Dermatology Maculopapular and Plaque Dermatitis By Stacey Singer-Leshinsky R-PAC

Maculopapular Description A Maculopapular rash is usually a large erythematous area with confluent bumps. Plaque

Allergic and Hypersensitivity Dematoses Inflammatory response Epidermal edema and separation of epidermal cells. Includes: Atopic dermatitis, Nummular eczema, Dyshidrotic eczema, Contact dermatitis, stasis dermatitis, Diaper dermatitis, perioral dermatitis, seborrheic dermatitis, lichen simplex chronicus, Psoriasis, lichen planus, seborrheic keratosis, Actinic keratosis

Atopic Dermatitis (Eczema) Type I (IgE) hypersensitivity inflammatory reaction Risk factors: Family history of atopy. Exacerbated by scratching, stress

Atopic Dermatitis (Eczema) Epidemiology: Usually begins prior to 6m of age. (FACE): flexor surfaces get adults, children extensor)

Atopic Dermatitis Clinical Manifestations Acute form Pruritus. Appear erythematous, edematous with papules/plaques. Scaling, weeping, and crusting

Atopic Dermatitis Clinical Manifestations Chronic form Lichenification painful fissures                                                                                                                  

Atopic Dermatitis Clinical Manifestations Infantile eczema Weeping inflammatory patches and crusted plaques on:

Atopic Dermatitis Clinical Manifestations Juvenile/adult Affects flexural areas Appear as dry, lichenified pruritic plaques

Atopic Dermatitis Diagnosis/ Complications History Serum IgE Differentiate from viral HSV Complications:

Atopic Dermatitis Management Avoidance of triggers. Avoid scratching Lubricants. Oral antihistamines Topical corticosteroids

Atopic Dermatitis Management Topical antibiotics for staphylococcus aureus infection Non-glucocorticoid anti-inflammatory agents now available such as pimecrolimus. Avoid oral steroids

Nummular Eczema Inflammatory response. Etiology: Risk factors: young and old. Fall and winter. Xerosis. Clinical manifestations Round coin like sharply demarcated erythematous papulovesicular patches/ plaques Intense pruritus, Lichenification

Nummular Eczema Diagnosis /Differentials History and physical exam Rule out secondary infection, allergy Differential diagnosis to include seborrheic dermatitis, psoriasis, contact dermatitis, tinea

Nummular Eczema Management Avoid scratching Lubricants Oral antihistamines Topical corticosteroids Intralesional triamcinolone Systemic antibiotics Phototherapy Complications:

Dyshidrotic Eczema Recurrent chronic relapsing form of vesicular hand and foot dermatitis No evidence of eccrine gland dysfunction dyshidrotic Intraepidermal vesicles Etiology/risks: Unknown etiology Epidemiology: Prior to age 40.

Dyshidrotic Eczema Clinical Manifestations Pruritus and burning Begins on lateral fingers and progress to palms and soles. Vesicles: 1-2mm with clear fluid resembling tapioca Later: desquamation and Lichenification

Dyshidrotic Eczema Diagnosis/Differentials Clinical Rule out secondary infection, allergy Differential diagnosis to include contact dermatitis, drug reaction Complications:

Dyshidrotic Eczema Management Burrow wet dressings High potency glucocorticoids and occlusive dressings Topical antipruritics. Severe need systemic steroids Intralesional Triamcinolone Systemic antibiotics

Contact Dermatitis Cell mediated reaction involving sensitized T lymphocytes. Etiology Irritant form: Chemical insult to skin. No previous sensitizing event. Allergic form is delayed-hypersensitivity reaction. Skin sensitized from initial exposure. During next exposure patient has reaction.

Contact Dermatitis Clinical manifestations Develop 24-96h post exposure Pruritus Acute present as vesicles with clear fluid on erythematous edematous skin. Sub-acute is edema and papules Chronic-

Contact dermatitis Diagnosis/Differential Diagnosis Clinical Rule out secondary infection. Patch testing Differential diagnosis to include seborrheic dermatitis, atopic eczema

Contact Dermatitis Treatment Remove etiologic agent Wet dressings with gauze soaked in Burow’s solution changed every 2-3 hours. Topical corticosteroids Systemic corticosteroids

Stasis Dermatitis Inflammatory skin disease that occurs on lower extremities Extravasation of plasma proteins and RBC into subcutaneous tissues. Becomes brown in color due to hemosiderin deposits Results in interstitial fluid accumulation . Leads to reduced capillary blood flow

Stasis Dermatitis Can progress to venous stasis ulcers and fibrosis Found in 6-7% of elderly population

Stasis Dermatitis Acute form: Initially medial aspect of ankle. Inflammation Weeping lesions Plaques/ Erythema Crusting/ Exudate

Stasis Dermatitis Chronic form Thin, shiny bluish brown irregularly pigmented scaling skin.

Stasis Dermatitis Diagnosis/Differentials Clinical Doppler Differential diagnosis to include contact dermatitis, Atopic dermatitis, cellulitis

Stasis Dermatitis Management Mid potency topical corticosteroids. Control chronic edema For ulcers: Unna venous boot changed every week. Wound care Advise patient to elevate legs and wear compression stockings Avoid standing or sitting for long time

Diaper Dermatitis Irritant dermatitis Cutaneous Candidiasis infection (C. Albicans ) Risks: areas where warmth and moisture lead to maceration of skin or mucous membranes

Diaper Dermatitis History and Physical Exam Pruritus, pain Erythematous papules/vesicles, edema Satellite lesions to Peri-genital, peri-anal, inner thigh, buttocks

Diaper Dermatitis Diagnosis/Differentials Diagnosis- KOH examination Differential diagnosis to include contact dermatitis, child abuse

Diaper Dermatitis Management Topical antifungal agents such as Nystatin, miconazole, or clotrimatzole Topical corticosteroids Complications Educate care givers

Perioral Dermatitis Facial dermatosis with confluent papulopustular lesions. Lead to inflammatory plaques. Unknown etiology. Risks: young women, prolonged use of topical steroids or steroid sprays

Perioral Dermatitis History and Physical Exam Lesions resemble rosacea Burning Follicular papules, vesicles and pustules on an erythematous base Grouped    

Perioral Dermatitis Diagnosis/ Differentials Clinical. Rule out secondary causes. Differentials Acne Vulgaris Contact dermatitis Rosacea seborrheic dermatitis

Perioral Dermatitis Management AVOID topical corticosteroids. Antibiotics Metronidazole, erythromycin topical Systemic antibiotics: Monocycline, Doxycycline, or tetracycline Wash with mild soap, use nonfluorinated toothpaste. Avoid oral contraceptives

Seborrheic Dermatitis Seborrhea Skin rash that occurs in areas of high sebaceous gland concentration Cutaneous inflammation to dermis Etiology: Immune response to endogenous yeast Pityrosporum Triggered by seasonal changes, scratching, emotional stress, medications.

Seborrheic Dermatitis Infants Affects scalp, flexural area and perioral Erythematous plaques Fine white scales Thick yellow brown greasy scaling

Seborrheic Dermatitis Adults Pruritus Burning Erythematous plaques with scaling

Seborrheic Dermatitis Diagnosis/Differentials History/Physical Differential diagnosis to include atopic dermatitis, candidiasis, lupus

Seborrheic Dermatitis Management Selenium sulfide shampoos, 2% ketoconazole shampoo, ketoconazole cream. Salicylic acid Corticosteroids Cradle cap- Treat for secondary infection

Lichen Simplex Chronicus End stage of pruritic and eczematous disorders. Skin responds to physical trauma by epidermal hyperplasia. Common areas Risk factors:

Lichen Simplex Chronicus History and Physical Exam Well circumscribed plaques with lichenified or thickened skin Pruritus- Hyperpigmentation Excoriation

Lichen Simplex Chronicus Diagnosis/Differentials Differential diagnosis to include psoriasis Vulgaris, contact dermatitis, fungal infection Diagnosis Clinical Biopsy shows hyperplasia acanthosis, hyperkeratosis KOH examination

Lichen Simplex Chronicus Management High potency topical glucocorticoids Oral antihistamines- Hydration Complications:

Psoriasis Increased epidermal cell proliferation due to a shortened epithelial cell cycle. Leads to hyperkeratosis. This results in keratinization defects, forming thick adherent scales . Patients have exacerbations and remissions. Can be triggered by stress, class I topical corticosteroids, or Koebner reaction. Etiology: Genetic abnormalities in the immune system

Psoriasis History and Physical Exam Plaque lesions most common Erythematous or salmon colored plaques with distinct borders covered with silvery white scales Extensor >flexor. Nails

Psoriasis History and Physical Exam Pustular psoriasis: Painful Deep sterile yellow pustules Pustules evolve into red macules

Psoriasis History and Physical Exam Guttate Psoriasis Could be immune Slight pruritus Small erythematous papules with fine scale Can be discrete or confluent

Psoriasis Diagnosis/Differentials Skin biopsy shows increased mitosis in keratinocytes Auspitz phenomenon Differential diagnosis to include lichen planus, eczema

Psoriasis Management Supportive care Hydrating creams Mid-potency topical glucocorticoids Retinoids such as tazarotene UV light combined with coal tar, salicylic acid, and anthralin Systemic immunosuppressive – Moderate, severe or disabling psoriasis

Lichen Planus Cell mediated immunologic reaction targeting keratinocytes. Etiology: Unknown, possibly genetic, liver disease. Involves skin and/or mucous membranes. Risks: age, HLA associated gene

Lichen Planus History and Physical Exam Pruritic, polygonal, purple, flat topped papules covered with fine scales Lesions Found on flexor areas, shins, and mucous membranes. Lesions resolve with post inflammatory hyperpigmentation.

Oral Lichen Planus Oral lesions involve the tongue and buccal mucosa Present with wickham’s striae Can then erode

Lichen Planus Diagnosis/Differentials Clinical inspection Skin biopsy Look for associated disorders Differential diagnosis to include chemical exposure, psoriasis, candidiasis, scabies Complications to include squamous cell carcinoma, alopecia

Lichen Planus Management Antihistamines Topical corticosteroids Systemic corticosteroids Topical and systemic retinoids Retinoids normalize epidermal differentiation and are anti inflammatory Immunosuppressant -Cyclosporine.

Seborrheic Keratosis Due to proliferation of Keratinocytes and melanocytes Etiology: Genetics Usually asymptomatic Benign, however must rule out malignant melanoma Spontaneous resolution rare

Seborrheic Keratosis Begin as sharply define light brown flat macules Then develop velvety to a warty surface with multiple plugged follicles Pasted on plaque Color from brown to black Size up to several centimeters.

Seborrheic Keratosis Diagnosis/Differentials Skin Biopsy Differentials Actinic Keratosis Carcinoma Warts

Seborrheic Keratosis Management Keratolytic agents-leads to desquamation of hornified epithelium- Ammonium Lactate lotion Trichloroacetic acid- cauterizes skin, keratin and tissues.

Actinic Keratosis Found in those with fair skin Sun exposure leads to damage to keratinocytes by UV radiation Hyperkeratotic form more prominent and palpable.

Actinic Keratosis Multiple, discrete flat or elevated Skin colored, yellow-brown or brown. Dry, rough, adherent scaly lesion 3-10mm

Actinic Keratosis Diagnosis/Differentials Diagnosis:Biopsy will show epidermal changes Differentials Squamous cell carcinoma Lupus Seborrheic keratosis

Actinic Keratosis Management Topical 5-fluorouracil: Surgical curettage or cryosurgery Retinoids Dermabrasion Avoid sun exposure.

Urticaria IgE or complement mediated edema of dermis or subcutaneous tissue Etiology: antigens Pathology: Mast cell stimulated to degranulate by IgE.

Urticaria Clinical: Pink Edematous Papules or plaques Vary in appearance Resolve within 24 hours Angioedema: Painless, deeper urticaria

Urticaria Diagnostics: Management: Eliminate cause Oral antihistamines

Review 1 In infants this lesion is found on extensor surfaces while in adults it is found on flexor surfaces. Pt presents with pruritic lesions that are erythematous What is this?

Review #2 Pruritus and burning prior to eruption Vesicles resemble tapioca No erythema What is this? Where is it found? How is it treated?

Review #3 This is the result of chronic venous insufficiency What is it? How is it managed?

Review #4 This rash occurs in areas with high sebaceous gland concentration. What is it? Describe this lesion What is the management?

Review #5 T-cell mediated autoimmune disease Abnormal growth of keratinocytes Erythematous plaques with distinct borders and silvery white scales What is this? Where is it found? How is it treated?

Review #6 What is the pathophysiology behind this? Describe this What are management options?

Review #7 What is this? What is the management of this?

Review #8 What is this? What causes this? What is the treatment for this?

Review #9 What is this? What is the cause of this? How is this treated?

Review #10 What is this? What is the cause of this? How is this managed?