COPD: Pathogenesis
Genetic Susceptibility Environmental insult to lungs
(i.e. a1-AT Deficiency) (i.e. long term smoking, pollution, infection)
Decreased Lung’s ability to
Free radicals Inactivation lung anti-
prevent damage to lung
produced in lungs proteases
tissue
Lung inflammation
Increased oxidative stress, inflammatory cytokines, amd
protease function
Increase proteolytic destruction
of lung parenchyma
Decreased
Decreased airway Permanent enlargement
structural
elasticity ( recoil of alveoli
supports for
ability)
airway patency
Trapping of air Airway narrowing Hyper- Bullae (easily
within lungs and collapse inflated ruptured air sacs) on
lungs lung surface
Emphysema
Chronic Obstructive Pulmonary Disease (COPD)
Clinical Findings Complications