Transcript Dermatology Maculopapular and Plaque Dermatitises

Dermatology
Maculopapular and Plaque
Dermatitis
By
Stacey Singer-Leshinsky R-PAC
Maculopapular
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Description
A Maculopapular rash is usually a large
erythematous area with confluent
bumps.
Plaque
Allergic and Hypersensitivity
Dematoses
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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)
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Type I (IgE) hypersensitivity
inflammatory reaction
Risk factors: Family history of atopy.
Exacerbated by scratching, stress
Atopic Dermatitis (Eczema)
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Epidemiology: Usually begins prior to
6m of age.
(FACE): flexor surfaces get adults,
children extensor)
Atopic Dermatitis
Clinical Manifestations
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Acute form
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Pruritus.
Appear erythematous,
edematous with
papules/plaques.
Scaling, weeping, and
crusting
Atopic Dermatitis
Clinical Manifestations
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Chronic form
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Lichenification
painful fissures
Atopic Dermatitis
Clinical Manifestations
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Infantile eczema
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Weeping
inflammatory
patches and
crusted plaques on:
Atopic Dermatitis
Clinical Manifestations
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Juvenile/adult
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Affects flexural areas
Appear as dry,
lichenified pruritic
plaques
Atopic Dermatitis
Diagnosis/ Complications
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Diagnosis
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History
Serum IgE
Differentiate from viral HSV
Complications:
Atopic Dermatitis
Management
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Avoidance of triggers. Avoid scratching
Lubricants.
Oral antihistamines
Topical corticosteroids
Atopic Dermatitis
Management
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Topical antibiotics for staphylococcus
aureus infection
Non-glucocorticoid anti-inflammatory
agents now available such as
pimecrolimus.
Avoid oral steroids
Nummular Eczema
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Inflammatory response.
Etiology:
Risk factors: young and old. Fall and winter.
Xerosis.
Clinical manifestations
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Round coin like sharply demarcated
erythematous papulovesicular patches/ plaques
Intense pruritus,
Lichenification
Nummular Eczema
Diagnosis /Differentials
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Diagnosis
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History and physical exam
Rule out secondary infection, allergy
Differential diagnosis to include
seborrheic dermatitis, psoriasis, contact
dermatitis, tinea
Nummular Eczema
Management
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Avoid scratching
Lubricants
Oral antihistamines
Topical corticosteroids
Intralesional triamcinolone
Systemic antibiotics
Phototherapy
Complications:
Dyshidrotic Eczema
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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
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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
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Diagnosis
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Clinical
Rule out secondary infection, allergy
Differential diagnosis to include contact
dermatitis, drug reaction
Complications:
Dyshidrotic Eczema
Management
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Burrow wet dressings
High potency glucocorticoids and
occlusive dressings
Topical antipruritics.
Severe need systemic steroids
Intralesional Triamcinolone
Systemic antibiotics
Contact Dermatitis
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Cell mediated reaction involving
sensitized T lymphocytes.
Etiology
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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
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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
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Diagnosis:
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Clinical
Rule out secondary infection.
Patch testing
Differential diagnosis to include
seborrheic dermatitis, atopic eczema
Contact Dermatitis
Treatment
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Remove etiologic agent
Wet dressings with gauze soaked in
Burow’s solution changed every 2-3
hours.
Topical corticosteroids
Systemic corticosteroids
Stasis Dermatitis
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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
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Can progress to venous stasis ulcers
and fibrosis
Found in 6-7% of elderly population
Stasis Dermatitis
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Acute form:
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Initially medial
aspect of ankle.
Inflammation
Weeping lesions
Plaques/ Erythema
Crusting/ Exudate
Stasis Dermatitis
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Chronic form
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Thin, shiny bluish
brown irregularly
pigmented scaling
skin.
Stasis Dermatitis
Diagnosis/Differentials
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Diagnosis:
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Clinical
Doppler
Differential diagnosis to include contact
dermatitis, Atopic dermatitis, cellulitis
Stasis Dermatitis
Management
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Mid potency topical corticosteroids.
Control chronic edema
For ulcers:
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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
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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
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Pruritus, pain
Erythematous
papules/vesicles,
edema
Satellite lesions to
Peri-genital, perianal, inner thigh,
buttocks
Diaper Dermatitis
Diagnosis/Differentials
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Diagnosis- KOH examination
Differential diagnosis to include contact
dermatitis, child abuse
Diaper Dermatitis
Management
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Topical antifungal agents such as
Nystatin, miconazole, or clotrimatzole
Topical corticosteroids
Complications
Educate care givers
Perioral Dermatitis
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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
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Lesions resemble
rosacea
Burning
Follicular papules,
vesicles and pustules
on an erythematous
base
Grouped
Perioral Dermatitis
Diagnosis/ Differentials
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Diagnosis:
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Clinical.
Rule out secondary causes.
Differentials
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Acne Vulgaris
Contact dermatitis
Rosacea
seborrheic dermatitis
Perioral Dermatitis
Management
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AVOID topical corticosteroids.
Antibiotics
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Metronidazole, erythromycin topical
Systemic antibiotics: Monocycline,
Doxycycline, or tetracycline
Wash with mild soap, use
nonfluorinated toothpaste.
Avoid oral contraceptives
Seborrheic Dermatitis
Seborrhea
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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
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Infants
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Affects scalp,
flexural area and
perioral
Erythematous
plaques
Fine white scales
Thick yellow brown
greasy scaling
Seborrheic Dermatitis
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Adults
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Pruritus
Burning
Erythematous plaques with
scaling
Seborrheic Dermatitis
Diagnosis/Differentials
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Diagnosis
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History/Physical
Differential diagnosis to include atopic
dermatitis, candidiasis, lupus
Seborrheic Dermatitis
Management
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Selenium sulfide shampoos, 2%
ketoconazole shampoo, ketoconazole
cream.
Salicylic acid
Corticosteroids
Cradle capTreat for secondary infection
Lichen Simplex Chronicus
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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
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Well circumscribed
plaques with lichenified
or thickened skin
PruritusHyperpigmentation
Excoriation
Lichen Simplex Chronicus
Diagnosis/Differentials
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Differential diagnosis to include
psoriasis Vulgaris, contact dermatitis,
fungal infection
Diagnosis
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Clinical
Biopsy shows hyperplasia acanthosis,
hyperkeratosis
KOH examination
Lichen Simplex Chronicus
Management
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High potency topical glucocorticoids
Oral antihistaminesHydration
Complications:
Psoriasis
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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
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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
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Pustular psoriasis:
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Painful
Deep sterile yellow
pustules
Pustules evolve into
red macules
Psoriasis
History and Physical Exam
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Guttate Psoriasis
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Could be immune
Slight pruritus
Small erythematous
papules with fine
scale
Can be discrete or
confluent
Psoriasis
Diagnosis/Differentials
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Skin biopsy shows increased mitosis in
keratinocytes
Auspitz phenomenon
Differential diagnosis to include lichen
planus, eczema
Psoriasis
Management
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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
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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
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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
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Oral lesions involve the
tongue and buccal
mucosa
Present with wickham’s
striae
Can then erode
Lichen Planus
Diagnosis/Differentials
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Diagnosis:
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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
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Antihistamines
Topical corticosteroids
Systemic corticosteroids
Topical and systemic retinoids Retinoids
normalize epidermal differentiation and
are anti inflammatory
Immunosuppressant -Cyclosporine.
Seborrheic Keratosis
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Due to proliferation of Keratinocytes
and melanocytes
Etiology: Genetics
Usually asymptomatic
Benign, however must rule out
malignant melanoma
Spontaneous resolution rare
Seborrheic Keratosis
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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
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Diagnosis:
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Skin Biopsy
Differentials
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Actinic Keratosis
Carcinoma
Warts
Seborrheic Keratosis
Management
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Keratolytic agents-leads to
desquamation of hornified epitheliumAmmonium Lactate lotion
Trichloroacetic acid- cauterizes skin,
keratin and tissues.
Actinic Keratosis
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Found in those with fair skin
Sun exposure leads to damage to
keratinocytes by UV radiation
Hyperkeratotic form more prominent
and palpable.
Actinic Keratosis
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Multiple, discrete
flat or elevated
Skin colored,
yellow-brown or
brown.
Dry, rough,
adherent scaly
lesion
3-10mm
Actinic Keratosis
Diagnosis/Differentials
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Diagnosis:Biopsy will show epidermal
changes
Differentials
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Squamous cell carcinoma
Lupus
Seborrheic keratosis
Actinic Keratosis
Management
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Topical 5-fluorouracil:
Surgical curettage or cryosurgery
Retinoids
Dermabrasion
Avoid sun exposure.
Urticaria
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IgE or complement mediated edema of
dermis or subcutaneous tissue
Etiology: antigens
Pathology: Mast cell stimulated to
degranulate by IgE.
Urticaria
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Clinical:
Pink
Edematous
Papules or plaques
Vary in appearance
Resolve within 24 hours
Angioedema: Painless, deeper urticaria
Urticaria
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Diagnostics:
Management:
Eliminate cause
Oral antihistamines
Review 1
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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
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Pruritus and
burning prior to
eruption
Vesicles resemble
tapioca
No erythema
What is this?
Where is it found?
How is it treated?
Review #3
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This is the
result of
chronic venous
insufficiency
What is it?
How is it
managed?
Review #4
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This rash occurs in
areas with high
sebaceous gland
concentration.
What is it?
Describe this lesion
What is the
management?
Review #5
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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
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What is the
pathophysiology
behind this?
Describe this
What are
management
options?
Review #7
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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
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What is this?
What is the
cause of this?
How is this
treated?
Review #10
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What is this?
What is the cause
of this?
How is this
managed?