Research Paper: Respiratory Infections

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[. . .] The patients with non-atopic asthma do not have elevated levels of IgE in blood serum and they do not have hypersensitivity to any allergens. However, there are certain immunologic mechanisms that have not been demonstrated Clark et al., 1999()

The risk factors of bronchial asthma usually lead to immunologic mechanisms whereby they cause irritation directly or indirectly as a result of denaturation of proteins. Bronchial asthma is also an occupational asthma and is suspected when the patient experiences these symptoms repeatedly when at work Chen, Schreier, Strunk, & Brauer, 2008()

Pathology

Bronchial asthma is a hereditary disease. When a person gets infected, there is IgE stimulation which causes mast cell degranulation which causes the asthma attack. The attack can then lead to an altered immunologic response that leads to the release of a chemical mediator which can either be histamine, prostaglandins, SRS-A, bradykinins, leukotrines Unger & Leon, 1954.

It can also cause increased resistance in the airway which causes mucus secretion as a result of bronchospasm inflammation which leads to audible expiratory ad inspiratory actions as well as breathing of the accessory muscles. It can also lead to nasal flaring and tachypnea or tachycardia. Bronchial asthma also causes increase lung compliance that causes the lungs to be hyper-inflated Lebowitz, Bronnimann, & Camilli, 1995()

Bronchial asthma can also cause impaired mucociliary function which causes an increase in production of mucus that causes a slowed down clearance of mucus. There is also increased water loss from mucus. Mucus also becomes increasingly viscous. At the same time, there can be wheezing and paroxysmal dyspnea. Bronchial asthma can also alter the exchange of O2 and CO2 which leads to increased resistance of the airway which makes the respiratory muscles to work harder. This causes muscular fatigue and exhaustion that causes respiratory alkalosis Flodin, Ziegler, Jonsson, & Axelson, 1996()

If there is no medical intervention, the individual compensates without an increase in respiration rate. This leads to respiratory alkalosis that causes mild hypoxemia. The mild hypoxemia then develops to severe hypoventilation that causes respiratory audoris which results in severe hypoxemia that can then lead to death. With medical intervention, there is O2 therapy as a result of the medication such as inhaled steroids, beta-2 adrenergic agents and bronchodilators (salbutamol). This leads to opening of the airway that causes a deep breathing and coughing exercise. With adequate rest, there is increased intake of fluids that then leads to relaxation of the body Flodin et al., 1996()

Bronchial asthma should be prevented by elevating HOB, limiting exposure to allergens and minimizing strenuous activities. Increasing fluid intake also helps to prevent bronchial asthma Flodin et al., 1996()

Symptoms

Bronchial asthma is usually characterized by attacks of coughs, dyspnea and expectoration of tenacious sputum that is mucous in nature. There is also wheezing in the patients as they breathe. The symptoms of bronchial asthma are usually mild and they can also occur in association with other respiratory infection. Classic atopic bronchial asthma usually begins in childhood and progresses in severity as the child grows. Hay fever usually accompanies atopic bronchial asthma Flodin et al., 1996()

Acute bronchial asthma is often characterized by dyspnea which is associated with wheezing and can be heard even without the use of a stethoscope. A cough may be present but it is often not the predominant symptom. There is a small group of patients with asthma who may have a paroxysmal cough as the predominant symptom. When bronchial asthma is prolonged, it presents as a severe wheezing that is intractable. This is known as status asthmaticus Flodin et al., 1996()

Differential diagnosis

For asthma, the most important differential diagnosis is for COPDs (chronic obstructive pulmonary diseases). This is because COPD can coexist with asthma. It can also occur as a complication of chronic asthma. At the late age of 65, most of the people who have obstructive airway disease will have asthma and COPD. COPD can be differentiated by the increased neutrophils in the airway and abnormally increased thickness of the wall as well as increased bronchi smooth muscle. COPD resembles asthma in terms of symptoms such as exposure to smoke and old age and also management such as long-acting beta agonists, corticosteroids and cessation of smoking Cerveri et al., 1987()

Other differential diagnoses include allergic rhinitis and allergic sinusitis in children. Other differential diagnoses in children include bronchopulmonary dysplasia, cystic fibrosis and viral bronchiolitis. In adults, the differential diagnoses include COPD, congestive heart failure, pulmonary embolism, pulmonary infiltration with eosinophilia and vocal cord dysfunction. Bronchial asthma is identified by an increase in the number of eosinophils in the peripheral blood cells Cerveri et al., 1987()

Treatment

The most effective way to control and treat bronchial asthma is to identify the triggers and to eliminate them. They include cigarette smoke, aspirin and pets. For smoking, the asthmatic person should avoid cigarette smoking as well as second-hand smoke. If avoidance of the trigger is insufficient, medical treatment can be given depending on the severity of the illness and how frequent the symptoms are. Medication for asthma is divided into long-acting and fast-acting medication. Bronchodilators are used for short-term relief of the symptoms of bronchial asthma. Those with mild persistent disease, say about two attacks in a week, low doses of glucocorticoids are given for inhalation or alternatively a mast cell stabilizer or leukotriene antagonist is given. For those who suffer from frequent attacks, say daily, a high dose of glucocorticoids is given for inhalation. Oral glucocorticoids are given for those with severe asthma exacerbation Unger & Leon, 1954()

Fast-acting medication for bronchial asthma includes SABA (short acting beta2-adrenoceptor agonists) such as salbutamol, anticholinergic medication such as ipratropium bromide and less selective adrenergic agonists such as inhaled epinephrine. Long-term medication includes glucocorticoids, LABA (long acting beta-adrenoceptor agonists) which have a 12-hour effect, leukotriene antagonists such as zafirlukast and mast cell stabilizers such as cromolyn sodium Unger & Leon, 1954()

Asthma medication is mostly delivered in metered-dose inhalers (MDIs) together with asthma spacers or as a dry powder inhaler. Nebulizers can also be used. Other complementary treatment options for asthma include air filtration to remove allergens and other triggers, use of mattress covers and other bedding encasement to prevent dust mites. Laundry can also be washed in hot water to control allergens. Another experimental method of treatment that does not have sufficient evidence to promote its use is the Buteyko breathing technique that controls hyperventilation Unger & Leon, 1954()

Exercise-induced bronchospasm

Exercise-induced bronchospasm (EIB) is a disorder that causes problems of breathing during or after doing exercise. The exact cause is usually unknown but there are several theories that try to explain this. One theory states that when there is rapid breathing, the airways become dry and thus easily irritated. This causes the airways to tighten and become smaller which is referred to as bronchoconstriction. Small air tubes make breathing to be harder. A second theory suggests that EIB is caused by bronchitis which causes injury to the layer of cells which causes a high flow of air through the airway during exercise. Research that has been conducted suggests that these theories may be on the right path of finding the real cause of EIB. The only risk factor of EIB is heavy exercise.

Etiology

EIB occurs both in people who have asthma and those without asthma. About 80% of the asthmatic people also have EIB. Another study showed that 80-90% of asthmatic patients also have EIB. However, not many of these patients who have EIB will experience the symptoms in other activities other than during exercise. Between 5-10% of non-asthmatic people will have EIB. Athletes have a higher rate of EIB as a result of the heavy exercise they do constantly. EIB occurs in about 20-50% of athletes who do not have asthma. The sad thing is that many of the athletes are not even aware that they are suffering from EIB. Additionally, people with sinus problems, allergies or family history of allergies are more at risk of contracting EIB Weiler, Emeritus, Anderson, & Randolph, 2010()

Pathology

EIB is caused by loss of water or heat or both from the lungs which is caused by heavy exercise. This stems from the hyperventilation of air that is cooler and drier that that which is in the respiratory tree. Heavy or strenuous exercise causes hyperpnea which in turn leads to the drying of the airways making them require humidification and often warming of large volumes of air over a short period of time. The loss of water in the airways also leads to an increase in the osmolarity of the airways surface. The increase in osmolarity of the airways is then postulated to induce the mast cells of the airways to degranulate and releasing chemical mediators that… [END OF PREVIEW]

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