Chapter 12
Why are antihistamines used to treat allergic rhinitis and allergic asthma? What symptoms of each disease, respectively, do they alleviate?
mast cells activated by inhaled allergens ni the type I hypersensitivity reaction that causes allergic Rhinitis or asthma release histamine. Binding of histamine to its receptors on smooth muscle causes the bronchial constriction typical of asthma and the difficulty in breathing. binding of histamine to receptors on vascular endothelium causes increased permeability of the epithelium ad inflammation of nearby tissue, causing the runny nose, and swollen eyes typical of allergic rhinitis, and accumulation of mucus and fluid in the bronchi typical of allergic asthma. By blocking histamine action, antihistamines help alleviate these symptoms.
12) Give me three ways in which a susceptible person can help minimize the risk of having an allergic reaction
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Describe 4 ways in which a type III hypersensitivity reaction differs from a type I reaction.
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Explain what causes farmers lung and its pathology. State what type of hypersensitivity reaction is involved.
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a) What is the tuberculin test used for and how does it work? b) What type of hypersensitivity reaction is involved? c) Why does vaccination render this test useless?
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a) what type of hypersensitivity reaction typically occurs when penicillin is administered to an individual allergic to the drug? b) Describe in chronological order the events leading to this reaction. c) What type of hypersensitivity reaction can penicillin cause in a non allergic individual?
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identify 4 different ways in which an individual may come into contact with an allergen, and provide 2 examples of allergens for each type of contact.
1) inhalation: house dust nite feces, animal dander 2) injection: drugs administered intravenously, wasp venom 3) Ingestion: peanuts, drug administered orally 4) Contact with skin: poison ivy, nickel in jewelry
Some allergies can be treated by a procedure called desensitization. Explain a) two current approaches to desensitize and B) the main disadvantage associated with it
a) I) one approach to de
a) describe three ways in which the immunoglobulins acting as antigen receptros on the surface of a mast cell differ from the immunoglobulins actin as the antigen receptors on the surface of a B cell. b) What is the essential different in response of these two cell types when antigen binds to these surface immunoglobulin.
a) I) the immunoglobuling on a mast cell is an IgE antibody that has become bound to the mast cells FCeRI receptor, whereas the immunoglobulin on a B cell is a transmembrane form made by the cell itself. ii) A B cell might have any class of immunoglobulin on its surface, whereas mast cells have only IgE. iii) IgE molecules of many different antigen specificties can be bound to the surface of an individual mast cell, whereas an individual B cell carries immunoglobulin molecules of only one specificity b) After binding to antigen, mast cells become operational as effector cells without the need to undergo proliferation or differentiation. In contrast, after antigen has bound to a surface immunoglobulin on a B cell, the cell must proliferate and differentiate to produce effector cells
a) describe in detail the mechanism responsible for mast cell activation during a type I hypersensitivity reaction? b) What are the products of mast cell activation?
a) in an individual becomes sensitized to antigen by making antibodies of the IgE isotype during first exposure, then a type I hypersensitivity reaction may result if antigen is encountered again. The IgE made initially binds stably via its Fc regions to very high affinity FceRI receptors on mast cell surfaces. When antigen binds to this IgE, cross linking of FceRI occurs, delivering an intracellular signal signal that activates the mast cell b) mast cells contain preformed granules containing a wide range of inflammatory mediators that are triggered to be released extracellularly through an exocytic mechanism called degranulation. The inflammatory mediators contained in the granules and released immediately include histamine, heparin, TNF- alpha, and proteases involved in the remodeling of connective tissue matrix. The proteases include tryptase an chymotryptase, cathepsin G, and carboxypeptidase. Additional inflammatory mediators are generated after mast cell activation, including IL-3, IL-4, IL-5, and IL-13, GM-CSF, CCL3, leukotrienes C4 and D4, and platelet activating factor.
Match the type of hypersensitivities in list A with the immune system components involved.
a3or5 b178 c1256 d1457
