COPD Midterm Notes PDF

4 1 RESPIRATORY – Chronic Obstruc.ve Pulmonary Disease (COPD) Chronic Obstruc.ve Pulmonary Disease (COPD) COPD is a chronic, progressive disease characterized by persistent airflow limita.on that is not f...

4 1 RESPIRATORY – Chronic Obstruc.ve Pulmonary Disease (COPD) Chronic Obstruc.ve Pulmonary Disease (COPD) COPD is a chronic, progressive disease characterized by persistent airflow limita.on that is not fully reversible. It encompasses two overlapping phenotypes: 1. Chronic Bronchi.s: Chronic inflamma@on of the bronchi with excessive mucus produc@on. 2. Emphysema: Destruc@on of alveolar walls, leading to loss of elas.c recoil and air trapping. 1. Most Likely Cause Cause: o Tobacco Smoking: The primary cause of COPD, accoun@ng for 70% of cases in high-income countries. o Exposure to Environmental Pollutants: This includes exposure to indoor air pollu.on (biomass fuels for cooking) and outdoor air pollu.on. o Occupa.onal Exposure: Chronic exposure to dust, vapors, and irritants in the workplace can cause lung damage, promo@ng COPD. o Gene.c Muta.on (α1-An.trypsin Deficiency): This gene@c muta@on increases suscep@bility to COPD, especially in non-smokers, as the α1-an.trypsin protein normally protects lung @ssue from damage. 2. Pathophysiology The pathophysiology of COPD varies depending on the subtype, chronic bronchi.s or emphysema, but it generally includes chronic inflamma@on, airway remodeling, and increased work of breathing. Pathophysiology of Chronic Bronchi.s 1. Inflamma.on: Inhaled irritants (e.g., cigareJe smoke) promote chronic inflamma@on, predominantly involving Th1 cells, macrophages, and neutrophils. 2. Mucus Produc.on: Cytokines like IL-1β and TNF-α promote an increase in the size and number of goblet cells and mucous glands, leading to excessive mucus produc@on 3. Impaired Ciliary Func.on: The cilia responsible for mucus clearance are impaired, leading to mucus accumula@on. 4. Airway Remodeling: Chronic inflamma@on promotes smooth muscle hypertrophy, narrowing of airways, and metaplasia of epithelial cells, transforming them into squamous cells that produce thicker mucus. 5. Airflow Limita.on: Increased mucus, smooth muscle hypertrophy, and airway narrowing contribute to expiratory flow limita.on. Pathophysiology of Emphysema 1. Alveolar Destruc.on: Chronic exposure to irritants like cigareJe smoke causes proteoly.c enzymes (released by neutrophils and macrophages) to destroy alveolar walls. 2. Loss of Elas.c Recoil: Destruc@on of elas.c fibers in the alveoli leads to the loss of recoil, resul@ng in air trapping during exhala@on.  2 3. Air Trapping: The inability to exhale fully causes air to remain in the lungs, leading to hyperinfla.on and increased work of breathing. 4. Ven.la.on/Perfusion Mismatch: Damaged alveoli cause an imbalance between ven@la@on and blood flow, leading to hypoxemia and hypercapnia. 5. Pulmonary Hypertension: Prolonged hypoxia leads to vascular remodeling, promo@ng pulmonary hypertension and, in severe cases, right-sided heart failure (cor pulmonale). 3. Disease Transmission Transmission: o Not transmissible. COPD is not an infec@ous disease. However, viral and bacterial infec.ons can cause acute exacerba@ons of COPD (AECOPD), which result in hospitaliza@on. o Viral and Bacterial Exacerba.ons: Approximately 50% of COPD exacerba.ons are triggered by respiratory infec@ons, oQen caused by viral infec.ons (like rhinoviruses) and bacterial pathogens (like Haemophilus influenzae and Streptococcus pneumoniae). 4. Risk Factors The risk factors for COPD can be divided into modifiable and non-modifiable factors. Modifiable Risk Factors Smoking: The number one cause of COPD, responsible for approximately 70% of cases in high-income countries. Occupa.onal Exposure: Long-term exposure to dust, vapors, chemicals, and fumes increases COPD risk. Air Pollu.on: Indoor air pollu.on (biomass fuels) and outdoor air pollu.on are significant risk factors, especially in low- and middle-income countries. Repeated Respiratory Infec.ons: Frequent infec@ons in childhood may cause lung damage, increasing the risk of developing COPD later in life. Non-Modifiable Risk Factors Age: COPD risk increases with age, especially in people over 40 years old. Gender: COPD is more common in men than in women, but rates are increasing in women due to smoking prevalence. Gene.c Predisposi.on (α1-An.trypsin Deficiency): Deficiency in α1-an.trypsin (a protein that protects against elastase) increases the risk of emphysema, especially in non-smokers. Ethnicity: Certain popula@ons are at higher risk due to differences in gene.c suscep.bility and socioeconomic factors. Summary Table Criteria Chronic Obstruc.ve Pulmonary Disease (COPD) Most Likely Smoking (70% of cases), air pollu.on, occupa.onal exposure (dust, Cause chemicals, fumes), and α1-an.trypsin deficiency.  3 Criteria Chronic Obstruc.ve Pulmonary Disease (COPD) Chronic bronchi.s: Inflamma@on, mucus hypersecre@on, airway narrowing, Pathophysiology and airflow limita@on. Emphysema: Alveolar destruc@on, loss of elas@c recoil, air trapping, and hyperinfla@on. Not transmissible. COPD is a non-infec@ous disease. However, bacterial and Transmission viral infec@ons can trigger COPD exacerba@ons (AECOPD). Modifiable: Smoking, air pollu@on, occupa@onal exposure, repeated Risk Factors respiratory infec@ons. Non-Modifiable: Age, gender, α1-an@trypsin deficiency.