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    Hypersensitivity 1

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    Oral Biology
    This document discusses the different types of hypersensitivity reactions. Type 1 is an immediate allergic reaction mediated by IgE antibodies and mast cells. Type 2 involves cytotoxic antibodies attacking antigens on cell surfaces. Type 3 occurs when immune complexes are deposited in tissues, activating complement and causing inflammation. Type 4 is cell-mediated and includes delayed hypersensitivity reactions and tuberculosis-type responses. The key mediators and clinical manifestations of each type are described.

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    Hypersensitivity 1

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    Oral Biology
    208 views30 pages
    This document discusses the different types of hypersensitivity reactions. Type 1 is an immediate allergic reaction mediated by IgE antibodies and mast cells. Type 2 involves cytotoxic antibodies attacking antigens on cell surfaces. Type 3 occurs when immune complexes are deposited in tissues, activating complement and causing inflammation. Type 4 is cell-mediated and includes delayed hypersensitivity reactions and tuberculosis-type responses. The key mediators and clinical manifestations of each type are described.

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    This document discusses the different types of hypersensitivity reactions. Type 1 is an immediate allergic reaction mediated by IgE antibodies and mast cells. Type 2 involves cytotoxic antibodies attacking antigens on cell surfaces. Type 3 occurs when immune complexes are deposited in tissues, activating complement and causing inflammation. Type 4 is cell-mediated and includes delayed hypersensitivity reactions and tuberculosis-type responses. The key mediators and clinical manifestations of each type are described.

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    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    208 views30 pages

    Hypersensitivity 1

    Uploaded by

    Oral Biology
    This document discusses the different types of hypersensitivity reactions. Type 1 is an immediate allergic reaction mediated by IgE antibodies and mast cells. Type 2 involves cytotoxic antibodies attacking antigens on cell surfaces. Type 3 occurs when immune complexes are deposited in tissues, activating complement and causing inflammation. Type 4 is cell-mediated and includes delayed hypersensitivity reactions and tuberculosis-type responses. The key mediators and clinical manifestations of each type are described.

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    of 30

    HYPERSENSITIVITY

    ALLERGIC REACTIONS.
    HYPERSENSITIVITY

     It is an exaggerated immune
    response.
     Sensitisation occurs on first exposure
    to the Antigen.
     Allergic response occurs on re
    exposure to the same/cross reacting
    antigen.
    Type 1 Hypersensitivity.

     Also known as ANAPHYLACTIC


    REACTION.
     An Ag induces IgE Ab .
     IgE Ab bind firmly to receptors on
    mast cells & basophils.
     Re exposure to the same Ag causes
    release of mediators leading to
    immediate allergic reaction.
    IMMEDIATE PHASE

     Pollen,animal dander,certain foods e.g


    nuts,shellfish etc.& various drugs
    cause production of large amounts of
    IgE in certain individuals.
     On re-exposure,cell bound
    IgE,crosslinks & degranulation of mast
    cells occurs releasing chemical
    mediators of anaphylaxis.
    CLINICAL
    MANIFESTATIONS.
     Asthma
     Edema.
     Erythema(wheal & flare).
     Itching.
     These occur within minutes,d/t release
    of histamine.
    LATE PHASE.

     Occurs after about 6 hrs. of exposure.


     Leukotriens(SRS-A)are synthesised
    after degranulation of mast
    cells,causing influx of neutrophils
    &eosinophils.
     Complement is not involved in these
    reactions.
    CLINICAL
    MANIFESTATIONS.
     Urticaria (hives).
     Eczema.
     Rhinitis & conjunctivitis(hay fever).
     Asthma.
     Diarrhea(in those who ingest
    allergens).
     Hay fever(in those who inhale
    allergens).
    Imp.Mediators of
    anaphylaxis.
     HISTAMINE.
     SLOW REACTING SUBSTANCE OF
    ANAPHYLAXIS(SRS-A).
     EOSINOPHIL CHEMOTACTIC FACTOR
    OF ANAPHYLAXIS(ECF-A).
     SEROTONIN.
     PROSTAGLANDINS.
     THROMBOXANES.
    TYPE 2
    HYPERSENSITIVITY.
     Also called CYTOTOXIC
    HYPERSENSITIVITY.
     Antigen is part of cell membrane.
     Ab directed at Ag activates
    complement.
     A membrane attack complex is formed
    that damages cell membrane.
    CAUSATIVE FACTORS.

     Hemolytic anaemias.
     ABO Transfusion reactions.
     Drugs e.g
    Penicillin,quinidine&phenacitin.
     Infections e.g Mycoplasma
    pneumoniae can induce Ab that cross
    react with RBC resulting in haemolysis.
     Good pasture’s syndrome.
    TYPE 3
    HYPERSENSITIVITY.
     Also known as IMMUNE COMPLEX
    HYPERSENSITIVITY.
     Immune complexes persist &get
    deposited in tissue.
     Complement is activated &results in
    inflamation & tissue damage.
    Manifestations.

     ARTHUS REACTION.
     Inflamation causedby deposition of
    immune complexes at a localised site.
     ALLERGIC ALVEOLITIS.
     FARMER’S LUNG.
     CHEESE WORKER’S LUNG.
     WOOD WORKER’S LUNG.
     WHEAT MILLER’S LUNG.
    SERUM SICKNESS.

     A systemic inflamatory response d/t


    deposition of immune complexes in
    many areas of the body.
    IMMUNE COMPLEX
    DISEASES.
     GLOMERULONEPHRITIS.
     RHEUMATOID ARTHRITIS.
     SYSTEMIC LUPUS ERYTHEMATOSIS.
    TYPE 4
    HYPERSENSITIVITY.
     CELL MEDIATED HYPERSENSITIVITY.
     It is due to cell mediated immunity.
     Can be transferred by T-cells.
    TYPES OF DELAYED
    HYPERSENSITIVITY.

     CONTACT HYPERSENSITIVITY.
     Caused by chemicals
    e.gNickle,formaldehyde,plant
    materiale.g poison ivy,poison
    oak,topically applied drugs e.g
    sulphonamides,neomysin,cosmetics&s
    oaps .
    TUBERCULIN TYPE
    HYPERSENSITIVITY.
     Occurs due to Ag of microorganisms.
     Tuberculin test is a typical example.
     PPD. Is injected I/D .
     Ina pt. who is previously exposed to
    infection redness & induration reaches
    a peak in 48-72 hrs.
    COMPLEMENT
    DEFICIENCY STATES.
     Deficiency of C5-C8---infections by
    Neisseriae sp.
     Def.of C3b---recurrent pyogenic
    infections.
     Def.of C1 Esterase inhibitor—
    angioedema.
     Def.Of decay accelerating factor—
    Haemolysis resembling Paroxysmal
    Nocturnal Haemoglobinuria.

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