Integumentary 2119 PDF

Alterations in Integumentary Function NUR 2119 A&P of the Integumentary System Assessment  Skin Scrapings Skin Scrapings Skin Biospy Patch Testing DIAGNOSTICS Tzanck Smear Cli...

Alterations in Integumentary Function NUR 2119 A&P of the Integumentary System Assessment  Skin Scrapings Skin Scrapings Skin Biospy Patch Testing DIAGNOSTICS Tzanck Smear Clinical Photographs Woods Light Examination Impetigo Superficial bacterial skin infection Common in children BB Contagious  Begin as small, red macules Impetigo which quickly become Manifestations discreet Vesicles rupture and become BB covered with honey crusts Smooth, red, moist surfaces under crusts Bullous impetigo Nonbullous impetigo  Topical antibacterial Impetigo therapy Management Systemic Antibiotics Bactericidal soap BB  Bathe at least once daily Impetigo Hand hygiene Nursing Use separate towel and Management washcloth BB Infected people should avoid contact with others until lesions heal.  Folliculitis Furuncle(Boil) Carbuncle Acute inflammation arising Inflammatory condition Abscess of the skin and deep in one or more hair of the cells within the subcutaneous tissue follicles ad spreading into hair follicles that represents an the surrounding dermis extension of a furuncle Bacterial, viral, fungal, Infection may progress and or parasitic infection involve skin and subcutaneous fatty tissue, High fever, pain, Single or multiple leukocytosis, and sepsis papules or pustules Tenderness, pain, and may occur appear close to the hair surrounding cellulitis may follicles develop Furnuncle Carbuncle  Systemic antibiotic therapy Folliculitis, Furuncle, Incision and drainage Carbuncle Intravenous (IV) fluids, Management fever reduction, and other BB supportive treatments Bactericidal soap  Warm, moist Folliculitis, Furuncle, compresses Carbuncle Antibacterial soap Management Antiobiotic oinment BB Dressings Standard precautions  Herpes Zoster “Shingles” Varicella-zoster virus (VZV) Painful vesicular eruption along the area of distribution of the sensory nerves (dermatome) from one or more posterior ganglia  Caused by reactivation of the dormant varicella-zoster virus Herpes Zoster in clients who have had chickenpox. “Shingles” Latent viruses are reactivated BB and travel by way of the peripheral nerves red rash of small fluid filled blisters  Pre eruptive, Herpes Zoster Acute eruptive Clinical Postherpetic Manefestations neuralgia(PHN) BB Herpes Zoster  Herpes Zoster Ophthalmicus Rare Trigeminal nerve is affected that innervates the ocular and periocular structures May cause significant pain,o cular complications, including blindness  Antiviral agents Herpes Zoster Pain managment Management Vaccination BB  Antivirals Pain Management Other Acyclovir NSAIDS Pregabalin or (Zovirax), Acetaminophen gabapentin, Valacyclovir Opiods tricyclic (Valtrex), antidepressants Famciclovir for Postherpetic (Famvir) neuralgia  Take medications as Herpes Zoster prescribed Nursing Management Keep f/u appts Pain managment BB Vaccination  Fungal Infections Tinea “Ringworm” Affects the head, body, groin, feet, and nails Tinea barbae Tinea capitis Tinea corporis Tinea cruris Tinea pedis Tinea unguium  TINEA Tinea Tinea Tinea cruris Tinea pedis Tinea Capitis/ Corporis unguium barbae Groin area; “athlete’s body “jock itch” foot” Toenails; red macule, small, red soles have hair shaft; onychomyc which scaling scaling, beard osis spreads to patches, mild Nails oval, scaling, a ring of spread to redness thicken, erythematou papules or form with crumble s patches vesicles circular maceration easily, and brittle hair, with elevated in the toe lack luster patchy central plaques webs alopecia clearing Pruritus Pruritus Tinea Capitis Tinea Corporis Tinea Cruris Tinea Pedis Tinea Unguium  Pediculosis Paraisitic skin infection Head louse – Pediculus humanus capitis Body louse – Pediculus humanus corporis Pubic or crab louse – Pediculosis pubis  PEDICULOSIS CAPITIS Infestation of the scalp eggs(nits) young lice hatch in about 6-9 days; reach maturity in about 7 days. Transmission Most commonly found along the back of the head and behind the ears. Eggs appear silvery, glistening oval bodies Pruritus Children Pediculosis Capitis  PEDICULOSIS CORPORIS Infestation of the body Affects people who live in close quarters. lives primarily in the seams of underwear and clothing Pruritus; excoriation Secondary lesion Long standing cases, skin may become thick, dry, and scaly with dark pigmented areas.  PEDICULOSIS PUBIS Infestation localized to the genital region and transmitted chiefly by sexual contact Pruritus, especially at night Reddish brown dust May coexist with STIs such as gonorrhea, herpes, or syphilis  Management Head & Pubic lice Pyrethrin containing Body lice shampoo; piperonyl Bathe with soap and water butoxide or Wash all bedding, towels, and clothing in hot water> at least 130 degrees permethrin. F or dry cleaned to prevent reinfestation. comb with fine toothed comb Education Nursing Do not share combs, brushes, hats Treatment for all family members and sexual contacts with body and or pubic lice Petroleum may be applied to eyelashes Upholstered furniture, rugs, and floors should be vacuumed frequently.  Scabies Infestation of the skin by the itch mite Sarcoptes scabiei Substandard hygienic conditions Frequently involve fingers  Scabies Symptoms typically develop 4 weeks after infestation Severe itching, esp. at night Small raised burrows Extensor surfaces of elbows, around nipples, axillary folds, under pendulous breasts, groin Secondary lesions Scabies  Scabies Gerontologic Considerations Long term care facilities susceptible to outbreaks  Scabies Diagnosis confirmed by scrapings of epidermis Warm soapy bath or shower Permethrin 5% Apply to skin from neck down, leave on 12-24 hours; repeat 1 week  Scabies Bedding and clothing washed in hot water and dried on the hot dryer cycle or dry cleaned Topical corticosteroid pruritis>oral antihistamines oral antibiotic if secondary infection Treat family memebers and close contacts  Acne Inflammatory disorder of sebaceous glands contiguous with hair follicles inflammatory (pustules, papules, and nodules) noninflammatory (closed and open comedones) lesions  Acne Pathophysiology androgens stimulate the sebaceous glands causing them to enlarge and secrete a natural oil (sebum) accumulated sebum plugs the pilosebaceous ducts inflammatory response.  Acne Clinical Manifestations Closed comedones>whitehead Open comedone>blackhead inflammation is seen clinically as erythematous papules, inflammatory pustules, and inflammatory cysts. Acne Acne  Acne Assessment and Diagnostic Findings Physical examination, evidence of lesions characteristic of acne and age Graded as mild, moderate, or severe based on number and type of lesions Mild Moderate Severe  Acne Goals of Management Reduce bacterial colonies Decrease sebaceous gland activity Prevent follicles from plugging Reduce inflammation Combat secondary infection Minimize scarring Eliminate predisposing factors Nutrition and Hygiene Therapy  Acne Pharmacologic Therapy Topical Therapy Benzoyl peroxide Salicylic acid preparations Topical retinoids Topical antibiotic Other> azelaic acid, dapsone gel  Acne Oral antibiotics>tetracycline, doxycycline, minocycline, erythromycin, azithromycin, trimethoprim-sulfamethoxazole Oral Retinoids> isotretinoin Estrogen therapy>progesterone- estrogen therapies Nursing Acne Monitor and manage potential of skin treatments Patient education> skin care techniques, managing potential problems related to skin disorder or therapy Prevention of scarring Educate about prescribed medications and self care Nursing Acne Monitor and manage potential of skin treatments Patient education> skin care techniques, managing potential problems related to skin disorder or therapy Prevention of scarring Educate about prescribed medications and self care  Psoriasis Chronic inflammatory multisystem disorder of the skin Silvery plaques on the skin over the elbows, knees, scalp, lower back, and buttocks Genetic predisposition Exacerbations and remissions  Psoriasis Pathophysiology Autoimmune Epidermis becomes infiltrated by activated T cells and cytokines Epidermal hyperplasia Rapid turnover of poorly matured cells resulting plaque like lesions that have silvery, scaly appearance Psoriasis  Psoriasis Red, raised patches of skin covered with silvery scales Scaly patches are formed from the buildup of living and dead skin  Psoriasis Complications Asymmetric rheumatoid factor-negative arthritis of multiple joints Rheumatology referral Generalized exfoliative dermatitis(erythroderma)  Psoriasis Presence of classic plaque like lesions generally confirms diagnosis  Psoriasis Goals of Medical Management Slow rapid turnover of epidermis Promote resolution lesions Control the natural cycles of the disease No known cure  Psoriasis Medical Management Topical Agents Phototherapy Systemic Agents  Psoriasis Medical Management Mild disease Topical agents, possibly in tandem with phototherapy Moderate and Severe disease Topical agents, phototherapy, and systemic treatment  Psoriasis Medical Management Topical Agents> used to slow the overactive epidermis Topical corticosteroids Anti Inflammatory effects  Psoriasis Medical Management Topical nonsteroidal agents>suppress epidermopoiesis and cause sloughing of the rapidly growing epidermal cells Calcipotrience(Dovonex)  Psoriasis Medical Management Topical nonsteroidal agents Continued Tazarotene(Tazorac)  Psoriasis Medical Management Intralesional injections Triamcinolone (Aristocort) Phototherapy Methotrexate- first line drug for treatment of moderate to severe Cyclosporine- considered in severe, therapy resistant cases  Psoriasis Medical Management Biologic agents-act by inhibiting activation and migration, eliminating the T-cells completely, slowing post secretory cytokines or inducing immune deviation Nursing Management Psoriasis Assess impact of disease on patient and coping strategies psychosocial and physical no cure and lifetime management provoking factors review and explain treatment emollients self care  Blistering Diseases Pemphigus Vulgaris Stevens Johnson Syndrome  Pemphigus Vulgaris Assessment and Diagnostic Findings Oral lesions painful, bleed easily, and heal slowly. Skin bullae enlarge, rupture, and leave large, painful eroded areas that are accompanied by crusting and oozing. Odor from bullae and the exuding serum Blistering or sloughing of uninvolved skin when minimal pressure is applied (Nikolsky sign)  Pemphigus Vulgaris Assessment and Diagnostic Findings Large areas of the body eventually are involved. Most common complications arise when disease process is widespread. Skin bacteria Fluid and electrolyte imbalance Pemphigus Vulgaris  Pemphigus Vulgaris Medical Management Prevent loss of serum and the development of secondary infection; promote re-epithelization (i.e., renewal of epithelial tissue). Corticosteroids Immunosuppressive agents Monoclonal antibody- rituximab(Rituxan) Intravenous immunoglobulin (IVIG) Immunosuppressant- cyclophosphamide (Cytoxan)  Pemphigus Vulgaris Nursing Management Nursing Management- p. 1847  Toxic Epidermal Necrolysis(TEN)/Stevens- Johnson Syndrome(SJS) TEN and SJS-potentially fatal acute skin disorders Widespread erythema and macule formation with blistering epidermal detachment or sloughing and erosion formation.  Toxic Epidermal Necrolysis(TEN)/Stevens-Johnson Syndrome(SJS) Up to 75% of cases of TEN and SJS are triggered by medication reactions Antibiotics (especially sulfonamides), anticonvulsants, NSAIDs, allopurinol (Zyloprim), and oxicam NSAIDs (e.g., meloxicam [Mobic]) frequently implicated  Toxic Epidermal Necrolysis(TEN)/Stevens-Johnson Syndrome(SJS) Occur in all ages and both genders Older adults who take multiple medications may be at greater risk. Genetic component Cell-mediated cytotoxic reaction  Toxic Epidermal Necrolysis(TEN)/Stevens-Johnson Syndrome(SJS) Clinical Manifestations Conjunctival burning or itching, cutaneous tenderness, fever, cough, sore throat, headache, extreme malaise, and myalgias Followed by a rapid onset of erythema involving much of the skin surface and mucous membranes, including the oral mucosa, conjunctiva, and genitalia.  Toxic Epidermal Necrolysis(TEN)/Stevens-Johnson Syndrome(SJS) Assessment and Diagnostic Findings Histologic studies History of medications known to precipitate TEN or SJS may confirm medication reaction esP. if the medications were prescribed within 4 weeks prior to the onset of illness  Toxic Epidermal Necrolysis(TEN)/Stevens-Johnson Syndrome(SJS) Assessment and Diagnostic Findings CBC results may show leukopenia and anemia. Skin biopsy results confirm the diagnosis  Toxic Epidermal Necrolysis(TEN)/Stevens-Johnson Syndrome(SJS) Medical Management Control of fluid and electrolyte balance, prevention of sepsis, and prevention of ophthalmic complications. Supportive care is the mainstay of treatment.  Toxic Epidermal Necrolysis(TEN)/Stevens-Johnson Syndrome(SJS) Medical Management Precipitating medications discontinued immediately. Treated in burn center Tissue samples for culture IV crystalloid fluids  Toxic Epidermal Necrolysis(TEN)/Stevens-Johnson Syndrome(SJS) Medical Management Thermoregulation, wound care, and pain management Total parenteral nutrition Systemic corticosteroids-controversial IVIG Immunosuppressants Topical agents for skin protection>antibacterial, anesthetic agents Biologic dressings  Toxic Epidermal Necrolysis(TEN)/Stevens-Johnson Syndrome(SJS) Nursing Management Nursing Management- p. 1849  Toxic Epidermal Necrolysis(TEN)/Stevens- Johnson Syndrome(SJS)