Pathophysiological Template for Paediatric Asthma - Essay Example

?Case Study Questions In Jason's case, as an infant some environmental factor, such as a respiratory infection or environmental allergy, triggereda bronchospasm that lead to his persistent cough. The bronchospasms result in increased sensitivity of the bronchial lining, making it more prone to future irritation. The large number of capillary blood vessels under the lining of the bronchial tract allows the inflammatory cells to be delivered rapidly and in large quantities. These cells cause the resultant swelling. His body is also improperly responding to the environmental irritants at a histological level, so that antibodies are not being produced in a normal fashion. 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. Because the cells cannot properly repair themselves after they are damaged by the inflammation of an acute attack, the response of Jason's body is to deposit more extracellular matrix between those cells, increase the number of cells being produced, and increase the size of the cells. The visible result is in the form of additional smooth muscle forming along the airways; in cases of more severe asthma, like in Jason's case, the amount of additional smooth muscle in the lining of the airways can be significant and may be permanent. It can also result in a thickening of the basement membrane of the inner lining in such severe cases. All three layers of the bronchial tract can be affected by airway diseases like asthma. This thickening affects his ability to draw in air to his lungs and further sensitizes the bronchial tubes to irritations, and may reduce the strength of his lung draw. 2. The wheezing Jason is experiencing when he arrives at the hospital is a result of the airway constriction that occurs with the inflammatory response of his bronchial lining. His body is of course still trying to pull air through the constricted path ways in order to provide air to his lungs. The wheezing is the sound that can be heard as the air passes through the confined space, similarly to the sounds produced by blowing air through a whistle. The fact that the wheezing can be heard both on inhale and exhale is due to the inflammation becoming more severe as the attack lengthens. Jason's body attempts to compensate for the constricted airways by increasing his respiratory rate, resulting in hyperventilation. The additional effort required to increase his respiratory rate, despite the inflammation and therefore constricted airways, results in a rapid heart rate. However, because he cannot either exhale or inhale without difficulty, the hyperventilation soon results in the pulmonary space becoming filled with air. This results in the dyspnoeic feeling; no matter how much or how fast Jason inhales, he cannot get enough fresh oxygen into his lungs, as there is simply not enough room to take in very much more air. In addition, no matter how fast he exhales, his lungs cannot force enough air out to make room, due to the inflammation and constriction of the airways. The dyspnoeia and the rapid heart rate combined most likely result in Jason's feelings of anxiety; he feels as if he is suffocating despite breathing rapidly and constantly. Due to his somewhat low oxygen saturation his brain is most likely not receiving enough oxygen, also contributing to his feelings of anxiety and probably resulting in minor disorientation. 3. In the case of an acute asthma attack, the administration of oxygen can be considered a drug. The oxygen is given in order to increase Jason's oxygen saturation. By breathing pure oxygen, the little air that Jason is able to pull into his lungs is enough to provide oxygen to his brain and other bodily organs. Increasing the oxygen saturation should help reduce Jason's respiratory rate, as his body will be less frantic to pull in more and more air, and therefore will reduce his heart rate, because less energy will need to be expending on simply breathing. Jason was also given inhaled salbutamol to reduce the bronchial spasms. Salbutamol is an ?2-adrenergic receptor agonist, and it reduces tension in the smooth muscle, acting as a bronchodilator. It will reduce inflammation and mucus production in the airways. Salbutamol stops the reflex reaction of the vagus nerve and inhibits the production of inflammatory mediators by the mast cells of the airway, helping to stop the feedback loop of constriction and allergenic response. Inhaled salbutamol can act directly on the bronchial lining, without needing to travel systemically first. Since Jason was experiencing symptoms of bronchoconstriction and hyperventilation, salbutamol is the obvious medication choice. Read More