dermatology maculopapular and plaque dermatitis by stacey singer-leshinsky r-pac

DermatologyMaculopapular and Plaque Dermatitis

ByStacey 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 DermatitisClinical Manifestations

Acute form Pruritus. Appear

erythematous, edematous with papules/plaques.

Scaling, weeping, and crusting


Chronic form Lichenification painful fissures


Infantile eczema Weeping

inflammatory patches and crusted plaques on:

Atopic DermatitisClinical Manifestations Juvenile/adult

Affects flexural areas

Appear as dry, lichenified pruritic plaques

Atopic DermatitisDiagnosis/ Complications Diagnosis

History Serum IgE Differentiate from viral HSV

Complications:

Atopic DermatitisManagement Avoidance of triggers. Avoid

scratching Lubricants. Oral antihistamines Topical corticosteroids

Atopic DermatitisManagement 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 EczemaDiagnosis /Differentials Diagnosis

History and physical exam Rule out secondary infection, allergy

Differential diagnosis to include seborrheic dermatitis, psoriasis, contact dermatitis, tinea

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

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

Dyshidrotic EczemaClinical 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 EczemaDiagnosis/Differentials Diagnosis

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 DermatitisClinical 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 dermatitisDiagnosis/Differential Diagnosis

Diagnosis: Clinical Rule out secondary infection. Patch testing

Differential diagnosis to include seborrheic dermatitis, atopic eczema

Contact DermatitisTreatment 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 DermatitisDiagnosis/Differentials Diagnosis:

Clinical Doppler

Differential diagnosis to include contact dermatitis, Atopic dermatitis, cellulitis

Stasis DermatitisManagement

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 DermatitisHistory and Physical Exam

Pruritus, pain Erythematous

papules/vesicles, edema

Satellite lesions to Peri-genital, peri-anal, inner thigh, buttocks

Diaper DermatitisDiagnosis/Differentials Diagnosis- KOH examination Differential diagnosis to include

contact dermatitis, child abuse

Diaper DermatitisManagement 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 DermatitisHistory and Physical Exam

Lesions resemble rosacea

Burning Follicular papules,

vesicles and pustules on an erythematous base

Grouped

Perioral DermatitisDiagnosis/ Differentials Diagnosis:

Clinical. Rule out secondary causes.

Differentials Acne Vulgaris Contact dermatitis Rosacea seborrheic dermatitis

Perioral DermatitisManagement AVOID topical corticosteroids. Antibiotics

Metronidazole, erythromycin topical Systemic antibiotics: Monocycline,

Doxycycline, or tetracycline Wash with mild soap, use

nonfluorinated toothpaste. Avoid oral contraceptives

Seborrheic DermatitisSeborrhea 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 DermatitisDiagnosis/Differentials Diagnosis

History/Physical Differential diagnosis to include

atopic dermatitis, candidiasis, lupus

Seborrheic DermatitisManagement 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 ChronicusHistory and Physical Exam

Well circumscribed plaques with lichenified or thickened skin

Pruritus- Hyperpigmentation Excoriation

Lichen Simplex ChronicusDiagnosis/Differentials Differential diagnosis to include

psoriasis Vulgaris, contact dermatitis, fungal infection

Diagnosis Clinical Biopsy shows hyperplasia acanthosis,

hyperkeratosis KOH examination

Lichen Simplex ChronicusManagement 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

PsoriasisHistory and Physical Exam Plaque lesions most

common Erythematous or

salmon colored plaques with distinct borders covered with silvery white scales

Extensor >flexor. Nails

PsoriasisHistory and Physical Exam Pustular psoriasis:

Painful Deep sterile

yellow pustules Pustules evolve

into red macules

PsoriasisHistory and Physical Exam Guttate Psoriasis

Could be immune Slight pruritus Small

erythematous papules with fine scale

Can be discrete or confluent

PsoriasisDiagnosis/Differentials Skin biopsy shows increased

mitosis in keratinocytes Auspitz phenomenon Differential diagnosis to include

lichen planus, eczema

PsoriasisManagement 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 PlanusHistory 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 PlanusDiagnosis/Differentials Diagnosis:

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 PlanusManagement 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 KeratosisDiagnosis/Differentials Diagnosis:

Skin Biopsy Differentials

Actinic Keratosis Carcinoma Warts

Seborrheic KeratosisManagement 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 KeratosisDiagnosis/Differentials Diagnosis:Biopsy will show

epidermal changes Differentials

Squamous cell carcinoma Lupus Seborrheic keratosis

Actinic KeratosisManagement 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

Diagnostics: Management: Eliminate cause Oral antihistamines

Urticaria

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?


cause of this? How is this

treated?


cause of this? How is this

managed?

dermatology maculopapular and plaque dermatitis by stacey singer-leshinsky r-pac

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