Asthma
Asthma is a chronic respiratory condition where the airway narrows and swells making it difficult to breathe. It is an inflammatory disease characterized by reversible episodic airway narrowing and hyper-responsiveness to different stimuli. According to Stern, Pier & Litonjua, (2020), major features from the definition include; presence of bronchial inflammation in all patients, airway hyper-responsiveness that causes easy narrowing from different stimulus, reversible obstruction that is evidenced by a change in lung function, and recurrent symptoms of wheeze, shortness of breath, tight chest and coughing. It affects over 300 million people worldwide and is the most common chronic disease in childhood. In childhood, it is twice common in males than females while in adulthood the ratio is the same. The peak age is about 3 years and it is more prevalent in developed countries and urban areas (Stern, Pier & Litonjua, 2020).
There are common risk factors for the disease. There is interplay between genetic and environmental factors. The non-modifiable factors include; gender wherein children males are at more risk while in adult females are at more risk. Others include; atopy, genetic predisposition, and airway hyper-responsiveness. Modifiable factors include; exposure to allergens, infections, air pollution, occupational exposures, tobacco smoking including passive smoking, helminthic infestation, viral infection, and breastfeeding for longer than 6 months. Common triggers for asthma attacks include; exercise, cold air, smoke, stress, paint and perfumes, medications, and allergens such as dust, mites, hormones, pollen, and pet fur (Stern, Pier & Litonjua, 2020).
The disease is more common in children with males at more risk while in adults the prevalence is the same with both genders but the risk is higher in females. Majority of asthma cases have a genetic basis. According to Willis-Owen, Cookson, & Moffatt (2018), it runs strongly in families and about 50% is due to genetic susceptibility. Five asthma genes have been identified and include; ADAM33, DPP10, SPINK5, GRPA, and PHF11. The functions of these genes are still unknown but the expression of the middle three in the differentiation of the epithelium suggests that they deal with threat or damage from the external environment. These genes express their effects on mucosal cells such as interleukin-13 which causes the production of mucus, activation of innate immune system, and triggering of mast cells. Lifestyle influences the disease in different ways.
Pathophysiology of the disease is complex. There is airway inflammation with the production of increased numbers of activated inflammatory cells due to exposure to triggers. Various chemical mediators are also produced. Mast cells initiate the bronchoconstriction response to stimuli and are activated through IgE dependent mechanism. They release bronchoconstrictor mediators such as histamine, cytokines, growth factors, chemokines, and leukotrienes. Eosinophils cause airway hyper-responsiveness (Boonpiyathad et al., 2019). They also release free oxygen radicals and the growth factors that are involved in airway remodeling. Neutrophils are responsible for resistance to the anti-inflammatory effects of corticosteroids. T-lymphocytes coordinate the inflammatory response and release cytokines (Lambrecht et al., 2019). They also release IL-5 which is responsible for eosinophilic inflammation and IL-13 which ensure IgE production. Structural cells such as epithelial, fibroblasts, and smooth muscle cells release cytokines which cause chronic inflammation (Boonpiyathad et al., 2019). These cause structural changes in the airway which result in functional changes. The overall result is chronic inflammation, edematous airway, vascular congestion, bronchoconstriction, and luminal occlusion with exudate.
These processes cause early closure of peripheral airways leading to hyperinflation of lungs and increased residual volume. There is increased airway resistance that brings about clinical features such as wheezing, difficulty breathing, coughing, and chest tightness. The symptoms worsen at night and early morning. Prodromal symptoms may include; chin itch, impending doom, and discomfort between the scapulae. Therefore, diagnosis is mainly clinical with the mentioned features contributing to the probability of asthma diagnosis. The time of onset, history of allergies, current medications such as beta-agonists, and exposure to triggers also contribute. Physical examination is often normal apart from the wheeze on auscultation (Tesse et al., 2018).
Investigations such as spirometry may be done. It will indicate airway obstruction and can be used to assess reversibility. There is reduced FEV, PEF, and FEV1/FVC ratio in lung function tests. Measuring PEF twice daily will confirm diurnal variation. In more than 12%, reversibility is evident after a therapeutic trial. A chest X-ray will be normal or demonstrate hyperinflammation. Blood samples show elevated serum IgE to the inhaled allergens. Other body systems are hardly affected by the condition. Skin tests may be done to confirm allergies, especially in occupational exposure. They are negative in intrinsic asthma (Tesse et al., 2018).
Complications of persistent asthma include; growth delay in children, airway remodeling, fibrosing bronchitis, respiratory failure, pneumonia, pneumothorax, atelectasis, emphysema, and status asthmaticus. If the disease is left untreated it will cause; lack of sleep, reduced physical activity, frequent hospitalization, and reduced quality of life(Tesse et al., 2018).
According to Christensen & Allen (2017), the treatment of asthma includes relievers for rapid relaxation of airway muscles and controllers for long-term prevention of attacks. Relievers include short-acting beta-agonists (salbutamol), anticholinergics (ipratropium bromide), xanthines (theophylline), and adrenaline. Short-acting beta-2 agonists such as albuterol are available in tablet form and are given one tab 2-3 times daily. Terbutaline is available as a subcutaneous injection at 0.25mg. They are also available as metered-dose inhalers. Their side effects include tachycardia and palpitations. Theophylline is given at 3-4mg/kg every 6hours through the oral route. Its side effects include anorexia, nausea, abdominal discomfort, diuresis, insomnia, tremors, seizures, and liver failure. Ipratropium bromide is given by inhalation and side effects include; tachycardia, agitation, urinary retention, and blurry vision. Adrenaline is injected subcutaneously (0.4ml of 1:1000 solution) or inhaled from a pressurized canister at 320mcg/puff. Side effects include tachycardia and worsening of angina.
Controllers include; corticosteroids (prednisolone and betamethasone), long-acting beta-2 agonists (salmeterol), and antileukotrienes (montelukast and zafirlukast). Combinations of these medications are used for maximal effects. A stepwise approach is recommended. Corticosteroids are given inhaled to prevent systemic effects. Beclomethasone 400mcg/day is given in 4 puffs twice. Side effects include; adrenal suppression, oral candidiasis, Cushing syndrome, and growth suppression. They are used in emergency and controller therapy for 10 days. Salmeterol potentiates the effects of inhaled corticosteroids and is combined (Christensen & Allen, 2017).
References
Boonpiyathad, T., Sözener, Z. C., Satitsuksanoa, P., & Akdis, C. A. (2019, December). Immunologic mechanisms in asthma. In Seminars in immunology (Vol. 46, p. 101333). Academic Press.
Christensen, H. D., & Allen, H. N. (2017). Antiasthmatics. In Therapeutic Drug Monitoring and Toxicology by Liquid Chromatography (pp. 237-268). Routledge.
Lambrecht, B. N., Hammad, H., & Fahy, J. V. (2019). The cytokines of asthma. Immunity, 50(4), 975-991.
Stern, J., Pier, J., & Litonjua, A. A. (2020, February). Asthma epidemiology and risk factors. In Seminars in Immunopathology (pp. 1-11). Springer Berlin Heidelberg.
Tesse, R., Borrelli, G., Mongelli, G., Mastrorilli, V., & Cardinale, F. (2018). Treating pediatric asthma according guidelines. Frontiers in pediatrics, 6, 234.
Willis-Owen, S. A., Cookson, W. O., & Moffatt, M. F. (2018). The genetics and genomics of asthma. Annual review of genomics and human genetics, 19, 223-246.