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Anaphylaxis Pathophysiology and Emergency Response

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Submitted By tabbyr
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Anaphylaxis is a respiratory disease that can be both acute and severe. It has a 3% mortality rate within Australia caused from a range of triggers that may or may not be known to the victim. Although anaphylaxis prevalence has increased, death rates have decreased due to understanding of the disease pathophysiology alongside better and faster management of life threatening symptoms (Liew, Williamson & Tang, 2009). This essay will discuss these points in detail as well as the pharmacological actions of adrenaline, the drug used to fight anaphylaxis in a pre-hospital setting.

Anaphylaxis is Type 1 hypersensitivity response as it is ‘IgE mediated’. This involves an antigen/antibody response. To develop hypersensitivity a person must first be exposed to the antigen. On the initial exposure, the antigen activates the immune system and a hyper-production of IgE (immunoglobin) antibodies, which are produced by plasma B cells. The IgE antibody is specific to only that antigen and will bind to basophils and mast cells in the blood and blood vessel tissues, remaining inactive until that same antigen is introduced to the body again. Upon secondary exposure to the antigen, many chemical reactions are undertaken at a rapid rate. The antigen binds to IgE resulting in degranulation of basophil and mast cells and release of chemical mediators such as histamine and leukotriene’s (Arnold & Williams, 2011). Histamine especially have a fast acting effect leading to symptoms of increased vascular permeability, vasodilation, contraction of smooth muscles in both gastro-intestinal tract and bronchial tree peaking within one to thirty minutes after antigen exposure depending on route into the body (Saunders 2012). Leukotrienes however have a more long-term effect causing symptoms such as bronchospasm (wheezing), coronary vasoconstriction

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