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32 Cards in this Set
- Front
- Back
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Hypersensitivity |
*excessive or inappropriate immune response *there are four types |
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Type 1 Hypersensitivity |
*IgE mdiated rxn -against foreign proteins commonly present in environment -atopic ag *Atopy |
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Allergens |
*antigens *exposure routes *tissue rich in mast cells |
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Type 1 Hypersensitivity Symptoms |
*match reactions in tissues involved *anaphylaxis -systemic -potentially life threatning |
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Initiation by IgE |
*regulation by tyype 2 helper cells -as opposed to type 1 helper cells (interferon gamma) *Th2 cells produce IL-3-5, 9, and 13 *IgE binds to mast cell receptors -ag binds -crosslinking causes degranulation |
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Mast cells |
*precursors in bone marrow *contain cytoplasmic granules -histamine 10x GT in basos |
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Basophils |
*histamine rich granules *high affinity receptors for IgE *respond to chemotactic stimulation -accumulated in inflammatory response -upregulation during allergic reaction |
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Mediators |
*preformed -histamine, heparin, eosinophil chemotactic factor of anaphylaxis, neutrophil chemotactic factor, and proteolytic enzymes |
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Clinical picture |
*localized skin rxn to systemic response *anaphylaxis (glycoproteins and large polypeptides, smaller molecules act as haptens) *symptoms begin w/in min (bronchospasm, laryngeal edema, vascular congestion, gives, etc |
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Asthma |
*chronic airflow obstruction |
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food allergies |
GI tract symptoms |
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Diagnostic testing |
*in vivo skin tests -cutaneous -intradermal
*in vitro tests -RIST -RAST -ImmunoCAP |
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RIST testing |
*total IgE -less sensitive, but also less traumatic |
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RAST |
*antigen-specific IgE *radioallergosorbent test |
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Ag-specific IgE testing (type of automated analysis) |
*solid phase is coated w/ specific allergen *reacted w/ patient serum *wash *add labeled IgE *amount of label is directly proportional to the amount of specific IgE in the patents serum |
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Type 2 hypersensitivity |
*cytotoxic *mediated by IgG and IgM ab binding to specific cells or tissues |
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Transfusion reactions |
*cellular destruction from ab combing w/ ag on RBC (ABO, Rh, Kell, Duffy, Kidd) |
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Hemolytic disease of the Newborn (HDN) |
*mom exposed to blood-group ag on baby's cells *IgG ab made in response -cross the placenta -destrcution of fetal RBCs |
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Autoimmune Hemolytic Anemia |
*ab to self-ag on RBC *Cold agglutinins -IgM class -peripheral circulation below 30 C -necrosis -intravascular hemolysis, if complement is activated -warm autoimmune hemolytic anemia -IgG ab -Accelerated clearance of ab-coated RBCs |
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Autoimmune thrombocytopenic pupura |
*increased plt destruction -in spleen by phagocytosis -drug induced |
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Goodpasture's Syndrome |
*ab against basement membrane protein |
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Type 2 testing |
*coombs direct antiglobulin test -detect ab or complement on RBCs *indirect Coombs -cross matching of blood *Plt agglutination test -ITP *Direct fluorescence -goodpastures |
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Type 3 Hypersensitivity |
*IgG or IgM, complement *ag is soluble |
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Arthus reaction |
*Classic ex: rabbit immunized to produce ab (mainly IgG) -ID injection of ag -localized inflammation -activation of complement is essential -rare in humans |
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Serum Sickness |
*Passive immunization w/ animal serum *symptoms 1-2 weeks after *sensitizing dose and shocking dose |
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Autoimmune diseases |
*triggered by autologous ag *SLE -abs against DNA and nucleohistones *RA -RF directed against IgG |
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Type 3 testing |
*specific abs *fluorescent staining tissue sections *complement levels |
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Type 4 hypersensitivity |
*sensitized T cells *ab and complement aren't directly involved *symptoms take several hours to develop *ex: poison ivy/oak/sumac |
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contact dermatitis |
*occupationally (environmental)--acquired illness |
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Hypersensitivity pneumonitis |
*sensitized T cells responding to inhaled allergens *IgG and IgM play a minor role *men btwn. 30-50 |
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Tuberculin-type hypersensitivity |
*Soluble ag of M. tuberculosis *ID challenge |
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Type 4 testing |
*skin tests -similar to testing for the presence of IgE
*patch test -Gold standard |
