Ch 45 Skin Disorders
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Inflammatory Disorders o Eczema
 Most common skin condition. When you hear eczema think dermatitis. Includes seborrheic and atopic o Allergic Contact Dermatitis o Irritant Contact Dermatitis o Atopic Dermatitis o Stasis Dermatitis o Seborrheic Dermatisis
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Allergic and Hypersensitivity Dermatoses o Type I (Allergies) sometimes called anaphylactic response
 Atopic Eczema
 Urticaria (hives)
 Characterized by vasodilation, increased capillary permeability, smooth muscle contraction, etc.
 Type II is a cytotoxic reaction
 Type III is immune complex reaction
 Type IV is a delayed or cellular reaction
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Urticaria o Lesions are raised areas of cutaneoud edema
 Drugs, foods, systemic diseases
 Histamine, vascular constriction, and edema
 Hives, wheals, welts
 Mild allergic response
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Cutaneous Vasculitis o Immune complexes deposited in small vessels after exposure to an antigen
 Drugs, allergens, bacteria, viruses
 Complement, chemotactic for WBC’s
 Type III response, inflammation of the small blood vessels in the skin after exposure to an antigen
 Purple discoloration, ischemia and something else result from something
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Eczema o Most common inflammatory disorder
 An inflammatory response of the skin caused by internal or external sources.
Kind of a general term for dermatitis. o Erythema, versicles, scales, and pruritis (itching)
 Characterized by these things

 Can also see edema, swelling, serous discharge, and when the drainage ruptures and dries, crusting.
 Chronic E makes leathery skin. It’s think and hyperpigmented (darker than all your other skin). Location is important when you are talking about the cause of dermatitis. IF you have a new laundry detergent and you have an allergic response to it, where you’re clothes are tight are where you would see that reaction! It’s where it’s touching you the most!
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Atopic Dermatitis o Affects approimately 10% of population o More common in infants, children o Associated with Inflammation,Allergies, Immune response. Sometimes hay fever or food allergies. Also an increased sensitivity to histamine.
 Mast cell activation
 Histamine, lymphokines
 T lymphocytes, Langerhans cells (immune cells of the skin),
 Monocytes, IgE production
 Chronic inflammation
 Incidence has increased over the last 30 years or so. Some people outgrow it, sometimes it hangs around for life.
 Common on the hands, feet, and flexor surfaces (the spots that bend, like the back of your knees and inside of your elbows)
 Lichenification= term for leathery, hyperpigmenation of the skin
 Treatment is low dose steroids or anti-histamines.
 Effected individuals should avoid herpes simplex exposure and vaccination with live virus (the effect could be hypersomething or other, super bad response)
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Allergic Contact Dermatitis o Erythema & edema, pruritis, vesicles (the same as atopic) o Allergy to Metal, chemicals, poison ivy o Cell mediated immune response o Delayed hypersensitivity response o Urticaria (wheals) can be present
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Irritant Contact Dermatitis o Prolonged exposure to acids or bases
 Wal-Mart sandles? Damn, her feet were messed up… o Nonimmunologically mediated inflammation o Lesions similar to Allergic Contact o Erythema & edema, pruritus, vesicles (same as allergic contact)
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Stasis Dermatitis o Venous Insufficiency  venous stasis ulcers, incompetent valves cause it o Venous stasis and edema

o Erythema, pruritis, scaling, petechiae, hyperpigmentation, Brawny (woody) edema (skin is tough and thick like green wood) o Ulcerated lesions may form - irregular borders, “weepy faucet”, champagne bottle appearance o Treatment: elevation, not standing for long periods, wearing lose clothing. Sometimes antibiotics are used when they get a secondary infection from their skin being all messed up.
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Cutaneous Infections o Bacterial o Viral o Fungal (tinneas vs. candidiasis/yeast) o Pretty common, generally localized and superficial. Occasionally sepsis can occur, which can be life threatening. We have all kinds of natural flora on our skin but kicks our ass when it gets in our body.
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Bacterial Infections o Folliculitis  furuncle  carbuncle o Cellulitis
 Skin and sometimes SubQ tissue as well o Difference is degree of tissue involved o Impetigo
 May lead to poststreptococcal hypersensitivity reactions
 These can cause glomerulonephritis o Boils are most commonly caused by Staph aureus.
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Acne o Disorder of sebaceous glands o Related to:
 Hormonal stimulation of sebaceous glands
 Increased number of sebaceous cells
 Increased sebum production
 Inflammatory response to bacteria in sebum
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Viral o Herpes Simplex
 Cold Sores o Herpes Zoster
 Varicella (shingles)
 Herpes invades dorsal root ganglia
 Caused when chickenpox herpes virus is reactivated
 Travels out nerve to skin and causes a new inflammation o Papillomavirus
 Warts
 Condyloma

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Venereal Warts
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Increased risk of Cervical cancer o Verrucae (warts)
 Benign Neoplasms (papillomas)
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Skin Infections of the fungal variety o Superficial fungal infections
 Ringworm, athlete’s foot
 Attack the keratinized (dead) cells
 Inflammatory reaction to toxins causes most signs and symptoms o Deep fungal infections
 Candidiasis, sporotrichosis
 Attack living tissue
 May attack other organs
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Fungi o Tineas o Candidiasis o Onychomycosis
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Vesiculobullous Disorders o Pemphigus Vulgaris
 Autoimmune
 IgG autoantibodies
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React with intracellular cement leading to loss of adhesion between epidermal and dermal cells
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Directed against the cell surface adhesion molecule desmoglein at the cell junction in suprabasal layer in epidermis.
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IgG and complement bind to desmoglein adhesion molecules (causing) destruction of cell to cell adhesion o Acantholysis o Blister formation
 2 drugs are associated with it: PCN and Captapril administration o Bullous Pemphigoid
 Milder form
 More often seen in people over the age of 60 o Erythmea Multiforme
 Acute inflammation with target-like lesions
 Rings of edema and inflammation
 Allergic reaction to drugs, herpes simplex
 Stevens-Johnson syndrome - mucus membrane involvement
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Drug-Induced Skin Eruptions o Erythema multiforme
 Occurs after herpes simplex; self-limiting

o Stevens-Johnson syndrome
 Skin detaches from body surface; <10% of body affected o Toxic epidermal necrolysis
 >30% of epidermis detaches
 30%–35% mortality rate
 Immune mediated
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Papulosquamous Dermatoses o Psoriasis
 You get papules, scales, plaques, and erythema. There are well demarcated, thick, silvery, scale, erythematous plaque on normal skin
 Patho:
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Chronic, noninfectious, T cell mediated inflammatory condition
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T cell  cytokine release (TNF-a),  inflammatory response  hyperproliferation of keratinocytes  thick inflamed plaques
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Red raised plaques c silvery scales o Pityriasis rosea- self limiting inflammatory disorder. Occurs in young adults in the winter. Probably herpes in origin. Begins with a single lesion (The Herald Patch) which is
3-4 cm, salmon pink, and clearly demarkated (you can tell where it is) o Lichen planus- benign auto immune inflammatory disorder of the skin and mucous membranes. It can occur after exposure to drugs or film processing chemicals. Causes non-scaling, violet colored puritic 2-4 mm papules on the wrist, ankles, lower legs, and genitalia. Patho might be the epithelial cells are considered foreign by the T cells, so the
T cells try and eat them.
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Pressure Ulcers o Risk Factors
 Immobilization
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Failure to move or turn
 Debilitation
 Incontinence
 Friction or Shear
 Use the Braden Scale to assess the risk factors, duh.
 Risks associated with certain chronic conditions
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Neurologic disorders
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Anemia
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Edema
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Renal Failure
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Malnutrition
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Sepsis o Patho
 Immobility
 Continuous Pressure

 Capillaries occlude with platelets
 Microthrombi form
 Occlusion of blood flow
 Anoxic necrosis
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Sun Exposure o Sun exposure increases the risk of skin cancer o Cumulative sun exposure increases risk of:
 Basal cell carcinoma
 Squamous cell carcinoma o Severe sun exposure with blistering increases risk of:
 Malignant melanoma
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Cancers arising from melanocytes
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Asymmetry
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Border irregularity
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Color variegation
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Diameter > 0.6 cm
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Evolving change over time
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Types of Melanomas o 70% are superficial spreading
 Raised edges; grow horizontally and vertically
 Ulcerate and bleed o 15%–30% are nodular
 Dome-shaped, blue-black o 4%–10% are lentigo maligna
 Slow growing, flat o 2%–4% acral lentiginous
 On palms, soles, nail beds, mucous membranes
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Skin Disorders of the Elderly o Actinic (solar) damage
 Keratoses: premalignant lesions
 Lentigines: liver spots o Vascular lesions
 Angiomas
 Telangiectases
 Venous lakes
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Benign Tumors o Suborheic Keratosis o Keratocanthoma o Actinic keratosis o Nevi
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Malignancies of the Skin

o Basal cell - most common, recurs often
 Originate from cells around hair follicles or glands o Squamous cells can become invasive
 Actinic (solar) keratosis is premalignant lesion o Melanoma can metastasize via lymph
 Arise from basalar epidermal cells or Nevi o Kaposi sarcoma - vascular malignancy
 Seen in immunodeficiency
 Herpes simplex-8
 Damage due to ? DNA sythesis, repair, replication; protooncogene activiation or inactivation of tumor suppression
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Sunburn Patho o Ultraviolet radiation hits the melanocytes. The melanin becomes oxidized which causes a tan. More melanin is produces which creates a delayed tanning effect. o Some of the UV reaches lower skin layers which damages your DNA and your immune cells. Inflammatory mediators are released. This causes the sunburn!
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Burns o 1 st Degree
 Partial thickness
 Outer layers of the epidermis o 2 nd Degree
 Superficial partial thickness, blistering, pain
 Deep partial thickness, dermis, no appendages
 Epidermis and Dermis
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Partial thickness is only part of the dermis
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Full thickness is the entire dermis o 3 rd Degree
 Full-thickness, entire epidermis, dermis, hypodermis, painless (because you burned away all your pain receptors)
 Extends into the subq tissue
 May damage muscle, bone, and blood vessels