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Dermatology > Eczematous Dermatitis & Urticaria- Wiss > Flashcards

Eczematous Dermatitis & Urticaria- Wiss Flashcards

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Dermatology Board Prep flashcards
1
Q

Name the subtypes of Eczematous Dermatitis

A
  • Atopic Dermatitis
  • Allergic Contact Dermatitis
  • Irritant Contact Dermatitis

Note: Eczema = Dermatitis

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2
Q

Describe how the appearance of Eczema changes as a function of time.

A

Acute:
-Erythema, Edema, Serous exudate, vesicles

Subacute:
-Erythema, thickening, scale

Chronic:
-Lichenification, Pigmenting, scale

Note: The swelling in the acute phase could look like Bulla.

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3
Q

What is Atopic Dermatitis?

A

A Pruritic Inflammatory Process

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4
Q

What is Atopy?

A

Tendency towards allergic diseases:

  • Atopic dermatitis
  • Asthma
  • Allergic Rhinitis

Note: Atopy is usually Familial.

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5
Q

Describe Atopic Dermatitis

A
  • First step in the Atopic March
  • 50% of children with AD will get asthma
  • 50-80% with AD will develop allergic rhinitis
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6
Q

Describe the pathophysiology of AD

A
  • T cell activation leading to overproduction of IgE
  • Hyper-responsiveness of Langerhans cells
  • Defective epidermal barrier

During flare:

  • Increased TH2 cells, resulting in IL-4 release
  • IL-4 stimulates B cells to produceIgE

Chronically:
-Increased TH1 cells and respective cytokines

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7
Q

Describe the T cell distribution as a function phase

A

Acute: T helper cells driven towards TH2
Chronic: T helper cells driven towards TH1

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8
Q

Describe the role of Langerhans cells in AD

A
  • Langerhans cells are Hyper-responsive and more numerous
  • They are IgE bearing

-Upon contact of allergen, they present to and activate T cells.

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9
Q

Describe the deficiency and the defect of the epidermal barrier in AD.

A

The epidermis in AD has decreased Ceramides:

  • This alters barrier integrity and inflammatory response.
  • Dry skin
  • Increased water loss
  • Increased penetration of irritants, allergen, microbes
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10
Q

Describe the general classes of triggers for AD

A

Allergens

  • Food
  • Aeroallergens

Infection

  • Staph aureus
  • Cutaneous viruses

Note: Infections worsen AD and AD worsens infections.

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11
Q

Describe why AD patients have increased risk of cutaneous infection. Which microbe is seen in up to 90 of AD patients%?

A

Reduced:

  • Ceramides (Epidermal barrier integrity, water retention)
  • Beta-Defensins (anti-microbial peptide)
  • Cathelicidins (anti-microbial peptide)

Staph aureus seen in up to 90% of AD cases. Commonly triggers flares.

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12
Q

Describe the clinical history of AD

A
  • 2/3 with personal or family history of atopy
  • manifestations usually seen within first 2yrs of life
  • Always Pruritic!
  • Dry skin
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13
Q

Aside from actual allergens and infection, what other things may worsen AD flares?

A
  • Temperature extremes
  • Stress
  • Wool
  • Soap
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14
Q

What visible feature will the poorly defined, erythematous, scaly plaques acquire chronically?

A

Lichenification

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15
Q

Describe the location of AD in an infant or toddler

A
  • Cheeks and face

- Spares the diaper area due to hydration and the inability to scratch.

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16
Q

Describe the location of AD in a child (2yrs to puberty)

A
  • Antecubital and popliteal fossa (flexures)
  • Wrists and ankles
  • Periorbital
17
Q

Is a child with atopic dermatitis still likely to have it in adulthood?

A

No. 95% resolved by age 20.

18
Q

Describe AD standard treatment

A
  • Topical steroids
  • Oral antihistamines
  • Topical and Oral antibiotics
  • Proper nutrition (allergy avoidance)
  • Address sleep disturbances
19
Q

Summarize atopic dermatitis temporally and pathologically

A
  • elevated TH2 activity resulting in IL4 release which activates B cells to produce IgE
  • Decreased Ceramides; reduced epidermal barrier
  • Flares and remits
  • Children

Note: 1st step in the Atopic March

20
Q

What are the two types of Contact Dermatitis?

A
  • Primary irritant

- Allergic

21
Q

Describe Primary Irritant Contact dermatitis

A
  • Non-immunologic; direct effect of irritant on the skin
  • Occurs in anyone with long enough exposure
  • Damages skin by direct contact

Examples:

  • Detergent, soap
  • Urine
  • Saliva (lip licking)
  • Stool
  • Water
22
Q

Describe Allergic Contact Dermatitis

A
  • Type IV (delayed) Hypersensitivity reaction
  • Occurs in allergic individuals

Initial Exposure:
-7 to 10 days to react

Repeated exposure:
-12 hours or more

Examples:

  • Poison Ivy
  • Nickel
  • Preservatives
23
Q

Describe the difference in histology between an atopic and allergic contact dermatitis biopsy

A

Atopic
-No lymphocytes in dermis

Allergic Contact
-Lymphocytes in dermis, acutely.

Spongiosis seen in both.

24
Q

Describe Allergic Contact Dermatitis Treatment

A
  • Identify cause
  • Wet dressings if acute
  • Topical and Oral steroids
  • Antihistamines
25
Q

What is Urticaria?

A
  • Hives
  • Pruritic eruption of transient wheals

Note: Angioedema is the more severe form (can result in anaphylaxis).

26
Q

Describe duration of Uritcaria and its 2 forms

A
  • Transient; lasts less than 24hrs.
  • Can be immunologic (type I) or non-immunologic

Note: Opiates and Radio-contrast dye are non-immunologic examples as they are mast cell degranulators.

Note: Shellfish and peanuts are immunologic.

27
Q

Describe the pathology of immunological urticaria

A

-IgE binds to the surface of Mast cells and basophils

28
Q

Describe cross reactivity

A

Patients allergic to allergens such as latex can also have cross reactivity to Kiwi, bananas, nuts, etc.

29
Q

Name Urticaria/Angioedema Rx

A
  • Avoid allergen
  • Antihistamines
  • Antipruritic lotions
  • Epinephrine if accompanied by Anaphylaxis

Dermatology (7 decks)

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