SM 256: Eczema and Itchy Skin Flashcards

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1
Q

What is Eczema?

A

A morphological pattern seen visually or microscopically

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2
Q

What are the types of Eczema?

A

Atopic Dermatitis Contact Dermatitis Drug-Induced Dermatitis

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3
Q

What are the two types of Contact Dermatitis

A

Allergic Dermatitis Irritant Contact Dermatitis

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4
Q

How does Eczema present?

A

Symmetric Patches or Plaques with Erosions

Ill-defined and hard to delineate start/stop of lesion

Erythematous pink-red appearance Lichenification

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5
Q

What is Lichenification?

A

Thickening of Skin and accentuation of skin lines due to scratching

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6
Q

Is this Eczema, why or why not?

A

Not Eczema due to the well defined circular nature of the Rash - Eczema is ill-defined

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7
Q

Where does Atopic Dermatitis tend to develop in infants?

A

Atopic Dermatitis tends to develop in the facial and scal regions in infants

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8
Q

Where does Atopic Dermatitis develop in Toddlers?

A

Extensor surfaces like the elbows

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9
Q

Where does Atopic Dermatitis tend to develop in Older children and adults?

A

Flexor areas like the Antecubital and Popliteal Fossas

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10
Q

Where does Atopic Dermatits develop in Adults only?

A

In adults alone, Atopic Dermatitis develops in the head and neck

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11
Q

Does Lichenification imply a chronic or acute Atopic Dermatitis?

A

Lichenification implies a chronic Atopic Dermatitis because it’s driven by itching, which takes a while to make the Lichenification appearance

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12
Q

What is Spongiosis?

A

Fluid between Epidermal cells on Histology, common in Atopic Dermatitis

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13
Q

What does Histology of Atopic Dermatisis show?

A

Spongiosis (top) and Perivascular Infiltrate (bottom)

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14
Q

What is the role of Biopsy in diagnosing Eczema?

A

Only narrows the diagnosis down to the Eczema family, and rules out other disorders, but does not diagnose a specific type of Eczema

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15
Q

What do biomarkers and blood test reveal in Atopic Dermatitis?

A

Nothing - biomarkers and blood tests are not useful

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16
Q

What is the age prevalence of Eczema?

A

Eczema is common in childhood and may persist into adulthood, and also has some adult-onset cases as well

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17
Q

What protein is implicated in the development of Atopic Dermatitis and how?

A

Filaggrin 1, which is a major component of Natural Mositerizing Factor and maintaining the skin barrier function, is often dysfunctional in Atopic Dermatitis

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18
Q

What does Filaggrin 1 form?

A

Natural Moisterizing Factor - helps maintain the barrier function of the skin

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19
Q

Describe the protein precursors and products of Filaggrin?

A

Profilaggrin is cleaved into Filaggrin, which is eventually broken down into amino acids that form Natural Moisterizing Factor

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20
Q

What is the role of Profilaggrin?

A

Profilaggrin is a major component of Keratocyte Granules in the Granular layer of the Epidermis

21
Q

Describe the mechanism of inflammation in Atopic Dermatitis?

A

Th2 cells produce IL-13 and Il-4, leading to decreased Fillagrin expression and compromising the barrier function of the skin

22
Q

What cells and cytokines mediate inflammation in Atopic Dermatitis?

A

Th2 cells produce IL-4 and IL-13, which drive inflammation in Atopic Dermatitis

23
Q

How does IgE drive Atopic Dermatitis pathophysiology?

A

It doesn’t - IgE elevation is a byproduct of IL-4 and IL-13 elevations due to Th2 cell activity

24
Q

What causes the Dry Skin and Itchiness that accompanies Atopic Dermatitis?

A

IL-4 and IL-13

25
Q

How does Atopic Dermatitis effect the development of allergies?

A

Allergies are more common and more severe in patients with Atopic Dermatitis, especially Asthma, respiratory allergies, and food allergies, due to compromised skin barrier function

26
Q

How does Atopic Dermatitis effect sleep?

A

Atopic Dermatitis leads to poor sleep quality

27
Q

How does Atopic Dermatitis effect Quality of Life?

A

Atopic Dermatitis can lead to self-consciousness, suicidality, inability to manage daily activities, etc.

28
Q

Why does Atopic Dermatitis lead to more allergies and other adverse reactions?

A

Atopic Dermatitis compromises the skin barrier function, lowering the irritant threshold and predisposing adverse reactions

29
Q

How does climate and environment effect Eczema?

A

High Humidity, High UV Exposure, and High Temperature all decrease Ezema prevalence and some patients may not need medications during vacations or seasonality

30
Q

What can cause Eczema flares?

A

Stress, air pollutants, bacteria/viruses/fungi

31
Q

What is the treatment of choice for Atopic Dermatitis?

A

Topical agents: Corticosteroids and Calcineurin inhibitors

32
Q

What is Tacrolimus?

A

A Calcineurin inhibitor used to treat Atopic Dermitis

Used in conjuction with Corticosteroids

33
Q

What systemic agents can treat Atopic Dermatitis and when are they used?

A

Cyclosporine, Mycophenolate, Methotrexate, etc. can be used in severe cases, and only sparingly

34
Q

How do light treatments effect Atopic Dermatitis?

A

Light therapy and lasers can use UV light to treat local patches of Eczema, in the same way that high environmental UV light exposure clears up Eczema

35
Q

What is the newest treatment for Atopic Dermatitis?

A

Dupilumab - mAb to IL-4 receptor

36
Q

What is Dupilumab?

A

A mAb against the IL-4 receptor used to treat Atopic Dermatitis

37
Q

What is Irritant Contact Dermatitis?

A

A type of dermatitis that does not require sensitization

Infrequent exposure to strong irritant OR frequent exposure to mild irritant

Occurs in Atopic Dermatitis due to impaired skin barrier and lower irritant threshold

38
Q

Does irritant contact dermatitis require sensitization?

A

Nope

Infrequent exposure to strong irritant OR frequent exposure to mild irritant

39
Q

What is Allergic Contact Dermatitis?

A

A dermatits that requires sensitization and can involve delayed reactions up to two weeks after exposure

40
Q

Which is a true allergy, Allergic Contact Dermatitis or Irritant Contact Dermatits?

A

Allergic contact dermatitis is a true allergy because it requires sensitization

41
Q

Why is sensitization significant in Allergic Contact Dermtatitis?

A

Sensitization leads to breakouts of Dermatitis even with minimal future exposures to common allergens like Poison Ivy

42
Q

Describe the mechanism of Irritant Contact Dermatitis?

A

Nonspecific junk from damaged cells causes the release of TNFalpha

43
Q

Describe the mechanism of Allergic Contact Dermatitis?

A

An Allergen crosses the skin barrier, and is engulfed the resident APC’s: Langerhans cells

Langerhans cells present to Tcells and cause a clonal expansion

44
Q

Why does Allergic Contact Dermatitis not have the same pathway as Atopic Dermatitis?

A

Atopic Dermatitis uses IL-4 and IL-13, while Allergic Contact Dermatitis uses IL-9 and IL-17

45
Q

Describe the mechanism of a food/seasonal allergy?

A

Immediate reaction mediated by Mast Cells, IgE, and Histamine with a risk of anaphylaxis

46
Q

How does Allergic Contact Dermatitis differ from Food/seasonal allergies?

A

ACD uses a Lymphocyte, Food allergies use Mast cells

ACD is driven by sensitization and IL-4/13, Food allergies are immediate and IgE/Histamine driven

47
Q

What are drawbacks to patch testing?

A

Itchiness from tape/positive reactions, can’t shower or do heavy activity while having a patch test

48
Q

How could a patch test sensitize someone to an allergy?

A

If you have a compromised skin barrier, the patch test will continually expose you to an allergen and potentially sensitizie you

49
Q

If you see new onset Eczema in an adult, what should you be thinking about?

A

Drug induced Eczema, especially from Calcium Channel Blockers