pathogenesis of emphysema

What is emphysema?

Emphysema is a form of chronic obstructive pulmonary disease (COPD) characterized by irreversible destruction of alveolar walls and permanent enlargement of airspaces distal to the terminal bronchioles, leading to reduced gas exchange surface area.

 Pathogenesis of Emphysema

The pathogenesis of emphysema involves an imbalance between proteases and antiproteases, oxidative stress, and chronic inflammation. Here's a step-by-step breakdown:

pathogenesis of emphysema


🔹 1. Exposure to Harmful Substances

  • Major risk factor: Cigarette smoking

  • Others: Air pollution, occupational dust, biomass fuel, genetic conditions like alpha-1 antitrypsin deficiency

🔹 2. Inflammatory Cell Activation

  • Inhaled irritants activate alveolar macrophages and epithelial cells.

  • These cells release chemotactic factors (like IL-8 and TNF-α) that recruit neutrophils and CD8+ T cells into the lungs.

🔹 3. Protease-Antiprotease Imbalance

  • Neutrophils and macrophages release proteolytic enzymes.

    • Elastase

    • Matrix metalloproteinases (MMPs)

  • Normally, these enzymes are controlled by antiproteases:

    • Mainly alpha-1 antitrypsin (A1AT)

  • In smokers or people with A1AT deficiency, this balance is disrupted → proteases dominate, degrading elastin and collagen in alveolar walls.

🔹 4. Oxidative Stress

  • Smoking and inflammation generate reactive oxygen species (ROS).

  • ROS further:

    • Inactivate alpha-1 antitrypsin

    • Damage lung tissue

    • Promote inflammation

🔹 5. Alveolar Wall Destruction

  • Elastin degradation causes loss of alveolar wall integrity.

  • Alveolar septa break down → coalescence of airspaces

  • Results in larger, fewer alveoli → ↓ surface area for gas exchange

🔹 6. Airflow Limitation

  • Loss of elastic recoil causes:

    • Air trapping

    • Hyperinflation

    • Difficulty in exhalation, especially during forced breathing

 Summary Table of Emphysema Pathogenesis

Step Description
1. Exposure Smoking, pollutants, A1AT deficiency
2. Inflammation Activation of macrophages, neutrophils
3. Enzyme Imbalance Protease (elastase) activity > antiprotease (A1AT)
4. Oxidative Stress ROS further damage tissue and inactivate A1AT
5. Alveolar Destruction Breakdown of elastin → loss of septa and alveolar walls
6. Airflow Limitation ↓ Elastic recoil → air trapping and hyperinflation

 Types of Emphysema (Based on Location)

  1. Centriacinar (Centrilobular) Emphysema

    • Affects respiratory bronchioles

    • Most common in smokers

    • Predominantly affects upper lobes

  2. Panacinar (Panlobular) Emphysema

    • Involves entire acinus

    • Associated with alpha-1 antitrypsin deficiency

    • Predominantly affects lower lobes

  3. Paraseptal (Distal Acinar) Emphysema

    • Involves distal part of acinus

    • Associated with spontaneous pneumothorax in young adults

  4. Irregular Emphysema

    • Scarring-related, often asymptomatic


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