COPD Fibrosis (1)

COPD Fibrosis (1) - COPD (Obstructive) Fibrosis...

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COPD (Obstructive) Fibrosis (Restrictive)
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C h a r a c t e r i s t i c s *breakdown of alveolar wall and chronic bronchitis (inflammation of the airway) – floppy airways - Air exhaled is much slower o Problem w/ exhalation NOT inhalation o FEV(1) = dec o FEV (1) / FVC = dec because force vital capacity decreased due to dec in exhalation (normal = 80%) o FRC = inc - The destruction of lung architecture (alveolar wall) abnormal lung function resulting in FLOW- LIMITING mechanism (3 factors) 1) Loss of radial traction of the airways (parenchyma) airway more easily compressed floppy airways [[more dynamic compression]] 2) Increased resistance of the peripheral airways (because the airways were destroyed along with the alveolar walls) AWR = increase decrease expiratory flow Elastic recoil = decrease **lungs not emptying as much air as it would normally** air-trapping 3) Driving pressure (Alveolar pressure – interpleural pressure) is reduced due to Compliance inc (compliance also increase lung volume) more dynamic compression b/c you decrease alveolar pressure - Compliance = inc decreased expiratory force - Elastic recoil = dec - Increase vol also decreases alveolar pressure leads to more dynamic compression (increasing work of breathing **These factors can be seen in normal patients during forced expiration BUT will be the normal breathing in COPD patients ***This flow-limiting mechanism LIMITS increase in ventilation trigger by exercise - V/Q mismatch Affects gas diffusion and is caused by destruction of the normal architecture o D(LCO) = dec o Loss of vascular cross sectional area (not due to increase in diffusion barrier) o Capillary destruction V/Q (increase) – Refer to the Ventilation More blood flow going to lower V/Q areas of the lungs (these area have partly
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This note was uploaded on 09/14/2011 for the course PHARM ps taught by Professor Staff during the Spring '11 term at UCSD.

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COPD Fibrosis (1) - COPD (Obstructive) Fibrosis...

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