Introduction

• Asthma and Chronic Obstructive Pulmonary Disease (COPD) are prevalent chronic respiratory diseases worldwide.
• Asthma-COPD Overlap (ACO) refers to patients who exhibit features of both asthma and COPD, often resulting in more severe symptoms, increased exacerbations, and higher hospitalisation rates.

Asthma

A. Key Features:

• Chronic airway inflammation, variable airflow limitation, and hyperresponsiveness.
• Symptoms are often triggered by environmental factors and allergens.

B. Pathophysiology:

1. Early Phase:

   • IgE antibodies activate mast cells, leading to the release of histamine, prostaglandins, and leukotrienes.
   • Causes smooth muscle contraction and airway tightening.

2. Late Phase:

   • Inflammatory cells like eosinophils and T-cells migrate to the lungs, enhancing bronchoconstriction and inflammation.
   • Th2 cells release cytokines (IL-4, IL-5, IL-13), leading to airway remodelling.

3. Airway Remodelling:

   • Persistent inflammation results in structural changes, including collagen deposition and epithelial thickening, potentially causing irreversible obstruction.

Chronic Obstructive Pulmonary Disease (COPD)

A. Key Features:

• Fixed and progressive airflow limitation, usually in response to long-term exposure to irritants like cigarette smoke.

B. Pathophysiology:

1. Inflammation:

   • Predominant inflammatory cells are macrophages and CD8+ T-cells, producing mediators (IL-8, IL-6, TNF-α) that cause tissue damage.
   • Oxidative stress exacerbates mitochondrial dysfunction and inflammation.

2. Emphysema:

   • Destruction of alveolar walls reduces surface area for gas exchange.
   • Loss of elastic recoil and alveolar integrity leads to airway collapse during exhalation.

3. Small Airway Disease:

   • Chronic inflammation causes structural changes and narrowing of small airways.
   • Diminished alveolar attachments contribute to airflow obstruction.

Asthma-COPD Overlap (ACO)

A. Pathophysiology:

• Likely involves a combination of mechanisms from both asthma and COPD, with contributions from eosinophilic and neutrophilic inflammation.
• Tobacco exposure and genetic predisposition are key factors.

B. Key Inflammatory Cells:

• Macrophages: Drive chronic inflammation.
• Lymphocytes: CD4+ T-cells in asthma, CD8+ T-cells in COPD, and Th17 cells in both.
• Eosinophils and Neutrophils: Both contribute to airway remodelling and tissue damage.

C. Cytokines and Chemokines:

• Elevated levels of cytokines like TSLP drive the chronic inflammatory state, contributing to ACO pathology.

D. Airway Remodelling:

• Shared mechanisms between asthma and COPD, including mucous hypersecretion and fibrosis, are worsened by tobacco smoke.

Clinical Significance for Pharmacists

• Understanding the pathophysiology of asthma, COPD, and ACO allows pharmacists to better support patient management.
• Pharmacist Role:
  • Educate on medication adherence, smoking cessation, and avoidance of known triggers.
  • Collaborate with healthcare teams to optimise individualised treatment plans for improved outcomes.

References

1. • Agarwal, A. K., Raja, A., & Brown, B. D. (2023, August 7). Chronic obstructive pulmonary disease. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK559281/

   • Hudler, A., Holguin, F., & Sharma, S. (2022). Pathophysiology of asthma-chronic obstructive pulmonary disease overlap. Immunology and Allergy Clinics of North America, 42(3), 521–532. https://doi.org/10.1016/j.iac.2022.04.008

   • Cukic, V., Lovre, V., Dragisic, D., & Ustamujic, A. (2012). Asthma and chronic obstructive pulmonary disease (COPD) – Differences and similarities. Materia Socio-Medica, 24(2), 100–105. https://doi.org/10.5455/msm.2012.24.100-105

   • Sinyor, B., & Perez, L. C. (2023, June 24). Pathophysiology of asthma. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK551579/

    

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