Skin

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skin

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Integumentary system- Integument. Largest organ of body: 16% of body weight. Skin differs anatomically and physiologically in different areas of the body. Thicker in areas of chronic friction. Mechanoreceptors- Merkel cell high in fingers.

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functions

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Protection: 1st defense for infection. If you loose; not if, but when and how many.

Sensation: cutaneous sensory receptors. Merkel- touch. Percinum corpuscles- vibration.

Thermoregulation: change BF to dissipate or conserve heat.

Immune system: Mast cells- histamine. Langerhans cells- antigen presenting cells.

Metabolism: it is an endocrine organ.

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skin endocrine/metabolism

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Metabolism: it is an endocrine organ. Precursor for Vitamin D found in skin. Release hormones- Leptin from subcutaneous.

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layers

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epidermis (5 layers)

dermis (2 layers)

subcutaneous- hypodermis

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epidermis

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Outermost layer that provides 1st barrier of protection (upper 1/3 of skin). Thickness varies according to location (but always 5 layers). Avascular: no blood vessels; nutrition via diffusion from lower dermal layer. Keratinocytes Non-Keratinocytes:

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Keratinocytes

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epidermis. (squamous cells): primary cell of epidermis; synthesize keratin (hard, thick, protective protein). Squamous cell CA.

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Non-Keratinocytes:

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epidermis.

Melanocytes: secrete melanin (skin pigment). Darker = more. Deeper. Protects against UV carcinogen. Absorbs UV light and dissipates it as heat. Protects cells from radiation and DNA damage.

Langerhans’ cells: immune cells.

Merkel cells: sensory to light touch.

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epidermis cell mov't

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Cells formed in lower layers (stratum basale) then push up to top and push dead cells off. Cells at top flatten, thinned as they are filled with keratin. ~14 days from creation --> top layer (stratum corneum). Live ~14 days at top layer until shed off. Desquamation: total lifespan of ~28 days; shedding of skin cells.

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dermis

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Provides thermoregulation and supports vascular network to supply nutrients to avascular epidermis. Papillary layer: Reticular layer:

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Reticular layer:

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Dermis. strength and elasticity to skin; much thicker and less organized; thicker, dense CT. Contents: Fibroblasts. Macrophages: initiate inflammation and repair. Mast cells: produce histamine Lymphatic glands: removal of microbes and excess interstitial fluid. Blood vessels N. fibers Epidermal appendages:

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Papillary layer

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Dermis top layer with free n. endings; well organized; thinner, loose CT.

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fibroblasts- dermis

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Reticular layer. secrete collagen, elastin and ground substance that provide support and elasticity of skin. Primary cell. Critical for wound healing.

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epidermal appendiges

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dermis.

eccrine units (sweat glands that open to skin surface)

apocrine units (sweat glands that open to hair follicles that develop during puberty- axilla and pubic).

hair follicles, nails, sebaceous glands.Originate in dermis and project into epidermis.

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subcutaneous

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(hypodermis) Energy storage in form of adipose tissue. Main function. Trauma protection. Endocrine organ: secretion of hormones (leptin, adiponectin, apelin).

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epidermis and aging

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Thinner: hyper-reactive to skin irritants and increases risk of skin tears.

Decreased # of melanocytes: increased risk of skin CA, loss of protection.

Decreased # of Langerhans’ cells: increased risk of skin CA, decreased immune function.

Decreased Vit D synth: increased risk of OP; less 7 dehydrocholesterol in skin (precursor).

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dermis and aging

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Decreased thickness and degeneration of elastin fibers (wrinkles).

Slower wound healing. Less fibroblasts. Increased risk of shear force trauma --> P ulcers.

Decreased BF. Altered thermoregulation. Slowed wound healing.

Less scar tissue/fibrosis b/c less fibroblasts. Decreased risk of hypertrophic scars.

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epidermal appendages and aging

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Decreased # and altered structure of sweat glands. Altered thermoregulation. Exercise in heat affected.

Decreased # and altered structure of n. endings: Decreased sensation as we age. Increased pain threshold- be careful w/ hot/cold modalities.

(baldness and gray hair).

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macule

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circumscribed (well delineated borders) flat discoloration; may be brown, blue, red or hypo-pigmented. Freckle. Café au lait spots/birth mark.

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pustule

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circumscribed collection of leukocytes and free fluid that varies in size. Acne (sebaceous gland). Folliculitis (hair follicle).

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vesicle

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circumscribed collection of free fluid < 0.5cm in diameter. Lesion filled w/ fluid/virus. Herpatic lesions. Clear fluid that contains viral particles.

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bulla

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circumscribed collection of free fluid >0.5cm in diameter. Lesion filled w/ fluid/virus. Herpatic lesions. Lupus erythematous.

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wheal

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firm edematous plaque resulting from infiltrations of dermis with fluid; transient (hrs). Dermis raised since filled with fluid. Hives. Insect bites.

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papule

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elevated solid lesion <0.5cm in diameter; color varies; can become confluent and form plaques. Very common! Melanoma. Seborrheic keratosis. Warts- contagious. Nevi- moles. Skin tags: usually in areas of chronic friction; benign, common.

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scale

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excess dead epidermal cells produced by abnormal keratinization and shedding. Eczema. Lupus- discoid or SLE. Psoriasis.

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crust

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collection of dried serum and cellular debris (scab like). Impetigo. Tinea capitis. Many are contagious.

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documenting skin lesions

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Any time you note a lesion during evaluation and tx that stands out as different, any time pt. reports sx of skin lesions (further eval. may be necessary). Med referral may be warranted. Location: Generalized (hives) or localized (contact dermatitis). Region of body. Unilateral/bilateral. Pattern: Characteristics:

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patterns

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Dermatomal (shingles). Flexor surfaces (eczema/dermatitis). Extensor surfaces (psoriasis/warts). Associated with contact (jewelry, accessories, etc.). Random.

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characteristics

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Size (measure dimensions) and shape. Anything larger than pencil eraser cause for concern. Color and temperature. Tenderness, pain, pruritus. Texture. Mobility. Elevated or depressed. Exudate: Color, odor, amount, consistency.

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Atopic Dermatitis (Eczema)

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Dermatitis = eczema. Atopy = allergy. Associated w/ infancy. Chronic inf skin dz; atopic is most common type. Often begins during infancy as red, oozing rash (occurs on face). W/ age skin becomes dry, thickened and brownish-gray in color. Common on face and flexor surfaces. Not contagious. To others or other areas. 2nd infection is the biggest prob.

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Atopic Dermatitis (Eczema) sx

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Abnormal drying (xerosis). Pruritus (intense itching).

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Atopic Dermatitis (Eczema) dx

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No definitive test for dx; clinical presentation and dx. Disappears in 1/2. Etiology is not fully known; likely immediate and cellular immune response.

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Atopic Dermatitis (Eczema) tx

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No cure; can resolve spontaneously (1/2). 90% controlled with therapy aimed to break inflammatory cycle. Personal hygiene: skin moisturizing, avoidance of irritants. Topical and/or systemic medications- antihistamines, ABX- treatment of secondary infections.

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Dermatitis (Eczema)

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When it reoccurs as an adult. 3 stages; acute, subacute, chronic. Common in older people. May be caused by hypoproteinemia, venous insufficiency, allergens (atopic), irritants, underlying malignancy, unknown. Can develop w/o having as infant.

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Eczema tips

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Provide edu on proper skin care and avoidance of exacerbating factors. Temped water temp. Non-irritant, no scent soap. Within 5 min, put on emollient- petroleum, no scent, retain moisture. No alcohol based. Urea based is helpful. Use 2-3x/d. In direction of hair. Avoid topical agents w/ alcohol.

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Rosacea

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Inflammatory skin condition that causes redness of face. Not associated with acne. Often cyclic with flare-ups lasting weeks - months. Epidemiology/Risk Factors: Adults (30-60 yrs) with fair skin. More common in women. 10% pop.

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Rosacea CP

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Red areas on the face (bridge of nose and face). Small red bumps or pustules on nose, cheeks, forehead and chin. Visible small blood vessels on nose and cheeks. Ocular rosacea: Burning or gritty sensation in eyes w/ blinking (1/3 of pts). Tendency to flush or blush easily. Rhinophyma:

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Rosacea Rhinophyma

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rare complication form of rosacea that occurs in severe cases. Hypertrophy of sebaceous glands in nose, leading to buildup of tissue on and around nose. More common in men and develops slowly over time. Surgery is only correction.

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Rosacea patho

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Unknown but likely genetic/environmental. Common theories: Blood vessel disorder, chronic bacterial inf (Pylori), mites in hair follicle. Alcohol doesn’t cause may worsen. Worsened by anything that increases BF to skin surface. Hot foods, beverages, alcohol, temp extremes, wind, sunlight, stress, embarrassment, strenuous exercise, hot baths, glucocorticoids, drugs that dilate (HTN).

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Rosacea tx

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Rarely clears up on its own; tends to worsen over time if left untx.tx more effective if started early. PT can be integral in referring early. Medications and self care. Permanent changes in face can be decreased with laser surgery and electro-surgery to reduce visibility of blood vessels.

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Rosacea meds

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Long term use of topical ABX (for anti-inflammatory component of ABX). Oral ABX.

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Rosacea self care

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minimize exposure to triggers that cause flare-ups. Minimize sun, wind, cold exposure to face. Avoid facial products with alcohol. Use non-comedogenic facial products (non-pore blocking). Avoid alcohol consumption.

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Psoriasis

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Chronic, hereditary inf dz that affects skin/nails. Itchy patches of thick, red skin covered by silvery scales- become silver w/ time. Speed up process of cells to surface; build up. Occur primarily on elbows, knees, legs, trunk, palms, soles and scalp (extensor surfaces). Cycles, flaring for few w-m, then subsiding/remission. Dz returns (rarely gone forever).

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Psoriasis epi/risks

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Slightly more females ~28 yrs. Caucasians (1-2% pop). High genetic component. Develops when ordinary life cycle of skin cells accelerates. Triggered by mechanical, chem injury, infections, rx drugs, psychological stress, smoking, preg, excessive sun exposure. Not sure. Not contagious: individual cannot spread condition to another person or to another part of body.

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Psoriasis patho

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develops when ordinary life cycle of skin cells accelerates.Skin cells normally die and flake off in scales 26-28d. Psoriasis accelerates to 3-4 days. 3-4 to move to surface. 14d living at surface. Build up. Not sure on triggers.

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Psoriasis tx

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No cure—tx. can offer significant relief. Goal is to slow cell turnover with fewest possible adverse effects. Challenging to tx- trying to limit ADRs. None cure turnover process. topical cream and phototherapy

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Psoriasis topical cream

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decrease cell turnover. Glucocorticoids (decrease immune system). Slow turnover, thin skin. Vitamin D analogues: decrease skin inflammation and help prevent skin cell proliferation. Coal tar: assumed to work by anti-mitotic effect. Effective; ADRs- stains everything!!! Harmful to good skin. Topical retinoid: normalize DNA activity in skin cells.

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Psoriasis phototherapy

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UV light decreases turnover. Tx. vs. trigger depends on dosage. Natural or artificial light. PUVA: psoralen medication + UVA light (increased risk of sunburn). Long term use increases risk of skin cancer.

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Psoriasis rpognosis

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Overall decreased QOL. Treatment relieves flare-ups in 85-90% of cases. Rate of infection of lesions (secondary infections) is high. Not life threatening, but shortens life expectancy- think it is from itching; decreased sleep quality.

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Psoriasis tips

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Flare-ups controlledw/ tx: meds and stress reduction techniques may reduce healing time. Teach proper application to topical cream: Rub down, not up. Apply only to lesions—not to surrounding skin (wear gloves) as it damages healthy skin. Reassure pt. that condition isn’t contagious. Psoriatic arthritis: ~5-8%. Lesions 10-20y prior. Tx by Rheumatologist.

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benign skin tumors

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Seborrheic keratosis

Nevi- moles

Lipomas

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Seborrheic keratosis

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Waxy, yellow, light to dark brown or black papules (solid). Usually appear as though “stuck-on”. Very common: appear >30 yrs in fair skinned people. Commonly misinterpreted as CA. Common on face and back. Usually medically insignificant (non-cancerous) but can be treated if repeatedly irritated- bras (or for cosmetic reasons). benign

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nevi

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Clusters of pigmented cells. Most people have 10-40 moles. Most moles develop by age 20 yrs; may change over time and may disappear.

Normal: Generally uniform in color (brown, black, blue) with distinct border separating the mole from surrounding skin. Oval or round in shape and about 6mm in diameter (size of pencil eraser). benign

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Lipomas

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Fatty tumors. May be single or multiple. Within dermal or subcutaneous layers. Soft and fairly mobile; feel doughy. Commonly located on neck, shoulders, back, arm, thighs. Take a long time to develop. They are benign. Removed if cosmetically upsetting, symptomatic, size >5cm. benign

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Dysplastic Nevi

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flat moles with irregular borders and a mixture of colors. More likely to become cancerous than normal moles.

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premalignant skin lesions

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Actinic Keratosis:

Bown's dz

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Actinic Keratosis:

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Solar keratosis (sun damage). Most common locations on sun exposed surfaces of fair skinned people (face,ears, lower arms/hands, bald scalps). Brown or dark pink rough, scaly plaques and well defined margins. Often recognized better by touch than sight- rough patches. premalignant skin lesions

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Actinic Keratosis: tx

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Treated by surgical excision or topic 5-Fluorouraceil (5-FU). Eats away top layers of CA cells- topical chemo. If untreated 2-5% progress to squamous cell carcinoma.

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bowen's dz

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Persistent brown to reddish brown scaly plaque with well-defined margins. Can occur anywhere on skin or mucous membranes. Most often on women on LE. Treated by surgical excision and topical 5-FU. premalignant skin lesions

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skin CA

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Malignant Skin Lesions (skin cancer): abnormal growth of skin cells.

3 Main Types: Basal cell and squamous cell cancer (non-melanomas). Melanoma.

Cancerous skin lesions can appear suddenly or develop slowly and appearance will vary depending on type of cancer. Majority of malignant cells develop from current moles.

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skin CA epidemiology

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Incidence of all types increasing. In F <40 yrs old incidence increasing BCC/SCC dramatically. <30 main association w/ indoor tanning. Develops primarily on areas of sun-exposed skin: scalp, face, lips, ears, neck, chest, arms, hands, legs. Dark skinned rarely affected (increased melanin protects).also forms on areas unexposure: palms, spaces between toes, genitals.

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Basal Cell Carcinoma (BCC)

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90% of skin CA cases. 65% located on sun-exposed surfaces of head/neck. Usually appear as: Pearly or waxy bump with rolled edges. Small blood vessels on surface (telangiectasia). Will sometimes bleed. Slowly grow in size. Lesions commonly bleed centrally from time to time. Very rarely metastasize. Usually painless.

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Basal Cell Carcinoma (BCC) and Squamous Cell carcinomas (SCC) dx

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biopsyand histologic exam.

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Basal Cell Carcinoma (BCC) prognosis

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Initial cure rate 90% but recurrences are common. 10% of BCCs recur at site of previous treatment. In scar or near scar. if untreated BCC invade surrounding tissues over months - years.; can destroy bone and cartilage tissue. Rarely met, but do spread locally.

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Basal Cell Carcinoma (BCC) and Squamous Cell carcinomas (SCC) tx

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cryosurgery. curettage and electrodessication. Chemo. surgical excision. Moh's surgery. Irradtion.

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cryosurgery

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freezing with liquid nitrogen. Successful but scars.

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Curettage and electrodessication:

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removal of growth with curet (blade) and destroy remaining cells with electric needle.

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Moh's surgery

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removal of skin growth layer by layer. Common in areas of thinner skin (eyelid). Delicate removal to preserve tissue.

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irradiaiton

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if surgery is not an option. Contraindicated if pt. if <50 yrs. of age.

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Squamous Cell Carcinomas (SCC):

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Often less distinctive appearance than BCC. Epidemiology: Peak incidence 60 yrs; more common in men. Usually occurs in sun damaged areas: ears, face, lips, mouth, dorsum of hand. Hard, horny crust. Risk of metastatic spread: Higher risk if lesion on unexposed skin, >1-2 cm in diameter, on nose, lip or ears.

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Squamous Cell Carcinomas (SCC): prognosis

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all major treatments have excellent cure ratesbut better with well-defined lesions.

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melanoma

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Malignant neoplasm originating from melanocytes- deeper. Comprises smallest percentage of all skin cancers but causes greatest number of deaths. Only ~4% of all skin cancers but ~74% of deaths. Classified into 4 types. Can occur anywhere on body but occurs most frequently- On upper back (M&F). Legs (females).

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melanoma epidemiology

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Lifetime risk 1/50 (increased >2000% since 1930's). Most common CA in women 25-29 yrs old. Higher female incidence in women birth-39 yrs. Higher male incidence in men >40 yrs. Median age diagnosis is 53 yrs.

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melanoma patho

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Majority associated with intensity rather than duration of sun exposure. Exact cause of all melanomas not clear (since many occur in less sun-exposed areas; only 65% in exposed areas). Intense bouts of UV exposure. UV radiation:

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UV radiation

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wavelength of sunlight in range too short for human eye to see.

UVA: damages melanocytes. Tanning beds.

UVB: cause burns, damage DNA of skin cells, create oncogene development.

UVC: not exposed to.

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melanoma risk factors

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Fair skin, sunburn hx, sunny high alt or equatorial climate, mole, family/personal hx, precancerous lesions (Bowen's dz, solar keratosis), weakened immune system, fragile skin, environmental hazard exposure, xeroderma pigmentosum.

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melanoma fair skin

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less melanin less protection from damaging UV radiation. Fair skinned people of N. European ancestry are of particular risk. Blond/red hair, light colored eyes, freckle/sunburn easy.

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melanoma burn hx

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>3 blistering sunburns before 20 yrs of age. Anything that peeled!!! >3 yrs of outdoor summer job experience.

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melanoma living location

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Sunny, high-altitude or equatorial climate: More common in AZ than MN. Altitude: 8-10% increase in UVB radiation for every 1000 ft elevation gain.

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melanoma mole risk

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Have 1 dysplastic mole doubles risk of melanoma. Have >50 ordinary moles.

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melanoma ABCDE

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Asymmetry: 1 side or half doesn’t look like other. Border: irregularity; edgesblurred, notched, ragged. Color: non-uniform in color of pigmentation as pts. other moles; often darker. Diameter: >6mm, size of eraser tip; any growth of current mole should be of concern. Evolving: changes in skin lesion over time. Ask pt.

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melanoma dx

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ABCDE. Often first sign is change in an existing mole or development of a new, unusual looking growth on skin. 70% melanomas arise from pre-existing mole. Suspicious changes in mole can include: scaliness, itching, change in texture, spreading of pigment from mole into surrounding skin, oozing, bleeding. Only way to diagnosis is with biopsy.

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melanoma tx

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Without evidence of metastatic spread will do surgical excision. Regional spread: surgery + radiation and/or chemotherapy.

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melanoma prognosis

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Prognosis depends on tumor thickness/depth of invasions. Deeper lesions are at higher risk for metastasis. 5yr w/ local met 65%. 5yr w/ distant met 30-35%. Met to brain, lungs, liver, bones, CNS most common; fatal in 1y.

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melanoma screening

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Monthly self exams: for everyone >18 yrs to learn moles, freckles, other skin marks that are normal for each individual. Skin screening exam: head to toe skin inspection by someone qualified to diagnosis skin cancer. Skin exams every 3 yrs. for adults 20-40 yrs w/ few risk factors. Yearly exams for everyone >40 yrs. People at risk may have more frequent screenings.

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skin CA prevention

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Avoid peak sunlight hours (10am-4pm) when sun’s rays are strongest. Clouds do not offer complete protects from UV rays. Wear broad-spectrum sunscreen year round (> 15 SPF). wear protective clothing. Avoid sun-tanning beds. Be aware of sun-sensitizing medications.

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Wear broad-spectrum sunscreen year round (> 15 SPF).

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Protects against UVA-UVB radiation. Best ingredients: avobenzone, titanium dioxide, zinc oxide. No all day, no water proof, no sun block. Most tests show very little diff b/n SPF 30 and anything >30. Use sunscreen on all exposed skin. Apply 30 mins before sun exposure and re-apply every 2 hrs throughout day. Reapply after swimming or exercising.

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protective clothing

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lightweight fabrics either treated with a UV inhibitor or woven to eliminate penetration of UV rays. Dark, tightly woven clothing that covers arms and legs (jeans, canvas). Broad-brimmed hat. Photoprotective clothing. Wear sunglasses that block both UVA and UVB. Choosing protective clothing may allow pts. to participate in outdoor activities.

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photoreceptive clothing

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UPF. Lightweight fabric either treated w/ a UV inhibitor or woven to eliminate penetration. 40-50 is most common. 98-99% UV blocked. 25-39 is 96-97%. 15-24 is 9-95%. Cotton rating is 7. Canvas and denim high but....

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SPF vs UPF

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SPF: sun protection factor; time it takes UV rays to cause skin to redden. UPF: ultraviolet protection factor; measures amount of UV radiation that penetrates and reaches the skin. No consideration needed for length of time of UV exposure.

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med and increased sun risk

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ABX. Cholesterol, HTN, DM. BCP. NSAIDs. Accutane (acne).