Allergy and atropy

Descripción

Mapa Mental sobre Allergy and atropy, creado por tanitia.dooley el 13/05/2013.
tanitia.dooley
Mapa Mental por tanitia.dooley, actualizado hace más de 1 año
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Resumen del Recurso

Allergy and atropy
  1. Allergy- A form of immediate or type 1 hypersensitivity reaction (IgE-production and mast cell activation)
    1. Atropy- propensity of an individual to produce IgE Abs in response to environmental stimuli and develop strong immediate hypersensitivity reactions (strong genetic component)
    2. Hayfever-most common, caused by inhalation of allergens. Disease of the upper respiratory tract. Clinical features include leukocyte infiltration, coughing and difficulty in breathing
      1. Allergic conjunctivitis- often associated with hay fever, itchy, irritated eyes
        1. Asthma- immediate hypersensitivity reaction in the lung-reversible airway obstruction, bronchial inflammation. Difficulty in breathing
          1. Eczema, Urticaria- allergic reaction in skin occurs when allergens come into direct contact with skin or after an allergen enters the system circ
            1. Anaphylaxis- systemic immediate hypersensitivity reaction characterised by edema, bronchoconstriction and/or hypotension (fall in blood pressure)
              1. Allergens
                1. House dust mites (their excreta), tree and grass pollen, food proteins especially egg and peanut, cat & dog dander-shed skin and hair-the allergen is a saliva protein, drugs
                  1. Dust mites thrive in warm humid conditions- bedding etc feed on dead kin and body fluids you excrete while you sleep
                    1. Wild grasses
                    2. Mechanisms
                      1. 1. Exposure to allergen 2. Activation of Th2 cells 3. IgE class switching in B-cells 4.Secretion of IgE 5. Binding of IgE to Fc on mast cells 6.Following re-exposure to Ag=cross linking of IgE 7.Activation of mast cells= degranulation and release of mediators
                        1. Mediators
                          1. Histamine, platelet-activating factor, leukotrienes, prostaglandin D
                            1. Early response= vasodilation, edema, bronchospasm/ late response=cellular recruitment, inflammation
                          2. Mast cell cytokines: IL-3 promotes mast cell proliferation, TNFa promotes inflammation, IL4 & IL13 promote TH2 differentiation, IL5 promotes eosinophil recruitment further eosinophil production and activation
                            1. time course graph
                              1. Production of IgE
                                1. IgE Ab is produced by B-cells stimulated with a Ag, IgE binds to mast cells, IgE binds to Fc receptor on mast cells, forming a multi-valent binding site for the Ag. The same Ag that stimulated B cells and IgE production subsequently binds to IgE on mast cells=degranulation. Atopic individual produce high levels of IgE following exposure to Ag. Normal individuals produce lower levels and or other isotopes
                              2. Activation of Th2 cells
                                1. IgE synthesis is dependent on activation of CD4+ T cells that secrete IL-4 & IL-13. Cytokines from type 2 T cells promote Ab class switchibg in B cells. T cells also secrete IL-5 and eotaxin which are involved in the recruitment and activation of eosinophils which are involved in the late phase of immediate hypersensitivity
                                2. Mast cells
                                  1. Mature mast cells are found throughout the body. Contains many pre-formed granules that contain histamine and other mediators. Following Ag cross-linking of Fc receptor bound IgE, there is three types of biological response -secretion of pre-formed mediators from granules -synthesis of further mediators -cytokine synthesis
                                  2. Eosinophils
                                    1. Migrate to sites of inflammation (move towards IL5). They secrete proteins (eg major basic protein) from granules- these proteins can directly damage host cells
                                    2. Genetic susceptibility
                                      1. IgE synthesis and atopy generally runs in families. The propensity to produce IgE is influenced by the inheritance of several genes (multi-genetic)
                                        1. Candidate genes: IL4 & 13-promote IgE class switching/ IL5 promotes eosinophil growth or activation/ MHC class II-certain alleles regulate T cell response to different Ags/ TNFa-mast cell mediator (inflammatory)/Fc receptor-mast cell receptor
                                      2. Treatment
                                        1. Anaphylaxis-Adrenaline which can be life-saving reverses bronchoconstriction, vasodilation & improve cardiac output/Antihistamines-antagonism of histamine receptors
                                          1. Asthma- corticosteroids-block the production of inflammatory cytokines/ sodium cromolyn-inhibits release of mast cell mediators
                                            1. Hayfever- antihistamines most common treatment
                                              1. Skin reactions- cutaneous corticosteroids
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