-Chronic inflammation of the airways, lung parenchyma (respiratory bronchioles and alveoli) and pulmonary blood vessels. Defining feature: NOT fully reversibel airflow limitation during forced exhalation, caused by loss of elastic recoinl and airflow obstruction from mucous hypersecretion, edma and bronospasm.
-Processes such as: airflow limitation, air trapping, gas exchange abornalities, muccus hypersecretion
-Main characteristic: inability to expire air (especially in smaller airways, getting trapped in expiration and lack of elastic recoil makes expiration deifficult -> hyperexpansion of lungs.
-Gas exchange abonormalities: Increase CO2 (hypercapnia) along with hypoxemia; V/Q mismatch occurs
-Pulmonary hypertension eventually leads to hypertropy of R ventricle (cor pulmonale) dilation and eventually right sided heart failure.
=> The predominant inflammatory cells in COPD:
- =>Primary process is inflammation: '
- Inhalation of noxious particles
- Mediators released cause damage to lung tissue and they start caussing damaage
- Airways inflamed
- Parenchyma destroyed (structures that support the alveoli)
neutrophils, macrophages, and lymphocytes which attract inflammatory mediatiors (leukotrienes) and result in structural lug changes.
^^ALL LEADING TO COPD where you have:
- COPD: Pathophysiology (schematic)
- -Breath in noxious particles leads to
- 1. Inflammation of central airways: Inflammatory cells (lymphocytes, macrophages, neutrophils) and mediators; release all wbc granulocytes
- 2. Peripheal airway remodeling
- 3. Parenchymal destruction: Imbalance b/w proteinase and antiproteinase
- 4. Pulmonary vasc changes: Thick vessels, infltration of inflammatory cells, collagen deposit and capillary bed destrcuction
Mucus Hypersecretion, cillia dysfunction, airflow limited, hyperinflated lungs, gas exchange abnormalities, pulmonary hypertension and cor pulmonale.