Atopic Dermatitis

Question 1

Define allergic contact eczema (dermatitis)

Answer 1

A red, itchy, weepy reaction where the skin has come into contact with a substance that the immune system recognises as foreign, such as poison ivy or certain preservatives in creams and lotions

Question 2

Define atopic dermatitis

Answer 2

A chronic skin disease characterised by itchy, inflamed skin.It is a chronic, system, relapsing, inflammatory disease- not a localised skin condition

Question 3

Define contact eczema (dermatitis)

Answer 3

A localised reaction that includes, redness, itching, and burning where the skin has come into contact with an allergen (an allergen-causing substance) or with an irritant such as acid, cleaning agent, or other chemical

Question 4

Prevalence of AD

Answer 4

15-30% of children, 1-3% of working adults

Question 5

Role of filaggrin in allergic skin disease

Answer 5

Mutations in filaggrin gene lead to filaggrin deficiency that leads to impaired barrier function and enhanced allergen exposure.

Question 6

Environmental RFs for AD

Answer 6

Air pollution, increased infant washing, increased water hardness, high latitudes

Question 7

Protective environmental factors for AD

Answer 7

Increased UV light exposure and increased outdoor temperature, increased humidity

Question 8

Pathophysiology of AD

Answer 8

1. Defects in skin barrier lead to penetration by antigens, which encounter Langerhans cells (a type of dendritic cell found in skin), which activate T helper 2 (Th2) cells.2. Th2 cells release cytokines IL-4, IL-5, and IL13. IL4 increases Th2 survival. These cytokines also drive lgE synthesis by B cells and recruitment of peripheral eosinophils but these cells are thought to be by-products of Th2 activation rather than pathogenic mediators of AD.3. Th2 cytokines disrupt the skin barrier function by inhibiting expression of filaggrin (a protein essential for skin barrier formation) and antimicrobial peptides (the first-line defence against infectious agents). This results in enhanced penetration of allergens and pathogens.4. Allergens and pathogens cause epithelial keratinocyte damage, leading to release of IL33, IL25 and TLSP. They activate both dendritic cells and group 2 innate lymphoid cells (ILC2) to drive the Th2 inflammatory responses.5. In chronic AD, TH22 cells release IL22 which induces thickening and discolouration of the skin. TH1 cells produce reduced lvls of IFN-y, a cytokine which suppresses. Th2 inflammation.

Question 9

Epidemiology of AD

Answer 9

Prevalence in caucasian population is higher than asian. Clinical phenotypes:- Asian: well demarcated erythematous plaque-like lesions- Caucasian: ill-defined flatter erythematous skin lessions

Question 10

Typical distribution of AD

Answer 10

cheeks, elbow (front and back), write (front), behind knee. groin area not affected

Question 11

Clinical features in diagnosis of AD

Answer 11

Essential features (must be present):- pruritis- eczema (acute, subacute, chronic): flexural lesions, sparing of groin and axillary regions, chronic or relapsing hxImportant features (seen in most cases, supports the diagnosis of AD): - early age of onset- atopy (genetic tendency to develop allergic diseases?): personal/family hx (of AR or asthma), lgE reactivity- xerosis (dry skin)

Question 12

Major and minor S&S of AD

Answer 12

Major indicators:- pruritus (intense itching)- characteristic rash in locations typical of disease- chronic or repeated occurring smx- personal or family hx of AD (eczema, hay fever, asthma)Selected minor indicators:- early age of onset- dry skin that may also have patchy scales or rough bumps- increased serum lgE- numerous skin creases on palms- hand or foot involvement- inflammation ard lips- nipple eczema- susceptibility to skin infection (bacteria): superficial (epidermis, dermis) or non-superficial -> as itching may cause broken/excoriated skin)- positive allergy skin tests

Question 13

Clinical presentation of AD in an infant

Answer 13

Red, if touch and it blanches, it is erythematous. Lichenification (hardness). No excoriation so less risk of infection

Question 14

Extensor pattern of AD

Answer 14

well defined, lichenfication

Question 15

Clinical presentation of AD in the popliteal fossa (behind knee joint)

Answer 15

skin lesions, papules, excoriated

Question 16

Hx taking: specific questions to ask patient

Answer 16

• Is itching present?- distribution of rash- fam hx of atopy- how freq they wash their skin- what type of water they use to wash?

Question 17

Measures of AD severity

Answer 17

SCORAD Score > 50: Severe ADSCORAD Score 25-50: Moderate ADSCORAD Score <25: Mild AD

Question 18

Non-pharm therapy of AD

Answer 18

Identify any triggers.- prevent overshowering- reduce stress- food hypersensitivity: egg, milk, wheat, fish, soya -> avoid- remove allergens (house dust mite, animal dander, moulds/pollens, cosmetics (contains preservations)

Question 19

Baseline: basic therapy for AD in adults

Answer 19

Educational programmes, emollients, bath oils, avoidances of clinically relevant allergens.

Question 20

How does Complete emollient therapy help?

Answer 20

emollient therapy is cornerstone of management of AD and acts through maintenance of skin barrier. It forms oclusive later, reduce water loss and exposure to bacteria.It improves smx of itch, pain, prolong time to a flare up, reduce potency and amt of CS used to control AD.It is used for all types (mild, mod, sev AD).For inflamed areas or those with genetic predeposition to AD and wishes to prevent it: lotions For dry skin: ointments.Example: suu balm menthol cream used BD-TDS everyday. Physiogel DMT cream.Ceramides (works as emollients?): re-inforce skin barrier and increases hydration

Question 21

MILD: SCORAD <25 or transient eczema therapy

Answer 21

Reactive therapy with topical GCS class II or depending on local cofactors: topical calcineurin inhibitors, antiseptics incl. silver/silver coated textiles.

Question 22

MODERATE: SCORAD 25-50 or recurrent eczema

Answer 22

Proactive therapy with topical tacrolimus, or class II or class III topical GCS, wet wrap therapy, UV therapy, psychosomatic counseling, climate therapy

Question 23

SEVERE: SCORAD >50 or persistent eczema

Answer 23

hospitalisation, systemic immunosuppression, cyclosporine, short couse of OCS, dupilumab, MTX, azathioprin, PUVA, alitretinoin, mycophenolate mofetil

Question 24

Least potent topical CS used in AD

Answer 24

hydrocortisone 1%, 2.5% in cream, lotions or ointments

Question 25

What is CI to topical CS use?

Answer 25

bacterial infection

Question 26

Adverse effects of topical CS

Answer 26

• redness- steroid telangiectasia: threadline red lines or patterns on skin (“spider veins”)- tinea faciei treated with topical steroid (shld nvr treat infection w steroids -> masks smx and worsens smx)- atrophy (thinning of skin)

Question 27

Counsel on wet wrap therapy

Answer 27

1. moisten the dressing in warm water until it is slightly damp2. wrap the moist dressing ard affected area3. wrap a dry dressing over wet one4. carefully put on clothes so as not to disturb bandages5. leave bandages on for several hrs or overnight

Question 28

How does topical calcineurin inhibitors (tacrolimus) help?

Answer 28

2nd line tx, mod-sev, no SE of thinning skin, good for thin skin (groin areas), response during 1wk.It inhibits calcineurin, preventing NFAT from being phosphorylated and stop it from entering nucelus. This alters gene expression, suppressing prdtn of inflammatory cytokines and T cell activation

Question 29

Combination therapy for preventing and treating flares of AD

Answer 29

Complete emollient therapy is used throughout for low severity.As severity increases:TCI: 2 x weekTCI: 2 x dayTCI - night, TCS - morningFor flares (peak severity): TCS: 2 x day.As severity decreases:TCI - night, TCS - morningTCI: 2 x dayTCI: 2 x week

Question 30

Examples of systemic tx of AD

Answer 30

AzathioprineCiclosporinDupilumab (IL4 antag, SC)MTXMycophenolate mofetilTofacitinib (JAK inhibitor, PO)

Question 31

How does JAK inhibitors work in AD?

Answer 31

stop downstream functions of inflammatory cytokines in AD. Inhibition of JAKs blocks their transphosphorylation, further inhibiting the phosphorylation and dimerisation of STATs

Question 32

Other systemic tx for smx and secondary infections arising due to AD

Answer 32

• oral antihistamines (eg. chlorphenramine, cetrizine): for pruritis, insomnia - antibiotics (eg. flucloxacillin): for sec infections- antivirals (eg. acyclovir): for sec infections

Question 33

Pathophysiology of allergic contact dermatitis (ACD)

Answer 33

Type 4 of delayed type of hypersensitivity reaction.1. haptens penetrate skin2. haptens bind to peptides at surface of langerhans cells3. langerhands cells migrate to local lymph nodes4. CD8+ T cells ‘primed’ to recognise peptide-hapten complex as antigen5. CD8+ T cells migrate to epidermis6. subsequent application of hapten leads to allergic rxnnote: AD is type 2 hypersensitivity rxn

Question 34

Clinical presentation of AD (areas)

Answer 34

corner of eye from wearing latex glove, bottom of ear, wrist (wearing watch), arms

Question 35

Causes and clinical presentation of irritant contact dermatitis

Answer 35

Esp children: cheeks, necks, around mouth. Pruritis is present

Question 36

Differential diagnosis for allergic and irritant dermatitis

Answer 36

fungal infection (lesions have defined advancing edge), psoriasis (lesions thickened and scaly), scabies (lesions located around wrists), medicine related or infection (sudden onset w assoc fever), dermatitis (lesions have poorly defined edge and/or vesicles)

Question 37

What age can AD medicines be used?

Answer 37

Emollient: from birth onwards (pregnancy and breastfeeding women is okay)Hydrocortisone: >10y/o (pregnancy and breastfeeding women is okay)Clobetasone: >12y/o