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(Ch12) Atopic Dermatitis Flashcards

1
Q

what is the epidemiology of AD ?

A

10–30% kids & 2–10% adults.

↓rural areas than urban/high- income areas

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2
Q

What are the subtypes of AD?

A
  1. Early Onset: (MC) AD in < 2 Yrs.
  2. Late Onset: AD after puberty.
  3. Senile Onset: Unusual
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3
Q

what percentage of children will have AD by age of 6 months?

A

Starts < 6 mo in 45%
1st year in 60%
< 5 years in 85%

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4
Q

what percentage of children will have allergen specific IgE by age of 2?

A

1/2 children develop allergen-specific IgE by 2 Yrs of age.

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5
Q

what percentage of children will develop remission by age of 12y?

A

60% go into remission at 12 years.

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6
Q

Strongest risk factor for AD?

A

Parental Hx of AD

stronger risk factor than asthma or allergic rhinitis

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7
Q

what are the major components in the pathogenesis of AD?

A
  1. Epidermal Barrier Dysfunction (↑TEWL, pH and permeability+altered lipids)
  2. ** Immune dysregulation**
  3. ** Altered microbiome**
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8
Q

What correlates with severity of AD ?

A

Level of TEWL in nonlesional skin

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9
Q

what can predict increased risk of AD in the 1st year of life ?

A

↑ level of transepidermal water loss (TEWL), on day 2 of life predicts ↑ risk of AD at 1 year of age.

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10
Q

what could reduce filaggrin level?

A

↑ local pH
protease activity
Th2 cytokine levels

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11
Q

what is filaggrin?

A

Keratin filament-aggregating protein.

Major structural component of SC

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12
Q

Strongest genetic risk factor for AD ?

A

Loss-of-function FLG Mx
(Both AD & ichthyosis vulgars)

Ass/w early-onset AD, ↑ severity, persistence into adulthood

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13
Q

Factors that contribute to impaired barrier function?

A
  1. abnormal Filaggrin and other structural proteins.

2.Alteration in SC lipids.

3.Imbalance between Proteases and protease inhibitors.

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14
Q

Mention few epidermal barrier proteins other than Filaggrin involved in barrier dysfunction?

A

loricrin, corneodesmosin, involucrin, SPRR3/4, claudin-1, and late cornified envelope protein 2B

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15
Q

Filaggrin and its breakdown products (e.g. histidine) contribute to?

A

1- epidermal hydration
2-acid mantle formation
3-lipid processing
4-barrier function

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16
Q

Epidermal barrier dysfunction can result in ?

A

↑TEWL, pH and permeability+altered lipids

also
1-Entry for irritants, allergens and microbes → ↑ immune responses → ↑ proinflammatory cytokines.

2- Epicutaneous sensitization to aeroallergens ➤ asthma + allergic rhinoconjunctivitis

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17
Q

How do SC lipids altered in AD?

A

1.Filaggrin-deficient cytoskeletal ➤ ✗ loading / secretion of lamellar bodies ➤ ✗ post-secretory lipid organization and processing.

2.Disruption of acidic mantle → ↓lipid-processing enzymes such as β-glucoscerebrosidase + acid sphingomyelinase.

3.Th2 cytokines also ↓ SC lipid
4.components.
Satph A colonization

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18
Q

mention 2 enzymes involved in lipid processing in AD ?

A

β-glucoscerebrosidase

acid sphingomyelinase

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19
Q

Which SPINK5 mutation associated with AD ?

A

SPINK5 polymorphisms ➤ ↑ risk of AD

Biallelic loss-of-function SPINK5 Mx ➤ Netherton syndrome.

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20
Q

Which endogenous serine proteases has ↑levels in AD skin?

A

Endogenous serine proteases e.g. kallikrein 5/7.

Imbalance in serine proteases enzymes and protease inhibitors such as lymphoepithelial Kazal-type trypsin inhibitor (LEKTI) encoded by SPINK5 lead to ↑levels of endogenous serine proteases e.g. kallikrein 5/7.

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21
Q

Which protease inhibitors encoded by SPINK5?

A

lymphoepithelial Kazal-type trypsin inhibitor (LEKTI)

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22
Q

How does LEKTI deficiency affect epidermal barrier function?

A

LEKTI deficiency ➤ ↓ Dsg1 → ✗ SC detachment → Disrupted epidermal barrier

S. aureus extracellular V8 protease (similar to S. aureus exfoliative toxins) also degrade Dsg1.

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23
Q

what is unique about adult onset AD

A

30% patients esp F have non-IgE- associated AD

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24
Q

what is the consistent feature of AD?

A

Epidermal barrier dysfunction

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25
which cytokine present in both acute and chronic AD
Th17 cytokines
26
Acute AD is mediated by Th?
Th2
27
Chronic AD mediated by Th?
Th1 & Th22
28
Master switch of allergic inflammation?
thymic stromal lymphopoietin (TSLP)
29
What Cytokines induce Th2 response in AD?
IL-1, IL-25 (17E), IL-33 & thymic stromal lymphopoietin (TSLP) all known as Keratinocyte-derived cytokines
30
Th2 response produce in AD?
IL-4, IL-5, and IL-13 Eosinophils and mast cells ↑ allergen-specific Ig results in: 1. ↓ terminal differentiation proteins: loricrin, filaggrin, and involucrin. 2.↓ β-defensin-2/3
31
3 main cell types involved in AD immune dysregulation?
Keratinocytes T cells  Antigen presenting cells(ILC) e.g. NK
32
IL involved in pruritis and receptors can be found in C nerve fibres as well as keratinocytes?
IL-31 Nemolizumab, anti-IL-31 receptor A subunit. Induced by Staphylococcal superantigen
33
Thymic stromal lymphopoietin (TSLP)
Expressed in acute and chronic AD (only in lesions skin) **Stimulated** by: allergens, viruses, trauma, and other cytokines (e.g. IL-1β, TNF) **Produced** by: keratinocytes, fibroblasts, and mast cells
34
Cytokines Characteristic of new-onset pediatric AD?
L-17 and IL-19 Produced by Th17
35
percentage of patient with AD colonized by Staph A
> 90% of AD colonized with S. aureus, During flare ↑Staphylococcus spp. from ~35% to ~90%
36
mention antimicrobial peptides reduced in AD?
cathelicidins, defensins2/3
37
How does Staph A affects AD?
1. Superantigenic exotoxins by S. aureus →↑ Th2 2. S. aureus δ-toxin →↑ mast cell degranulation and Th2. 3. ↓Filaggrin increases susceptibility of KC to S. aureus α-toxin-induced cytotoxicity
38
IL-4 and IL-13
IL-4 Function→ IMP for ↑Th2 cell differentiation, ↑IgE and ↑eosinophil IL-4 and IL-13 heterodimeric receptors contain IL- 4Rα subunit and STAT6 → naive T cells into Th2
39
what is the age-dependent sequence, referred to as Atopic March?
1. Atopic dermatitis – in first 2 years of life (infants and young children) 2.Food allergies – in first 2 years of life (infants and young children) 3. Asthma – around 2-5 years (older children) 4.Allergic rhinitis – 10 years + (predominates in adolescents) 5.Eosinophilic esophagitis (rare
40
Predictors of persistence of AD into adulthood?
1.Young age at onset 2.Concurrent asthma and/or allergic rhinoconjunctivitis 3.Low socioeconomic status 4.non-White ethnicity 5. filaggrin mutations
41
Essential features of AD? Must be present and sufficient for dx
1. Pruritus 2.Typical eczematous morphology or Age-specific distribution 3. Chronic or relapsing course
42
Important Features of AD?
1. Onset during infancy or early childhood 2. Personal or fam hx of Atopy 3. Xerosis
43
Triggers of AD
1. Climate extremes or low humidity 2. Irritants 3. infections 4. Environemental Allergies 5. Food Allergies
44
Mention 5 mutations As/w AD
Encodes Epidermal protein: 1. FLG 2. FLG2 3. SPINK5 Encodes immunologic proteins 4. IL4&R, IL13&R, IL31&R 5- TSLP
45
AD subtypes based on Age
1. Infantile 2. childhood 3. Adolescent/ adult 4.Senile
46
which anatomical locations not affected by AD ?
Axilla and groins
47
which eczema variant common in skin of colour?
papular eczema SOC eczema associated with Th17
48
Regional Variants of AD?
1. Cheilitis sicca 2. Ear eczema 3. Eyelid eczema 4. Head and neck dermatitis 5. Juvenile plantar dermatosis 6. Atopic hand eczema 7. Prurigo AD 8. Nummular / Discoid AD 9. Frictional lichenoid eruption 10. Nipple eczema
49
Hallmark of eczema
Pruritus
50
Pathophysiology of Pityriasis alba
low-grade eczematous dermatitis disrupts transfer of melanosomes to K
51
itch that rashes
Rubbing & scratching initiate flares or exacerbate existing dermatitis
52
infantile AD vs diaper rash or Seboderm
Sparing of diaper area in AD
53
Atopic Stigmata (associated features)
1. Xerosis 2. Icthyosis Vulgaris 3. Palmoplanter hyper linearity 4. Keratosis pilaris 5. Dennie Morgan lines 6. Allergic Shiners 7. Ant neck folds 8. Hertoghe 9. White dermatographism 10. Follicular prominence
54
Complications of AD
1. Bacterial and viral infections (strep P, HSV, Molluscum) 2. risk of ↑ cardiovascular complications 3. Anterior Subcapsular cataracts 4. Psychological/emotional impact
55
Ophthalmological complication As/w AD?
Anterior Subcapsular cataracts
56
AD pruritus worst timing?
in the evening
57
Mention few scoring systems to assess severity of AD?
1. EASI (Eczema Area Scoring Index) 2. SCORAD (SCORing Atopic Dermatitis 3. Diepgen score 4. POEM (Patient-Oriented Eczema Measure.
58
“Soak and smear” technique
TCS or anti-inflammatory Rx immediately after bathing, prior to moisturizer
59
6 + 3 rule
6 minutes in bath 3min after bath window for occlusion
60
Name 2 risk factors for hand eczema development in AD patients?
-FLG mutation -Frequent exposure to water and other irritants
61
What is the Ddx of pityriasis alba?
-PIH from other inflammatory skin conditions (e.g. seb derm, PLC) -Pityriasis versicolor: more sharply demarcated, scale -Vitiligo: sharply demarcated, depigmented not hypopigmented -Hypopigmented MF: extrafacial involvement
62
What is the treatment of pityriasis alba?
Sunscreen, photoprotection, emollients
63
What clinical features help to distinguish infantile AD vs. seb derm?
AD: mainly in extensors + cheeks Seb derm: mainly in folds; earlier onset (1 wk post-birth); a/w yellow-white greasy adherent scales; surrounded by satellite lesions; absence of pruritus, irritability and sleeplessness
64
Ddx of AD
Seborrheic dermatitis Contact dermatitis (ACD or ICD) Psoriasis Asteatotic eczema LSC Scabies Dermatophytosis
65
Name 5 immunodeficiencies that are part of the AD Ddx?
Wiskott-Aldrich Hyper IgE syndromes IPEX (immune dysregulation, polyendocrinopathy, enteropathy, X-linked) Omenn syndrome DiGeorge syndrome Ig deficiencies (X-linked hypogammaglobulinemia, IgA deficiency) Ataxia telangiectasia
66
What should you think of if a patient with AD is not improving, or worsening despite, regular use of TCS?
Allergic contact dermatitis
67
What are the 3 objectives of maintenance therapy in AD?
- Prevent triggers - Control subclinical inflammation - Restore barrier
68
What is the minimum age approved for the use of TCIs for AD?
≥ 2 yo
69
What is the therapeutic ladder of treatment for AD?
General Educational interventions: disease mechanisms and course, triggers, appropriate use of therapies, goals of management, support groups and organizations, psychological interventions Gentle skin care: bath/shower guidelines, avoidance of fragrance, soap cleansers and hot water, moisturizer after bath Moisturizer: immediately after bath/shower, apply liberally and frequently daily Topical TCS TCI Crisaborole Topical tofacitinib Phototherapy NBUVB UVA1 PUVA Systemic First line Dupilumab CsA AZA MTX MMF SCS Second line Omalizumab: anti IgE monoclonal Ab Nemolizumab Tofacitinib Rituximab IFN-gamma IVIg Other: crude coal tar, HCQ, ECP Adjunctive Wet wraps Bleach baths Antimicrobials and antiseptics – if superinfection Antihistamines – sedating effects for pruritus control Leukotriene antagonists Sodium cromoglycate Probiotics Vit. D supplementation and other dietary supplements Systemic allergen-specific immunotherapy Management of co-existing allergic diseases (food, aeroallergens, ACD)
70
Explain how to do a wet wrap?
1. Application of TCS 2. Inner wet layer 3. Outer dry layer of cotton gauze or garments 4. Leave in place for 8-24 hours per day 5. Treatment duration should not exceed 2 weeks
71
What are the 5 MC food allergies associated with AD?
1. Eggs *most often a/w AD exacerbations 2. Milk 3. Peanuts 4. Soy 5. Wheat
72
Is there an association between food allergies and AD? percentage of children with AD who has food allergy
In 10-30% of infants and young children with AD, exposure to food allergens may exacerbate their eczema (especially in those with severe, recalcitrant dz)
73
Name 5 side effects of TCS?
1.Atrophy 2. Telangiectasias 3. Steroidal acne 4. Poor wound healing 5. Perioral dermatitis 6. Cataracts 7. Iatrogenic Cushing’s 7. Hypopigmentation 8. Hypertrichosis 9. Milia, folliculitis.
74
Name 2 primary preventive strategies for AD development?
1. For infants with +famhx of atopy: exclusive breastfeeding during first 3-4mos of life may decrease risk (longer exclusive feeding does not confer additional benefit/protection against developing AD) 2. Maternal vitamin D supplementation
75
MOA of Crisaborole, Roflumilast
PDE4 inhibitors (PDE4 degrades cAMP which increases cytokines like IL-10 and IL-4 so Crisaborole decreases the pro-inflammatory cytokines)
76
MOA of Tralokinumab
targets IL-13R alpha1 and IL13R a2 🡪 decreases IL-23
77
MOA of AZA and MMF
AZA: inhibitor of purine synthesis that reduces leukocyte proliferation MMF: inhibits the de novo pathway of purine synthesis, resulting in suppression of lymphocyte function
78
MOA of CSA
CsA: potent inhibitor of T-cell-dependent immune responses and IL-2 production
79
Role of Phototherapy in AD
Phototherapy: immunomodulatory effects occur via induction of T-cell apoptosis, reduction of dendritic cells, and decreased expression of Th2 cytokines such as IL-5, IL-13, and IL-31

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