COPD Midterm Notes PDF

**RESPIRATORY -- *Chronic Obstructive Pulmonary Disease (COPD)*** **Chronic Obstructive Pulmonary Disease (COPD)** COPD is a chronic, progressive disease characterized by **persistent airflow limitation** that is **not fully reversible**. It encompasses two overlapping phenotypes: 1. **Chronic B...

**RESPIRATORY -- *Chronic Obstructive Pulmonary Disease (COPD)*** **Chronic Obstructive Pulmonary Disease (COPD)** COPD is a chronic, progressive disease characterized by **persistent airflow limitation** that is **not fully reversible**. It encompasses two overlapping phenotypes: 1. **Chronic Bronchitis**: Chronic inflammation of the bronchi with excessive mucus production. 2. **Emphysema**: Destruction of alveolar walls, leading to **loss of elastic recoil** and **air trapping**. **1. Most Likely Cause** - **Cause:** - **Tobacco Smoking**: The primary cause of COPD, accounting for **70% of cases** in high-income countries. - **Exposure to Environmental Pollutants**: This includes exposure to **indoor air pollution** (biomass fuels for cooking) and **outdoor air pollution**. - **Occupational Exposure**: Chronic exposure to **dust, vapors, and irritants** in the workplace can cause lung damage, promoting COPD. - **Genetic Mutation (α1-Antitrypsin Deficiency)**: This genetic mutation increases susceptibility to COPD, especially in **non-smokers**, as the **α1-antitrypsin protein** normally protects lung tissue from damage. **2. Pathophysiology** The pathophysiology of COPD varies depending on the subtype, **chronic bronchitis** or **emphysema**, but it generally includes chronic inflammation, airway remodeling, and increased work of breathing. **Pathophysiology of Chronic Bronchitis** 1. **Inflammation**: Inhaled irritants (e.g., cigarette smoke) promote chronic inflammation, predominantly involving **Th1 cells, macrophages, and neutrophils**. 2. **Mucus Production**: 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 production 3. **Impaired Ciliary Function**: The cilia responsible for mucus clearance are impaired, leading to mucus accumulation. 4. **Airway Remodeling**: Chronic inflammation promotes **smooth muscle hypertrophy**, **narrowing of airways**, and **metaplasia of epithelial cells**, transforming them into **squamous cells** that produce thicker mucus. 5. **Airflow Limitation**: Increased mucus, smooth muscle hypertrophy, and airway narrowing contribute to **expiratory flow limitation**. **Pathophysiology of Emphysema** 1. **Alveolar Destruction**: Chronic exposure to irritants like cigarette smoke causes **proteolytic enzymes** (released by **neutrophils and macrophages**) to destroy **alveolar walls**. 2. **Loss of Elastic Recoil**: Destruction of **elastic fibers** in the alveoli leads to the loss of recoil, resulting in **air trapping** during exhalation. 3. **Air Trapping**: The inability to exhale fully causes air to remain in the lungs, leading to **hyperinflation** and increased work of breathing. 4. **Ventilation/Perfusion Mismatch**: Damaged alveoli cause an imbalance between ventilation and blood flow, leading to **hypoxemia** and **hypercapnia**. 5. **Pulmonary Hypertension**: Prolonged hypoxia leads to **vascular remodeling**, promoting pulmonary hypertension and, in severe cases, **right-sided heart failure (cor pulmonale)**. **3. Disease Transmission** - **Transmission:** - **Not transmissible**. COPD is not an infectious disease. However, **viral and bacterial infections** can cause acute exacerbations of COPD (AECOPD), which result in hospitalization. - **Viral and Bacterial Exacerbations**: Approximately **50% of COPD exacerbations** are triggered by respiratory infections, often caused by **viral infections** (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**. - **Occupational Exposure**: Long-term exposure to **dust, vapors, chemicals, and fumes** increases COPD risk. - **Air Pollution**: **Indoor air pollution** (biomass fuels) and **outdoor air pollution** are significant risk factors, especially in low- and middle-income countries. - **Repeated Respiratory Infections**: Frequent infections 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. - **Genetic Predisposition (α1-Antitrypsin Deficiency)**: Deficiency in **α1-antitrypsin** (a protein that protects against elastase) increases the risk of emphysema, especially in **non-smokers**. - **Ethnicity**: Certain populations are at higher risk due to differences in **genetic susceptibility** and **socioeconomic factors**. **Summary Table** **Criteria** **Chronic Obstructive Pulmonary Disease (COPD)** ----------------------- ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------ **Most Likely Cause** **Smoking** (70% of cases), **air pollution**, **occupational exposure** (dust, chemicals, fumes), and **α1-antitrypsin deficiency**. **Pathophysiology** **Chronic bronchitis**: Inflammation, mucus hypersecretion, airway narrowing, and airflow limitation. **Emphysema**: Alveolar destruction, loss of elastic recoil, air trapping, and hyperinflation. **Transmission** **Not transmissible**. COPD is a non-infectious disease. However, bacterial and viral infections can trigger COPD exacerbations (AECOPD). **Risk Factors** **Modifiable:** Smoking, air pollution, occupational exposure, repeated respiratory infections. **Non-Modifiable:** Age, gender, α1-antitrypsin deficiency.