1 Structure, Function, and Disorders of the Integument Chapter 44.
Transcript of 1 Structure, Function, and Disorders of the Integument Chapter 44.
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Structure, Function, and Disorders of the IntegumentChapter 44
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Layers of the Skin Epidermis Dermis Subcutaneous
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Layers of the Skin
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Layers of the Skin Epidermis
Stratum basale Stratum germinativum Stratum spinosum Stratum lucidum Stratum corneum
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Layers of the Skin Epidermis
Keratinocytes Keratin
Melanocytes Langerhans cells Merkel cells
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Layers of the Skin Dermis
Collagen, elastin, reticulum, and a gel-like ground substance
Hair follicles, sebaceous glands, sweat glands, blood vessels, lymphatic vessels, nerves
Fibroblasts, mast cells, macrophages Subcutaneous layer
Adipocytes Dermal and subcutaneous collagen are continuous
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Layers of the Skin Dermal appendages
Nails Hair Sebaceous glands Eccrine and apocrine sweat glands
Blood supply Papillary capillaries
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Nails
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Aging and Skin Integrity The integumentary system reflects numerous
changes from genetic and environmental factors The skin becomes thinner, drier, wrinkled, and
demonstrates a changes in pigmentation Shortening and decrease in the number of capillary loops Fewer melanocytes and Langerhans cells Atrophy of the sebaceous, eccrine, and apocrine glands Changes in hair color Fewer hair follicles and growth of thinner hair
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Clinical Manifestations of Skin Dysfunction Macule Papule Patch Plaque Wheal
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Clinical Manifestations of Skin Dysfunction Nodule Tumor Vesicle Bulla Pustule
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Clinical Manifestations of Skin Dysfunction Cyst Telangiectasia Scale Lichenification Keloid Scar
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Clinical Manifestations of Skin Dysfunction Excoriation Fissure Erosion Ulcer Atrophy
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Clinical Manifestations of Skin Dysfunction Pressure ulcers
Pressure ulcers result from any unrelieved pressure on the skin, causing underlying tissue damage Pressure Shearing forces Friction Moisture
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Clinical Manifestations of Skin Dysfunction Pressure ulcers
Stages Nonblanchable erythema of intact skin Partial-thickness skin loss involving epidermis or
dermis Full-thickness skin loss involving damage or loss of
subcutaneous tissue Full-thickness skin loss with damage to muscle, bone,
or supporting structures
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Clinical Manifestations of Skin Dysfunction Keloids
Elevated, rounded, and firm Clawlike margins that extend beyond the original
site of injury Excessive collagen formation during dermal
connective tissue repair Common in darkly pigmented skin types and
burn scars Type III collagen is increased.
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Keloids
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Clinical Manifestations of Skin Dysfunction Pruritus
Itching Most common symptom of primary skin disorders Itch is carried by specific unmyelinated C-nerve fibers
and is triggered by a number of itch mediators The CNS can modulate the itch response Pain stimuli at lower intensities can induce itching Chronic itching can result in infections and scarring due
to persistent scratching
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Disorders of the Skin Inflammatory disorders
The most common inflammatory disorder of the skin is dermatitis or eczema
There are various types of dermatitis The disorders are generally characterized by
pruritus, lesions with indistinct borders, and epidermal changes
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Inflammatory Disorders Allergic contact dermatitis
Caused by a hypersensitivity type IV reaction The allergen comes in contact with the skin, binds
to a carrier protein to form a sensitizing antigen; Langerhans cells process the antigen and carry it to T cells, which become sensitized to the antigen
Manifestations Erythema, swelling, pruritus, vesicular lesions
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Allergic Contact Dermatitis
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Inflammatory Disorders Atopic dermatitis
Type I hypersensitivity—activation of mast cells, eosinophils, T lymphs, and other inflammatory cells
Causes red, weeping crusts and chronic inflammation, lichenification
Irritant contact dermatitis Nonimmunologic inflammation of the skin Chemical irritation from acids or prolonged exposure to
irritating substances Symptoms similar to allergic contact dermatitis Treatment—remove stimulus
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Atopic Dermatitis
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Inflammatory Disorders Stasis dermatitis
Occurs in the legs as a result of venous stasis, edema, and vascular trauma
Sequence of events: erythema, pruritus, scaling, petechiae, ulcerations
Seborrheic (sebōrēik) dermatitis Inflammation of the skin involving the scalp, eyebrows,
eyelids, nasolabial folds, and ear canals Scaly, white, or yellowish plaques
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Stasis and Seborrheic Dermatitis
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Papulosquamous Disorders Psoriasis
Chronic, relapsing, proliferative skin disorder T cell immune–mediated skin disease Scaly, thick, silvery, elevated lesions, usually on the
scalp, elbows, or knees caused by a high rate of mitosis in the basale layer
Shows evidence of dermal and epidermal thickening Epidermal turnover goes from 26-30 days to 3-4 days Cells do not have time to mature or adequately keratinize
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Psoriasis
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Papulosquamous Disorders Psoriasis
Plaque psoriasis Inverse psoriasis Guttate psoriasis Pustular psoriasis Erythrodermic psoriasis
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Papulosquamous Disorders Pityriasis rosea
Benign, self-limiting inflammatory disorder Usually occurs during the winter months Herald patch
Circular, demarcated, salmon-pink, 3- to 4-cm lesion
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Pityriasis Rosea Herald Patch
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Papulosquamous Disorders Lichen planus
Benign, inflammatory disorder of the skin and mucous membranes
Unknown origin, but T cells, adhesion molecules, inflammatory cytokines, and antigen presenting cells are involved
Nonscaling, violet-colored, 2- to 4-mm lesions Wrists, ankles, lower legs, genitalia
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Lichen Planus
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Papulosquamous Disorders Acne vulgaris
Inflammatory disease of the pilosebaceous follicles Acne rosacea
Inflammation of the skin that develops in adulthood Lesions
Erythematotelangiectatic, papulopustular, phymatous, and ocular Associated with chronic, inappropriate vasodilation resulting in
flushing and sensitivity to the sun
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Papulosquamous Disorders Lupus erythematosus
Inflammatory, autoimmune disease with cutaneous manifestations
Discoid lupus erythematosus Restricted to the skin Photosensitivity Butterfly pattern over the nose and cheeks
Systemic lupus erythematosus
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Discoid Lupus Erythematosus
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Vesiculobullous Disorders Pemphigus
Rare, chronic, blister-forming disease of the skin and oral mucous membranes
Blisters form in the deep or superficial epidermis Autoimmune disease caused by circulating IgG
autoantibodies The antibodies are against the cell surface adhesion
molecule, desmoglein in the suprabasal layer of the epidermis
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Vesiculobullous Disorders Pemphigus
Tissue biopsies demonstrate autoantibody presence
Types Pemphigus vulgaris (severe) Pemphigus foliaceus Pemphigus erythematosus
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Vesiculobullous Disorders Bullous pemphigoid
More benign disease than pemphigus vulgaris Bound IgG and blistering of the subepidermal
skin layer Subepidermal blistering and eosinophils
distinguish pemphigoid from pemphigus
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Bullous Pemphigoid
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Vesiculobullous Disorders Erythema multiforme
Acute, recurring disorder of the skin and mucous membranes
Associated with allergic or toxic reactions to drugs or microorganisms
Caused by immune complexes formed and deposited around dermal blood vessels, basement membranes, and keratinocytes
“Bull’s-eye” or target lesion Erythematous regions surrounded by rings of alternating edema
and inflammation
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Vesiculobullous Disorders Erythema multiforme
Bullous lesions form erosions and crusts when they rupture
Affects the mouth, air passages, esophagus, urethra, and conjunctiva
Severe forms Stevens-Johnson syndrome (bullous form) Toxic epidermal necrolysis
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Erythema Multiforme
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Infections Bacterial infections
Folliculitis Furuncles Carbuncles Cellulitis Erysipelas Impetigo
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Furuncle
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Infections Viral infections
Herpes simplex virus Herpes zoster and varicella
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Herpes Simplex Virus
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Warts Benign lesions caused by the human
papillomavirus (HPV) Diagnosed by visualization Condylomata acuminata
Venereal warts
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Fungal Infections Fungi causing superficial skin lesions are
called dermatophytes Fungal disorders are called mycoses; mycoses
caused by dermatophytes are termed tinea Tinea capitis (scalp) Tinea pedis (athlete’s foot) Tinea corporis (ringworm) Tinea cruris (groin, jock itch) Tinea unguium (nails) or onychomycosis
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Tinea Pedis
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Fungal Infections Candidiasis
Caused by Candida albicans Normally found on the skin, in the GI tract, and in the
vagina C. albicans can change from a commensal organism to a
pathogen Local environment of moisture and warmth, systemic
administration of antibiotics, pregnancy, diabetes mellitus, Cushing disease, debilitated states, age younger than 6 months, immunosuppression, and neoplastic diseases
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Vascular Disorders Cutaneous vasculitis
Results from immune complexes in the small blood vessels Develops from drugs, bacterial infections, viral
infections, or allergens
Lesions Palpable purpura progressing to hemorrhagic bullae
with necrosis and ulceration
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Cutaneous Vasculitis
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Vascular Disorders Urticaria
Due to type I hypersensitivity reactions to allergens
Histamine release causes endothelial cells of the skin to contract Causes leakage of fluid from the vessels
Treatment Antihistamines and steroids
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Urticaria
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Vascular Disorders Scleroderma
Sclerosis of the skin that can progress to the internal organs
The disease is associated with several antibodies Lesions exhibit massive deposits of collagen with
inflammation, vascular changes, and capillary dilation
Skin is hard, hypopigmented, taut, and tightly connected to underlying tissue
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Vascular Disorders Scleroderma
Facial skin becomes very tight Fingers become tapered and flexed; nails and
fingertips can be lost from atrophy Mouth may not open completely 50% of patients die within 5 years
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Scleroderma
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Insect Bites Ticks Mosquitos Flies
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Benign Tumors Seborrheic keratosis Keratoacanthoma Actinic keratosis Nevi (moles)
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Cancer Basal cell carcinoma Squamous cell carcinoma Malignant melanoma Kaposi sarcoma
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Frostbite Skin injury caused by exposure to extreme cold Usually affects fingers, toes, ears, nose, and cheeks The “burning reaction” is caused by alternating
cycles of vasoconstriction and vasodilation Inflammation and reperfusion are both part of the
pathophysiology
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Disorders of the Hair Male-pattern alopecia
Genetically predisposed response to androgens Androgen-sensitive and androgen-insensitive
follicles Female-pattern alopecia
Associated with elevated levels of the serum adrenal androgen dehydroepiandrosterone sulfate
No loss of hair along the frontal hairline
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Disorders of the Hair Alopecia areata
Autoimmune T cell–mediated inflammatory disease against hair follicles that results in baldness
Hirsutism Androgen-sensitive areas
Abnormal growth and distribution of hair on the face, body, and pubic area in a male pattern that occurs in women
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Disorders of the Nail Paronychia
Acute or chronic infection of the cuticle Onychomycosis
Fungal or dermatophyte infection of the nail plate