Chronic obstructive pulmonary disease. Clinicopathological forms. Pathomorphological changes in the lungs and heart
COPD is a type of irreversible obstructive lung disease characterised by long-term poor airflow with dyspnea, cough and sputum production. It is a combination of chronic bronchitis and emphysema (see above questions that explain each condition in turn).
Smoking is the principal cause of COPD, as is clear from the clear relationship between smoking, emphysema and chronic bronchitis.
Pathologically, we see emphysema (abnormal enlargement of air spaces distal to the terminal bronchiole and destruction of alveolar walls without fibrosis) and chronic bronchitis (hypertrophy of the submucosal glands, hyperplasia of the goblet cells and metaplasia of the pseudostratified epithelium on the bronchi).
Remember: the two classic clinical ends of COPD:
- Pink puffer (emphysema predominant): thin, very dyspnoeic, hyperventilates through pursed lips, barrel chest, blood gases near normal until late
- Blue bloater (chronic bronchitis predominant): productive cough, cyanosis, hypoxaemia and hypercapnia, oedema from cor pulmonale
The earliest pathologic changes that are focal collections of brown-pigmented macrophages in the respiratory bronchiole and sparse infiltrate of neutrophils and lymphocytes in the walls of the terminal bronchioles. This process will continue until the almost complete mucous plugging of various distal airways, squamous cell metaplasia, goblet cell hyperplasia and smooth muscle hypertrophy.
COPD also causes increased vascular resistance, this increases pulmonary pressure (pulmonary hypertension) and causes right sided heart failure due to the increased effort (although not before right sided hypertrophy occurs). This is known as cor pulmonale.