Pathophysiology of Chronic Obstructive Pulmonary Disease

COPD types
Chronic Bronchitis Emphysema Bronchiectasis destruction and widening of large airways Asthma

General COPD Progression

Most cases are a result of exposure to noxious stimuli, most often cigarette smoke. Pathogenic mechanisms are unclear Increased numbers of PMN leukocytes and macrophages release elastases in a manner that cannot be counteracted effectively by anti-proteases, resulting in lung destruction.

Chronic Bronchitis
Defined as presence of a chronic productive cough for 3 months during each of 2 consecutive years Mucous gland hyperplasia is the histologic hallmark Damage to endothelium impairs mucociliary response Contrast to emphysema, has relatively undamaged pulmonary capillary bed.

Histologic hallmark

Emphysema
Defined as abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Airway limitation is due to loss in elastic recoil and increase in airway resistance. Permanent enlargement of airspaces distal to the terminal bronchioles. Gradual destruction of alveolar septae and pulmonary capillary bed leads to decreased ability to oxygenate blood 2 mechanisms of airflow limitation
Loss of alveolar walls results in decrease in elastic recoil Loss of alveolar supporting structure leads to airway narrowing.

Chronic Bronchitis inflammation, or irritation, in the bronchioles of the lungs. Body responds by decreasing ventilation and increasing cardiac output

Emphysema permanent enlargement of the airways in your lungs, accompanied by alveoli destruction Body responds by hyperventilation and decreasing cardiac output

V/Q mismatch leading to hypoxemia(blue) V/Q mismatch leads to hypoxia(relatively and polycythemia pink) Hypercapnia and respiratory acidosis Lack of radial traction on bronchioles leads to marked tendency to collapse during expiration due to expiratory positive pleural pressures Patient breathes through mouth with gradual release of pressure so there is more intra bronchial pressure to prevent airway collapse(Purse lip breathing) In other words, patient puffs breathing.

Pulmonary artery vasoconstriction and Cor Pulmonale(alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system) Right heart fibrillation leading to edema(bloaters)

References
http://emedicine.medscape.com/article/2976 64-overview#showall http://www.prep4usmle.com/forum/thread/7 4374/