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Hypersensitivity and autoimmune diseases

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    Hypersensitivity and autoimmune diseases Hypersensitivity and autoimmune diseases Presentation Transcript

    • Hypersensitivity and autoimmune diseases
    • • Medical news reports a rise of hypersensitivity reactions to various foodstuffs, particles and even personal stuff. In what 3 ways do you think would help you as well as the patient in preventing catastrophic events arising from hypersensitivity reactions in the dental clinic?
    • Hypersensitivity • The phenomenon of damage caused by the immune system while trying to combat an insult. • Precipitating factor (external), instead of the immune system coping and restoring the body’s homeostasis, the immune response is altered and becomes the “internal” cause of disease.
    • Type I hypersensitivity • Anaphylactic • Release of allergic mediators • Asthma, eczema, hay fever and reactions to certain food • Grass pollen, house dust mite feces or seafoods
    • • Immediate injections of epinephrine • Antihistamine or steroids as back up medications • Avoidance of allergens
    • Type II hypersensitivity • Antibody dependent cytotoxic hypersensitivity • Antibodies react with antigens fixed to the surface of various types of cells and cause damage • Complement fixing (the antibodies cause the destruction of the target cell or damage the surrounding cells)
    • • Functional fixing (antibodies interfere with cell function) • Drug reactions where a binding of a drug may alter a normal self antigen and thus produce something that can no longer be tolerated
    • Type II hypersensitivity - Rhesus incompatibility
    • Type III hypersensitivity • Immune complex mediated hypersensitivity • Antibody driven process • The antibodies react with free antigen and under the right circumstances they form soluble immune complexes that circulate in the blood giving rise to “serum sickness”
    • Type III hypersensitivity – Farmer’s Lung Alveolitis
    • Type IV hypersensitivity • Cell mediated (delayed type) hypersensitivity • T lymphocytes which over several hours and days recruit and activate other T cells and macrophages and produce local tissue damage and granuloma formation
    • Type IV hypersensitivity – Mantoux Test
    • Autoimmune Diseases General Principles • Autoimmunity arises through some combination of susceptibility genes (causing loss of self tolerance) and environmental triggers (specially infection)
    • • Self antigens or abnormal immune cells develop that incite the immune response into abnormal or excessive activity of T or B lymphocytes • Once induced tend to be progressive, albeit with occasional relapses and remissions
    • • Most autoimmune disorders are complex multigenic disorders - associated with specific histocompatibility molecule HLA alleles - defects in pathways that normally regulate either peripheral or central tolerance - polymorphisms in other genes (PTPN- 22, NOD-2, IL-2 and IL-7) • Role of infection
    • • GI: primary biliary cirrhosis, ulcerative colitis and atrophic gastritis • Cardiovascular: pernicious anemia, hemolytic anemia, idiopathic thrombocytopenia and leukopenia • Endocrine: insulin dependent diabetes, thyrotoxicosis and Hashimoto’s thyroiditis • Musculoskeletal: mixed connective tissue diseases, rheumatoid arthritis, systemic lupus erythematosus, myasthenia gravis • Dermatology: dermatomyositis and scleroderma
    • Rejection of Tissue Transplants • Mechanisms of recognition: - Class I molecules are expressed on all nucleated cells. Class I molecules bind peptide fragments derived from endogenous proteins - Class II molecules are confined to APC including dendritic cells, macrophages, B cells and activated T cells
    • - Class II molecules bind peptide fragments derived from exogenous proteins and presents these processed antigens to CD4+ T lymphocytes • Host T cells recognize either by direct or indirect pathways
    • Rejection of solid organs: • Following lymphocyte activation, rejection is mediated by the following: - direct CTL-mediated parenchymal and endothelial cytolysis - macrophage mediated damage - cytokine mediated vascular and parenchymal dysfunction - microvasccular injury - antibody mediated responses
    • • Rejection: - hyperacute - acute - chronic
    • Immunodeficiency Syndrome • Primary immunodeficiencies - are usually hereditary and manifest between 6 months and 2 years of life as maternal protection is lost • Secondary immunodeficiencies - result from altered immune function due to infections, malnutrition, aging, immunosuppression, irradiation, chemotherapy and autoimmunity
    • • Acquired immunodeficiency syndrome - retrovirus human immunodeficiency virus (HIV) characterized by profound suppression of T cell mediated immunity leading to opportunistic infections, secondary neoplasms and neurologic disorders
    • Amyloidosis • Amyloid is a heterogenous group of fibrillar proteins that share the ability to aggregate into an insoluble, cross-beta pleated sheet tertiary conformation • Amyloid fibrils accumulate extracellularly in tissues due either to excess synthesis or resistance to catabolism
    • • As amyloid accumulates, it produces pressure atrophy of adjacent parenchyma • Depending on tissue distribution and degree of involvement, the clinical effects of amyloid can range from life threatening to an asymptomatic incidental finding at autopsy
    • Do you have any questions?