Tissue Responses to Injury and Infection - Hypersensitivity Reactions PDF

1 1 TISSUE RESPONSES TO INJURY AND INFECTION – Hypersensi)vity Reac)ons 1. Type I Hypersensi.vity (Immediate/Allergic Reac.ons) Cause: o Caused by exposure to environmental allergens such as...

1 1 TISSUE RESPONSES TO INJURY AND INFECTION – Hypersensi)vity Reac)ons 1. Type I Hypersensi.vity (Immediate/Allergic Reac.ons) Cause: o Caused by exposure to environmental allergens such as pollen, pet dander, food allergens (e.g., peanuts), insect venom, and certain medica.ons. Pathophysiology: o Sensi.za.on Phase: Ini7al exposure to the allergen promotes the produc7on of IgE an.bodies that bind to mast cells and basophils. o Re-exposure: Upon re-exposure to the same allergen, cross-linking of the IgE on the surface of mast cells triggers mast cell degranula.on, releasing histamine, leukotrienes, and prostaglandins, leading to increased vascular permeability, smooth muscle contrac.on, and mucus secre.on. o Clinical Manifesta.ons: These include ur.caria (hives), allergic rhini.s (hay fever), asthma, and in severe cases, anaphylaxis. Transmission: o Not transmissible. It is an immune-mediated response triggered by exposure to allergens. Risk Factors: o Gene.c predisposi.on to atopy (family history of allergies, asthma, or eczema). o Environmental exposure to allergens (e.g., pollen, pets, dust mites). o Occupa.on-related exposure (e.g., healthcare workers exposed to latex). 2. Type II Hypersensi.vity (Cytotoxic Reac.ons) Cause: o Autoimmune disorders (like Graves’ disease and Myasthenia gravis) and blood transfusion reac.ons occur when.ssue-specific an.gens are targeted by the immune system. Pathophysiology: o An.body-Mediated Destruc.on: IgG or IgM an.bodies bind to an.gens on cell surfaces, leading to: § Opsoniza.on and phagocytosis of cells by macrophages. § Ac.va.on of the complement system, forming the membrane aSack complex. § Cell lysis and death through the release of cytotoxic molecules from immune cells. o Examples: § Graves' disease: An7bodies bind to TSH receptors, leading to overs7mula7on of the thyroid. § Myasthenia gravis: An7bodies block acetylcholine receptors at the neuromuscular junc7on. Transmission: o Not transmissible. It is caused by the body's immune response to self-an.gens or foreign an.gens.  2 Risk Factors: o Gene.c predisposi.on (family history of autoimmune diseases). o Autoimmune disorders like Graves' disease and Myasthenia gravis. o Blood transfusions from incompa7ble blood types. 3. Type III Hypersensi.vity (Immune Complex-Mediated) Cause: o Caused by the forma7on of immune complexes (an7gen-an7body complexes) that are deposited in 7ssues and cause inflamma.on. o Autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthri.s (RA) fall under this category. Pathophysiology: o Immune Complex Forma.on: Circula7ng an.gen-an.body complexes become trapped in the walls of blood vessels or 7ssues. o Ac.va.on of the Complement System: This leads to the recruitment of neutrophils, which release lysosomal enzymes that cause.ssue damage. o Inflammatory Response: This process causes inflamma.on and.ssue necrosis in organs like the kidneys, joints, and blood vessels. o Examples: § Systemic lupus erythematosus (SLE): Immune complexes are deposited in the kidneys (lupus nephri7s). § Rheumatoid arthri.s (RA): Complexes deposit in the synovial fluid of joints, causing inflamma7on. Transmission: o Not transmissible. It occurs due to the body's immune response to self or foreign an7gens. Risk Factors: o Autoimmune diseases like SLE and RA. o Chronic infec.ons (e.g., chronic hepa77s) that lead to persistent immune complex forma7on. 4. Type IV Hypersensi.vity (Delayed/Cell-Mediated) Cause: o Triggered by environmental an.gens (like poison ivy), medica.ons, or infec.ous agents such as Mycobacterium tuberculosis. Pathophysiology: o Sensi.za.on Phase: Memory T cells are generated aPer the ini7al exposure to an an7gen. o Re-exposure: Upon re-exposure, the an7gen-presen7ng cells ac7vate memory T cells, resul7ng in the release of cytokines (e.g., IFN-γ, TNF-α). o Delayed Inflammatory Response: Recruitment of macrophages to the site of exposure leads to the forma7on of granulomas and.ssue destruc.on. o Examples: § Contact derma..s: Triggered by exposure to agents like poison ivy.  3 § Tuberculosis (TB) skin test: A posi7ve Mantoux test indicates prior exposure to Mycobacterium tuberculosis. § Type 1 diabetes: T cells destroy pancrea7c beta cells. Transmission: o Not transmissible. It results from T-cell-mediated immune responses. Risk Factors: o Exposure to allergens like poison ivy, nickel, and topical medica.ons. o Contact with certain chemicals (e.g., formaldehyde, latex). o Infec.ous diseases like tuberculosis can induce Type IV hypersensi7vity reac7ons. Summary Table Type Cause Pathophysiology Transmission Risk Factors Family history, Type Allergens (pollen, IgE-mediated (mast cell Not environmental I food) degranula7on) transmissible exposure Type Autoimmune (Graves, IgG/IgM an.bodies Not Blood transfusions, II Myasthenia) aVack self-7ssue transmissible autoimmune diseases Type Immune complex Immune complex Not Autoimmune diseases, III diseases (SLE, RA) deposi.on in 7ssues transmissible chronic infec7ons Type Environmental T-cell-mediated Not Exposure to allergens, IV allergens (poison ivy) inflamma.on transmissible infec7ons