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Premium member Presentation Transcript HYPERSENSITIVITY DISORDERS: HYPERSENSITIVITY DISORDERS Over reaction to a substance, or hypersensitivity, is referred to as an allergic response Hypersensitivity designates an increased immune response to the presence of an antigen that results in tissue destructionHYPERSENSITIVITY DISORDERS: HYPERSENSITIVITY DISORDERS Four distinct types Type I: IgE mediated allergic reactions Type II: when bodies own tissue is recognized as foreign Type III: immune-complex-mediated reactions Type IV: cell mediated reactions Reactions can be immediate or delayed Immediate: occur in minutes to a few hours Delayed: may take several hours and are at maximum severity days after re-exposure to the antigenType I Hypersensitivity : Type I Hypersensitivity (Immediate Hypersensitivity, Allergic Disorders, Anaphylaxis) Hay fevers, allergic rhinitis, urticaria, asthma and anaphylactic shock Characterized by production of antigen-specific IgE by B cells Requires repeated exposure so person is “sensitized” When IgE meets the pathogen (antigen), histamine is released with other inflammatory factors contracts smooth muscle bronchial constriction increases vascular permeability edema causes vasodilation increasing blood flowPowerPoint Presentation: Immediate Hypersensitivity Allergic Disorders Anaphylaxis Wheezing, hypo-tension, swelling, urticaria, rhinnorhhea. If response becomes systemic, develops vasodilation, broncho-spasm, increased mucous secretion and edema Anaphylaxis can be life threateningType II Tissue Specific Reactions: Type II Tissue Specific Reactions (Cytotoxic Reactions to Self-Antigens) When the body's own tissue is not recognized as “self” or is recognized as foreign Activation of complement Agglutination, cell destruction and phagocytosis of cells Especially common for blood cells and platelets Examples: Blood transfusion reactions, hemolytic disease of newborns, myasthenia gravis Cross reaction of exogenous pathogen with endogenous pathogens Rheumatic fever- develops 2-3 wks after strep infection; cross reactivity can involve heart, skin, joints Guillain-Barre- immune response to foreign antigens but miss target and damage host nerve tissue leading to paralysisType III Hypersensitivity : Type III Hypersensitivity (Immune Complex Mediated Reactions) Immune complexes (antibody-antigen) are not cleared from the body and deposit in tissues around vessels Causes acute inflammation and local tissue injury Vasculitis Skin (urticaria), synovial joints, kidney (nephritis), pleura (pleuritis) and pericardium (pericarditis) SLE antigen of individual’s own nuclei and anti-nuclear antibody (ANA) and deposit in skin, joints and kidney.Type IV Hypersensitivity : Type IV Hypersensitivity (Cell Mediated Immunity) Delayed hypersensitivity response after sensitization to an allergen Cosmetic, adhesive, topical med, poison ivy Antigen is processed by macrophages and presented to T cells Example: Graft rejection and latex sensitivityFibromyalgia (Rheumatologic): Fibromyalgia (Rheumatologic) Chronic muscle pain syndrome which is widespread in at least 11 of 18 tender points Biologic disorder associated with neurohormonal dysfunction of the ANS Commonly associated with hypothyroid, RA, SLE, CFS Systemic problem with localized myofascial pain Perpetuating and initiating factors Psychological stress, primary sleep disorder inflammatory RA, acute febrile illness Reciprocal relationship between immune and sleep wake systemsPowerPoint Presentation: Incidence 6 million Americans > RA. Women > men 14- 68 years Risk Factors Prolonged anxiety, emotional stress, trauma Rapid steroid withdrawal , hypothyroid, viral and non viral infections, anxiety, depression. Extra capsular silicone Pathogenesis Both central and peripheral Hypothalamic pituitary axis ANS Reproductive hormone axis Immune systemPathogenesis : Stress System PathogenesisClinical Manifestations: Clinical ManifestationsMedical Management: Medical Management Dx: No definitive test Widespread pain in 4 quadrants > 3 months Subjective report with palpation in 11 of 18 sites Rx: metabolic rehabilitation, holistic, and multidisciplinary Education, stress management, work simplification, medications, modalities for pain, nutraceuticals Prognosis: Symptoms usually remain unchangedRehabilitation Implications: Rehabilitation Implications Accurate assessment (tender points) Directing individuals to reach goals of lessening pain, fatigue, sleep difficulties Outcomes using scales Monitor vitals Modalities – very little study US Soft tissue Exercise Cardio flexibilitySummary: Summary Immune dysfunction can potentially impact the rehabilitation setting in a variety of ways including direct involvement of the system and as a comorbidity. 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HYPERSENSITIVITY DISORDERS end podcast aSGuest125455 Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 29 Category: Entertainment License: All Rights Reserved Like it (0) Dislike it (0) Added: January 31, 2012 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript HYPERSENSITIVITY DISORDERS: HYPERSENSITIVITY DISORDERS Over reaction to a substance, or hypersensitivity, is referred to as an allergic response Hypersensitivity designates an increased immune response to the presence of an antigen that results in tissue destructionHYPERSENSITIVITY DISORDERS: HYPERSENSITIVITY DISORDERS Four distinct types Type I: IgE mediated allergic reactions Type II: when bodies own tissue is recognized as foreign Type III: immune-complex-mediated reactions Type IV: cell mediated reactions Reactions can be immediate or delayed Immediate: occur in minutes to a few hours Delayed: may take several hours and are at maximum severity days after re-exposure to the antigenType I Hypersensitivity : Type I Hypersensitivity (Immediate Hypersensitivity, Allergic Disorders, Anaphylaxis) Hay fevers, allergic rhinitis, urticaria, asthma and anaphylactic shock Characterized by production of antigen-specific IgE by B cells Requires repeated exposure so person is “sensitized” When IgE meets the pathogen (antigen), histamine is released with other inflammatory factors contracts smooth muscle bronchial constriction increases vascular permeability edema causes vasodilation increasing blood flowPowerPoint Presentation: Immediate Hypersensitivity Allergic Disorders Anaphylaxis Wheezing, hypo-tension, swelling, urticaria, rhinnorhhea. If response becomes systemic, develops vasodilation, broncho-spasm, increased mucous secretion and edema Anaphylaxis can be life threateningType II Tissue Specific Reactions: Type II Tissue Specific Reactions (Cytotoxic Reactions to Self-Antigens) When the body's own tissue is not recognized as “self” or is recognized as foreign Activation of complement Agglutination, cell destruction and phagocytosis of cells Especially common for blood cells and platelets Examples: Blood transfusion reactions, hemolytic disease of newborns, myasthenia gravis Cross reaction of exogenous pathogen with endogenous pathogens Rheumatic fever- develops 2-3 wks after strep infection; cross reactivity can involve heart, skin, joints Guillain-Barre- immune response to foreign antigens but miss target and damage host nerve tissue leading to paralysisType III Hypersensitivity : Type III Hypersensitivity (Immune Complex Mediated Reactions) Immune complexes (antibody-antigen) are not cleared from the body and deposit in tissues around vessels Causes acute inflammation and local tissue injury Vasculitis Skin (urticaria), synovial joints, kidney (nephritis), pleura (pleuritis) and pericardium (pericarditis) SLE antigen of individual’s own nuclei and anti-nuclear antibody (ANA) and deposit in skin, joints and kidney.Type IV Hypersensitivity : Type IV Hypersensitivity (Cell Mediated Immunity) Delayed hypersensitivity response after sensitization to an allergen Cosmetic, adhesive, topical med, poison ivy Antigen is processed by macrophages and presented to T cells Example: Graft rejection and latex sensitivityFibromyalgia (Rheumatologic): Fibromyalgia (Rheumatologic) Chronic muscle pain syndrome which is widespread in at least 11 of 18 tender points Biologic disorder associated with neurohormonal dysfunction of the ANS Commonly associated with hypothyroid, RA, SLE, CFS Systemic problem with localized myofascial pain Perpetuating and initiating factors Psychological stress, primary sleep disorder inflammatory RA, acute febrile illness Reciprocal relationship between immune and sleep wake systemsPowerPoint Presentation: Incidence 6 million Americans > RA. Women > men 14- 68 years Risk Factors Prolonged anxiety, emotional stress, trauma Rapid steroid withdrawal , hypothyroid, viral and non viral infections, anxiety, depression. Extra capsular silicone Pathogenesis Both central and peripheral Hypothalamic pituitary axis ANS Reproductive hormone axis Immune systemPathogenesis : Stress System PathogenesisClinical Manifestations: Clinical ManifestationsMedical Management: Medical Management Dx: No definitive test Widespread pain in 4 quadrants > 3 months Subjective report with palpation in 11 of 18 sites Rx: metabolic rehabilitation, holistic, and multidisciplinary Education, stress management, work simplification, medications, modalities for pain, nutraceuticals Prognosis: Symptoms usually remain unchangedRehabilitation Implications: Rehabilitation Implications Accurate assessment (tender points) Directing individuals to reach goals of lessening pain, fatigue, sleep difficulties Outcomes using scales Monitor vitals Modalities – very little study US Soft tissue Exercise Cardio flexibilitySummary: Summary Immune dysfunction can potentially impact the rehabilitation setting in a variety of ways including direct involvement of the system and as a comorbidity.