The etiology and pathogenesis of COPD

The pathogenesis of COPD defines the development of the threat lung disease with serious complications. Disease is an actual problem because of its prevalence and risk of disability of the person. Many research centers worldwide are engaged in the study of disease and methods of combating it.

The who has developed a number of criteria to help you assess the severity of the disease. Installed the pathogenesis of COPD helps to use these criteria and to develop a scheme of treatment, prevention and rehabilitation of patients.

The essence of the disease

Chronic obstructive pulmonary disease (COPD) is a disease that generates an irreversible decrease of airflow within the respiratory channels. The change in flow is continuously shifted in the direction of its restriction, and is caused by reaction of the lung tissue of an inflammatory nature to the exposure to various particles and gas. Pathology initially occurs in the bronchial mucous membrane, where, in response to pathogenic exposure to altered secretion of enzymes: increases the production of mucus, violated the separation of bronchial secretions. To this is added the infection process, resulting in a range of reflexive reactions that ultimately lead to destructive phenomena in the bronchi, bronchioles and alveoli.

The etiology of the disease

The etiology and pathogenesis of COPD is based on the mechanism of mutual influence of genetic factors and factors associated with exposure to the external environment.

Question about the etiology of the disease to date is under dispute and debate scientists.

The reasons for not raising the doubts in authenticity, are the internal parameters – the lack of alpha-antitrypsin; external influences, including Smoking and harmful substances used in professional activities (cadmium, silicon, etc.).

With a high degree of probability the etiology of COPD due to the following reasons: internal – birth pathology, particularly prematurity, bronchial hyperreactivity, heredity, elevated levels of lgE; external – contaminants in the air, the way of life and diet, passive Smoking, especially in children.

Finally, the possible reasons can be considered to be a genetic predisposition in people with blood group A (II), infection with adenovirus, the lack of vitamin C.

The main precipitating factor of the disease is recognized, the Smoking, the proportion of smokers and COPD patients reaches 80% of all registered casesdisease. Shortness of breath caused by this disease, in smokers appears around the age of 40, almost 15 years earlier than non-smokers.

The second most common cause of COPD is the professional factor caused by the inhalation of dust with content of silicon and cadmium.

In this respect, the most harmful is considered to be the mining industry, and profession, included in the maximum risk is miners, builders, concrete workers, metallurgists, railway workers; workers involved in the processing of pulp, wheat and cotton.

The pathogenesis of the disease

The pathogenesis of COPD is based on the following typical processes such as inflammatory response, the imbalance in proteinase and antiproteinase, oxidative stress.

Inflammation of a chronic nature extends to most areas of the respiratory system, parenchyma and pulmonary vessels. Chronic inflammation leads to progressive destruction of lung tissue and irreversible pathologies. The other two process of pathogenesis is also due to the development of the inflammatory response in conjunction with the influence of external and internal factors.

As a result of inflammatory reactions is a significant increase in the concentration of the so-called cells of inflammation: neutrophils, macrophages and T-lymphocytes that cause pathogenic imbalance. Thus, the neutrophils increase the secretion of proteases of different types. Macrophages secrete tumor necrosis factor, leukotriene, and T-lymphocytes contribute to the cytolysis of epithelial cells of the alveoli.

The most significant role in the development of COPD is played by the tumor necrosis factor and interleukin, which actively destroy the lung structure and amplify neutrophilic inflammation.

In the process of inflammation is actively formed oxidants which can destroy proteins, fats, nucleic acids, causing the necrosis of the cells.

As a result of oxidative stress increases proteinazy imbalance. Under its influence is detected by the obstruction of the bronchi reversible.

Pathological physiology

The pathogenesis of this disease develops in the direction of occurrence of pathological disorders such as excessive production of mucus, impaired function of the cilia, the bronchial obstruction, destruction of parenchyma, and emphysema, impaired gas exchange, pulmonary hypertension, the appearance of "pulmonary heart disease", systemic pathology.

In the course of disease progression need to note the following key elements of pathophysiology:

1. The restriction of movement of air flow, barriers to flow. The process of pathogenesiscause of bronchial obstruction that impedes the flow outlet when you exhale; that appears, hyperinflation leads to a reduction of the volume of air inhaled, dyspnea, and premature fatigue, which in turn, disrupts contractile function of respiratory muscles.
2. Abnormality of gas exchange: developing hypoxemia and hypercapnia, there is an accumulation of carbon dioxide and decreased oxygen transport.
3. Excessive production of mucus leads to the characteristic cough.
4. Pulmonary hypertension: due to the spasm of pulmonary arteries of small size and develops in the later stages of COPD; the progression of pulmonary hypertension leads to atrophy of the right heart ventricle and the appearance of "pulmonary heart".
5. Worsening respiratory manifestations, provoked by the accession of a viral or bacterial infection, the influence of external factors (harmful component of air); increases inflammatory response, further decreases airflow due to increased hyperinflation and the emergence of new sources of resistance to flow; a ventilation imbalance can lead to complicated by hypoxia, worsening respiratory signs of COPD may be due to cardiac insufficiency, pneumonia.
6. Systematic violation: a violation of the respiratory rhythm and hyperinflation affect the functioning of the cardiovascular system and metabolism in the body, which leads to the beginning of other diseases (ischemia, diabetes, depression, etc.), a significant reduction in muscle tone and cachexia.

Pathological morphology

The progression of the disease leads to morphological changes in the structure of lung tissue, bronchi, vascular system, etc. of Such changes include metaplasia of the epithelium, necrosis of cilia atrophy of glands, and pathology of the smooth respiratory muscles. An excess of phlegm and mucus, worsening of bronchial drainage function, constrict the bronchi. Violation of muscle activity and hypoventilation of the alveoli gives rise to chronic hypercapnia and vascular spasms.

Clinical features of the disease

Clinic COPD is characterized by the following features:

1. Cough: the first symptom of COPD signs and symptoms – at first occasionally, then constantly; if the aggravation of the disease is not present, then a dry cough.
2. Sputum: in the early stages of the amount of release is small (most often in the morning and slimes), the transition in the acute phase – the added volume and there is a purulent mass.
3. Shortness of breath: is detected at a late stage, at first only during exercise, then may progress to severe respiratory failure.

Given the importance of the latter feature in the assessment of disease progression forclassification of dyspnea adopted by the international scale:

1. Degree 0 (weight not measured): shortness of breath occurs only during very fast and long walking.
2. Stage 1 (severity - mild): shortness of breath manifests while walking or travelling uphill.
3. Stage 2 ( degree - average): shortness of breath makes you move slower than peers.
4. Stage 3 (degree - heavy): you have to stop every 100 m.

At last, stage 4) shortness of breath appears even in dressing. Leaving the house is simply not strong enough. The forecast for the last 2 stages adverse.