NURS 3056 Final Info Test 2. Integumentary – Ch. 11,22,23, updated spring 2021 complete guide

NURS 3056 Final Info Test 2. Integumentary – Ch. 11,22,23 Anatomy review • Epidermis-5 layers o Passive circulation from dermis o Cell types in epidermis  Keratinocytes (90%) • Essential for the skin’s protective ...

NURS 3056 Final Info Test 2. Integumentary – Ch. 11,22,23 Anatomy review • Epidermis-5 layers o Passive circulation from dermis o Cell types in epidermis  Keratinocytes (90%) • Essential for the skin’s protective barrier function  Melanocytes (5%) • Protection against UV sunlight  Langerhans’ • Essential for skin immunity  Merkel cells • Touch receptors • Dermis o Highly vascular o Collagen  Critical in wound healing  Responsible for skin’s mechanical strength o Elastic fibers and reticular fibers • Subcutaneous Tissue o Connective tissue and fat cells o Function:  Insulation  Cushioning  Temp regulation  Energy storage • Glands o Sebaceous  Sebum 1) waterproofs 2) lubricates skin and 3) promotes absorption of fat-soluble substances o Apocrine sweat  Become active at puberty  Located in axillae, breast areola, umbilical and anogenital areas, external auditory canals, eyelids o Eccrine sweat  Widely distributed  Function: Cool body by evaporation, excrete waste products, moisturize surface cells • Hair and nails o Rooted in the dermis o Form from specialized keratin • Nails o Protection Functions of the Skin • Protection • Insulation • Sensation • Fluid balance • Temperature regulation • Vitamin production • Immune response function • Can act as a delivery system for drugs Primary vs. Secondary Lesions • Primary lesions o Develop on previously unaltered skin o Macule  Circumscribed, flat area with a change in skin color, <0.5cm diameter. If lesion is >0.5cm, it’s a patch  Ex. Freckles, petechiae, measles, flat mole (nevus), café-au-lait spots, vitiligo (complete depigmentation) o Papule  Elevated, solid lesion, <0.5cm diameter. If >0.5cm diameter it’s a nodule  Ex. Wart (verruca), elevated moles, lipoma, basal cell carcinoma o Vesicle  Circumscribed, superficial collection of serous fluid. <0.5cm diameter  Ex. Varicella (chickenpox), herpes zoster (shingles), second-degree burn o Plaque  Circumscribed, elevated, superficial, solid lesion. >0.5cm diameter  Ex. Psoriasis, seborrheic and actinic keratoses o Wheal  Firm, edematous, irregularly shaped area, diameter variable  Ex. Insect bite, urticaria o Pustule  Elevated, superficial lesion filled with purulent fluid  Ex. Acne, impetigo • Secondary skin lesions o Change with time o Occur because of secondary factors (scratching, infection, etc.) o Fissure  Linear crack or break from epidermis to dermis, dry or moist  Ex. Athletes foot, cracks at corner of the mouth o Scale  Excess, dead epidermal cells produced by abnormal keratinization and shedding  Ex. Flaking skin after drug reaction or sunburn o Scar  Abnormal formation of connective tissue that replaces normal skin  Ex. Surgical incision, healed wound o Ulcer  Loss of epidermis, extending into dermis, crater-like irregular shape  Ex. Pressure ulcer, chancre o Atrophy  Depression in skin resulting from thinning of the epidermis or dermis  Ex. Aged skin, striae o Excoriation  Area in which epidermis is missing, exposing the dermis  Ex. Abrasion, scratch Lesion distribution Term Description Annular Circular, begins in center and spreads to periphery (tinea corporis - ringworm) Asymmetric Unilateral distribution Confluent Merging together (urticaria - hives) Discrete Distinct individual lesions that remain separate (acne) Gyrate Twisted, coiled spiral, snakelike Grouped Clusters of lesions (multiple vesicles of contact dermatitis) Localized Limited areas of involvement that are clearly defined (confined to one area) Polycyclic Annular (circular) lesions grow together (psoriasis) Solitary Single lesion Symmetric Bilateral distribution Zosteriform Linear arrangement along a dermatome area (herpes zoster) Assessment • Subjective: health history, medications, surgery or other treatments, functional health patterns (ex: nutrition) • Objective – Physical Assessment - inspection and palpation o Nails  Color  Texture  Consistency  Thickness  Shape/angle of nail o Hair  Color  Texture  Distribution  Quantity o Skin  Color  Texture  Turgor  Temperature  Moisture  Lesions?  Vascular changes?  Skin changes can point to other disease processes that we will study throughout this year Effects of Drugs on Integumentary System • Drugs that cause photosensitivity (Table 23-2 for full list) o Examples of common offenders:  Antidepressants: amitriptyline, venlafaxine (Effexor)  Antidysrhythmics: amiodarone  Antihistamines: diphenhydramine (Benadryl), cetirizine (Zyrtec)  Antimicrobials: tetracycline, azithromycin (Zithromax), ciprofloxacin (Cipro)  Antifungals: griseofulvin, ketoconazole  Antipsychotics: haloperidol  Diuretics: furosemide (Lasix), hydrochlorothiazide  Hypoglycemics: glipizide, glyburide  NSAIDS: diclofenac (Voltaren), sulindac Categories Examples Antidepressants amitriptyline, doxepin, venlafaxine Antidysrhythmics quinidine, amiodarone (Cordarone) Antihistamines diphenhydramine, chlorpheniramine, clemastine, cetirizine (Zyrtec) Antimicrobials tetracycline, sulfamethoxazole, azithromycin (Zithromax), ciprofloxacin (Cipro) Antifungals griseofulvin, ketoconazole Antipsychotics chlorpromazine, haloperidol Chemotherapy methotrexate, dacarbazine (DTIC), 5-fluorouracil (5-FU) Diuretics furosemide (Lasix), hydrochlorothiazide Hypoglycemics tolbutamide, glipizide (Glucotrol), glyburide Nonsteroidal antiinflammatory drugs diclofenac (Voltaren), piroxicam (Feldene), sulindac Diagnostic tools • Inspection and history • Dermatoscopy • Biopsy • Potassium hydroxide (KOH) • Tzanck test • Stains and cultures • Curretage • Mineral oil slides • Wood’s lamp • Patch testing Study Description and Purpose Nursing Responsibility Biopsy Punch Special punch biopsy instrument of appropriate size used. Instrument rotated to appropriate level to include dermis and some fat. Suturing may or may not be done. Provides full-thickness skin for diagnostic purposes Before: Verify that consent form is signed (if needed). During: Assist with site preparation, anesthesia, procedure, and hemostasis. Properly identify specimen. After: Apply dressing, give postprocedure instructions to patient. Excisional Used when good cosmetic results and/or entire lesion removal desired. Skin closed with subcutaneous and skin sutures Same as above Incisional Wedge-shaped incision made in lesion too large for excisional biopsy. Useful when larger specimen than shave or punch biopsy is needed Same as above Shave Single-edged razor blade used to shave off superficial lesions or small sample of a large lesion. Provides thin specimen for diagnostic purposes Same as above Microscopic Tests Potassium hydroxide (KOH) Hair, scales, or nails examined for superficial fungal infection. Specimen put on glass slide and 10%-20% concentration of KOH added Before: Instruct patient regarding purpose of test. During: Prepare slide. Tzanck test (Wright's and Giemsa's stain) Fluid and cells from vesicles examined. Used to diagnose herpes infections. Specimen put on slide, stained, and examined microscopically Before: Inform patient of purpose of test. During: Use sterile technique for collection of fluid. Culture Test identifies fungal, bacterial, and viral organisms. For fungi, scraping or swab of skin performed. For bacteria, material obtained from intact pustules, bullae, or abscesses. For viruses, vesicle or bulla and exudate taken from base of lesion Before: Instruct patient regarding purpose and procedure. During: Properly identify specimen. Follow instructions for storing specimen if not immediately sent to laboratory. Mineral oil slides To check for infestations, scrapings are placed on slide with mineral oil and viewed microscopically. Before: Instruct patient about purpose of test. During: Prepare slide. Immunofluorescent studies Some skin diseases have specific, abnormal antibody proteins that can be identified by fluorescent studies. Both skin tissue and serum can be examined. Before: Inform patient about purpose of test. During: Assist in obtaining specimen. For punch biopsy, place specimen in special fixative (e.g., Michel's) and not formalin. Miscellaneous Wood's lamp (black light) Examination of skin with long-wave ultraviolet light causes specific substances to fluoresce (e.g., Pseudomonas fungal, infections, vitiligo). Before: Explain purpose of examination. Inform patient it is not painful. During: Darken room. Patch test (Fig. 22-10) Used to assess for allergic dermatitis and photoallergic reactions. Application of allergens to the patient's skin (usually on the back) for 48 hr. Test sites examined 48 hr later for a reaction, characterized by the presence of erythema, papules, vesicles, or all of these. Additional readings beyond 48 hr may be done. Before: Explain purpose and procedure to patient. After: Instruct patient that patches are left in place for 48 hr, during which time it is important not to wash the area or play vigorous sport because if the adhesive tapes peel off the process will have to be repeated. The patches should not be exposed to sunlight or other sources of ultraviolet (UV) light. Skin care • Environmental Hazards o Sun exposure  Ultraviolet (UV) rays • UVA—tanning • UVB—sunburn  Sun protection • Protective clothing • Sunscreen • Risk factors o Fair skin o Blonde or red hair, blue eyes o Outdoor sunbathing o Living near the equator or high altitudes o History of skin cancer Nonmelanoma skin cancers • Actinic keratosis o Premalignant skin lesions • Basal cell carcinoma o Most common type of skin cancer o Least deadly Inflammatory response • Clinical Manifestations o Local response to inflammation  Redness  Heat  Pain  Swelling  Loss of function o Systemic response to inflammation  Increased WBC count with a shift to the left  Malaise  Nausea and anorexia  Increased pulse and respiratory rate  Fever  Beneficial aspects of fever include: • Increased killing of microorganisms • Increased phagocytosis • Increased proliferation of T cells • Types of inflammation o Acute  Healing occurs in 2 to 3 weeks, usually leaving no residual damage  Neutrophils are predominant cell type at site of inflammation o Subacute  Has same features as acute inflammation but persists longer o Chronic  May last for years  Injurious agent persists or repeats injury to site  Predominant cell types involved are lymphocytes and macrophages  May result from changes in immune system (e.g., autoimmune disease) Nursing and interprofessional management • Nursing Implementation o Health Promotion  Prevention of injury  Adequate nutrition  Early recognition of inflammation  Immediate treatment • Acute Intervention o Observation  Immunosuppressed—classic manifestations masked; just “don’t feel well” o Vital signs o Fever management  Determine cause  Administer antipyretic or antibiotics  Monitor for seizures or delirium (>104° F) • Drug therapy o Aspirin o Acetaminophen o NSAIDs o Corticosteroids • RICE o Rest—O2 and nutrients for repair; wound healing o Ice (first 24 hours)—reduced swelling and pain o Compression and immobilization—reduce edema and stabilize o Elevation—reduce edema and pain Inflammation healing process • The final phase of the inflammation process is healing • Healing includes two major components: o Regeneration  Replace cells and tissues with same type o Repair  Connective tissue replaces lost cells  Primary, secondary, or tertiary intention Types of wound repair • Primary intension o Wound margins are neatly approximated  Ex: surgical incision or paper cut  Incision with blood clot  edges approximated with sutures  fine scar • Secondary intention o Wounds occurring from trauma, ulceration, infection o Typically have large amounts of exudate o Wide, irregular wound margins with extensive tissue loss o Often has a greater defect and more gaping wound edges than wounds healing by primary intention o Irregular, large wound with blood clot  granulation tissue fills in wound  large scar • Tertiary Intention o Also known as delayed primary intention o This type of healing is used when:  A contaminated wound is left open and is sutured together after infection is controlled  Infected wound is opened and allowed to granulate before restoring o Typically results in larger/deeper scar than healing by primary or secondary intention o Contaminated wound  granulation tissue  delayed closure with sutures Effect of Nutrition on Wound Healing • Vitamin A: maintenance of normal cell structure, wound healing • Vitamin B complex: needed for metabolic function • Vitamin C ascorbic acid: connective tissue formation and wound healing • Vitamin K: essential for synthesis of clotting factors • Protein: cell growth and wound healing Nursing Management of Dermatologic Concerns • Wet compresses • Baths • Topical medications • Control of pruritus o Break the itch/scratch cycle o Cool environment o Hydration, wet compresses, moisturizers o Topical drugs • Prevention of spread • Prevention of secondary infections • Specific skin care Chronic Dermatologic Problems • Psychologic effects o Reinforce prescribed regimen o Support groups o Camouflage Common Bacterial Infections • Impetigo o Etiology and Patho  Caused by Group A beta-hemolytic strep, staphylococci, or both  Associated with poor hygiene  Contagious o Clinical manifestations  Most commonly on the face  Thick, honey-colored crusts surrounded by erythema  Pruritic (itchy) o Treatment  Topical: warm saline soaks followed by soap and water removal of crusts, antibiotic cream/ointment  Systemic: antibacterial: oral penicillin or clindamycin for widespread or systemic manifestations • Folliculitis o Etiology and Patho  Usually staphylococci  Increased incidence in those with diabetes mellitus o Clinical manifestations  Present in areas of increased friction, moisture, rubbing, or oil  Tender, small pustule at opening of hair follicle with minimal erythema  Crusting  Common on scalp, beard, extremities in men o Treatment  Antistaphylococcal soap and water cleansing  Topical antibiotics (ex: mupirocin)  Warm compresses • Furuncle o Etiology and Patho  Deep infection with staph around hair follicle  Associated with severe acne or seborrheic dermatitis o Clinical manifestations  Tender, erythematous area around hair follicle with draining pus  Common on face, back of neck, axilla, breasts, buttocks, perineum, thighs o Treatment  Incision and drainage  Antibiotics  Warm, moist compresses • Carbuncle o Etiology and Patho  Multiple, connected furuncles o Clinical manifestations  Multiple pustules with localized erythema o Treatment  Same as for furuncles  Often recur  Heal slowly  Scars may form • Cellulitis o Etiology and Patho  Deep inflammation of subcutaneous tissues  Causative agents: Staphylococcus aureus and strep  Often follows a break in the skin o Clinical manifestations  Hot, tender, erythematous, edematous area with diffuse borders  Chills, malaise, fever o Treatment  Topical: moist heat, immobilization, elevation  Systemic: antibiotics, hospitalization for IV antibiotics if severe • Erysipelas o Etiology and Patho  Superficial cellulitis involving the dermis  Caused by group A beta-hemolytic strep o Clinical manifestations  Red, hot, painful  Sharply demarcated plaque with induration  Bacteremia may be possible. Toxic signs: fever, increased WBC count, headache, malaise o Treatment  Systemic antibiotics (typically penicillin)  Hospitalization likely required Etiology & Pathophysiology Manifestations Treatment and Prognosis Impetigo • Group A β-hemolytic streptococci, staphylococci, or combination of both • Associated with poor hygiene • Primary or secondary infection. Contagious • Vesiculopustular lesions that develop thick, honey-colored crust surrounded by erythema • Pruritic • Most common on face as primary infection Topical: • Wound care with warm saline or aluminum acetate soaks followed by soap-and-water removal of crusts and application of topical antibiotic cream or ointment (mupirocin [Bactroban], retapamulin [Altabax]) • Meticulous hygiene essential Systemic: • Systemic antibiotics (e.g., cephalosporins, amoxicillin, clindamycin) for widespread infections or systemic manifestations Folliculitis • Usually staphylococci • Present in areas subjected to friction, moisture, rubbing, or oil • Increased incidence in patients with diabetes mellitus • Small pustule at hair follicle opening with minimal erythema • Development of crusting • Most common on scalp, beard, extremities in men • Tender to touch • Antistaphylococcal soap (e.g., Hibiclens, Lever 2000, Dial) and water cleansing • Topical antibiotics (e.g., mupirocin) • Warm compresses of water or aluminum acetate solution • Usually heals without scarring • If lesions extensive and deep, possible scarring, loss of involved hair follicles, and treatment with systemic antibiotics Furuncle • Deep infection with staphylococci around hair follicle • Often associated with severe acne or seborrheic dermatitis • Tender erythematous area around hair follicle that is painful • Draining pus and core of necrotic debris on rupture • Most common on face, back of neck, axillae, breasts, buttocks, perineum, thighs • Incision and drainage (possibly with packing), antibiotics, meticulous care of involved skin, frequent application of warm, moist compresses Furunculosis • Increased incidence in patients who are obese, diabetic, chronically ill, or regularly exposed to moisture, pressure • Lesions as above • Malaise, regional adenopathy, elevated body temperature Topical: • Incision and drainage of painful nodules • Warm, moist compresses to erythematous plaques • Measures to reduce surface staphylococci include antimicrobial cream to nares, armpits, and groin and antiseptic to entire skin. • Meticulous personal hygiene Systemic: • Systemic antibiotic effective against MRSA pending culture and sensitivity results • Often recurrent with scarring Carbuncle • Multiple, interconnecting furuncles • Many pustules appearing in erythematous area • Most common at nape of neck • Treatment same as for furuncles • Often recurrent despite production of antibodies • Heal slowly with scar formation Cellulitis • Inflammation of subcutaneous tissues • Possibly secondary complication or primary infection • Often following break in skin • Staphylococcus aureus and streptococci usual causative agents • Deep inflammation of subcutaneous tissue from enzymes produced by bacteria • Hot, tender, erythematous, and edematous area with diffuse borders • Chills, malaise, and fever Topical: • Moist heat, immobilization, and elevation Systemic: • Systemic antibiotic therapy • Hospitalization if severe for IV antibiotic therapy (dalbavancin [Dalvance], vancomycin, linezolid [Zyvox], ceftaroline fosamil [Teflaro], daptomycin [Cubicin]) • Progression to gangrene possible if untreated Erysipelas • Superficial cellulitis primarily involving the dermis • Group A β-hemolytic streptococci • Red, hot, sharply demarcated plaque that is indurated and painful • Bacteremia possible • Most common on face and extremities • Toxic signs: fever, ↑ WBC count, headache, malaise • Systemic antibiotics, usually penicillin • Hospitalization often required Common Viral Infections • HSV1 and HSV2 o Etiology and Patho  Recurrent, lifelong viral infections  Oral: Herpes Simplex Virus-1  Genital: Herpes Simplex Virus-2  Contagious (transmitted via respiratory droplet or fluid containing virus)  Exacerbated by sun, trauma, menses, stress, systemic infection o Clinical manifestations  Symptoms occur 2 days-2 weeks after contact  Painful single or grouped vesicles on erythematous base with/without systemic symptoms (fever, malaise) o Treatment  Symptomatic: soothing moist compress, white petrolatum to lesions  Antiviral drugs: acyclovir, famciclovir, valacyclovir • Herpes Zoster (Shingles) o Etiology and Patho  Incidence increases with age  Activation of varicella-zoster virus  Can be contagious to anyone who has not had chickenpox or is immunosuppressed o Clinical manifestations  Linear distribution of grouped vesicles and pustules on an erythematous base along a dermatome  Usually on trunk, face, lumbosacral area  Burning, pain, neuralgia prior to outbreak  Mild/severe pain during outbreak o Treatment is symptomatic  Topical: wet compresses, Silvadene for ruptured vesicles  Systemic: antivirals within 72 hrs to prevent postherpetic neuralgia, analgesia, gabapentin for postherpetic neuralgia • Verruca Vulgaris (common warts) o Etiology and Patho  Caused by HPV  Mildly contagious in autoinoculation phase  Prevalence greater in young and immunosuppressed  May spontaneously disappear in 1-2 years o Clinical manifestations  Circumscribed, hypertrophic, flesh-colored papule  Painful if laterally compressed o Treatment  Surgery  Liquid nitrogen  Blistering agent (cantharidin)  Salicylic acid  CO2 laser destruction Common Fungal Infections • Candidiasis o Etiology and Patho  Caused by Candida albicans  Appears in warm, moist areas (groin, oral mucosa, submammary folds)  Immunosuppression allows yeast to become pathogenic o Clinical manifestations  Mouth: white, cheesy plaque (think milk curds!)  Vagina: Red, edematous, painful vaginal wall with white patches. Vaginal discharge and itching. Pain with urination and intercourse  Skin: Diffuse papular erythematous rash with pinpoint satellite lesions around edges of affected area o Treatment and prognosis  Azole antifungals  Sexual abstinence or use of a condom  Skin hygiene (goal to keep skin clean/dry)  Powder for non-mucosal surfaces to prevent recurrence • Tinea o Tinea corporis (ringworm)  Ring-like in shape, scaly, well-defined, erythematous o Tinea cruris (jock itch)  Well-defined, scaly plaque in groin o Tinea pedis (athlete’s foot)  Scaling and maceration in interdigital space  Plantar surfaces may have erythema and blistering  Can be pruritic and painful o Tinea unguium (onychomycosis)  Incidence increases with age  Toenails more commonly affected than fingernails  Scaliness under distal nail plate  Brittle/thickened, broken, yellowed nails Common Infestations • Pediculosis (lice) o Etiology and Patho  Can be on the head, body, or pubic area  Parasites suck blood, excrete and leave eggs on skin and hair  Transmission of pubic lice is by sexual contact o Clinical manifestations  Small, red, noninflammatory  Starts flush with skin. May progress to more of a papular/wheal-like shape  Pruritic. May see excoriation from pruritis  Nits/eggs are firmly attached to hair shift on head/body o Treatment  γ-Benzene hexachloride or pyrethrins to treat body  Spinosad (Natroba) topical suspension to treat scalp/hair  Close contacts should be screened/treated • Scabies o Etiology and Patho  Caused by Sarcoptes scabei  Allergic reaction to the eggs, feces, and mite parts  Spread by direct contact o Clinical manifestations  Erythematous papules/vesicles with possible crusting  Severe itching, especially at night  Burrows in interdigital webs, flexor surface of the wrists, genitalia, and anterior axillary folds o Treatment  5% permethrin topical lotion, one overnight application with second application 1 wk later. May yield 95% eradication.  Treat all family members with plastic covering for 5 days, launder all clothes and linen with bleach.  Antibiotics if secondary infection present • Ticks o Etiology and Patho  Borrelia burgdorferi causes Lyme disease  Ticks are endemic in the NE, Mid-Atlantic, parts of Midwest and West o Clinical manifestations  Spreading, ringlike, warm, itchy, painful rash commonly seen in groin, buttocks, axilla, trunk, upper arms, and legs (appearing 3-4 weeks post tick bite)  Flu-like symptoms  Cardiac, arthritic, and neurologic symptoms possible o Treatment  Oral antibiotics: doxycycline, tetracycline  IV antibiotics if arthritic, neurologic or cardiac symptoms present  Rest/healthy diet Common Reactions • Allergic Contact Dermatitis o Etiology and Patho  Type IV delayed hypersensitivity response • Notes: The allergic agent is absorbed through the skin and acts as an antigen. Sensitization occurs after one or more exposures to the irritant  Lesions appear 2-7 days after allergic contact o Clinical manifestations  Sharply circumscribed red papules/plaques  May see occasional vesicles  Pruritic  Dermatitis typically takes shape of causative agent (ex: dermatitis around finger from ring) o Treatment  Topical or oral corticosteroids (systemic If severe)  Antihistamines  Skin lubrication  Elimination of allergic agent • Atopic Dermatitis o Etiology and Patho  Type 1 hypersensitivity  Genetic influence  Typically, chronic and relapsing in nature  Associated with allergic rhinitis/asthma o Clinical manifestations  Pruritic  Can be erythematous or scaly  May see lichenification from itching o Treatment  Lubrication  Topical immunomodulators (Elidel and Protopic)  Stress reduction  Corticosteroids or phototherapy if severe  Antibiotics if secondary infection from chronic scratching Acne • Etiology and Patho o Inflammatory disorder of sebaceous glands o More common in teens but can persist into adulthood o Flares can occur: 1) before menses, 2) with use of corticosteroids or 3) androgen dominant BCP • Clinical manifestations o Noninflammatory: Open comedones (blackheads) and closed comedones (whiteheads) o Inflammatory: papules and pustules • Treatment o Topical: mechanical removal via extraction, topical benzoyl peroxide, retinoids, antimicrobials o Systemic: systemic antibiotics, Accutane (severe nodulocystic acne) Psoriasis • Etiology and Patho o Autoimmune chronic dermatitis involving excessive turnover of epidermal cells o Family predisposition o Typically develops before age 40 • Clinical manifestations o Well-demarcated silvery, scaly plaques on reddened skin o Commonly located on scalp, elbows, knees, palms, soles, fingernails o Itching, burning, pain • Treatment o Topical: corticosteroids, tar, salicylic acid, calcipotriene, anthralin, intralesional steroid injection o Systemic: Natural/artificial UVB light, PUVA, methotrexate, Otezla, biologic therapy (moderate to severe disease) Seborrheic Keratosis • Etiology and Patho o Benign o Familial o Usually occur after age 40 • Clinical manifestations o Irregularly round/oval verrucous papules or plaques o Stuck-on appearance o Pigment increase with time o May be itchy • Treatment o Removed via curettage or cryosurgery to eliminate itching or for cosmetic reasons o Biopsy may be necessary to distinguish between SK and melanoma Lentigo (age spot) • Etiology and Patho o Increased number of normal melanocytes in the basal layer of the epidermis r/t sun exposure and aging • Clinical manifestations o Hyperpigmented brown/black macule or patch on a sun-exposed area • Treatment o Treatment is only for cosmetic reasons: liquid nitrogen, laser resurfacing o Biopsy if trying to differentiate between lentigo and melanoma Atypical or Dysplastic Nevi • Etiology and Patho o Can be a precursor for malignant melanoma • Clinical manifestations o Typically, greater than 5mm o Irregular border o Variegated color o At least one flat portion, often at edge of mole • Treatment o Closely monitor those with family history of melanoma or dysplastic nevi o Biopsy for suspicious looking lesions Premalignant Skin Lesion: Actinic Keratosis • Etiology and Patho o Caused by sun damage o Premalignant and common in older whites o Most common type of skin cancer; least deadly • Clinical manifestations o Dry, keratotic, scaly papule o Can appear as a rough, adherent scale on an erythematous base, which recurs when it is removed • Treatment o Cryosurgery o Topical application of 5-FU, Aldara, or diclofenac o Chemical peels o Laser resurfacing o Photodynamic therapy Malignant Neoplasms of Skin: • Basal Cell Carcinoma o Etiology and Patho  Continuous division of basal cells, causing formation of a mass  Related to sun exposure, genetic skin type, radiation, scars, some types of nevi o Clinical manifestations  Superficial BCC: erythematous, pearly, well-defined, slightly elevated plaque  Nodular/ulcerative BCC: Small, slowly growing papule that is pearly in appearance. Can develop into ulceration or erosion. May see overlying telangiectasia o Treatment  5-FU and imiquimod for superficial lesions  Surgical excision, electrodessication and curettage, cryosurgery, radiation therapy, topical or systemic chemo, photodynamic therapy • Squamous Cell Carcinoma o Etiology and Patho  Often occurs on previously damaged skin (sun, radiation, area of scarring)  Malignant tumor of squamous cells in epidermis o Clinical manifestations  Commonly seen on sun exposed areas (think hands and face!)  Superficial SCC: thin, scaly, erythematous plaque  Early SCC: firm nodule with unclear border, scaling, ulceration  Late SCC: Lesion is covered with a scale or horn, may see ulceration o Treatment  Surgical excision  Cryosurgery  Radiation/chemotherapy  Electrosurgery • Malignant Melanoma o Etiology and Patho  Neoplastic growth of melanocytes  Classified according to histological spread  Can metastasize o Risk factors: red or blonde hair, light-colored eyes, fair skin that freckles, chronic sun exposure, family history o Clinical manifestations  Irregular color, surface, border  Can be flat or elevated  May be ulcerated or eroded  Typically, less than 1 cm in size o Diagnosis  Dermoscopy  Incisional biopsy  Tumor thickness  Breslow measurement  Clark level o Treatment  Treatment determined by  Site of original tumor  Stage of the cancer  Surgical excision with potential sentinel lymph node evaluation • Table 23.4 – Premalignant and Malignant Conditions of the Skin Etiology and Pathophysiology Clinical Manifestations Treatment and Prognosis Actinic Keratosis • Actinic (sun) damage • Premalignant skin lesions • Common in older whites • Flat or elevated, dry, hyperkeratotic scaly papule. Often multiple • Possibly flat, rough, or verrucous (wartlike) • Rough adherent scale on red base, which returns when removed • Often on erythematous sun-exposed area • Increase in number with age • Cryosurgery. Topical application of 5-FU, imiquimod (Aldara) or diclofenac (Solaraze), chemical peels, laser resurfacing, photodynamic therapy (PDT, with 5-aminolevulinic acid [5-ALA] or methyl aminolevulinate [MAL] followed by light irradiation) • Recurrence possible even with adequate treatment Atypical or Dysplastic Nevi • Morphologically between common acquired nevi and melanoma • May be precursor of malignant melanoma • Often >5 mm. Irregular border, possibly notched. Frequently multiple • Variegated color of tan, brown, black, red, or pink within single mole • Presence of at least one flat portion, often at edge of mole • Most common site on back, but possible in uncommon mole sites such as scalp or buttocks (Fig. 23-5) • Increased risk for melanoma • Careful monitoring of persons suspected of familial tendency to melanoma or dysplastic nevi • Excisional biopsy for suspicious lesions Basal Cell Carcinoma • Change in basal cells. No maturation or normal keratinization • Continuing division of basal cells and formation of enlarging mass • Related to excessive sun exposure, genetic skin type, x-ray radiation, scars, and some types of nevi Nodular and ulcerative: • Small, slowly enlarging papule • Borders semi-translucent or “pearly” with overlying telangiectasia • Erosion, ulceration, and depression of center • Normal skin markings lost Superficial: • Erythematous, pearly, sharply defined, barely elevated plaques • Surgical excision, electrodessication and curettage, cryosurgery, radiation therapy, topical or systemic chemotherapy, and photodynamic therapy • 90% cure rate with primary lesions • Slow-growing tumor that invades local tissue. Metastasis rare • 5-FU and imiquimod for superficial lesions, photodynamic therapy for small lesions, vismodegib (Erivedge) or sonidegib (Odomzo) for metastatic or recurrent locally invasive lesions Squamous Cell Carcinoma • Frequent occurrence on previously damaged skin (e.g., from sun, radiation, scar) • Malignant tumor of squamous cell of epidermis. Invasion of dermis, surrounding skin • Most common on sun-exposed areas such as face and hands • Superficial: Thin, scaly erythematous plaque without invasion into the dermis • Early: Firm nodules with indistinct borders, scaling, and ulceration • Late: Covering of lesion with scale or horn from keratinization, ulceration • Surgical excision, cryosurgery, radiation therapy, chemotherapy, electrosurgery • Untreated lesion may metastasize to regional lymph nodes and distant organs. • 13-cis-retinoic acid and interferon alfa-2A for metastatic lesions • High cure rate with early detection and treatment Malignant Melanoma • Neoplastic growth of melanocytes anywhere on skin, eyes, or mucous membranes • Classification according to major histologic mode of spread • Potential invasion and widespread metastases • Irregular color, surface, and border Variegated color, including red, white, blue, black, gray, brown • Flat or elevated. Eroded or ulcerated • Often <1 cm in size • Most common sites in males are back, then chest. In females are legs, then back (Fig. 23-2) • Surgical excision and possible sentinel lymph node evaluation • Possible use of adjuvant therapy after surgery if lesion >1.5 mm in depth • Correlation between survival rate and depth of invasion • Poor prognosis unless diagnosed and treated early • Spreading by local extension, regional lymphatic vessels, and bloodstream Cutaneous T-Cell Lymphoma • Origins in skin. Localized chronic, slowly progressing disease • Possibly related to environmental toxins and chemical exposure • Mycosis fungoides (MF) is most common form. • Sézary syndrome is an advanced form of MF. • Prevalence twice as high in men as in women • Classic presentation involves 3 stages: patch (early), plaque, and tumor (advanced). • History of persistent macular eruption followed by gradual appearance of indurated erythematous plaques on trunk that appears similar to psoriasis • Pruritus, lymphadenopathy • Treatment usually controls symptoms but is not curative. UVB, PUVA, corticosteroids, topical nitrogen mustard, radiation therapy in patch and plaque stage of disease • Interferon, systemic chemotherapy, extracorporeal photopheresis, romidepsin (Istodax) for progressive disease • Bexarotene (Targretin), denileukin diftitox (Ontak), and vorinostat (Zolinza) for advanced disease • Disease course is unpredictable. 10% will have progressive disease. • Cultural and Ethnic Integumentary Problems o African Americans and Hispanics have a lower incidence of skin cancer than whites. o In the United States, rates of BCC and SCC are increasing among Hispanic and Asian women. o Melanoma can occur in dark-skinned persons but often goes unrecognized until the advanced stages. o When darker skin heals after injury or inflammation, it tends to be hypopigmented or hyperpigmented. o African Americans and Asians are more likely to develop a keloid at the site of an injury. Patient Education • Self-monitoring for Skin Cancer o Patients should self-examine monthly o Teach them ABCDE  A: Asymmetry  B: Border  C: Color change/variation  D: Diameter greater than 6mm  E: Evolving lesion • Sun Damage o Sun damage to skin is cumulative o Greatest risk for sun damage between 10am-2pm o Sunscreens are not completely water resistant; reapply sunscreen after swimming o Ears, toes, lips need sunscreen as well o Reapply every 2 hours o Certain medications can potentiate the sun’s effects (ex: Cipro can cause photosensitivity) o Apply sunscreen with at least SPF 15 if normal risk; SPF 30 if history of skin cancer or problems with sun sensitivity. Look for sunscreen that is broad-spectrum o Teach patients to wear sunglasses, a large-brimmed hat, darker-colored, long-sleeve shirt with tightly woven fabric or carry an umbrella o There is still a risk of sun damage on cloudy days, up to 80% of sun’s UV rays can penetrate clouds o Table 23.12 – Drug Therapy Agent Therapeutic Considerations Powder Promotion of dryness. Lubricates skinfold areas to prevent irritation. Base for antifungal preparations. Protect patient from inhaling. Lotion Emulsions of water, alcohol, and/or oil. Cooling and drying. Some leave residual powder film after evaporation of water. Useful in subacute pruritic eruptions Cream Emulsions of oil and water. Most common base for topical medications. Lubrication and protection Ointment Oil with differing amounts of water added in suspension. Lubrication and prevention of dehydration. Petrolatum most common Paste Mixture of powder and ointment, used when drying effect necessary because moisture is absorbed Gel Non-greasy combination of propylene glycol and water. May contain alcohol Cutaneous Drug Reactions • Steven Johnson syndrome (SJS) • Toxic epidermal necrolysis (TEN) o Stop offending drugs o Supportive care Wounds Pathophysiology review • Inflammatory response=reaction to cell injury o Purpose:  Neutralize/dilute inflammatory agent  Remove necrotic material  Create an appropriate environment for healing o Made up of:  Vascular response to injury • Cell injuredBrief vasoconstrictionrelease of chemical mediatorslocal vasodilation and increased blood flow increased capillary permeability and localized edema redness, heat, swelling at injury site  Cellular response to injury • Neutrophils and monocytes move from circulation to site of injury  Exudate is formed  Healing Assessment: wound classification • Cause • Depth of affected tissue • Color • Location • Size Nursing Assessment • Location • Size (longest length and widest width) • Depth • Undermining and tunneling • Wound margin (normal, macerated, erythema) • Wound base (eschar, slough, exudate) • Document o Consistency, color, odor of drainage o COCA = Color, odor, consistency, amount **************************CONTINUES****************************