Understanding Chronic Bronchitis
PKGhatak,MD
Chronic bronchitis is hardly discussed as such nowadays, it is currently grouped together with pulmonary emphysema and is known as chronic obstructive pulmonary disease.
Shortly after the first World War one, cigarette smoking became a socially cool thing and spread quickly worldwide. It did not take long before doctors in England noticed a sharp increase in chronic cough and sputum production in cigarette smokers. Doll and Hill published their landmark research paper in 1969 on the adverse effects of cigarette smoking and demonstrated the direct correlation between the number of cigarettes smoked with the incidence of lung cancer. Pathologists reported gradual changes of the respiratory epithelium of the bronchial tree to the squamous epithelium and an increase in the proliferation of mucus producing cells, Goblet cells, in smokers. Subsequently, the further transformation of squamous cells to cancer cells was demonstrated. Even then, Chronic bronchitis continued to increase and became a very common malady of that time.
It did not take long to notice that non-smokers were having chronic bronchitis too. Secondhand smoking, a new term, was coined; subsequently, coal burning smoke from factories, at home coke or firewood burning stove fumes were linked to chronic bronchitis. It is now accepted that repeated exposures to noxious fumes, like chlorine, ammonia, etc. lead to the development of chronic bronchitis in both non-smokers and smokers.
Inhaled air travels in a laminar flow down the tracheobronchial tree to the alveoli of the lungs. Because of the changed respiratory epithelium and increased goblet cells, the airflow becomes eddy flow at points of irregularities of the surface. The flow rate decreases in proportion to the irregular surface area. During inspiration, in a normal lung, the airway elongates and narrows. The combined effects, of surface changes and changes in the caliber of airways during inspiration, result in decreased air entry in the lungs. During expiration the electric recoil of the lung and the chest wall, is the sole force, to push air out of the lungs. The force generated by the elastic tissue is directly proportional to the stretched length of elastic fibers. As lungs are less inflated during inspiration, the air low during expiration is reduced. In clinical practice, decreased airflow during expiration is utilized to categorize the degree of severity of chronic bronchitis and is also used as a reliable tool for monitoring the effects of medical therapy. The test is quickly learned by the patients and the gadget costs only a few dollars and is covered by insurance. The test is called Air Flow Meter.
Behind the scenes in the Lab.
In an earlier time, learning Inflammation and infection was not difficult. With the knowledge of the immunity - innate and adaptive, the role of individual subsets of immunocytes, the importance of cell to cell communication, powerful enzymatic actions of cytokines, bradykinins, chemokines, the role of prostaglandins, interleukins, cellar growth promoting factors, vascular endothelial growth factor, etc. and the role, of the master programmer, the genes and messenger RNA, if not complicated enough, then add gene mutation, age related Telomere gene deletion, point mutations, etc. made medical study akin to study FBI agents receive at the academy.
That aspect is voluminous and better studied under the heading of inflammation, repair and remodeling. In the study of chronic bronchitis, there is no way out other than, at the minimum, to mention some of the processes at critical points of symptom development.
Age and lung function.
At birth, the lung structure and maturity cells are not fully developed. Lungs continue to grow and cells mature during childhood. Lung growth accelerates during adolescence. By the time the longitudinal growth of the long bone ceases, the lungs also stop growing. The lung is an exceptional organ because it begins to lose function after mid 20s. It is estimated that an individual loses 1 % of lung reserve each year. Until the loss of volume is greater than 50%, the patients remain asymptomatic. In cigarette smokers, the rate of decline of lung functions is much faster, and they become symptomatic earlier.
In addition, the changes in genes due to age manifest in a variety of ways. Every chromosome has several genes, and each gene has a beginning and end part. The end part of the gene is called Telomere. In advanced age, the telomere portion of the gene is lost. Depending on the gene function, the symptoms vary. Telomere deletion leads to decreased immune functions, specially the repair and remodeling of the lungs.
Symptoms and progression of chronic bronchitis.
Patients become symptomatic after considerable lung damage. Some inhaled chemicals are direct toxins to respiratory cells or due to the generation of free radicals at the local level. Some inherited conditions, like alpha1 antitrypsin deficiency, dyskinesia of ciliary epithelium of the respiratory tract, congenital mitochondrial diseases and macrophage enzyme deficiency, accelerate these changes.
Cough and increased mucoid mucus production are mostly observed in the morning after waking up. Later, more frequent symptoms are noticed during the evening and night. At this stage, the chest x-ray may be negative, but the vital capacity is reduced and also FEV1(expired air volume in the 1st second of expiration). Similarly, the flow rate is reduced. Frequent respiratory infections due to respiratory viruses are common and occasional bacterial infections are seen.
Each new episode of viral, bacterial infection or exposure to toxins produces destruction of the lamina propria, smooth muscles and elastic fibers.
Repair and remodeling do not progress normally because of repeated inflammations. Haphazard laying down of new cells, generated by the resident progenitor cells of the endothelium, fibroblasts, and myeloblasts produce irregular remodeling and more obstruction to airflow. Bronchioles less than 2 mm in diameter show a 40 to 50 % reduction of the caliber and can be demonstrated by HTCT (high regulation CT). Loss of elastic fibers distorts the delicate alveoli and capillaries. The surface area of the alveoli is reduced. A mismatch between ventilation and circulation occurs. The arterial oxygen saturation falls during exercise and later at rest. Continuation of infections, abnormal repairs and remodeling produce hypoventilation and Carbon dioxide retention. After each bout of infections, patients experience progressively worsening shortness of breath.
Chest x-ray shows heavy bronchovascular markings and is in association with patches of infiltrates. Hyperinflation of sub-segmental lobes, most marked in the upper zone of the lungs is seen. Still later, the radiological picture becomes a combination of chronic bronchitis and emphysema. The progression of the disease takes several years. It is not unusual that patients to live with chronic bronchitis for 40 to 50 years. At the final stage, the pulmonary arterial pressure increases in a step-wise fashion in line with the damage to the lung. Right ventricular hypertrophy develops as a compensatory mechanism, and later right heart fails to keep up and congestive heart failure develops.
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