Bronchitis & Emphysema (COPD-2)

Bronchitis

Bronchitis is an inflammation of the bronchial tubes, which carry air to and from your lungs. There are two main types:

Acute Bronchitis: Typically caused by viruses, often the same viruses that cause colds and flu. It can also be caused by bacterial infections or exposure to irritants like tobacco smoke, dust, fumes, and air pollution

Duration: Short-term, usually lasts for a few weeks, often following a cold or respiratory infection

Symptoms:

  • Cough (often with or without mucus)
  • Fatigue
  • Shortness of breath
  • Slight fever and chills
  • Chest discomfort

Chronic Bronchitis

Chronic Bronchitis: is defined by the presence of a persistent cough that produces mucus and lasts for at least 3 months, with episodes occurring for at least 2 consecutive years.

Causes: Most commonly caused by smoking. Long-term exposure to air pollution, dust, or toxic gases can also contribute.

Duration: It’s a long-term condition that requires ongoing management.

Symptoms: (Blue Bloaters)

  • Persistent cough (often with mucus) for at least three months and recurring for at least two consecutive years
  • Shortness of breath
  • Frequent respiratory infections
  • Wheezing
  • Fatigue

1. Chronic Inflammation:

  • Exposure to Irritants:
    • Chronic bronchitis is often caused by prolonged exposure to irritants such as cigarette smoke, air pollution, and occupational dust.
  • Immune Response:
    • These irritants trigger an inflammatory response in the bronchial walls. The immune system responds by releasing inflammatory cells, including neutrophils, macrophages, and lymphocytes.

2. Mucus Hypersecretion:

  • Goblet Cell Hyperplasia:
    • The constant irritation leads to an increase in the number and size of goblet cells in the bronchial mucosa.
  • Submucosal Gland Hypertrophy:
    • The submucosal glands also become enlarged and produce excessive mucus.
  • Increased Mucus Production:
    • This results in excessive mucus production, which can clog the airways and lead to further obstruction.

3. Airway Obstruction:

  • Thickening of Bronchial Walls:
    • The chronic inflammation causes thickening of the bronchial walls due to edema, fibrosis, and infiltration by inflammatory cells.
  • Narrowing of Airways:
    • The thickened walls and excessive mucus reduce the diameter of the airways, making it difficult for air to flow in and out of the lungs.

4. Impaired Mucociliary Clearance:

  • Ciliary Dysfunction:
    • The cilia, which normally help to clear mucus from the airways, are damaged by inflammation and irritants.
  • Mucus Stasis:
    • This dysfunction leads to mucus stasis, increasing the risk of infections and further inflammation.

5. Recurrent Infections:

  • Bacterial Colonization:
    • The stasis of mucus provides a breeding ground for bacteria, leading to recurrent respiratory infections.
  • Exacerbations:
    • Each infection exacerbates the inflammatory response, causing further damage to the airways.

6. Structural Changes:

  • Fibrosis:
    • Chronic inflammation can lead to fibrosis, a process where the lung tissue becomes scarred and stiff.
  • Loss of Elasticity:
    • The structural changes reduce the elasticity of the bronchial walls, contributing to airflow limitation.

7. Gas Exchange Abnormalities:

  • Ventilation-Perfusion Mismatch:
    • The obstruction and structural changes lead to areas of the lung that are well-perfused but poorly ventilated, resulting in impaired gas exchange.
  • Hypoxemia:
    • This mismatch causes hypoxemia (low blood oxygen levels) and can lead to hypercapnia (high blood carbon dioxide levels) in advanced stages.

8. Systemic Effects:

  • Inflammatory Mediators:
    • The chronic inflammatory state can release mediators into the bloodstream, leading to systemic effects such as muscle wasting and cardiovascular disease.

Emphysema

Emphysema: (Entrapped air) Damage and enlarged alveoli causing the loss of lung elasticity & air trapping.

Causes

  • Smoking: The leading cause of emphysema. Cigarette smoke irritates and damages the alveoli.
  • Air pollution: Long-term exposure to air pollutants, chemical fumes, and dust can contribute to the development of emphysema.
  • Genetics: A rare genetic condition known as alpha-1 antitrypsin deficiency can cause emphysema, even in non-smokers. (Alpha-1 antitrypsin, a serine protease inhibitor (SERPIN) produced by the liver and released into the bloodstream, prevents the enzyme neutrophil elastase from damaging lung tissue. A deficiency in alpha-1 antitrypsin results in unregulated elastase activity, leading to the destruction of elastin fibers in the alveolar walls and the onset of early emphysema. This process is known as the protease-antiprotease hypothesis of emphysema development.)
  • Occupational exposure: Exposure to certain dust and chemicals at work can increase the risk. (coal miners)

Symptoms (Pink Puffers)

  • Shortness of breath: Initially during physical activities, but eventually even at rest as the disease progresses.
  • Chronic cough: Often with mucus production.
  • Wheezing: A whistling or squeaky sound when breathing.
  • Chest tightness: Discomfort or a feeling of constriction in the chest.
  • Fatigue: Persistent tiredness and lack of energy.
  • Weight loss: Unintended weight loss in advanced stages due to increased energy expenditure in breathing.

Diagnosis

  • Spirometry: A test to measure lung function and airflow obstruction.
  • Chest X-ray: Can show signs of lung damage and help rule out other conditions.
  • CT scan: Provides detailed images of the lungs to assess the extent of damage.
  • Arterial blood gas analysis: Measures the levels of oxygen and carbon dioxide in the blood.
  • Alpha-1 antitrypsin blood test: Detects a deficiency in the enzyme, which can cause emphysema.

Pathophysiology

  1. Alveolar Destruction:
    • In healthy lungs, alveoli are small, elastic structures that expand and contract with each breath, facilitating gas exchange (oxygen in, carbon dioxide out).
    • In emphysema, the walls between alveoli break down, creating larger but fewer alveoli. This reduces the surface area available for gas exchange.
  2. Loss of Elasticity:
    • The lung tissue loses its elasticity, making it difficult for the lungs to expel air. This trapped air can cause the lungs to overinflate, leading to further damage and a decrease in lung function.
  3. Protease-Antiprotease Imbalance:
    • Normally, enzymes called proteases that break down proteins are balanced by antiproteases like alpha-1 antitrypsin.
    • In emphysema, this balance is disrupted, often due to smoking or genetic factors, leading to unregulated protease activity and destruction of alveolar walls.