Pathophysiology of COPD

Pathophysiology of COPD

COPD, or chronic obstructive pulmonary disease, is a progressive inflammatory disease connecting the airways, lung parenchyma, and vasculature. It causes the hurt and remodeling of the airways and lung tissue. obliging functioning of lungs is rejected continuously by COPD. Over a period of time, these changes result in more severe conditions such as pulmonary hypertension and apt heart failure. The sincere pathophysiology of COPD is unidentified.

The inflammatory process is a driving aspect in the pathophysiology of COPD. original verification suggests that the inflammatory response results in a number of effects, including an arrival of inflammatory cells such as macrophages, neutrophils and lymphocytes. Thickened airways and structural changes such as increased still muscle and fibrosis may also be manifested. Cigarette smoking causes an inflammatory response in the lungs. This response does not stay with the removal of the stimulus, but progresses for an unlimited period of time. COPD is a subset of obstructive lung diseases that includes cystic fibrosis, bronchiectasis and asthma. Degeneration and destruction of the lung and supporting tissue are characteristic of COPD. These processes result in emphysema, chronic bronchitis, or both. Emphysema begins with a diminutive airway disease and progresses to alveolar destruction, with a predominance of limited airway narrowing and mucous gland hyperplasia.

The pathophysiology of COPD is not entirely understood. Chronic inflammation of the cells lining the bronchial tree plays a major role. Smoking and, seldom, other inhaled irritants, perpetuates an ongoing inflammatory response that results in airway narrowing and hyperactivity. Airways become edematous, excessive mucus production occurs and cilia function weakly. Patients face increasing pain clearing secretions with disease progression. Accordingly, they compose a chronic productive cough, wheezing and dyspnea.

The basic pathophysiologic process in COPD consists of increased resistance to airflow, loss of elastic recoil and decreased expiratory scamper rate. The alveolar walls frequently fracture because of the increased resistance of air flows. The hyper inflated lungs flatten the curvature of the diaphragm and enlarge the rib cage. The altered configuration of the chest cavity places the respiratory muscles, including the diaphragm, at a mechanical disadvantage and impairs their force-generating capacity. Consequently, the metabolic work of breathing increases, and the sensation of dyspnea heightens.