Integumentary Inflammatory Skin Disorders Midterm Notes PDF

2 1 INTEGUMENTARY – Inflammatory Disorders of the Skin Derma&&s Derma((s, also known as eczema, is a general term used to describe a group of inflammatory skin condi&ons. It results in itchy, red, and inflame...

2 1 INTEGUMENTARY – Inflammatory Disorders of the Skin Derma&&s Derma((s, also known as eczema, is a general term used to describe a group of inflammatory skin condi&ons. It results in itchy, red, and inflamed skin lesions. Derma((s can be classified into several types, including atopic derma&&s, contact derma&&s, seborrheic derma&&s, and stasis derma&&s. 1. Most Likely Cause The most likely causes of derma((s vary by type: Atopic Derma&&s (AD): o Cause: Thought to be a result of a type I hypersensi&vity reac&on. This is mediated by IgE an&bodies and is oAen associated with a family history of asthma, allergic rhini&s, and eczema. o Triggers: Environmental allergens, food allergens, irritants, and microbial an(gens. o Gene&cs: Muta(ons in the filaggrin gene (FLG), which is crucial for maintaining the integrity of the skin barrier, are associated with atopic derma((s. Allergic Contact Derma&&s (ACD): o Cause: A result of a type IV hypersensi&vity reac&on (delayed-type hypersensi(vity) where T cells mediate the immune response. o Allergens: Common allergens include poison ivy, nickel, fragrances, latex, and certain medica&ons. Irritant Contact Derma&&s (ICD): o Cause: Caused by direct skin contact with irritants, which leads to skin inflamma(on without the involvement of the immune system. o Irritants: Chemicals, soaps, detergents, and repeated exposure to water are common irritants. Stasis Derma&&s: o Cause: Results from chronic venous insufficiency (poor blood flow in the veins) that causes blood pooling in the lower legs. o Risk Factors: Older age, varicose veins, deep vein thrombosis (DVT), and obesity. Seborrheic Derma&&s: o Cause: Associated with overgrowth of Malassezia yeast, as well as excessive sebum produc(on. o Triggers: Stress, cold weather, and immunosuppression can exacerbate seborrheic derma((s. 2. Pathophysiology The pathophysiology of derma((s depends on its type. However, the general pathway involves immune system ac&va&on, skin barrier dysfunc&on, and inflamma&on. Atopic Derma&&s (AD):  2 o Impaired Skin Barrier: Deficiency in the filaggrin protein leads to increased water loss and permeability of the skin, allowing allergens and irritants to penetrate. o Type I Hypersensi&vity Reac&on: Exposure to allergens leads to the produc(on of IgE an&bodies, which trigger mast cell degranula&on and the release of histamines, resul(ng in itching (pruritus), redness (erythema), and swelling (edema). o Chronic Inflamma&on: Persistent an(gen exposure ac(vates T-helper cells (Th2), resul(ng in the release of interleukins (IL-4, IL-13), which further disrupts the skin barrier and drives chronic inflamma(on. Allergic Contact Derma&&s (ACD): o Type IV Hypersensi&vity Reac&on: Ini(al exposure to an allergen sensi(zes Langerhans cells (dendri(c cells), which present the an(gen to T cells, leading to the produc(on of memory T cells. o Re-exposure: Subsequent exposure results in T cell ac&va&on, leading to the produc(on of cytokines and chemokines, which aTract inflammatory cells to the site, causing swelling, erythema, and vesicle forma(on. Irritant Contact Derma&&s (ICD): o Direct Damage to Skin: Unlike ACD, ICD does not involve the immune system. Instead, irritants damage the kera&nocytes and disrupt the skin barrier, causing inflamma&on, erythema, and edema. o Repeated Exposure: Chronic exposure to irritants such as water, soaps, or solvents leads to skin desquama(on and barrier breakdown. Stasis Derma&&s: o Venous Hypertension: Chronic venous insufficiency causes blood to pool in the lower extremi(es, increasing capillary pressure and leading to plasma leakage into the dermis. o Inflammatory Cascade: Proteins from plasma ac(vate inflammatory cells, which release cytokines that cause fibrosis and skin discolora&on. Seborrheic Derma&&s: o Malassezia Yeast Overgrowth: Excessive coloniza(on by the yeast triggers an inflammatory response due to its release of pro-inflammatory metabolites. o Excess Sebum: Seborrheic derma((s typically occurs in areas rich in sebaceous glands (scalp, face) due to overproduc(on of sebum. 3. Disease Transmission Transmission: o Not transmissible. Derma((s is not an infec(ous disease and cannot be transmiTed from person to person. o Seborrheic Derma&&s: While it is associated with Malassezia yeast, it is not considered a transmissible infec(on. 4. Risk Factors Risk factors vary depending on the type of derma((s.  3 Atopic Derma&&s (AD) Gene&cs: Family history of atopy (asthma, eczema, allergic rhini&s). Environmental Triggers: Pollen, dust mites, animal dander, and harsh weather. Skin Barrier Dysfunc&on: Filaggrin muta&ons and exposure to harsh detergents/soaps. Age: Commonly seen in infants and children, but it can persist into adulthood. Allergic Contact Derma&&s (ACD) Allergen Exposure: Poison ivy, nickel, latex, perfumes, and certain cosme(cs. Occupa&onal Risk: Healthcare workers, beau(cians, construc(on workers, and cleaners are at increased risk. Irritant Contact Derma&&s (ICD) Occupa&onal Exposure: Frequent hand washing, handling chemicals, and exposure to irritants are key risk factors. Dry Skin: Individuals with exis(ng dry skin condi(ons are more vulnerable. Stasis Derma&&s Venous Insufficiency: Condi(ons like varicose veins and deep vein thrombosis (DVT) increase risk. Obesity and Prolonged Standing: Increases venous pressure and impairs blood flow. Seborrheic Derma&&s Infants and Adults: Occurs in infants ("cradle cap") and in adults, especially males. Immunosuppression: Pa(ents with HIV/AIDS or Parkinson's disease are at higher risk. Stress and Weather: Cold weather and stress can trigger flare-ups. Summary Table Criteria Derma&&s Most Likely Atopic: Type I hypersensi(vity; Contact: Allergens/irritants; Stasis: Venous Cause insufficiency; Seborrheic: Malassezia yeast. Involves immune response, skin barrier dysfunc(on, and chronic Pathophysiology inflamma(on. Transmission Not transmissible. Risk Factors Family history, allergens, environmental exposure, obesity, occupa(on.  4 Ur&caria (Hives) Ur(caria, commonly known as hives, is a type I hypersensi&vity reac&on of the skin. It is characterized by itchy, raised, and red welts (wheals) that appear suddenly on the skin. It can be acute (las&ng less than 6 weeks) or chronic (las&ng more than 6 weeks). 1. Most Likely Cause Cause: o Ur(caria is primarily caused by a type I hypersensi&vity reac&on. This reac(on is IgE-mediated, meaning the immune system reacts to allergens, leading to the release of histamine from mast cells and basophils. o Common triggers include: § Allergens: Foods (e.g., shellfish, nuts, eggs), insect s(ngs, and certain medica(ons (e.g., penicillin, NSAIDs). § Environmental Factors: Exposure to extreme temperatures, sunlight, and water pressure (aquagenic ur(caria). § Physical Triggers: Fric(on, pressure on the skin, and exercise. § Infec&ons: Viral, bacterial, and parasi(c infec(ons can trigger ur(caria. 2. Pathophysiology The pathophysiology of ur(caria involves immune system dysregula&on, leading to excessive release of histamine and other inflammatory mediators from mast cells and basophils in the skin. 1. Sensi&za&on: o The ini(al exposure to an allergen (e.g., food, drug, or insect venom) causes IgE an&bodies to be produced. o These IgE an(bodies bind to mast cells and basophils, "arming" them for a future reac(on. 2. Re-Exposure and Ac&va&on: o Upon re-exposure to the allergen, it binds to the IgE receptors on the surface of mast cells and basophils. o This triggers the degranula&on (release of contents) of mast cells and basophils. 3. Release of Histamine and Other Mediators: o Histamine is released, which binds to H1 and H2 histamine receptors in the skin. o This leads to vasodila&on, increased capillary permeability, and edema (swelling), forming the characteris(c wheals and welts on the skin. o Other inflammatory mediators like leukotrienes and prostaglandins further promote inflamma(on. 4. Clinical Manifesta&on: o Ur(caria presents as pruri&c (itchy) wheals that can vary in size and shape. o The wheals are transient, meaning they appear and disappear in different loca(ons on the skin. 3. Disease Transmission  5 Transmission: o Not transmissible. Ur(caria is not an infec(ous disease. o However, infec&ous diseases (like viral or bacterial infec(ons) can trigger ur&caria due to immune system ac(va(on. 4. Risk Factors Risk factors for ur(caria include individual predisposi&ons, environmental exposures, and certain medical condi&ons. Modifiable Risk Factors Food Allergens: Exposure to foods like shellfish, nuts, eggs, and wheat can trigger ur(caria in allergic individuals. Medica&on Use: Certain medica(ons, especially NSAIDs, an&bio&cs (e.g., penicillin), and ACE inhibitors, are known to trigger ur(caria. Environmental Exposures: Extreme temperatures (heat or cold), exposure to water (aquagenic ur(caria), and UV light (solar ur(caria) are known triggers. Stress and Anxiety: Psychological stress can trigger or exacerbate chronic ur(caria. Non-Modifiable Risk Factors History of Atopy: Individuals with a history of asthma, eczema (atopic derma&&s), and allergic rhini&s are more likely to develop ur(caria. Age: Ur(caria is more common in children and young adults. Gender: Females have a higher prevalence of chronic ur&caria compared to males. Autoimmune Diseases: Individuals with autoimmune condi(ons like thyroid disease and systemic lupus erythematosus (SLE) are at higher risk of chronic ur(caria【. Summary Table Criteria Ur&caria (Hives) Most Likely IgE-mediated Type I hypersensi&vity reac&on to allergens like foods, drugs, Cause and insect s&ngs. 1. Sensi&za&on (IgE produc(on) → 2. Re-exposure (mast cell degranula(on) Pathophysiology → 3. Histamine release → 4. Vasodila&on, leakage, and wheals. Not transmissible. It is an allergic immune response, but infec(ons can Transmission trigger it. Modifiable: Allergens (food, drugs), extreme temperatures, exposure to UV Risk Factors light, stress. Non-Modifiable: Age, gender (more common in females), atopy (asthma, eczema), autoimmune diseases.  6 Acne Vulgaris Acne vulgaris is a common chronic skin condi&on involving inflamma&on of the pilosebaceous unit (hair follicle + sebaceous gland) and typically affects adolescents and young adults, though it may persist into adulthood. 1. Most Likely Cause The most likely cause of acne vulgaris is mul(factorial, involving the following key elements: Hormonal Changes: Androgens (male sex hormones) s(mulate increased produc(on of sebum (skin oil) in sebaceous glands Cu&bacterium acnes (formerly Propionibacterium acnes): This bacterium shiAs from a symbio&c to a pathogenic role, triggering inflamma(on. Hyperkera&niza&on: Excess produc(on of kera(n leads to clogging of the hair follicle (plug forma(on). Sebaceous Gland Overac&vity: Increased sebum produc(on clogs the follicle, which provides a growth environment for bacteria. 2. Pathophysiology The development of acne vulgaris follows a well-established process involving four key pathological changes: 1. Hyperkera&niza&on: o Excess produc(on of kera(n (protein that forms skin) occurs in the follicular epithelium. o This excess kera(n forms a plug (microcomedone) in the hair follicle, which traps sebum and debris. 2. Increased Sebum Produc&on: o Androgens (e.g., during puberty) s(mulate the sebaceous glands to produce excess sebum. o Excess sebum accumulates behind the follicular plug, crea(ng an ideal environment for bacterial growth. 3. Coloniza&on of Cu&bacterium acnes: o Cu&bacterium acnes, a normal skin commensal, colonizes the sebaceous follicle. o As it feeds on the sebum, it releases lipases, which convert triglycerides in sebum into free fa`y acids. o These faTy acids irritate the follicle wall, further promo(ng inflamma(on. 4. Inflamma&on and Rupture: o The follicular wall may rupture due to the pressure of accumulated sebum and bacteria. o This rupture releases sebum, C. acnes, and debris into the dermis, triggering an intense immune response with the recruitment of inflammatory cells (macrophages, neutrophils). o The result is the development of inflamed lesions like papules, pustules, nodules, and cysts.  7 3. Disease Transmission Transmission: o Acne vulgaris is not a transmissible disease. It is a chronic inflammatory condi(on driven by internal factors (hormonal, gene(c, and microbial). o While Cu&bacterium acnes is involved, it is a normal commensal of human skin, not an infec(ous agent. 4. Risk Factors Several risk factors contribute to the development and progression of acne vulgaris. Intrinsic Risk Factors Hormonal Changes: Puberty, menstrua(on, pregnancy, and condi(ons like polycys&c ovary syndrome (PCOS) increase androgens, s(mula(ng sebaceous gland ac(vity. Gene&cs: Family history of acne increases the likelihood of developing the condi(on. Skin Type: Oily skin increases sebum produc(on and promotes follicular plugging. Lifestyle and Environmental Factors Diet: Diets high in refined sugars, dairy, and processed foods are associated with acne development. Stress: Stress triggers the release of cor&sol, which can exacerbate sebaceous gland ac(vity. Cosme&c Use: Use of oil-based cosme(cs can clog pores, leading to acne (commonly called acne cosme&ca). Medica&ons: Certain medica(ons, such as steroids, lithium, and isoniazid, are associated with acne. Environmental Factors: Humid environments and excessive swea(ng can clog hair follicles, increasing acne risk. Summary Table Criteria Acne Vulgaris Most Likely Androgenic hormones, C. acnes coloniza&on, follicular hyperkera&niza&on, Cause sebum overproduc&on. 1. Plug forma&on (hyperkera&niza&on) → 2. Sebum accumula&on → 3. Pathophysiology Coloniza&on of C. acnes → 4. Follicular rupture and inflamma&on. Not transmissible. It is an inflammatory condi(on linked to gene(cs, Transmission hormones, and microbial ac(vity. Intrinsic: Hormonal changes (puberty, pregnancy, PCOS), gene(cs, skin type Risk Factors (oily skin). Lifestyle: Diet (sugars, dairy), stress, cosme(cs, medica(ons (steroids, lithium).