosus Industrial carcinogens Arsenic slowly evolving |
SQUAMOUS CELL CARCINOMA
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form of cancer of the carcinoma type that may occur in many different organs, including the skin, lips, mouth, esophagus, prostate, lungs, vagina, and cervix.
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SQUAMOUS CELL CARCINOMA
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This type of cancer is characterized by red, scaly skin that becomes an open sore.]
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SQUAMOUS CELL CARCINOMA
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squamous cell in situ
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BOWEN'S DISEASE
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Usually a solitary lesion on exposed skin
Slowly enlarging, erythematous macule, sharp border, little or no infiltration, usually slight scaling, some crusting Treatment: Excision Moh’s surgery in difficult sites Cryotherapy Efudex [phototoxicity, very irritating, crusts over - it will look very ugly] Imiquimod Prognosis: Mortality rate is very low |
BOWEN'S DISEASE
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is a sunlight-induced skin disease, considered either as an early stage or intraepidermal form of squamous cell carcinoma
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BOWEN'S DISEASE
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typically presents as a gradually enlarging, well demarcated erythematous plaque with an irregular border and surface crusting or scaling.
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BOWEN'S DISEASE
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occurs predominantly in women (70-85% of cases); about three-quarters of patients have lesions on the lower leg (60-85%), usually in previously or presently sun-exposed areas of skin. A persistent progressive non-elevated red scaly or crusted plaque which is due to an intradermal carcinoma and is potentially malignant
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BOWEN'S DISEASE
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Clinically and histologically resembles Bowen’s disease but occurs on the penis
5-Fluorouracil Imiquimod Nd:YAG or CO2 laser |
ERYTHROPLASIA OF QUEYRAT
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Fleshy, granulating, friable, crusted nodules
Has the capacity to metastasize Any persistent nodule, plaque or ulcer, especially in areas of sun-exposure, radiation dermatitis, old burn scars or on the genitalia must be biopsied Treatment: Excision Accutane Prognosis: SCC has an overall remission rate after therapy of 90% |
INVASIVE SQUAMOUS CELL CARCINOMA
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Solitary or multiple dermal or subcutaneous nodules, from a distant noncontiguous primary malignant neoplasm
[likely if they had a history of cancer, very cachetic] Age: Any age but usually older Incidence: 3-4% of malignant tumors metastasize Most frequent primary sites: breast, stomach, lung, uterus, colon, kidney, prostate, ovary, liver History of primary internal cancer Average survival: 3 months except for contiguous spread of breast cancer, may last for years |
METASTIC CARCINOMA
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Jewish and persons of Mediterranean descent , >50yrs old
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KAPOSI'S SARCOMA
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in Sub-Saharan Africa
Epidemic or AIDS-associated homosexual males, thought to be sexually transmitted Associated with Human Herpes Virus 8 |
KAPOSI'S SARCOMA
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Presentation:
Ecchymotic-like macule Asymptomatic Plaques Nodules Ulcerate and bleed easily Progressive edema of extremities Urethral and anal canal lesions can cause obstruction Treatment: Radiotherapy Cryosurgery Laser or excisional surgery Intralesional vinblastine or interferon Systemic chemotherapy |
KAPOSI'S SARCOMA
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not curable, in the usual sense of the word, but it can often be effectively palliated for many years and this is the aim of treatment
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KAPOSI'S SARCOMA
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Malignant neoplasm - unilateral nipple or areola
Simulates chronic eczematous dermatitis Represents primary carcinoma of the intraductal and intraepidermal area of the breast Age: 30-50 years Insidious onset up to a year Biopsy any lesion that persists longer than a few weeks or is resistant to topical treatment Treatment: Surgery |
PAGET'S - Mammary
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Anogenital and axillary skin
Histologically and clinically similar to Paget’s of the breast Often represents an intraepidermal extension of a primary adenocarcinoma of underlying secretory glands Age: >40 years Gender: Females>Males Treatment: Moh’s surgery |
PAGET'S - Extramammary
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Simulates eczematous dermatitis:
Months to years Pruritis, often intractable [pruritis is out of proportion to what they have, may be better in summer, have high index of suspecion] May be asymptomatic Unresponsive to topical therapy Cigarette paper appearance Age: 50 years (range, 5 to 70years) Gender Male:Female ratio 2:1 Incidence 2 per 1,000,000 Early stages histologic confirmation may not be possible despite repeated biopsies |
CUTANEOUS T-CELL LYMPHOMA
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T-cell typing may be helpful
Peripheral blood for abnormal lymphocytes (Sezary cells) High index of suspicion in patients with atypical or refractory psoriasis or eczema Treatment - dependant on stage: PUVA Topical nitrogen mustard Total electron beam therapy X-ray Chemotherapy Bexarotene (Targretin) |
CUTANEOUS T-CELL LYMPHOMA
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is a class of non-Hodgkin's lymphoma, which is a type of cancer of the immune system. Unlike most non-Hodgkin's lymphomas (which are generally B-cell related), caused by a mutation of T cells. The malignant T cells in the body are pushed to the surface of the skin in a biological process used to rid the body of offending material, causing various lesions to appear on the skin. These lesions change shape as the disease progresses, typically beginning as what appears to be a rash and eventually forming plaques and tumors before metastatizing to other parts of the body.
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CUTANEOUS T-CELL LYMPHOMA
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[nuclei look like "little brians"]
Rare variant of CTCL Generalized or universal erythroderma Peripheral lymphadenopathy Cellular infiltrates of atypical lymphocytes (Sezary cells) in the skin and blood [shed cells] Age: Over 60 Gender: Male>Female Progressive course without treatment Treatment: Chemotherapy PUVA no remission of lymph node involvement, effective for erythroderma Photophoresis is an option |
SEZARY'S SYNDROME
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