Bronchitis
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Bronchitis
Pathology
Bronchitis is a respiratory system disease usually characterized by airway irritation that leads to inflammation, with the main symptom being cough and sputum production. Acute and chronic bronchitis are two forms of bronchitis, and they exhibit a wide variation in terms of symptom presentation and etiological factors. Acute bronchitis is usually a respiratory illness often caused by a viral infection. It lasts for 1-3 weeks, with cough being the most common symptom in healthy individuals and other constitutional symptoms such as fatigue and body aches (Solomon et al., 2016). Chronic bronchitis is a form of chronic obstructive pulmonary disease that results from irreversible, usually incomplete, obstruction of the airways that usually produce a decrease in maximal expiratory airflow. The disease is clinically defined by the presence of persistent cough production for more than three months in at least two consecutive years with no identifiable underlying cause.
The disease is more common among habitual smokers and those living in smog-laden cities, indicating that environmental pollutants play a key role in causing the infection. Chronic obstructive pulmonary disease(COPD) comprises obstructive airway diseases that decrease the maximal expiratory airflow, usually leading to breathing-related symptoms. Chronic bronchitis is one of the most common forms of COPD, with emphysema, characterized by alveolar destruction, is the other major manifestation. Both forms of bronchitis are usually characterized by persistent sputum-producing cough, but they vary when the cough lasts. In the acute form, the cough persists for about 1-3 weeks, while for the chronic form, the cough persists for more than 3 months in 2 consecutive years, and there is no identifiable cause isolated. With acute infection being a lower respiratory illness, usually of viral etiology, the risk of superimposed bacterial infection is considerably high. These individuals are vulnerable to develop infections such as otitis media and pneumonia.
Normal Anatomy of Respiratory System
The respiratory system is vital because it can achieve the required blood oxygen gas levels. Anatomically, the respiratory system is divided into the upper and lower respiratory tract. The upper respiratory tract comprises the nose, pharynx, and larynx, which are all outside the thorax. The lower respiratory tract comprises the trachea, bronchus, bronchioles, and lungs. Additionally, the respiratory system is usually divided into two parts based on functionality. One of the parts is the conducting zone, which runs from the nose to the bronchioles, and the respiratory zone runs from the alveolar duct to the alveoli (Anzueto & Miravitlles, 2017). The conducting zone is usually responsible for transmitting the inhaled down the respiratory tree to the respiratory zone, where the actual gaseous exchange occurs.
The nose and the nasal cavity are usually divided into two parts by the nasal septum. On the lateral wall of the nose, there are three turbinates/conchae, the superior, middle, and inferior turbinates. The clinical significance of the three turbinates is that the passage inferior to inferior is the preferred route for the nasal gastric tube passage. The pharynx is the tube-like passage that usually connects the posterior nasal and oral cavities to the larynx and the esophagus. The pharynx is usually divided into three parts, the nasopharynx, oropharynx, and laryngopharynx. The clinical relevance of this is that any increase in soft tissue usually results in an anatomical imbalance, which reduces the space available for air passage.
Additionally, it is important to understand the microscopic structure of the alveolar wall. The alveolar wall comprises the capillary epithelium that lines the intertwining network of anastomosing capillaries, the basement membrane and the surrounding tissue, the alveolar epithelium, and the alveolar macrophages. The alveolar epithelium comprises two cell types, the type 1 pneumocytes and the type 2 pneumocytes. The type 1 pneumocytes are flattened and plate-like, and round type 2 pneumocytes responsible for surfactant production.
Normal Physiology of the Respiratory System
Ventilation refers to the inhalation and the exhalation of the gas. This is to achieve gas exchange to maintain the blood oxygen levels within the normal limits. The respiratory system has a close neural control, whereby the central nervous system tightly controls it. The brainstem is the part that is responsible for the control of ventilation. The brain has some centers that can sense the blood oxygen and, in turn, respond by increasing the ventilation rate if the oxygen levels are low. The medulla oblongata is the primary respiratory control center in the brain, and its main function is to send signals to the muscles that control respiration, making breathing occur. There is great physiologic control on the ventilation, which is the air movement into and out of the lungs. The breathing rate is around 10-12 breaths per minute. The rate is usually determined by the number of impulses that the diaphragm and the muscles receive from the brain. The breathing mechanism is a process that is regulated by the pressures (Eapen et al., 2018). When the diaphragm moves downwards, the thoracic cavity volume increases, which results in the movement of air down the pressure gradient, and the air thus enters the lungs, causing inflation.
The active phase of ventilation where the air moves into the lungs is called ventilation. During expiration, the diaphragm flattens, decreasing the thoracic vole and increasing the pressure, which makes the air move out of the lungs leading to exhalation. Perfusion is another component of respiration, which refers to blood circulation through the capillaries, and the process facilitates a proper nutrient exchange. Diffusion is another component of respiration that entails the gas’s movement across the alveolar wall (Anzueto & Miravitlles, 2017). The alveolar wall is thin enough to reduce the diffusion distance, enhancing a proper gaseous exchange between the lung and the blood. The lungs are inflatable, and they actively distend when air enters the lungs. In normal respiration, the negative pleural pressure is sufficient to distend the lungs during the inspiratory phase. It is vital to understand these respiratory mechanics. The clung compliance is also key in achieving normal respiration because diseases that decrease lung compliance affect the lung volumes because the lungs cannot achieve the normal ling volumes, which may affect the blood gas levels.
Mechanism of Pathophysiology
A long-standing irritation of respiratory mucosa seems to be key in the genesis of chronic bronchitis, with substances such as tobacco increasing the likelihood of developing the condition. 90% of patients who develop chronic bronchitis usually have a history of smoking. However, other environmental pollutants such as dust from grains, cotton, and silica are also key in exacerbating the disease’s risk (Eapen et al., 2018). The chronic irritation of the mucosa leads to mucus hypersecretion on the large airways, resulting from hypertrophy of the submucosa glands of the trachea and the bronchi. Additionally, the proteases secreted by the neutrophils, such as elastase, cathepsin, and matrix metalloproteinases, further stimulate the hypersecretion. As chronic bronchitis persists, there is a marked increase in the goblet cells in the bronchi and the bronchioles that further increases the mucus secretion leading to airway obstruction. The submucosal gland hypertrophy in the trachea and the bronchi, together with the hyper-proliferation of goblet cells in bronchi and bronchioles, is a protective metaplastic reaction environmental irritants and tobacco smoke.
The respiratory system’s damage usually leads to the recruitment of the inflammatory cells, with neutrophils being the prominent cells that are recruited. The recruitment of the inflammatory cells results from the upregulation of adhesion molecules such as ICAM-1 and the E-selectin on the subepithelial blood vessels. Additionally, the macrophages and the CD8+ cells infiltrate the sub-epithelial space. The high number of inflammatory cells is suggestive that inflammation of the glands is key in addition to the hypertrophy of the mucus-producing glands. Thus, the main pathogenesis that underlies the increased mucus production in patients with chronic bronchitis is the hypertrophy of the submucosal glands in the trachea and bronchi and the goblet cell hyper-proliferation in the bronchi and bronchioles. The hypertrophy of the submucosal glands and the hyper-proliferation of the goblet cells are metaplastic changes aimed at being protective against tobacco smoke and other environmental irritants (Anzueto & Miravitlles, 2017). The role of infection in the pathogenesis of chronic bronchitis is secondary because it is not responsible for the initiation but rather for the maintenance and production of some acute exacerbations of symptoms. Additionally, tobacco smoking interferes with the normal ciliary function, directly damages the airway epithelium, and may inhibit the leukocytes’ ability to clear the bacteria.
Acute bronchitis pathogenesis usually stems from the viral colonization of the epithelial cells. In response to the colonization, there is the production of cytokines that, in turn, recruit some immune cells to the site of epithelial cell damage. Thus, acute bronchitis’s main pathogenesis is due to the immune responses that result from the inflammatory process.
Prevention of Bronchitis
With tobacco smoke being an important initiation factor for the disease’s pathogenesis, the disease can be prevented by the cessation of smoking in these individuals. The metaplastic changes such as submucosal gland hypertrophy and goblet cell proliferation do not occur by quitting smoking and thus reduces the risk of developing bronchitis (Solomon et al., 2016). Additionally, with other environmental factors being key initiating factors for the disease, the disease can be prevented by wearing respirators for all workers working in places that they might be predisposed to such respirators. Infections play a key role in maintaining and exacerbating the disease’s symptoms, and thus offering prophylactic antibiotics to individuals at risk can be key in preventing the disease occurrence. The cessation of smoking can be done by helping these patients quit smoking and can be done by giving the patients some nicotine gums to curb the smoking urge.
Treatment
Glucocorticoids are the mainstay in the treatment because inflammation is key in the pathogenesis of bronchitis, thus preventing these responses. Antibiotics, especially broad-spectrum antibiotics such as amoxicillin, should also be given to the patient because the superimposed infections are crucial in maintaining bronchitis (Itkin et al., 2016). Beta-2 adrenoceptor agonists are also important in standard therapy because they are used to dilate the airways relieving the patient of airway obstruction symptoms. Anticholinergics are also important in patients with bronchitis because they lead to dilatation of the airways leading to relief of the airway obstruction symptoms. Additionally, mucolytics can relieve the symptoms of accumulated mucus because they act by lysing the mucus preventing its accumulation.
References
Anzueto, A., & Miravitlles, M. (2017). Pathophysiology of dyspnea in COPD. Postgraduate Medicine, 129(3), 366-374. https://www.tandfonline.com/doi/abs/10.1080/00325481.2017.1301190
Eapen, M. S., Hansbro, P. M., Larsson‑Callerfelt, A. K., Jolly, M. K., Myers, S., Sharma, P., … & Larby, J. (2018). Chronic obstructive pulmonary disease and lung cancer: underlying pathophysiology and new therapeutic modalities. Drugs, 78(16), 1717-1740. https://link.springer.com/article/10.1007/s40265-018-1001-8
Itkin, M. G., McCormack, F. X., & Dori, Y. (2016). Diagnosis and treatment of lymphatic plastic bronchitis in adults using advanced lymphatic imaging and percutaneous embolization. Annals of the American Thoracic Society, 13(10), 1689-1696. https://www.atsjournals.org/doi/full/10.1513/AnnalsATS.201604-292OC
Solomon, G. M., Raju, S. V., Dransfield, M. T., & Rowe, S. M. (2016). Therapeutic approaches to acquired cystic fibrosis transmembrane conductance regulator dysfunction in chronic bronchitis. Annals of the American Thoracic Society, 13(Supplement 2), S169-S176. https://www.atsjournals.org/doi/full/10.1513/AnnalsATS.201509-601KV