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Me > (Ch12) Atopic Dermatitis > Flashcards

(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
Q

which cytokine present in both acute and chronic AD

A

Th17 cytokines

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26
Q

Acute AD is mediated by Th?

A

Th2

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27
Q

Chronic AD mediated by Th?

A

Th1 & Th22

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28
Q

Master switch of allergic inflammation?

A

thymic stromal lymphopoietin (TSLP)

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29
Q

What Cytokines induce Th2 response in AD?

A

IL-1, IL-25 (17E), IL-33 & thymic stromal lymphopoietin (TSLP)

all known as Keratinocyte-derived cytokines

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30
Q

Th2 response produce in AD?

A

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

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31
Q

3 main cell types involved in AD immune dysregulation?

A

Keratinocytes
T cells
Antigen presenting cells(ILC) e.g. NK

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32
Q

IL involved in pruritis and receptors can be found in C nerve fibres as well as keratinocytes?

A

IL-31
Nemolizumab, anti-IL-31 receptor A subunit.
Induced by Staphylococcal superantigen

33
Q

Thymic stromal lymphopoietin (TSLP)

A

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
Q

Cytokines Characteristic of new-onset pediatric AD?

A

L-17 and IL-19
Produced by Th17

35
Q

percentage of patient with AD colonized by Staph A

A

> 90% of AD colonized with S. aureus,
During flare ↑Staphylococcus spp. from ~35% to ~90%

36
Q

mention antimicrobial peptides reduced in AD?

A

cathelicidins, defensins2/3

37
Q

How does Staph A affects AD?

A
  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
Q

IL-4 and IL-13

A

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
Q

what is the age-dependent sequence, referred to as Atopic March?

A
  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)

  1. Asthma – around 2-5 years (older children)

4.Allergic rhinitis – 10 years + (predominates in adolescents)

5.Eosinophilic esophagitis (rare

40
Q

Predictors of persistence of AD into adulthood?

A

1.Young age at onset

2.Concurrent asthma and/or allergic rhinoconjunctivitis

3.Low socioeconomic status

4.non-White ethnicity

  1. filaggrin mutations
41
Q

Essential features of AD?
Must be present and sufficient for dx

A
  1. Pruritus

2.Typical eczematous morphology or Age-specific distribution

  1. Chronic or relapsing course
42
Q

Important Features of AD?

A
  1. Onset during infancy or early childhood
  2. Personal or fam hx of Atopy
  3. Xerosis
43
Q

Triggers of AD

A
  1. Climate extremes or low humidity
  2. Irritants
  3. infections
  4. Environemental Allergies
  5. Food Allergies
44
Q

Mention 5 mutations As/w AD

A

Encodes Epidermal protein:
1. FLG
2. FLG2
3. SPINK5

Encodes immunologic proteins
4. IL4&R, IL13&R, IL31&R
5- TSLP

45
Q

AD subtypes based on Age

A
  1. Infantile
  2. childhood
  3. Adolescent/ adult
    4.Senile
46
Q

which anatomical locations not affected by AD ?

A

Axilla and groins

47
Q

which eczema variant common in skin of colour?

A

papular eczema

SOC eczema associated with Th17

48
Q

Regional Variants of AD?

A
  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
Q

Hallmark of eczema

A

Pruritus

50
Q

Pathophysiology of Pityriasis alba

A

low-grade eczematous dermatitis disrupts transfer of melanosomes to K

51
Q

itch that rashes

A

Rubbing & scratching initiate flares or exacerbate existing dermatitis

52
Q

infantile AD vs diaper rash or Seboderm

A

Sparing of diaper area in AD

53
Q

Atopic Stigmata (associated features)

A
  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
Q

Complications of AD

A
  1. Bacterial and viral infections (strep P, HSV, Molluscum)
  2. risk of ↑ cardiovascular complications
  3. Anterior Subcapsular cataracts
  4. Psychological/emotional impact
55
Q

Ophthalmological complication As/w AD?

A

Anterior Subcapsular cataracts

56
Q

AD pruritus worst timing?

A

in the evening

57
Q

Mention few scoring systems to assess severity of AD?

A
  1. EASI (Eczema Area Scoring Index)
  2. SCORAD (SCORing Atopic Dermatitis
  3. Diepgen score
  4. POEM (Patient-Oriented Eczema Measure.
58
Q

“Soak and smear” technique

A

TCS or anti-inflammatory Rx immediately after bathing, prior to moisturizer

59
Q

6 + 3 rule

A

6 minutes in bath
3min after bath window for occlusion

60
Q

Name 2 risk factors for hand eczema development in AD patients?

A

-FLG mutation
-Frequent exposure to water and other irritants

61
Q

What is the Ddx of pityriasis alba?

A

-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
Q

What is the treatment of pityriasis alba?

A

Sunscreen, photoprotection, emollients

63
Q

What clinical features help to distinguish infantile AD vs. seb derm?

A

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
Q

Ddx of AD

A

Seborrheic dermatitis
Contact dermatitis (ACD or ICD)
Psoriasis
Asteatotic eczema
LSC
Scabies
Dermatophytosis

65
Q

Name 5 immunodeficiencies that are part of the AD Ddx?

A

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
Q

What should you think of if a patient with AD is not improving, or worsening despite, regular use of TCS?

A

Allergic contact dermatitis

67
Q

What are the 3 objectives of maintenance therapy in AD?

A
  • Prevent triggers
  • Control subclinical inflammation
  • Restore barrier
68
Q

What is the minimum age approved for the use of TCIs for AD?

A

≥ 2 yo

69
Q

What is the therapeutic ladder of treatment for AD?

A

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
Q

Explain how to do a wet wrap?

A
  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
Q

What are the 5 MC food allergies associated with AD?

A
  1. Eggs *most often a/w AD exacerbations
  2. Milk
  3. Peanuts
  4. Soy
  5. Wheat
72
Q

Is there an association between food allergies and AD?
percentage of children with AD who has food allergy

A

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
Q

Name 5 side effects of TCS?

A

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
Q

Name 2 primary preventive strategies for AD development?

A
  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
Q

MOA of Crisaborole, Roflumilast

A

PDE4 inhibitors

(PDE4 degrades cAMP which increases cytokines like IL-10 and IL-4 so Crisaborole decreases the pro-inflammatory cytokines)

76
Q

MOA of Tralokinumab

A

targets IL-13R alpha1 and IL13R a2 🡪 decreases IL-23

77
Q

MOA of AZA and MMF

A

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
Q

MOA of CSA

A

CsA: potent inhibitor of T-cell-dependent immune responses and IL-2 production

79
Q

Role of Phototherapy in AD

A

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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