COPD Pathogenesis & Clinical Findings PDF

# COPD: Pathogenesis ## Author: Yan Yu Reviewers: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* *MD at time of publication* ## Genetic Susceptibility - (i.e. a1-AT deficiency) ## Environmental Insult to Lungs - (i.e. long-term smoking, pollution, infection) ### Lung's ability to...

# COPD: Pathogenesis ## Author: Yan Yu Reviewers: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* *MD at time of publication* ## Genetic Susceptibility - (i.e. a1-AT deficiency) ## Environmental Insult to Lungs - (i.e. long-term smoking, pollution, infection) ### Lung's ability to prevent damage to lung tissue: ↓ ### Free radicals produced in lungs ### Inactivation of lung anti-proteases ## Lung Inflammation - ↑ oxidative stress, inflammatory cytokines, and protease function ### Continued, repeated injury to the bronchial tree **Infiltration of inflammatory cells, esp. neutrophils** **Goblet cell proliferation, ↑ mucus production** **Death of airway epithelium ciliated cells** **↓ airway elasticity (recoil ability)** **↑ proteolytic destruction of lung parenchyma** **↓ structural supports for airway patency** **Permanent enlargement of alveoli** **Airway fibrosis and narrowing** **Mucus trapped in airways, serves as nidus for infection** **Trapping of air within lungs** **Airway narrowing and collapse** **Hyper-inflated lungs** **Bullae (easily ruptured air sacs) on lung surface** **Chronic Bronchitis** **Emphysema** # Chronic Obstructive Pulmonary Disease (COPD) ## Clinical Findings (See relevant slides) ## Complications (See relevant slides) ## Legend: - **Pathophysiology** - **Mechanism** - **Sign/Symptom/Lab Finding** - **Complications** ## COPD: Clinical Findings ### Lung Tissue Damage - If occurring around airways - ↓elastic recoil to push air out of lungs on expiration - Lungs don't fully empty, air is trapped in alveoli (lung hyperinflation) - ↑ lung volume means diaphragm is tonically contracted (flatter) ### Airflow Obstruction - ↑ mucus production - Total expiration time takes longer than normal - Prolonged expiration - Diaphragm can't flatten much further to generate deep breaths - Breathes are rapid & shallow - To breathe, chest wall must expand out more - Barrel chest - If end-stage: diaphragm will be "flat". Continued inspiratory effort further contracts diaphragm, pull the lower chest wall inwards - Hoover's sign (paradoxical shrinking of lower chest during inspiration) ### During expiration, positive pleural pressure squeezes on airways → ↑ obstruction - More effort needed to ventilate larger lungs - Respiratory muscles must work harder to breathe - Dyspnea (Shortness of breath, especially on exertion) - Turbulent airflow in narrower airways is heard on auscultation - Expiratory Wheeze - ↓ ventilation of alveoli - ↓oxygenation of blood (hypoxemia) - ↓perfusion of body tissues (i.e. brain, muscle) - Patient tries to expire against higher mouth air pressure, forcing airways to open wider - If end-stage: Chronic fatigue causes deconditioning - Fatigue; ↓ exercise tolerance - ↓ number of epithelial ciliated cells to clear away the mucus (the cells have been killed by airway inflammation) - Chronic cough with sputum - Patient breathes with accessory muscles as well as diaphragm to try to improve airflow - Pursed-lip breathing - Muscle weakness and wasting - Tripod sitting position (activates pectoral muscles) - Neck (SCM, Scalene) muscles contracted ## Legend: - **Pathophysiology** - **Mechanism** - **Sign/Symptom/Lab Finding** - **Complications**