Est1 Task 2
What type of reaction is the health care provider concerned about and why?
The health care provider in this patient scenario is concerned that E.O. might have type 1-hypersensitivity. The patient has indications of this reaction as written in the provided patient history. Having an allergy to bee stings, and being a diagnosed asthma patient makes the Health care provider cautious in prescribing E.O. a course of penicillin, which is a broad spectrum antibiotic and a possible cause of human anaphylaxis as indicated in the textbox 10-1 (Copstead & Banasik, 2013). The bee sting allergy indicates that the patient has hypersensitivity and having asthma indicates the physiological mechanisms to a type 1 reaction. Type 1-hypersensitivity reactions …show more content…
Genetic mechanisms influence type 1-hypersensitivity with strong hereditary linkage regarding the IgE response to allergens, which are usually environmental. Immunoglobulin E (IgE) is the primary antibody mediating this reaction. It is produced by plasma cells and circulates in small amounts in the blood. It usually takes repeated exposure to cause significantly high levels of IgE in the blood. Environmental pollutants may play a role by increasing mucosal permeability and increasing antigen entry into the body (Copstead & Banasik, 2013). The chief effector cell of type 1-hypersensitivity is the mast cell even though they are many others. These mast cells are found in loose connective tissue and they are covered with IgE receptors and are filled with vesicles or granules containing vasoactive, proinflammatory chemical mediators that produce inflammation when released. The IgE antibody binds to the mast cell surface receptor are presented to passing antigens. The initial onset of the type 1-hypersensativity is the cross-linkage of two IgE receptors to one antigen on the mast cell. This leads to an increase in intracellular calcium that results in immediate, massive, local mast cell degranulation of preformed proinflmmatory mediators. This release causes the inflammatory response (Copstead & Banasik, 2013). Once the mast cell is coated with IgE
The health care provider in this patient scenario is concerned that E.O. might have type 1-hypersensitivity. The patient has indications of this reaction as written in the provided patient history. Having an allergy to bee stings, and being a diagnosed asthma patient makes the Health care provider cautious in prescribing E.O. a course of penicillin, which is a broad spectrum antibiotic and a possible cause of human anaphylaxis as indicated in the textbox 10-1 (Copstead & Banasik, 2013). The bee sting allergy indicates that the patient has hypersensitivity and having asthma indicates the physiological mechanisms to a type 1 reaction. Type 1-hypersensitivity reactions …show more content…
Genetic mechanisms influence type 1-hypersensitivity with strong hereditary linkage regarding the IgE response to allergens, which are usually environmental. Immunoglobulin E (IgE) is the primary antibody mediating this reaction. It is produced by plasma cells and circulates in small amounts in the blood. It usually takes repeated exposure to cause significantly high levels of IgE in the blood. Environmental pollutants may play a role by increasing mucosal permeability and increasing antigen entry into the body (Copstead & Banasik, 2013). The chief effector cell of type 1-hypersensitivity is the mast cell even though they are many others. These mast cells are found in loose connective tissue and they are covered with IgE receptors and are filled with vesicles or granules containing vasoactive, proinflammatory chemical mediators that produce inflammation when released. The IgE antibody binds to the mast cell surface receptor are presented to passing antigens. The initial onset of the type 1-hypersensativity is the cross-linkage of two IgE receptors to one antigen on the mast cell. This leads to an increase in intracellular calcium that results in immediate, massive, local mast cell degranulation of preformed proinflmmatory mediators. This release causes the inflammatory response (Copstead & Banasik, 2013). Once the mast cell is coated with IgE