Airflow Limitation
by Jessica Pal - CD | Burnaby
1. Cellular Adaption
1.1. Hyperplasia of the goblet cells in the surface epithelium
1.2. Hypertrophy and hyperplasia of the submucosal glands in the large bronchi
1.3. Metaplasia for example ciliated epithelial cells change to stratified squamous epithelial cells
2. Acute Inflammatory Response
2.1. Triggered by cell injury. AIR eliminates the irritant and prevents it from spreading. In turn initiating wound healing
2.1.1. AIR process: chemical mediators, vascular response and cellular response
3. Mucus Hypersecretion
3.1. Hyperplasia of the goblet cells secondary to chemical mediators, histamine, and leukotriene.
4. Ciliary Dysfunction
4.1. Thick mucus makes it difficult for cilia to function.
4.2. Can be secondary to smoking.
4.3. Once ciliated epithelial cells are replaced by stratified squamous epithelial cells, it is difficult for cilia to function.
5. Pulmonary Hyperinflation
5.1. Caused by blockages in the air passages or by air sacs that are less elastic, which interferes with the expulsion of air from the lungs.
6. Pulmonary Hypertension
6.1. Alveolar hypoxia leads to compensatory vasoconstriction of the pulmonary capillaries and larger vessels. This allows blood to divert from areas of low alveolar oxygen to high. Initially this compensatory response will improve the ventilation and perfusion match.
7. Initiating Event or Irritant
7.1. long term exposure to an irritant, such as smoking and asbestos.
7.1.1. This stresses the tracheobronchial cellular environment, causing cellular adaptation to take place along with AIR process.
8. Airflow Restriction
8.1. Bronchitis
8.1.1. Inflammation of airways
8.1.2. Increased mucus production
8.1.3. Mucus plug
8.1.4. Bronchoconstriction
8.1.5. Cellular adaption
8.1.6. Airway fibrosis
8.2. Emphysema
8.2.1. Loss of elastic recoil and radial retraction