Dermatitis Flashcards

1
Q

Atopic Eczema/Dermatitis

A
  • Common allergic skin disease
  • Comes and goes over time, usually starts in childhood
  • Primary symptom is itchy skin
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2
Q

Epidemiology of Atopic Eczema/Dermatitis

A

Atopic eczema affects 5-20% children worldwide

  • 11% in the US
  • Slight F > M predominance
  • Majority of cases have an onset before age 5
    • 60% of cases occur in the 1st year of life
    • 85% by 5 years of age
  • May persist into adulthood for up to half of those diagnosed during childhood
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3
Q

Characteristics of Atopic Eczema/Dermatitis

A

•Chronic, non-contagious, inflammatory skin disease
•Disruption of the skin barrier:
o Filaggrin(FLG) gene mutation
o Allergens or other triggers
•Type I hypersensitivity reaction (IgE mediated)
•Viscous cycle of pruritis and disruption of the skin surface; “the itch that rashes”
•Begins early in life, with chronic exacerbations and remissions.

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4
Q

Contributing Factors of Atopic Eczema/Dermatitis

A

•Genetic defects/family history (70%)

•Environment
-foods, dust mites, molds, pollens, animal dander, season (winter/low humidity), clothing, emotional stress

Atopic triad:
•atopic dermatitis
•allergic rhinitis (hay fever)
•asthma

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5
Q

Clinical Presentation of Atopic Eczema/Dermatitis

A
  • Ranges from ill-defined, erythematous, scaling patches to edematous papules and vesicles
  • Cheeks, scalp & extensor surfaces common in infants
  • Flexural surfaces, hand/foot (older children/adults)

Acute - pruritic, erythematous papulovesicular lesions; serous exudate

Chronic - lichenification, papules, and excoriation

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6
Q

Distribution of Atopic Eczema/Dermatitis by Age

A

Babies - Concentrated near or around the face

Toddler & Children - Concentrated in areas with folds and creases, such as elbows and knees

Adults - Concentrated on the hands, feet, as well as head and neck region.

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7
Q

Features to Consider in the Diagnosis of Atopic Dermatitis

A
Essential Features:
Required
•Pruritus
•Eczema (acute, subacute, chronic)
•Typical morphology and age-specific patterns
•Chronic or relapsing history
Important Features:
Observed in majority of cases; adds support to diagnosis:
•Early age of onset
•Atopy
•Personal and/or FH
•IgE reactivity
•Xerosis
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8
Q

Complications of Atopic Eczema/Dermatitis

A
  • Excoriations
  • Lichenification
  • Thickened, dry, irritated skin due to chronic scratching
  • Skin lines are accentuated
  • Fissures (palms, fingers, soles) –can be very painful
  • Secondary cellulitis
  • Skin is often highly colonized with Staph aureus •Eczema Herpeticum –disseminated viral infection, typically primary infection of HSV 1
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9
Q

Atopic Eczema/Dermatitis Treatment

A

Optimal management includes:
•Patient education
•Avoid exacerbating factors (allergens/irritants)
•Hydrate the skin & restore the skin barrier function
•Pharmacologic treatment of skin inflammation
•Topical/oral steroids
•Calcineurin Inhibitors
•+/-Antihistamines/antibiotics

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10
Q

Topical Corticosteroid Use for Atopic Eczema/Dermatitis

A
  • Mild disease: low potency, applied 1-2x daily for 2-4 weeks
  • Moderate disease: medium to high potency
  • Acute flares: intermediate to super high potency preparations may be used for up to 2 weeks, then replaced with a lower potency until lesions resolve.

•IMPORTANT:Use extreme caution when using topical corticosteroids on thinned-skin areas (face, neck, and skin folds). Higher absorption and risk of adverse effects!

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11
Q

Absorption of Topical Corticosteroids

A
Regional differences in percutaneous absorption (percent of the total dose absorbed across the body) are as follows:
•Sole of foot –0.14 %
•Palm –0.83 %
•Forearm –1.0 %
•Scalp –3.5 %
•Forehead –6.0 %
•Mandible –13 %
•Genitalia –42 %
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12
Q

Adverse Effects of Coricosteroid Use

A
Skin atrophy
Acneiform or rosacea-like eruptions
Striae
Bruising
Telangiectasias
Hypertrichosis
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13
Q

Topical Calcineurin Inhibitors

A

Pimecrolimus (Elidel) cream and Tacrolimus (Protopic) ointment:
•Steroid-sparing, anti-inflammatory agents
Efficacious for acute flares and maintenance therapy in adults and children ≥ 2 years old
•0.1% formulation for adults
•0.03% formulation for patients 2-15 years old
MOA –inhibits calcineurin-dependent T cell activation, impeding production of pro-inflammatory cytokines
•Applied twice daily for mild to moderate eczema of the face, eyelids, neck and skin folds.
•Maintenance -apply 2-3x per week to recurrent sites of involvement to reduce relapse.
•Side effects: burning, stinging and pruritis (most common during 1st week)

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14
Q

Other Pharmacologic Treatments for Atopic Eczema/Dermatitis

A
  • Oral antihistamines prn pruritus (to break the itch-scratch-itch cycle)
  • Antibiotics if secondary infection
  • Oral steroids reserved for severe cases
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15
Q

Lichen Simplex Chronicus

A
  • Aka “Neurodermatitis”
  • Affects F>M, age 30-50 years old
  • Secondary skin condition; lichenified plaque caused by excessive scratching or rubbing
  • Exaggerated skin markings, dry, leathery appearance, pigmentation
  • Common areas: scalp, back of neck, wrists, forearms, lower legs and genitals
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16
Q

Causes of Lichen Simplex Chronicus

A
  • Atopic Dermatitis
  • Contact Dermatitis
  • Psoriasis
  • Lichen Planus
  • Fungal Infection
  • Insect Bite
  • Neuropathy (DM)
  • Anxiety/stress
17
Q

Lichen Simplex Chronicus Treatment

A

Treatment is to stop rubbing!

  • High potency topical steroids
  • Moisturizers
  • Antidepressants: SSRIs –Paroxetine (Paxil), Sertraline (Zoloft) or tricyclic antidepressants
  • 1st generation antihistamine, Hydroxyzine (Vistaril), or tricyclic antidepressant (Doxepin) can be used for nocturnal pruritus.
18
Q

Dyshidrotic Eczema

A
  • Aka “dyshidrosis” or “pompholyx”
  • NOT a problem with the sweat glands
  • Deep seated vesicles with “tapioca-like” appearance
  • Vesicles coalesce and rupture
  • Location: hands (80%), sides of fingers, palms and soles
  • INTENSELY PRURITIC
  • Emotional stress & hot weather precipitating factors, also found in those with nickel allergy
  • Episodes usually weeks to months apart, spontaneous remission after 2-3 weeks
  • Management-reassurance, wet dressings (Burow’ssoaks, aka Domeborosolution), topical steroids
19
Q

Keratosis Pilaris

A
  • Disorder of keratinization
  • Forms horny plugs in hair follicles
  • Rough, raised papules (flesh, red or brownish)
  • Usually worse in winter months
  • Outer upper arms, thighs, cheeks, upper back
  • Improves with age
  • Can try creams, exfoliating scrubs, topical retinoids (avoid in children), urea, salicylic acid, alpha-hydroxy acids
20
Q

Classification of Contact Dermatitis

A

•Allergic Contact Dermatitis - a delayed-type hypersensitivity reaction
- Poison ivy (genus Toxicodendron), nickel, etc.

•Irritant Contact Dermatitis –80% of all contact dermatitis
- Household duties: hands in water, detergents, solvents, etc.
- The most common occupational skin disease
- Healthcare workers, chemical industry workers,
hairdressers, construction workers, etc.

21
Q

Allergic Contact Dermatitis

A
  • Dominant symptom is itch
  • Localized to skin areas that came in contact with the allergen
  • Hands, face and eyelids common
  • Erythematous, papular dermatitis with indistinct margins; often blisters and edema
  • Can take 1-2 days to appear
  • Poision ivy, oak, and sumac (urushiol oil)
  • Nickel, rubber; latex, preservatives, cosmetics, Neomycin (in topical creams/ointments)
22
Q

Irritant Contact Dermatitis

A
  • Burning, stinging pain
  • Hands are most common
  • Erythema, chapped skin, dryness and fissuring
  • More immediate onset (minutes to hours)
23
Q

Contact Dermatitis - Treatment

A
  • Discontinue exposure to allergen or irritant.
  • Decrease frequency of hand-washing if that is playing a role; use mild soap.
  • Wear gloves or protective clothing.
  • Apply bland emollient (Vaseline, Aquaphor, etc.)
  • Topical steroids 1-2x daily for 7-14 days
  • Consider an oral corticosteroid for ACD involving face or >20% BSA.
  • Prednisone 0.5-1mg/kg/day (max 60mg/day) for 7 days
24
Q

Drug Hypersensitivity

A

Immune-mediated response to a drug in a sensitized patient

25
Q

Drug Allergy

A

Type I immune reaction mediated by IgE (urticaria, angioedema, bronchospasm, pruritis, V/D, anaphylaxis)

26
Q

Adverse Cutaneous Drug Reactions

A
  • Aka “Drug Eruptions” occur in ~2% of patients
  • 90-95% are drug-induced exanthems (Type IV)
  • Often described as “morbilliform” or “rubelliform” because pattern resembles a viral exanthem.
  • 5% are drug-induced urticarial (Type I)
  • Rarely, severe non-allergic hypersensitivity cutaneous reactions occur (EM major, SJS/TEN and DIHS)
27
Q

Drug-Induced Exanthems

A
  • Account for 90% of all adverse cutaneous drug reactions•Develops within 5-14d of exposure
  • Morbilliform rash -erythematous macules, papules (rarely pustules/bullae)
  • Involves trunk and proximal extremities; mucosal involvement is absent
  • PCNs and sulfonamides common
28
Q

Urticaria

A

“hives”

Intensely pruritic, circumscribed, raised, erythematous eruption with central pallor

29
Q

Angioedema

A

Swelling deeper in dermis and subQ tissue (face/lips)
- Tongue swelling, laryngeal edema -> Airway
obstruction

30
Q

Treatment of Common Cutaneous Drug Reactions

A
  • Discontinue the offending drug!
  • Supportive and/or symptomatic care•Systemic corticosteroids
  • Topical steroids or antihistamines prn pruritus
  • Resolution is typically within 5-14 days
  • Post-inflammatory hyperpigmentation may occur
  • Counsel regarding avoidance and cross-reacting drugs in the future
31
Q

Severe Cutaneous Drug Reactions

A

Drug-Inducing Hypersensitivity Syndrome (DIHS)

Steven-Johnson Syndrome / Toxic Epidermal Necrolysis (SJS/TEN)

32
Q

Drug-induced Hypersensitivity Syndrome

A
A serious drug-induced reaction characterized by:
•Fever (100.4-104°F)
•Facial edema
•Rash (morbilliform eruption)
•Lymphadenopathy 
•Blood abnormalities
•Visceral involvement

Causes: antiepileptic agents, allopurinol, sulfonamides, minocycline, vancomycin and dapsone

Morbidity is 5-10%

33
Q

Stevens-Johnson Syndrome & Toxic Epidermal Necrolysis

A

•Rare, acute, potentially LIFE THREATENING mucocutaneous reactions!

  • Nearly always caused by medications
  • Epidermal necrosis and sloughing of the mucous membranes and skin; Fas/Fasligand-induced apoptosis
34
Q

SJS/TEN – Epidemiology & Etiology

A
  • Affects all age groups and races
  • Incidence is 100-fold higher in HIV-infected individuals
  • Malignancy, genetic factors (HLA type) and SLE are also risk factors
  • Overall mortality ranges from 10-30%
  • Commonly implicated medications:
  • Allopurinol
  • Anticonvulsants (phenobarbital, phenytoin, carbamazepine, and lamotrigine*)
  • Sulfonamides*
  • NSAIDs
  • Other causes: Mycoplasma pneumoniae*

*Most common causes in pediatrics

35
Q

SJS/TEN – Clinical Presentation

A
  • Prodrome: fever often >39C (102.2F) and flu-like sxs 1-3 days before lesions develop
  • Skin lesions: tender erythematous, purpuric macules, vesicles/bullae form, skin sloughing
  • Denudation: skin detachment
  • SJS < 10% TBSA
  • TEN >30% TBSA

•Nikolsky Sign: the elicitation of skin blistering as a result of gentle mechanical pressure on the skin.

Mucosal involvement (90%)
•Erythema and edema of lips
•Intraoral bullae; ruptured bullae, painful friable raw surfaces and hemorrhagic crusts
•Oral, genital, and/or ocular involvement (conjunctival itching, burning, pain, corneal ulceration and photophobia)

36
Q

SJS/TEN - Diagnosis

A

Clinical initially; skin biopsy and cultures (blood, wound, mucosal lesions)

37
Q

SJS/TEN - Treatment

A
  • Discontinue offending medication
  • Hospital admission -if extensive skin denudation, ICU/burn unit
  • Supportive care:
    • Nutritional and fluid replacement (via IV and NG tubes)
    • Temperature maintenance
    • Pain relief
    • Ocular management
    • Wound care/sterile handling
38
Q

Complications of SJS/TEN

A
Acute Phase (lasts 8-12 days)
•Fatal complications
•Dehydration and acute malnutrition
•Infection: skin, mucous membranes, lungs (pneumonia), and septicemia(S. aureus and P. aeruginosa) 
•GI ulceration and perforation
•Acute respiratory distress syndrome
•Shock and multiple organ failure
•Thromboembolism 

Long-term sequelae
•Cutaneous, mucosal, ocular, and pulmonary complications