Dermatitis and Urticaria Quiz

A general term for a group of inflammatory skin conditions that cause itchy, red, and inflamed skin lesions.

It is characterized by a type I hypersensitivity reaction mediated by IgE antibodies. This is often associated with a family history of asthma, allergic rhinitis, and eczema. Triggers include environmental allergens, food allergens, irritants, and microbial antigens.

It is caused by direct skin contact with irritants which leads to skin inflammation without involving the immune system. Common irritants include chemicals, soaps, detergents, and repeated exposure to water.

It is a result of a type IV hypersensitivity reaction (delayed-type hypersensitivity) where T cells mediate the immune response. Common allergens include poison ivy, nickel, fragrances, latex, and certain medications.

Results from chronic venous insufficiency (poor blood flow in the veins) that causes blood pooling in the lower legs. Risk factors include older age, varicose veins, deep vein thrombosis (DVT), and obesity.

It is associated with overgrowth of Malassezia yeast, as well as excessive sebum production. Stress, cold weather, and immunosuppression can exacerbate seborrheic dermatitis.

The common pathway of dermatitis involves immune system activation, skin barrier dysfunction, and inflammation. But the specific causes and mechanisms differ depending on the type of dermatitis.

Atopic dermatitis is caused by a type I hypersensitivity reaction where IgE antibodies are involved. It's commonly seen in families with history of allergies like asthma or eczema.

Seborrheic dermatitis is linked to an overgrowth of Malassezia yeast and is often triggered by stress, cold weather, and immunosuppression.

Urticaria, also known as hives, is caused by a type I hypersensitivity reaction triggered by various factors like food allergies, medications, or infections.

Dermatitis isn't contagious. It's not spread from person to person, but can be triggered by environmental factors or underlying medical conditions.

Atopic dermatitis (AD) is a skin condition characterized by an impaired skin barrier due to a deficiency in filaggrin, leading to increased water loss and permeability. This allows allergens and irritants to penetrate the skin, triggering a type I hypersensitivity reaction.

Allergic contact dermatitis (ACD) is a type IV hypersensitivity reaction triggered by exposure to specific allergens. Initial exposure sensitizes Langerhans cells, which then present the allergen to T cells, leading to the production of memory T cells. Subsequent exposure results in T cell activation, triggering an inflammatory response.

Irritant contact dermatitis (ICD) is a direct skin reaction to irritants, causing damage to keratinocytes and disrupting the skin barrier. Unlike ACD, ICD doesn't involve the immune system. Repeated exposure to irritants like soaps or solvents can exacerbate this condition.

Seborrheic dermatitis is characterized by an overgrowth of Malassezia yeast, which triggers an inflammatory response due to the release of pro-inflammatory metabolites. This condition is often linked to areas rich in sebaceous glands, such as the scalp and face, due to excessive sebum production.

In Atopic Dermatitis, the deficiency of filaggrin protein leads to a compromised skin barrier, resulting in increased water loss and permeability. This allows for the entry of allergens and irritants, contributing to the symptoms of AD.

In Allergic Contact Dermatitis, a type IV hypersensitivity reaction occurs when T cells recognize and react to allergens. This response involves the release of cytokines and chemokines, which attract inflammatory cells to the site, causing swelling, erythema, and vesicle formation.

In Irritant Contact Dermatitis, direct contact with irritants leads to damage to the skin's keratinocytes, disrupting the barrier function. This damage triggers inflammation, resulting in erythema and edema. Repeated exposure to irritants can exacerbate the condition.

A skin condition characterized by itchy, red, and inflamed skin lesions.

An allergic reaction triggered by the immune system's response to allergens, such as food, drugs, or insect stings.

Exposure to foods like shellfish, nuts, eggs, and wheat can trigger Urticaria in allergic individuals.

Certain medications, especially NSAIDs, antibiotics, and ACE inhibitors, are known to trigger Urticaria.

Extreme temperatures, exposure to water, and UV light are known triggers for Urticaria.

Acne is a result of inflammation of the pilosebaceous unit (hair follicle + sebaceous gland) and affects mainly adolescents and young adults.

Hormonal changes, particularly androgens (male sex hormones) that stimulate sebum production in sebaceous glands, contribute to acne.

C. acnes, a bacterium normally found on skin, shifts to a pathogenic role and causes inflammation, which is one of the key contributors to acne.

A type of allergic reaction characterized by itchy, raised welts called wheals which appear and disappear suddenly.

The process by which the immune system overreacts to allergens, causing the release of histamine.

An immune system response that involves the production of IgE antibodies. These antibodies bind to mast cells and basophils.

The allergen binds to IgE receptors on mast cells and basophils, causing them to release histamine and other inflammatory mediators.

Histamine, a chemical released from mast cells, binds to histamine receptors in skin, causing redness, swelling, and itching.

Urticaria is not contagious.

Individuals with a predisposition to allergies, exposure to triggers, and certain medical conditions.

Urticaria is not a specific disease but a symptom of an underlying allergic reaction.

The process of acne development involves several steps. First, excess keratin builds up inside the hair follicle, forming a plug. Second, increased sebum production traps more oil and debris beneath the plug. Third, Cutibacterium acnes bacteria colonize the follicle and release irritants. Lastly, the follicular wall ruptures, releasing bacteria and triggering inflammation.

Hyperkeratinization is the excessive production of keratin, a protein found in the skin. This leads to a buildup of keratin in the hair follicle, forming a plug that traps sebum and debris.

Increased sebum production is a key factor in acne. It results from the stimulation of sebaceous glands by androgens (e.g., during puberty). The excess sebum contributes to the formation of comedones (blackheads and whiteheads) and provides nourishment for C. acnes bacteria.

Cutibacterium acnes (formerly Propionibacterium acnes) is a common skin bacteria that plays a role in acne. It feeds on sebum and produces inflammatory substances that contribute to the development of acne lesions.

The follicular wall may rupture due to the pressure of trapped oil and bacteria. This rupture releases inflammatory substances, triggering an immune response and leading to red, inflamed lesions.

Acne is not contagious. It's a chronic condition caused by a combination of internal factors like hormonal changes, genetics, and microbial imbalances.

Hormonal changes, particularly increased androgen levels, can stimulate sebaceous gland activity and contribute to acne. This is why acne is common during puberty, menstruation, and pregnancy.

Genetics plays a role in acne susceptibility. People with a family history of acne are more likely to develop the condition. This suggests that genetic predisposition can influence sebum production and follicle responsiveness.