Skin and Respiratory Health - Atopic Dermatitis Flashcards
Q1: What is atopic dermatitis (AD)?
A1: Atopic dermatitis (AD), also known as eczema, is a chronic inflammatory skin disease characterized by an impaired skin barrier and immune dysregulation. It leads to dry, itchy skin, redness, and inflammation, often occurring in areas such as the flexor surfaces, face, scalp, neck, wrists, and ankles.
Q2: What are the common symptoms and clinical presentation of AD?
A2: Common symptoms include:
Pruritus (itching): Often intense, leading to scratching.
Dry, erythematous (red) skin: Commonly on flexor or extensor surfaces.
Lichenification: Thickened, hyperpigmented plaques due to scratching.
Papulovesicular lesions: Small blisters or vesicles formed in the skin.
Q3: What is the “atopic triad” in AD?
A3: The “atopic triad” refers to the co-occurrence of three common allergic conditions: atopic dermatitis, allergic rhinitis, and asthma. Around 30%–50% of people with AD may have this combination of conditions.
Q4: What are the two types of atopic dermatitis, and what differentiates them?
A4:
Exogenous / Extrinsic AD: This form is IgE-mediated (allergy-related) and affects 70–80% of cases.
Endogenous / Intrinsic AD: This form is non-IgE-mediated, affecting 20–30% of cases. It is associated with a defect in the immune system and skin barrier.
Q5: What are the underlying causes and risk factors for developing AD?
A5: Key factors include:
Genetics: Filaggrin gene mutations are the strongest known risk factor.
Immune health: Imbalance between Th1 and Th2 cells, often with heightened Th2 activity.
Environmental triggers: Stress, pollution, allergens, and infections (e.g., S. aureus).
Nutritional deficiencies: Deficiency in vitamin D, zinc, and essential fatty acids (EFAs) are linked to AD.
Q6: How does dysbiosis (microbial imbalance) contribute to AD?
A6: Dysbiosis, especially early-life antibiotic use, disrupts the gut microbiome. This can lead to an overgrowth of harmful bacteria (e.g., S. aureus, Clostridia, E. coli) while decreasing beneficial bacteria like Bifidobacteria. These imbalances can exacerbate immune responses that trigger AD flare-ups.
Q7: What are the common triggers that worsen AD symptoms?
A7: Common triggers include:
Environmental allergens: Pollutants, dust, and plant pollens.
Food allergens: Cow’s milk, eggs, peanuts, soy, and wheat, especially in children.
Topical irritants: Harsh soaps, detergents, and fragrances.
Heat, humidity, and stress: These can worsen itching and skin inflammation.
Q8: What laboratory tests are typically used to diagnose AD?
A8: Key diagnostic tests include:
Blood tests: Complete blood count (eosinophils), serum IgE levels.
Allergy testing: Food and environmental allergy testing (e.g., Cyrex).
Stool testing: To check for gut dysbiosis or microbial imbalances.
Genetic panels: Testing for filaggrin gene mutations (FADS2, VDR).
Q9: What are the conventional treatment options for AD?
A9: Conventional treatments often include:
Topical corticosteroids: These are anti-inflammatory but can lead to skin thinning over prolonged use.
Antihistamines: For reducing itching.
Immunosuppressants: Used when other treatments fail, but flare-ups often return once the treatment stops.
Q10: What natural approaches can help manage AD?
A10: Natural approaches focus on:
Elimination diets: Avoiding common allergens like milk, eggs, peanuts, and wheat.
Anti-inflammatory foods: Omega-3 fatty acids (found in fish, flaxseeds), quercetin-rich foods (apples, kale).
Probiotics: To improve gut health and balance the immune system.
Stress management: Yoga, meditation, or other relaxation techniques.
Q11: How does vitamin D influence AD?
A11: Vitamin D helps regulate immune function by normalizing Th1/Th2 cytokine balance. Adequate vitamin D levels can reduce IgE production and prevent mast cell activation, both of which are involved in allergic reactions seen in AD.
Q12: How do essential fatty acids (EFAs) affect AD?
A12: EFAs like omega-3 fatty acids (EPA) and gamma-linolenic acid (GLA) play a crucial role in reducing inflammation. EPA increases the production of anti-inflammatory prostaglandins (PG3), while GLA helps reduce pro-inflammatory arachidonic acid metabolites.
Q13: Can probiotics help with AD?
A13: Yes, probiotics can support a healthy gut microbiome and reduce inflammation. Specific strains like Lactobacillus rhamnosus and Bifidobacterium lactis are particularly beneficial for enhancing intestinal barrier function and reducing Th2 inflammation.
Q14: What topical treatments can be used to soothe AD symptoms?
A14: Topical treatments include:
Aqueous creams or lotions: Avoid oily preparations that may increase skin heat.
Herbal applications: Calendula, chamomile, and lavender have anti-inflammatory properties.
Magnesium baths: Bathing in magnesium salts (e.g., Dead Sea salts) supports skin hydration and barrier function.
Q15: What dietary changes can help manage AD symptoms?
A15: Key dietary changes include:
Increase omega-3 fatty acids: Found in fish, flaxseeds, chia seeds.
Avoid inflammatory foods: Such as processed sugars, refined carbs, and trans fats.
Include anti-inflammatory foods: Like quercetin-rich fruits (apples, onions) and vegetables (spinach, kale).
Q16: Can magnesium help with AD?
A16: Magnesium plays a role in reducing inflammation and improving skin barrier function. Magnesium baths (such as using Dead Sea salts) can help moisturize the skin and alleviate itching, promoting healing in individuals with AD.
