Skin Disorders Spring 2024 PDF

D R. M A D E LY N S P R I N G C A R E Y 2 0 2 4 A LT E R E D T I S S U E INTEGRITY DERMIS Below epidermis; thicker layer Contains: Blood vessels Skin appendages Sensory receptors for pain, touch, temperature Smooth and skeletal muscle cells Two layers Papillary layer (superficial) Reticular layer (t...

D R. M A D E LY N S P R I N G C A R E Y 2 0 2 4 A LT E R E D T I S S U E INTEGRITY DERMIS Below epidermis; thicker layer Contains: Blood vessels Skin appendages Sensory receptors for pain, touch, temperature Smooth and skeletal muscle cells Two layers Papillary layer (superficial) Reticular layer (thicker and deeper) EPIDERMIS Upper layer of skin Stratified squamous epithelial cells; keratinocytes Melanocytes, T lymphocytes, dendritic (Langerhans) cells, tactile (Merkel) cells Avascular; no lymphatic vessels TYPES OF WOUND HEALING Primary Intention (Primary Closure) Surgical closure of wound Repair: formation of new ECM Regeneration: reepithelialization Little granulation tissue Secondary Intention (Secondary Or Spontaneous Closure) Full thickness wound heals without closure attempt Large amount of granulation tissue or exudate Longer healing time; larger scar Skin grafting; skin substitutes Tertiary Intention (Delayed Primary Closure) Combination of primary and secondary intention Contaminated wound cleaned, left open drainage Scarring ˃ primary intention and < secondary intention Localized ischemic lesion of skin and underlying tissue P R E SS U R E INJURIES Over bony prominence External pressure impairs flow of blood and lymph Etiology and pathogenesis Immobility Reactive hyperemia Microthrombi Shearing forces Risk factors Immobility or inactivity Poor perfusion (including diabetes) Skin status; maceration P R E SS U R E INJURIES Clinical manifestations Pressure decreases gradually from bony area toward periphery Discoloration to blisters or areas of denuded superficial skin to deep tissue damage with necrosis Graded or staged to classify degree of tissue damage N U T R I T I O N A L S TAT U S Major role in wound healing Essential macronutrients: carbohydrates and fats Malnutrition: Impaired immune and inflammatory responses Delayed wound healing; increased wound infection Diminished angiogenesis Reduced matrix formation and remodeling Vitamin and mineral deficiencies Associated with chronic, nonhealing wounds in nutritionally debilitated individuals ACUTE SKIN DISORDERS ACUTE SKIN CONDITIONS Bacterial or fungal infection Contact with offending organism or allergen Parasites and insects Medications Disorders of nail Possible transition to chronic skin conditions Life-threatening inflammatory disorders CELLULITIS Diffuse painful inflammation of skin and subcutaneous layers Most at risk: Athletes Children Men who have sex with men Military recruits Prisoners Residents of long-term care facilities Intravenous drug users Prior MRSA exposure C L I N I C A L M A N I F E S TAT I O N S Painful, red, swollen area of the skin that is hot and tender to touch. Fever and chills Vesicles, bullae, plaques (with Staphylococcus) Tachycardia, hypotension, confusion, headache Lymphadenitis and lymphangitis CELLULITIS Diagnosis Treatment Physical examination Manage and prevent spread of infection Cultures and blood tests Topical antibiotic ointment Oral antibiotic medication Intravenous antibiotics Pain medication Teaching: treatment and prevention IMPETIGO Acute, highly contagious skin infection Types Nonbullous impetigo (impetigo contagiosa) Bullous impetigo CLINICAL M A N I F E S TAT I O N S Red pimples, fluid-filled blisters, oozing rash with yellow crusts Bacteria live under crust and in blisters IMPETIGO Diagnosis Treatment Physical examination Prescription ointments Culture Severe: oral antibiotics are ordered Parent Teaching: Take medication as prescribed Good hand hygiene, use of antibacterial soap and water, and use of a separate washcloth and hand towel are necessary. Airflow is needed for healing; therefore, loose dressings may be used. FOLLICULITIS Inflammation of hair follicle Infectious Bacteria (S. aureus), virus, fungi, or parasite Noninfectious Trauma Inflammation Damaged or blocked follicles EGFR receptor inhibitors Autoimmune diseases FOLLICULITIS Clinical Manifestations Diagnosis & Treatment Pruritus, burning, or mild discomfort Diagnosis Multiple small papules and pustules with a red base around single hair follicle; break and crust over Treatment Based on signs and symptoms Dependent on etiology Treatment of infection or fungus and inflammation FURUNCLES AND CARBUNCLES Furuncle (boil) Extension of folliculitis or infection of sebaceous gland Carbuncle Cluster of infected hair follicles Primary causative agent: S. aureus and MRSA FURUNCLES AND CARBUNCLES Clinical Manifestations Diagnosis & Treatment Area firm, red, painful; tips white; purulent drainage Diagnosis Physical examination Culture Treatment Moist heat Oral antibiotics Incision and drainage of lesion Hygiene CANDIDIASIS Infection of skin or mucous membranes with any species of Candida (C. albicans most common) Mouth, throat, lungs, vagina, folds of skin, bowel Usually secondary condition: those immunosuppressed, are taking certain antibiotics, or are being treated for cancer are at risk for candidiasis. Etiology Candida normal in skin and mucous membranes Warmth, moisture, breaks in epidermis can cause infection Life threatening if in bloodstream CANDIDIASIS Clinical Manifestations Diagnosis & Treatment Thrush: white covering of tongue, mouth, throat Diagnosis Common secondary condition to those taking certain antibiotics Vaginal yeast infection: itching; foul odor; white discharge Balanitis: flattened pustules, edema, burning, tenderness Diaper rash: dark red patches in skin folds; fluid-filled spots Physical examination Skin scraping Treatment Antifungal drugs TINEA Contagious infection by different types of fungus Superficial infections; called dermatophytoses Named by location on body Spread by direct contact Thrive in warm, damp environments Common causative organisms Trichophyton rubrum T. tonsurans Microsporum canis TINEA Clinical Manifestations Diagnosis & Treatment Scaly plaque with erythema Diagnosis Crust, papules, vesicles, and bullae Skin scrapings, fungal culture, polymerase chain reaction assay, skin biopsy, or Wood light examination Physical examination Treatment OTC and prescription medications Inflammation and irritation of the skin Caused by contact with irritant or allergen Irritant contact dermatitis (80% of all cases) Allergic contact dermatitis (immune response) C O N TA C T D E R M AT I T I S C O N TA C T D E R M AT I T I S Clinical Manifestations Diagnosis & Treatment Irritant: hyperemia, itching, skin lesions, vesicular or pustular skin eruptions, itching Diagnosis Allergic: weeping vesicles, hives, itching Full examination and history “Use” test Skin biopsy Treatment Avoidance of cause OTC medications Home remedies Witch hazel cream and St. John’s wort SEBORRHEIC AND E X F O L I AT I V E D E R M AT I T I S Seborrheic dermatitis (SD) Chronic skin inflammation; exacerbations and remissions Papulosquamous disorder on the sebum glands Linked to immunologic abnormalities involving Malassezia Exfoliative dermatitis (ED) Widespread skin inflammation from preexisting skin disorders, drugs, cancer, or unknown C L I N I C A L M A N I F E S TAT I O N S Seborrheic Rounded, irregular or circular lesions covered with yellow or brown-gray greasy scales; itching Exfoliative Erythematous and scaly; patches that spread; pruritus, malaise, chills SEBORRHEIC AND E X F O L I AT I V E D E R M AT I T I S Diagnosis Seborrheic Distribution of involvement Skin biopsy; fungal culture Exfoliative Dermatologist; skin biopsy Treatment Ketoconazole, naftifine, or ciclopirox creams and gels Calcineurin inhibitors, sulfur or sulfonamide combinations, or propylene glycol U RT I C A R I A (H I V E S ) Welts on skin that often itch Acute urticaria more common than chronic urticaria Numerous causes Reactions to drugs, contact with allergens, exposure to water, emotional stimuli, physical stimuli, etc. Pathogenesis Immunoglobulin E (IgE) initiates release of histamine, bradykinin, leukotrienes, prostaglandins This causes extravasation of plasma into the dermis U RT I C A R I A Clinical Manifestations Diagnosis & Treatment Sudden eruption of pale wheals or papules that cause severe itching Diagnosis Allergy testing Skin biopsy Treatment Antihistamines, calamine lotion, cortisone creams (itching) Topical emollients and aluminum acetate (dry skin) LICHEN PLANUS Noncontagious inflammatory disorder of skin, mouth, nails, scalp, and mucous membranes Unknown cause; may be allergic or autoimmune response LICHEN PLANUS Clinical Manifestations Diagnosis & Treatment Slow or quick onset Diagnosis Rash with flat-topped, firm, reddish to purple bumps with symmetrical sides and sharp border; Wickham striae Itching Skin biopsy Laboratory work Treatment Might not be needed; no cure Oral antihistamines, corticosteroids, retinoic acid, PUVA therapy N E C R O T I Z I N G FA S C I I T I S “Flesh-eating disorder” Rapidly spreading infection caused by bacteria Caused by a mixture of aerobic and anaerobic organisms affecting subcutaneous tissues and fascia Starts from contagious ulcer, wound, untreated skin infection, complication of surgery, abscess Occlusion of small subcutaneous vessels; tissue ischemia, infarction, necrosis N E C R O T I Z I N G FA S C I I T I S Clinical Manifestations Treatment Skin red, hot, swollen, malodorous Antibiotics Pain Surgical debridement Septicemia and gangrene Pain control Amputation of limbs Hyperbaric oxygen STEVENS-JOHNSON SYNDROME Rare disorder of skin and mucous membranes Cell death causes epidermis to separate from dermis Milder form of toxic epidermal necrolysis (TEN) Etiology More than 200 medications Infectious causes Delayed hypersensitive reaction STEVENS-JOHNSON SYNDROME Clinical Manifestations Diagnosis & Treatment Flulike symptoms Diagnosis Symmetric burning rash; red, purple target lesions Physical examination CBC with CD4+ and CD8+ T lymphocytes Electrolytes Kidney function studies Ocular examination Treatment Stopping all non-essential medications Fluid replacement, nutrition, wound and eye care Pain medications, antihistamines, antibiotics, topical steroids B E E A N D WA S P S T I N G S Vespids vs. apids Female of each species has stinging apparatus and sac containing venom Bee can sting only one time Wasps can sting multiple times B E E A N D WA S P S T I N G S Clinical Manifestations Treatment Swelling, redness, itching, mild pain Remove stinger Anaphylactic reactions Apply cool compress immediately to site Oral and topical antihistamines, analgesics Emergency management of anaphylaxis: EpiPen TIC BITES Blood-sucking arachnids (parasites) Embed head into skin and grow as they feed Risk factors for bites Outdoor activities Contact with animals C L I N I C A L M A N I F E S TAT I O N S Allergy: usual allergic reactions Associated diseases: flulike symptoms; rash over entire body; neck stiffness; swollen lymph nodes Lyme disease: red bump with ringed red rash resembling bulls-eye; fever; headache; fatigue; erythema migrans Rocky Mountain spotted fever: dots on ankles and wrists T R E AT M E N T Remove tick with tweezers Swab bite with alcohol Treat infection or symptoms of severe disease Topical antihistamines and corticosteroids Calamine lotion and benzocaine spray Ice pack Severe symptoms: tests for specific tick disease Acute stage of Lyme disease: oral antibiotics PEDICULOSIS Infestation of parts of body or clothing with lice eggs, larvae, adults of lice Pediculosis humanus capitis Pediculosis humanus corporis Pthiriasis Most do not cause diseases PEDICULOSIS Clinical Manifestations Diagnosis & Treatment Pruritus Diagnosis Itching and sores from scratching Visible body lice in crevices and skinfolds Symptoms and appearance of nits Wood lamp; yellow-green fluorescence of lice and nits Treatment Pediculicides Nit comb Wash clothes and linens SCABIES Intense pruritic rash caused by a mite; very contagious Pathogenesis Sarcoptes scabei mite burrows into skin and lays eggs Clinical manifestations Rash and itching Diagnosis Physical examination and skin scraping Treatment Antiscabies medications Antihistamine BEDBUG BITES Cimex lectularius; ectoparasite Blood-sucking insects that are more pest than risk High-risk areas Places with high turnover of human guests (e.g., hotels, hospitals) Sanitation not a factor Clinical manifestations Asymptomatic or redness around site with darker red spot in middle; stinging; itching Treatment Antihistamine Ice packs Antiseptic cream or lotion Clean linens and furnishings ACNE VULGARIS Formation of comedones, papules, pustules, nodules, cysts when hair follicles and sebaceous glands become inflamed due to obstruction Types Noninflammatory acne Inflammatory acne Mixed Classifications: mild, moderate, severe Treatment Medications Diet therapy Procedures ROSACEA Chronic red rash involving central part of face and is characterized Recurring, persistent, transient Unknown cause Various triggers: hot drinks, spicy foods, alcohol, temperature extremes, sunlight or wind, emotions, exercise, cosmetics, and vasodilating drugs Risk factors Being female and fair skinned Age > 30 Smoking Family history ROSACEA Clinical Manifestations Treatment Facial redness; telangiectasia Skin care Can lead to eye problems, such as dryness, irritation, swelling, reddened eyelids, styes, conjunctivitis. Medications for redness and pimples Oral antibiotics Referral: ophthalmologist can help with your dry eyes and irritation Alternative therapies Gentle massage DISORDERS OF THE NAIL: BRITTLE NAILS Easily crack, chip, split, or peel Onychoschizia: brittle or soft nails with splitting Causes Aging; long-term nail polish use; exposure to moisture; dryness Diseases; chemotherapy; chemicals Prevention Keep nails short Avoid nail polish remover with acetone Use gloves to avoid getting wet; use emollients DISORDERS OF THE NAIL: NAIL INFECTIONS Onychomycosis (fungal infection) Causes Tinea unguium, yeasts, Candida albicans, molds Clinical manifestations White or yellow spot under tip of nail Appears dull, becomes distorted, thickens Pain and odor Treatment Oral antifungals Laser and light-based therapies; ultrasound DISORDERS OF THE NAIL: N A I L T R AU M A O R LO SS Cut, torn, smashed, nail Causes Crushing, smashing leads to subungual hematoma Nail lifts completely from nail bed Diabetes, circulatory problems, AIDS, chemotherapy Clinical manifestations Pain, bleeding, swelling, warmth Treatment Dressing; stitches; antibiotics CHRONIC SKIN DISORDERS CHRONIC SKIN CONDITIONS Long term Relapses common May or may not resolve Viral Infections HERPES SIMPLEX VIRUS Herpes simplex virus type 1 (HSV-1) Herpes simplex virus type 2 (HSV-2) Affected body regions HSV-2 is spread via oral, vaginal, or anal sexual contact with an individual who is shedding the virus. Herpes labialis: (lips; cold sores) Herpetic keratitis (eye) Transmission commonly occurs from contact with an infected partner who does not have visible lesions and may not know they are infected Herpetic whitlow (digits or hands) Causes most sexually-transmitted anogenital herpes Most common HSV-1 infection Herpes gladiatorum (torso of wrestlers) Herpetic sycosis (beard follicles) Usually contracted during childhood Recurrences persist into old age Lesions on genitals, perineum, or anus May cause cold sores Less common cause than HSV-1 HERPES SIMPLEX VIRUS Virus enters skin or mucous membrane via microscopic tear Virus travels to sensory root ganglion Virus becomes dormant and permanent resident of ganglion Cell-mediated immune system is triggered Viral activation occurs Virus travels from neuron to skin innervated by neuron Virus enters dermal and epidermal cells Viral replication causes recurrent rash outbreak C L I N I C A L M A N I F E S TAT I O N S May have asymptomatic herpes or mild fever Usually begins with prodrome (fever or flu-like symptoms) Red, swollen area of skin or mucous membrane develops Eruption of painful vesicles Vesicular rash Dermatome eruption in localized skin region Innervated by single sensory spinal nerve Pattern may lead to misdiagnosis (herpes zoster or shingles) Regional lymph nodes swell Lesions open and form painful ulcers that crust and begin healing Primary genital herpes: May cause dysuria and urinary retention, especially in women HERPES SIMPLEX VIRUS Diagnosis Treatment May be based on clinical findings Antiviral medications Patient history and observation of lesions Laboratory tests Analgesics Viral culture Cool compresses Antigen testing Sitz baths Direct fluorescent antibody (DFA) testing Polymerase chain reaction (PCR) assays Serologic tests HERPES ZOSTER Chronic viral skin condition Also known as shingles Caused by varicella-zoster virus (VZV) Member of the herpesvirus family VZV also causes chickenpox First VZV infection causes chickenpox Latent VZV is reactivated Virus is released into the skin and replicates Painful rash develops C L I N I C A L M A N I F E S TAT I O N S Prodromal Phase Pain on one side of the body Sensatory changes at site of impending rash eruption Tingling, itching, burning, numbness Malaise, fever, chills, myalgia, headache, nausea Skin lesions Usually present on one side of the body or head Typically affects one dermatome May spread to more than one dermatome Initial presentation Macules and papules on erythematous base Vesicles spread over the dermatome Vesicles open and crusts form Painful skin lesions persist Rash present for 10 days to one month CRANIAL NERVE DAMAGE HZ ophthalmicus Involves ophthalmic division of trigeminal nerve May cause visual impairment Requires emergent treatment by ophthalmologist Ramsay-Hunt syndrome or HZ oticus Involves facial nerve (CN7) Risk of hearing loss or permanent facial weakness Emergent treatment required HERPES ZOSTER Diagnosis Treatment History and physical examination Antiviral medications Usually sufficient for diagnosis after rash appears Atypical or recurrent rashes (more than episodes) May require laboratory testing to identify cause Laboratory testing Direct immunofluorescent assay PCR assay Glucocorticoids Analgesics Cool compresses WA RT S H U M A N PA P I L L O M AV I R U S (HPV) Various types of human papillomavirus (HPV) Sites of occurrence Anywhere on skin or mucous membranes Malignancy Most lesions caused by HPV are benign Some HPV types linked to dysplasia and cancer 90% of cervical and anal cancers 70% of vaginal and vulvar cancers 60% of penile cancers 70% of oropharyngeal cancers C L I N I C A L M A N I F E S TAT I O N S Lesion presentation varies due to selectivity of HPV Specific serotypes affect specific areas Examples Flat Papular Pedunculated T R E AT M E N T Treatment of cutaneous warts Does not eradicate HPV or prevent HPV transmission HPV does not respond to antiviral medication Spontaneous recovery 50 percent resolve without treatment within 1 year First Line: Salicylic Acid Second Line: Cryotherapy Surgical AT O P I C D E R M AT I T I S Eczema General term Describes inflammatory skin disorders Includes atopic dermatitis (AD) Most severe form of eczema Atopic Dermatitis Chronic, recurring, itchy, inflammatory disorder Associated with increased serum IgE Affected individuals often have other atopic disorders E.g., asthma, allergic rhinitis Most often affects children May persist into adulthood AT O P I C D E R M AT I T I S High risk for bacterial, viral, and fungal infection Contributing factors Dysfunctional epidermal barrier Impaired immune systems Clinical Manifestations Exacerbation and remission of dry, itchy, red skin Begins in infancy Constant pruritus Prevailing symptom Precedes eczematous rash Skin excoriations and lichenification Xerosis and crusting lesions Negative impact on overall quality of life E.g., sleep disturbances, depression AT O P I C D E R M AT I T I S Diagnosis Treatment No reliable biomarkers or laboratory tests available Topical agents Diagnosis based on clinical findings Cool-mist humidifiers History Appearance and distribution of the rash Associated signs and symptoms Lukewarm baths Wet-wrap therapy PSORIASIS Immune-mediated disease Genetic and environmental causation Pathogenesis Hyperproliferation of keratinocytes Decreased epidermal cell turnover rate Inflammation Thickening of dermis and epidermis Clinical Manifestations Varies based on type of psoriasis Plaque psoriasis – Skin lesions usually round or oval, well-demarcated plaques Treatment Corticosteroid therapy Vitamin D analogs Topical retinoids (teratogenic) Calcineurin inhibitors Phytotherapy Biologic agents BENIGN NEOPLASMS Noncancerous types of tissue proliferation Usually harmless but may become problematic Subject to friction/rubbing Enlarged to the point of compressing organs May be mistaken for cancer May be premalignant Examples Moles, lipomas, actinic keratosis P H O T O D E R M AT I T I S Immune response to UV rays Numerous factors can promote increased skin sensitivity Photodermatitis reaction to sunlight may also be idiopathic Clinical Manifestations: Urticaria in sun-exposed skin Potential acute signs and symptoms: Wheezing, dizziness, fainting, erythema, pruritus, papules, vesicles, eczema, skin pain, chills, headache, fever, nausea Potential chronic effects: Skin thickening and scarring Treatment: varies ACTINIC K E R AT O S I S Primary cause: Cumulative skin damage from sun or tanning-device May also develop after extensive exposure to x-rays or certain industrial chemicals Clinical Manifestations: Thick, rough, crusting or scaly areas Common sites: Bald head, face, ears, lips, backs of the hands and forearms, shoulders, neck Lesion size and color may vary Treatment: Aimed at destroying lesions Office procedures (e.g., cryotherapy, chemical peel, curettage, laser resurfacing) Medications (e.g., 5-fluorouracil [5-FU] cream, diclofenac sodium gel, imiquimod cream, ingenol mebutate gel) HEMANGIOMAS, MOLES, AND S K I N TA G S Hemangiomas Congenital lesions Occur in 10–12% of all infants Moles Also called nevi May be congenital or may occur later in life Usually benign but may become cancerous Skin tags Also called acrochordons Soft papules on a stalk Develop in body regions where skin rubs on skin E.g., neck, axillae, groin LIPOMA Familial tendency exists for all lipomas Solitary lipomas linked to changes in chromosome 12 Multiple lipomas not linked to chromosome 12 changes Pathogenesis Benign lumps Arise from the mesoderm (middle embryonic layer) Comprise mature adipose cells in a fibrous sheath Grow under normal skin in subcutaneous tissues Manifestations Lesions may be single or multiple Smooth, usually soft, doughy, rubbery, painless masses Single lipomas usually found on trunk, upper arms, or neck Size varies Treatment Treatment needed only if complications or changes develop Treatments include liposuction and surgical excision EPIDERMAL INCLUSION CYSTS Squamous epithelium of the epidermis becomes trapped or implanted in the dermis Pathogenesis Dermal cavity fills with keratinocytes and debris Benign lesions form Manifestations Flesh-colored, firm nodules Central punctum (sharp tip or point) Adults: Usually found on face, scalp, neck, and trunk Newborns (milia): Cheeks, forehead, nose, nasolabial folds Treatment No treatment unless EIC ruptures beneath skin Ruptured EIC requires incision and drainage or antibiotics Cysts may be surgically removed SKIN CANCER Most common types of skin cancer Basal cell carcinoma Squamous cell carcinoma Most dangerous type of skin cancer Melanoma BASAL CELL CARCINOMA Most often caused by early (childhood) radiation therapy, repeated, or prolonged exposure to ultraviolet light (UV) A and B rays from sun or tanning devices Arises from the bottom layer (base) of cells of the epidermis, hair follicles, and eccrine sweat glands UV rays damage DNA in cell nucleus Damage to genes that control skin cell growth Manifestations Most often found on sun-exposed areas May appear on skin exposed to arsenic and radiation, within areas of chronic inflammation, burn scars, or tattoos Lesions vary in appearance Treatment Definitive diagnosis requires biopsy Treatment usually requires removal of lesion Topical medications (early lesions) SQUAMOUS CELL CARCINOMA Cumulative UV light exposure Arises from damaged, unrepaired DNA in the nucleus of squamous cells of the epidermis UV radiation triggers cancerous keratinocyte transformation Impaired keratinocytes extend into dermis Manifestations Often, SCC is a nonhealing sore that bleeds easily. Firm, smooth, or hyperkeratotic papules or plaques with an ulcer in the center on sun-exposed skin. May present as large wart, cutaneous horn, or slow-growing, scaly, red plaque Typically occurs in sun-exposed areas May also occur in body regions that are not sun exposed Treatment Diagnosis confirmation requires biopsy Treatment usually requires removal of lesion Topical chemotherapy may be used for surface SCC Radiation or chemotherapy needed if metastasis present MELANOMA Etiology not fully understood Most often due to unrepaired DNA damage to melanocytes Inherited genetic mutations linked to melanoma Damaged melanocytes multiply rapidly and form cancerous tumors Manifestations Most often brown or black in color Colors vary widely (e.g., tan, pink, red, purple, blue, white) May occur anywhere on skin or mucous membranes May appear as unusual sores, lumps, spread of pigmented areas, new moles after age 30, color changes in the skin, or changes in an existing mole Treatment Dermoscopic examination with biopsy or complete excision Lymph node removal if node metastasis present Treatment depends on stage and size of melanoma Interventions include surgery, immunotherapy, targeted therapy, chemotherapy, and radiation Warning signs of changes to existing moles (ABCDE) Asymmetry Asymmetric appearance Two halves differ in shape Borders Irregular borders Uneven, notched, or scalloped Color Color changes within a mole Unusual color Multicolored Diameter More than 1/4 inch wide (the size of a pencil eraser) Evolving New mole in an individual over age 30 changing mole “Ugly duckling” mole that differs from all others VITILIGO Multifactoral disorder; exact cause unknown Genetic and environmental elements involved Considered a marker for certain autoimmune disorders Pathogenesis Loss of functional melanocytes in areas of the skin, hair, or mucous membranes Manifestations Milky-white or chalk-white hypopigmented macules or patches on the skin Common sites include hands, arms, feet, trunk, and face Distribution may be localized, generalized, or universal Treatment No treatment will restore skin color in all patients Treatment options include systemic phototherapy, laser therapy, steroid therapy, topical tacrolimus ointment, and depigmentation therapy Use of high–sun protection factor (SPF) sunscreen is encouraged Cosmetic cover-ups may be preferred CAFÉ AU LAIT SPOTS Increase in melanin in spots on the skin May also be seen in other inherited disorders Manifestations Flat, light brown or dark brown lesions Irregular or smooth borders Lesions vary in size Lesions are present at birth and darken with age Treatment No treatment required for lesions Treatment of any associated genetic disorder is needed SOLAR LENTIGO Caused by ultraviolet (UV) light exposure Manifestations Tan-brown or black macules Well demarcated and surrounded by normal skin Variable in size Irregular in shape Typically found on sun-exposed skin of the hands forearms, face, neck, and shoulders Treatment Typically benign and do not require treatment Dermoscopy or biopsy may be needed to rule out precancerous lesion or melanoma Treatments aimed at reducing appearance of lesions ALOPECIA Alopecia has various causes Causes are classified as scarring or nonscarring Hair growth cycle shortens Affected hair follicles stop replacing lost hair Pregnancy: usually produces a prolonged anagen phase, followed in postpartum by a prolonged telogen phase; telogen effluvium may persist for up to 1 year. Manifestations Signs and symptoms depend on the cause Androgenic alopecia begins with hair loss around the temples and progresses to hair loss over the top of the scalp Treatment Treatment varies based on cause Males: Treatment of androgenic alopecia may include minoxidil or finasteride Finasteride: Not used in women (considered teratogenic) Females: Hormonal modulators may help relieve female-pattern alopecia (e.g., birth control pills or spironolactone) ALOPECIA A R E ATA Well-demarcated patches of hair loss on scalp or beard Single or multiple patches of hair loss may be present Patches of hair loss are asymmetric over the head and face May progress to alopecia totalis (AT) or alopecia universalis (AU)