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Efren N. Aquino M.D. Jan. 6, 2009 May 19, 2009 1 Fungal infections are caused by microscopic organisms (fungi) that can live on the skin. They can live on the dead tissues of the hair, nails, and outer skin layers. 2 3 Superficial fungal infections are known as dermatophytoses. The most common are: tinea capitis, tinea corporis, tinea cruris, and tinea pedis. 4 Tinea refers to the common disorder known as “ringworm.” The name comes from its characteristic ring-shaped lesion and the location of infection. 5 Etiology/pathophysiology Microsporum audouinii major fungal pathogen Tinea capitis - Ringworm of the scalp Tinea corporis - Ringworm of the body Tinea cruris - Jock itch Tinea pedis (most common) Athlete’s foot 6 Tinea capitis Erythematous around lesion with pustules around the edges and alopecia at the site The hair can break off at the scalp, and hair loss is typically not permanent. 7 (From Habif, T.P. [2004]. Clinical dermatology: a color guide to diagnosis and therapy. [4th ed.]. St. Louis: Mosby.) Tinea capitis. 8 Clinical manifestations/assessment Tinea corporis Tinea corporis refers to ringworm of the body. Flat lesions—clear center with red border, scaliness, and pruritus Outbreaks are typically in hairless areas. 9 Tinea Corporis 10 Clinical manifestations/assessment Tinea cruris Brownish-red lesions in groin area, severe pruritus with skin excoriation due to intense scratching These lesions migrate outward from the groin region. 11 Tinea cruris, also known informally as crotch itch or jock itch in American English and dhobi itch or scrot rot in British English, is a dermatophyte fungal infection of the groin region in either sex, though more often seen in males. 12 The type of fungus that most commonly causes tinea cruris is called Trichophyton rubrum. Some other contributing fungi are Candida albicans, Trichophyton mentagrophytes and Epidermophyton floccosum. 13 14 15 16 Clinical manifestations/assessment Tinea pedis Fissures and vesicles around and below toes Tinea pedis is also known as “athlete’s foot.” This infection is associated with more skin maceration than the other types of tinea. 17 18 19 Diagnostic tests Visual inspection Ultraviolet light for tinea capitis Infected hair becomes fluorescent (blue-green) under the light 20 Medical management Griseofulvin—oral Antifungal soaps and shampoos Tinactin or Desenex Burrow’s solution (tinea pedis) 21 Nursing Interventions The feet should be cleaned and dried thoroughly, paying special attention to the toes. Proper application of medications and warm compresses Excellent foot care is stressed. Wearing sandal-type shoes or going barefoot helps decrease foot moisture. 22 23 Superficial inflammation of the skin is known as dermatitis. It can be caused by numerous agents, such as drugs, plants, chemicals, metals, and food. The nurse first observes erythema and edema, followed by the eruption of vesicles that rupture and encrust. Pruritus is always present, which promotes further skin excoriation. 24 1. Contact dermatitis 2. Dermatitis venenata, exfoliative dermatitis, and dermatitis medicamentosa 3. Urticaria 4. Angioedema 5. Eczema (atopic dermtitis) 6. Acne vulgaris 7. Psoriasis 8. Systemic lupus erythematosus 25 Contact dermatitis – The epidermis is inflammed and damaged Etiology/pathophysiology Direct contact with agents of hypersensitivity Detergents, soaps, industrial chemicals, plants 26 Clinical manifestations/assessment Burning Pain Pruritus Edema Papules and vesicles 27 Diagnostic tests Health history – (1) tried a new soap, (2) been traveling and using different personal items, or (3) been working with plants or flowers 28 Diagnostic tests Intradermal skin testing Elimination diets Elevated serum IgE levels and eosinophilla support the diagnosis. It is thought that both tests relate to abnormalities of T-cell function. 29 Medical management/nursing interventions Remove cause Burrow’s solution Corticosteroids to lesions Cold compresses Antihistamines (Benadryl) 30 Nursing Interventions The primary goal is to identify the offensive agent so as to rest the involved skin and protect it from further damage. Wet dressings, using Burow’s solution, help promote the healing process. A cool environment with increased humidity decrease the pruritus. Cold compresses may be applied to decrease circulation to the area (vasoconstriction). 31 Nursing Interventions Daily baths to cleanse the skin should be taken with an application of oil. Fingernails should be cut at the level of the fingertips to decrease excoriation from scratching. Clothing should be lightweight and loose to decrease trauma of the involved area. 32 Prognosis Removal of the offensive agent results in full recovery. Desensitizing the individual may be necessary if recurrences are frequent. 33 Dermatitis venenata, exfoliative dermatitis, and dermatitis medicamentosa Etiology/pathophysiology Dermatitis venenata: Contact with certain plants Exfoliative dermatitis: Infestation of heavy metals, antibiotics, aspirin, codeine, gold, or iodine Dermatitis medicamentosa: Hypersensitivity to a medication 34 Clinical manifestations/assessment Mild to severe erythema and pruritus Vesicles Respiratory distress (especially with medicamentosa) 35 Exfoliative Dermatitis 36 Medical management/nursing interventions All dermatitis Colloid solution, lotions, and ointments Cordicosteroids 37 Medical management/nursing interventions Dermatitis venenata Thoroughly wash affected area Cool, wet compresses Calamine lotion 38 Medical management/nursing interventions Dermatitis medicamentosa Discontinue use of drug 39 Etiology/pathophysiology Presence of wheals or hives in an allergic reaction commonly caused by drugs, food, insect bites, inhalants, emotional stress, or exposure to heat or cold. The wheals (round elevation of the skin; white in the center with a pale red periphery) of urticaria appear suddenly. Urticaria or hives is caused by the release of histamine in an antigen-antibody reaction. 40 Etiology/pathophysiology Clinical manifestations/assessment Pruritus Burning pain Wheals 41 42 43 Diagnostic tests Health history Allergy skin test Serum examination for immunoglobulin E (IgE) Medical management Identify cause and alleviate symptoms Antihistamine (Benadryl) Epinephrine 44 Nursing Interventions Identify and alleviate cause Therapeutic bath Teach patient possible causes and prevention The signs and symptoms of an anaphylactic reaction should be reviewed to include shortness of breath, wheezing, and cyanosis. 45 Prognosis Patient recover fully when the offensive agent is determined and avoided. Compliance with the therapeutic treatment regimen influences the outcome. 46 Etiology/pathophysiology Form of urticaria Occurs only in subcutaneous tissue Same offenders as urticaria Common sites: eyelids, hands, feet, tongue, larynx, GI, genitalia, or lips 47 Clinical manifestations/assessment Burning and pruritus Acute pain (GI tract) Respiratory distress (larynx) Edema of an entire area (eyelid, feet, lips, etc.) 48 Angioedema 49 Medical management Antihistamines (Benadryl®) Epinephrine Corticosteroids (Solu-Medrol®) Cold compresses 50 Nursing interventions Cold compresses Respiratory assessment, continuous Medical alert Education and teaching for prevention Prognosis With early treatment, the prognosis is good 51 Etiology/pathophysiology Allergen causes histamine to be released and an antigen-antibody reaction occurs Primarily occurs in infants The common allergies are to chocolate, eggs, wheat, and orange juice. 52 Clinical manifestations/assessment Pruritus Papules and vesicles on scalp, forehead, cheeks, neck, and extremities The vesicles generally rupture, discharging a yellow, tenacious exudates that dries and encrusts. the skin may depigment and become shiny with dry scales. Erythema and dryness of area 53 54 55 Eczema (atopic dermatitis) (continued) Diagnostic tests Health history (heredity) Diet elimination Skin testing 56 Medical management/nursing interventions Reduce exposure to allergen Hydration of skin Topical steroids Lotions—Eucerin, Alpha-Keri, Lubriderm, or Curel 3-4 times/day 57 Etiology/pathophysiology Occluded oil glands Androgens increase the size of the oil gland Influencing factors Diet Stress Heredity Overactive hormones 58 Clinical manifestations/assessment Tenderness and edema Oily, shiny skin Pustules Comedones (blackheads) Scarring from traumatized lesions Diagnostic tests Inspection of lesion Blood samples for androgen level 59 Comedones with a few inflammatory pustules 60 Papulo-pustular acne 61 Medical management/nursing interventions Keep skin clean Keep hands and hair away from area Wash hair daily Water-based makeup 62 Medical management/nursing interventions Topical therapy Benzoyl peroxide, vitamin A acids, antibiotics, sulfur-zinc lotions Systemic therapy Tetracycline, isotretinoin (Accutane) 63 Etiology/pathophysiology Noninfectious, hereditary, chronic, proliferative epidermal disorder Skin cells divide more rapidly than normal Clinical manifestations/assessment Raised, erythematous, circumscribed, silvery, scaling plaques Located on scalp, elbows, knees, chin, and trunk 64 (Courtesy of the Department of Dermatology, School of Medicine, University of Utah.) Psoriasis. 65 66 Objective of treatment: decrease inflammation Reduces shedding of the outer layer of skin Slow down the proliferation of skin epithelium Topical steroids e.g: betamethasone, hydrocortisone decrease inflammation 67 Keratolytic agents Tar preparations Salicylic acid Reduces shedding of the outer layer of skin Photochemotherapy PUVA ( Oral psoralen + Ultraviolet light) Methotrexate and vit D reduce epidermal proliferation 68 Prognosis: Psoriasis is a chronic disease. The clinical course is variable, but less than half of the patients followed for a prolonged period will have a prolonged remission; severity may range from a minimal cosmetic problem to a life-threatening emergency. 69 Etiology/pathophysiology Also referred to as systemic red wolf skin Autoimmune disorder Inflammation of almost any body part Skin, joints, kidneys, and serous membranes Affects women more than men Chronic, incurable, and multicausal disease Contributing factors Immunological, hormonal, genetic, and viral 70 Clinical manifestations/assessment Erythema butterfly rash over nose and cheeks Alopecia Photosensitivity Oral ulcers Polyarthralgias and polyarthritis Pleuritic pain, pleural effusion, pericarditis, and vasculitis Renal disorders Neurological signs (seizures) Hematological disorders 71 Systemic Lupus Erythematosus (SLE) – The 72 Diagnostic tests Antinuclear antibody DNA antibody Complement CBC Erythrocyte sedimentation rate Coagulation profile Rheumatoid factor • • • • • • Rapid plasma reagin Skin and renal biopsy C-reactive protein Coomb’s test LE cell prep Urinalysis Chest x-ray 73 Medical management/nursing interventions Medications Nonsteroidal antiinflammatory agents Ibuprofen, ASA antimalarial drugs - hydroxychloroquine (Plaquenil®) or chloroquine Corticosteroids - methylprednisolone antineoplastic drugs – azathioprine (Imuran) antiinfective agents - Ciprofloxacin Analgesics diuretics 74 Medical management/nursing interventions No cure treat symptoms induce remission aleviate exacerbations Avoid direct sunlight Balance rest and exercise Balanced diet 75 Prognosis There is no known cure for SLE. Management of the disease depends on the nature and severity of the manifestations and the organs affected. 76 77 Etiology/pathophysiology Lice infestation Three types of lice Head lice (capitis) Attaches to hair shaft and lays eggs Body lice (corporis) Found around the neck, waist, and thighs Found in seams of clothing Pubic lice (crabs) Looks like crab with pincers Found in pubic area 78 Clinical manifestations/assessment Nits and/or lice on involved area Pinpoint raised, red macules Pinpoint hemorrhages Severe pruritus Excoriation Diagnostic tests Physical exam 79 (From Baran R., Dawber, R.R., & Levene, G.M. [1991]. Color atlas of the hair, scalp, and nails. St. Louis: Mosby.) Eggs of Pediculus attached to shafts of hair. 80 Medical management/nursing interventions Lindane (Kwell); pyrethrins (RID) Cool compresses Corticosteroid ointment Assess all contacts Wash bed linens and clothes in hot water Properly clean furniture or nonwashable materials 81 Etiology/pathophysiology Sarcoptes scabiei (itch mite) Mite lays eggs under the skin Transmitted by prolonged contact with infected area Clinical manifestations/assessment Wavy, brown, threadlike lines on the body Pruritus Excoriation 82 Diagnostic tests Microscopic examination of infected skin Medical management/nursing interventions Lindane (Kwell), pyrethrins (RID), crotamiton (Eurax), 4-8% solution of sulfur in petrolatum Treat all family members Wash linens and clothing in hot water 83 Keloids Angiomas Verruca (wart) Nevi (moles) Basal cell carcinoma Squamous cell carcinoma Malignant melanoma 84 Keloids Overgrowth of collagenous scar tissue; raised, hard, and shiny May be surgically removed, but may recur Steroids and radiation may be used Angiomas A group of blood vessels dilate and form a tumor-like mass Port-wine birthmark Treatment: electrolysis; radiation 85 (From Zitelli, B.J., Davis, H.W. [2002]. Atlas of pediatric physical diagnosis. [4th ed.]. St. Louis: Mosby.) Keloids. 86 Verruca (wart) Benign, viral warty skin lesion Common locations: hands, arms, and fingers Treatment: cauterization, solid carbon dioxide, liquid nitrogen, salicylic acid Nevi (moles) Congenital skin blemish Usually benign, but may become malignant Assess for any change in color, size, or texture Assess for bleeding or pruritus 87 Basal cell carcinoma Skin cancer Caused by frequent contact with chemicals, overexposure to the sun, radiation treatment Most common on face and upper trunk Favorable outcome with early detection and removal 88 Squamous cell carcinoma Firm, nodular lesion; ulceration and indurated margins Rapid invasion with metastasis via lymphatic system Sun-exposed areas; sites of chronic irritation Early detection and treatment are important 89 (From Belcher, A. E. [1992]. Cancer nursing. St. Louis: Mosby.) Basal cell carcinoma. 90 (Courtesy of the Department of Dermatology, School of Medicine, University of Utah.) Squamous cell carcinoma. 91 Malignant melanoma Cancerous neoplasm Melanocytes invade the epidermis, dermis, and subcutaneous tissue Greatest risk Fair complexion, blue eyes, red or blond hair, and freckles Treatment Surgical excision Chemotherapy Cisplatin, methotrexate, dacarbazine 92 (From Habif, T.P. [2004]. Clinical dermatology: a color guide to diagnosis and therapy. [4th ed.]. St. Louis: Mosby.) The ABCDs of melanoma. 93 Prevention of Skin Cancer The American Academy of Dermatology (AAD) has recommended these three preventive steps for prevention of skin cancer: Wear protective clothing, including a hat with a 4-inch brim. Apply sunscreen all over the body and avoid sun from 10 am to 3 pm. Regularly use a broad-spectrum sunscreen with a skin protection factor (SPF) of 15 or higher, even on cloudy days. 94 Prevention of Skin Cancer The following six steps have been recommended by the AAD and the Skin Cancer Foundation to help reduce the risk of sunburn and skin cancer: 1. Minimize exposure to the sun at midday-between 10 AM and 3 PM. 2. Apply sunscreen, with at least an SPF 15 or higher that protects against both ultraviolet A (UVA) and ultraviolet B (UVB) rays, to all areas of the body that are exposed to the sun. 3. Reapply sunscreen every 2 hours, even on cloudy days. Reapply after swimming or perspiring. 95 Prevention of Skin Cancer 4. Wear clothing that covers the body and shades the face. Hats should provide shade for both the face and back of the neck. Wearing sunglasses reduces the amount of rays reaching the eyes by filtering as much as 80% of the rays, and protecting the eyelids as well as the lenses. 96 Prevention of Skin Cancer 5. Avoid exposure to UV radiation from sunlamps and tanning parlors. 6. Protect children. Keep them from excessive sun exposure when the sun is stronger (10 AM to 3 PM), and apply sunscreen liberally and frequently to children ages 6 months and older. 97 • • END DONE 98