Question

In your own words, explain the pathophysiology of COPD and how it affects Jim.

Answer 1

*Cigarette smoking is the leading cause of COPD.

*For people with COPD, pathophysiology is starts with damage to the airways and tiny air sacs in the lungs. Symptoms progress from a cough with mucus to difficulty in breathing.

There are various factors that causes the airflow limitation and other complications in COPD:-

Like Inflammation, Infection and Air flow obstruction.

1) INFLAMMATION:-

The inhalational exposure trigger an inflammatory response in the alveoli and airway that leads to disease in genetically susceptible individuals.

This process is mediated by an increase in protease activity and decrease in antiprotease activity.

Lung proteases like neutrophil elastase, matrix metalloproteinases, and cathepsins, break down elastin and connective tissue in the normal process of tissue repairing.

Their activity is normally balanced by antiproteases like alpha-1 antitrypsin, airway epithelium–derived secretory leukoproteinase inhibitor, elafin, and matrix metalloproteinase tissue inhibitor. In patients with COPD, activated neutrophils and other inflammatory cells release proteases as part of the inflammatory process; protease activity exceeds antiprotease activity, and it will result in the tissue destruction and mucus hypersecretion.

2) INFECTION:-

Respiratory infections also amplify progression of lung destruction.

Bacteria, especially the Haemophilus influenzae, colonize the lower airways in approximately 30% patients with COPD.

Colonization with Pseudomonas aeruginosa or other gram-negative bacteria are common in the patients who have a history of previous hospitalisations.

Smoking and airflow obstruction may lead to impaired mucus clearance in lower airways, which predisposes to respiratory infections.

3) AIRWAY NARROWING/OBSTRUCTION/LIMITATION:-

Airflow limitation is a cardinal pathophysiologic feature of COPD. It results due to airway narrowing or obstruction, loss of elastic recoil, or both.

Airway narrowing and obstruction are caused by inflammation-mediated mucus hypersecretion, mucus plugging, mucosal edema, bronchospasm, peribronchial fibrosis, and remodelling of the small airways or a combination of these mechanisms.

There is destruction of alveolar septas, reducing parenchymal attachments to the airways and thereby facilitating airway closure during expiration.

Enlarged alveolar spaces sometimes consolidate into bullae which are defined as the airspaces ≥ 1 cm in diameter. Bullae may be entirely empty or have strands of lung tissue traversing them in areas of locally severe emphysema; they occasionally occupy the entire hemithorax.

These changes results in loss of elastic recoil and hyperinflation of lungs.

Increased airway resistance increases the work of breathing.

Lung hyperinflation also increases the work of breathing. Increased work of breathing may lead to alveolar hypoventilation with hypoxia and hypercapnia.

Complications are :-

✓Pulmonary hypertension

✓Respiratory infection

✓Weight loss