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Disorders of Immunity and Inflammation

Hypersensitivity. Exaggerated Immune Response. Hypersensitivity Types. AllergyExogenous, non-human antigenIsoimmunity (alloimmunity)Exogenous, human antigenAutoimmunityEndogenous antigen. Hypersensitivity Mechanisms. Type I: IgE mediatedType II: Tissue specificType III: Immune complex mediatedType IV: Cell mediated.

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Disorders of Immunity and Inflammation

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    1. Disorders of Immunity and Inflammation

    3. Hypersensitivity Types Allergy Exogenous, non-human antigen Isoimmunity (alloimmunity) Exogenous, human antigen Autoimmunity Endogenous antigen

    4. Hypersensitivity Mechanisms Type I: IgE mediated Type II: Tissue specific Type III: Immune complex mediated Type IV: Cell mediated

    5. Type I Immediate hypersensitivity IgE mediated Exogenous antigen

    6. Type I: Mechanism Repeated antigen exposure causes increased IgE production IgE binds to mast cells Sensitization occurs

    7. Type I: Mechanism Antigen binds to IgE on mast cell membrane Mast cell releases histamine, chemotaxic factors Inflammatory response occurs

    8. Type I: Signs/Symptoms Clinical signs, symptoms = response to histamine release GI, skin, respiratory system High mast cells numbers Most sensitive

    9. Type I: Signs/Symptoms Histamine effects Vasodilatation Increased capillary permeability Non-vascular smooth muscle spasm

    10. Type I: Signs/Symptoms Skin: flushing, itching, edema, urticaria, hives Respiratory: bronchospasm, laryngospasm, laryngeal edema Cardiovascular: tachycardia, hypotension GI: nausea, vomiting, cramping, diarrhea

    11. Type I: Atopia “Allergy prone” individuals Genetic predisposition More IgE More mast cell receptors for antibodies than normal

    12. Type I: Anaphylaxis Severe, generalized Type I reaction Life-threatening Loss of airway Ventilatory failure Hypoperfusion

    13. Type II Tissue specific Reaction to tissue-specific antigens Causes target cell destruction, dysfunction Exogenous or endogenous antigen

    14. Type II Most commonly affected cells Red blood cells Thyroid cells

    15. Type II: Mechanisms Antibody binds to cell membrane, triggers compliment-mediated lysis Examples Reaction to transfused blood Hemolytic disease of newborn

    16. Type II: Mechanisms Antibodies promote target cell clearance by macrophages

    17. Type II: Mechanisms Antibodies bind to target cells and cytotoxic T-cells Trigger release of toxins to destroy target cells

    18. Type II: Mechanisms Antibody binds to cell membrane, causes alterations in target cell function Example: Graves' disease Antibody binds to thyroid cell membrane Mimics Thyroid Stimulating Hormone action Causes production of excessive amounts of thyroid hormone Results in common form of hyperthyroidism

    19. Type III Mediated by antigen/ antibody complex deposition in tissues Exogenous or endogenous antigen

    20. Type III: Mechanism Ag-Ab complex deposited in tissues Especially sensitive tissues are blood vessels, GI, respiratory system Causes complement activation, increased neutrophil activity Neutrophils have trouble digesting complexes, release lysosomes causing damage

    21. Type III Immune complex quantity varies over time Symptomatic periods alternate with periods of remission

    22. Type III: Serum Sickness Repeated intravenous antigen injections Immune complexes deposited in tissues Fever, rash, pain, lymphadenopathy

    23. Type III: Raynaud’s Phenomenon Temperature governs immune complex deposition in peripheral circulation Exposure to cold causes redness, pain of fingers, toes followed by numbness, cyanosis, gangrene

    24. Type III: Arthus Reaction Occurs after repeated LOCAL exposure to exogenous antigen Immune complexes in vessel walls Examples Celiac disease from wheat protein Hemorrhagic alveolitis from moldy hay inhalation

    25. Type IV Delayed Mediated by Td (lymphokine-producing) or Tc (cytotoxic) cells No antibody involved

    26. Type IV Examples Graft rejection Contact allergic reactions (poison ivy)

    27. Hypersensitivity Targets Allergins Pollen (hay fever) Drug reactions Foods

    28. Hypersensitivity Targets Neoantigens Hapten binds to protein molecule Changes its antigenicity Causes it to become an allergen

    29. Hypersensitivity Targets Autoantigens Sequestered cells (cornea, testes) Foreign antigen triggered (infection) Suppressor T-cell malfunction Genetic causes

    30. Hypersensitivity Targets Isoantigens Tissue grafts, transplants Rh negative sensitivity

    31. Autoimmune Disease Clinical disorder produced by immune response to normal tissue component of patient’s body

    32. Graves’ Disease Antibody stimulates thyroid hormone over production Produces hyperthyroidism Antibody, disease can be passed through placenta

    33. Rheumatoid Arthritis Antibody reaction to collagen in joints Causes inflammation, destruction of joints

    34. Myasthenia Gravis Antibodies destroy acetylcholine receptors on skeletal muscle Produce episodes of severe weakness Antibodies can cross placenta, affect newborn

    35. Immune Thrombocytopenic Purpura Antibodies destroy platelets Produces clotting disorders, hemorrhaging Antibodies can cross placenta, affect newborn

    36. Isoimmune Neutropenia Antibodies attack, destroy neutrophils Can cross placenta, affect newborn

    37. Other Autoimmune Diseases Type I diabetes mellitus Primary myxedema Rheumatic fever Crohn’s disease Ulcerative colitis Systemic Lupus Erythematosis (SLE)

    38. SLE Chronic, multi-system auto-immune disease Highest incidence Women, 20-40 years of age Black, Hispanic women Mortality after diagnosis averages 5% per year

    39. SLE Antibody against nucleic acid components (ANA, anti-nuclear antibody) Immune complex precipitates in tissues, causes widespread destruction Especially affected are renal system, blood vessels, heart

    40. SLE Signs/Symptoms Facial rash/skin rash triggered by sunlight exposure Oral/nasopharyngeal ulcers Fever Arthritis

    41. SLE Signs/Symptoms Serositis (pleurisy, pericarditis) Renal injury/failure CNS involvement with seizures/psychosis Peripheral vasculitis/gangrene Hemolytic anemia

    42. SLE Chronic management Anti-inflammatory drugs Aspirin Ibuprofen Corticosteroids Avoidance of emotional stress, physical fatigue, excessive sun exposure

    43. Disorders of Immunity Immunodeficiency Diseases

    44. Immunodeficiency Disease Patient unable to fight off infection Hallmarks Repeated infections Opportunistic infections

    45. Immunodeficiency Disease Most are defects in T cells or B cells T cells, macrophage defects = fungal, viral infections B cells, complement defects = bacterial infections

    46. Immunodeficiency Disease Congenital Acquired

    47. Congenital B-cell Deficiency IgA Deficiency DiGeorge’s Syndrome Severe Combined Immunodeficiency

    48. B Cell Deficiency Agammaglobulinemia Hypogammaglobulinemia

    49. IgA Deficiency Most common immune deficiency disorder Genetic condition Failure of IgA synthesis Patient has repeated, recurrent sinus, lung, GI infections

    50. DiGeorge’s Syndrome Thymic hypoplasia Severe decrease in T-cell production, function Defects of face, ears, heart

    51. Severe Combined Immunodeficiency Thymus development arrested at ~6-8 weeks gestation. Deficiency, defective maturation of stem cells that produce B and T cells Little to no antibody production

    52. SCID Two types Autosomal recessive X-linked disease recessive

    53. SCID Recurrent, frequently overwhelming infections Particularly respiratory, gastrointestinal Most die in first few years of life, usually by one year of age Death usually due to opportunistic infection

    54. Acquired Nutritional deficiency Iatrogenic (drugs, radiation) Trauma (prolonged hypoperfusion) Stress Infection (HIV)

    55. Immune Deficiency Therapies B-cell deficiency: Gamma globulin SCID: Bone marrow transplants, enzyme replacement DiGeorge’s Syndrome: Fetal thymus transplants Gene therapy

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