Compose a 1750 words essay on Case study: Pathophysiological template for paediatric astha and 3 case study questions. Needs to be plagiarism free!Since his mother reports that she has hay fever Jason

Compose a 1750 words essay on Case study: Pathophysiological template for paediatric astha and 3 case study questions. Needs to be plagiarism free!

Since his mother reports that she has hay fever Jason's asthma may be allergenic. The possibility of allergenic asthma is further increased by the fact that Jason's brother has eczema. the skin cells related to allergic response and eczema flare-ups are the same as those involved in an asthma response. Since the lining of the airways cannot be penetrated by the allegen or irritant, it is a surface membrane response that leads to all three conditions: asthma, hay fever allergies, and eczema. When Jason's body was exposed to environmental irritants or allergens, his body produced elevated levels of Immunoglobulin E (IgE). This occurs through an allergenic cascade. when Jason is exposed to the allergen, the cells with the allergenic substance attached are attacked by his body's T-cells. These T-cells produce cytokines, which trigger the B-lymphocytes into producing IgE. This production usually takes place within the first few weeks after exposure to the allergen. Some of the IgE will attach to the mast cells of the bronchial lining, while others will remain free-floating. When Jason is re-exposed to the same allergenic trigger, the free-floating IgE will link with the IgE bound to the mast cells and trigger them to produce histamine, prostaglandins and leukotrienes. These inflammatory mediators then result in the bronchial inflammation and mucus production, as Jason's body tries to rid itself of the allergen that caused the initial response. Once the mast cells are activated, they will produce other chemicals that attract neutrophils. These neutrophils produce lysosomes, which attack the cells of the mucosal lining. When these cells are under attack, they add to the inflammatory effect of the asthma attack. This response does not occur for several hours after exposure to the allergen, explaining why Jason's asthma attack has continued even after removal from the trigger. The spasms that result from the production of IgE, however, are not necessarily the direct result of the inflammatory mediators on the smooth muscle layer of Jason's airways. Instead, the spasms could be the result of the mediators stimulating the vagus nerve. The vagus nerve then responds by constricting the bronchial pathways. Chronic asthmatics like Jason may have an overly sensitive vagus nerve reflex, causing the spasms to occur more often than in a healthy person. This overly-sensitive reflex can also be related to an imbalance of brain chemicals, such as beto-adrenoceptors, alpha-adrenoceptors, and catecholamines, or an abnormally high number of cholinergic receptors. A combination of the allergic and reflex responses is most likely the cause of Jason's asthma attack in this situation. Jason's lungs and airways respond to the irritation and spasms by producing thick mucus and mucus plugs in his air tracts, reducing the flow of air to his lungs. In addition, over the course of the years that Jason has had asthma, the bronchospasms are damaging to the lining of his airways, resulting in airway remodeling. The repeated inflammation and irritation of the lining prevents the extracellular matrix of his esophageal cells from repairing themselves properly.