Pharmacotherapy of Asthma and Chronic Obstructive Pulmonary Disease (COPD)

This PowerPoint presentation provides an in-depth overview of the pharmacotherapy approaches for managing asthma and Chronic Obstructive Pulmonary Disease (COPD). It covers the pathophysiology of these respiratory conditions, the various classes of medications used, their mechanisms of action, indications, side effects, and the latest treatment guidelines. Designed for students, healthcare professionals, and anyone interested in respiratory pharmacology, this presentation offers a comprehensive understanding of current therapeutic strategies and advancements in the field.

1. Pharmacotherap y of Asthma and COPD 1 Presented By: Hrithik Dey M. Pharm Pharmacology (2 nd Sem) LIMT Presented To: Dr. Syed Salman Ali Associate Professor Department of Pharmacology ADVANCED PHARMACOLOGY – II ( MPL 201T )

2. 2 CONTENT

3. 3 ASTHMA

4. 4 What is asthma? Asthma is a chronic respiratory disease characterized by inflammation and narrowing of the airways, leading to difficulty breathing. The primary features of asthma include: Airway Inflammation : Persistent inflammation of the bronchial tubes. Bronchoconstriction : Tightening of the muscles around the airways. Hyperresponsiveness : Increased sensitivity of the airways to various stimuli. Reversible Obstruction : Unlike some other respiratory conditions, airway obstruction in asthma is typically reversible with treatment or spontaneously.

5. 5 Symptoms of asthma Common symptoms of asthma include: Wheezing : A high-pitched whistling sound when breathing. Shortness of Breath : Difficulty in breathing or feeling out of breath. Chest Tightness : A feeling of tightness or pressure in the chest. Coughing : Often worse at night or early in the morning.

6. 6 How does someone get asthma? The exact cause of asthma is not fully understood, but it is believed to result from a combination of genetic and environmental factors. Genetic Factors Family History : Asthma often runs in families. If one or both parents have asthma, their children are more likely to develop it. Atopy : A genetic tendency to develop allergic diseases such as asthma, eczema, and allergic rhinitis (hay fever). Atopic individuals are more prone to produce IgE antibodies in response to allergens.

7. 7 How does someone get asthma? Environmental Factors Allergens : Common allergens include pollen, dust mites, mold, pet dander, and cockroach droppings. Irritants : Exposure to tobacco smoke, air pollution, chemical fumes, and strong odors can trigger asthma. Respiratory Infections : Viral infections, particularly in early childhood, can increase the risk of developing asthma. Occupational Exposures : Exposure to certain workplace chemicals or dust can cause occupational asthma. Physical Activity : Exercise-induced asthma occurs when physical exertion triggers symptoms. Weather Conditions : Cold air, weather changes, and high humidity can exacerbate asthma symptoms.

8. 8 Pathogenesis Sensitization : Initial exposure to an allergen in a genetically predisposed individual leads to the production of specific IgE antibodies. Mast Cell Activation : Upon re-exposure to the same allergen, IgE antibodies on mast cells recognize the allergen, triggering mast cell degranulation and release of mediators like histamine, leukotrienes, and prostaglandins. Early Phase Reaction : These mediators cause immediate bronchoconstriction, mucus production, and vascular permeability, leading to the early phase symptoms of asthma. Late Phase Reaction : Several hours later, inflammatory cells (eosinophils, T-helper cells, neutrophils) are recruited to the airways, perpetuating inflammation and causing ongoing symptoms and airway hyperresponsiveness.

9. 9 Pathogenesis

10. 10 COPD

11. 11 What is COPD? Chronic Obstructive Pulmonary Disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. It encompasses two main conditions: Chronic Bronchitis : Long-term inflammation of the bronchial tubes, leading to mucus production and chronic cough. Emphysema : Destruction of the alveoli (air sacs) in the lungs, resulting in reduced surface area for gas exchange and difficulty in exhaling air.

12. 12 Symptoms of COPD Common symptoms of COPD include: Chronic cough: Often with mucus production. Shortness of breath: Particularly during physical activities. Wheezing: A high-pitched whistling sound when breathing. Chest tightness. Frequent respiratory infections. Fatigue. Unintended weight loss (in later stages).

13. 13 How does someone get COPD? The primary cause of COPD is long-term exposure to irritants. Environmental Factors Tobacco Smoke: The most significant risk factor. Both smoking and exposure to secondhand smoke can lead to COPD. Air Pollution: Long-term exposure to outdoor air pollution, particularly in urban areas. Occupational Exposures: Dust, fumes, and chemicals in certain work environments can contribute to COPD. Indoor Air Pollutants: Exposure to smoke from burning fuels used for cooking and heating in poorly ventilated homes. Genetic Factors Alpha-1 Antitrypsin Deficiency: A rare genetic disorder that can cause COPD. Alpha-1 antitrypsin is a protein that protects the lungs, and its deficiency can lead to lung damage.

14. 14 Pathogenesis Inflammatory Response : Long-term exposure to irritants like cigarette smoke leads to an inflammatory response in the airways and lungs. Key inflammatory cells involved are neutrophils, macrophages, and CD8+ T-lymphocytes. Chronic Bronchitis : Mucus Hypersecretion : Goblet cells and submucosal glands in the bronchi enlarge, leading to excessive mucus production and a chronic cough. Airway Inflammation : Persistent inflammation causes thickening and narrowing of the airways.

15. 15 Pathogenesis Emphysema : Alveolar Destruction : Inflammation leads to the release of proteases (enzymes that break down proteins), such as elastase, destroying alveolar walls. Loss of Elastic Recoil : The lungs lose their ability to recoil and push air out, leading to air trapping and hyperinflation. Airflow Obstruction : Both chronic bronchitis and emphysema contribute to the narrowing of the airways and difficulty in expelling air, resulting in airflow obstruction. Gas Exchange Abnormalities : The destruction of alveoli and capillaries reduces the surface area for gas exchange, leading to hypoxemia (low oxygen levels in the blood) and hypercapnia (high carbon dioxide levels).

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17. 17 Differences between Asthma & COPD Etiology : COPD is primarily caused by long-term exposure to lung irritants, especially tobacco smoke, whereas asthma is often linked to genetic predisposition and environmental allergens. Pathogenesis : Asthma involves reversible airway inflammation and hyperresponsiveness, whereas COPD is characterized by irreversible airflow obstruction and lung damage. Cellular Mechanisms : Asthma mainly involves mast cells, eosinophils, and Th2 cells, while COPD involves neutrophils, macrophages, and CD8+ T-lymphocytes. Age of Onset : Asthma can occur at any age, often starting in childhood, while COPD typically develops in middle-aged or older adults after long-term exposure to irritants.

18. 18 Pharmacotherapy of Asthma Quick-Relief Medications Short-Acting Beta2-Agonists (SABAs): Medications: Albuterol , Levalbuterol. Mechanism: Relax bronchial smooth muscle by stimulating beta2-adrenergic receptors. Use: Immediate relief of acute asthma symptoms and prevention of exercise-induced bronchospasm. Anticholinergics: Medications: Ipratropium. Mechanism: Block muscarinic receptors, reducing bronchoconstriction. Use: Often used in combination with SABAs during severe exacerbations.

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21. 21 Pharmacotherapy of Asthma Long-Term Control Medications Inhaled Corticosteroids (ICS) : Medications: Fluticasone, Budesonide, Beclomethasone. Mechanism: Reduce airway inflammation by inhibiting inflammatory cells and cytokines. Use: First-line therapy for persistent asthma. Long-Acting Beta2-Agonists (LABAs): Medications: Salmeterol, Formoterol. Mechanism: Similar to SABAs but with a longer duration of action. Use: Used in combination with ICS for long-term control; not for monotherapy.

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23. 23 Pharmacotherapy of Asthma Leukotriene Modifiers: Medications: Montelukast, Zafirlukast. Mechanism: Block leukotriene receptors, reducing bronchoconstriction and inflammation. Use: Alternative or adjunct to ICS, particularly for patients with allergic asthma. Theophylline: Mechanism: Bronchodilator that relaxes smooth muscle and has mild anti-inflammatory effects. Use: Adjunct therapy for persistent asthma; requires monitoring due to narrow therapeutic window.

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26. 26 Pharmacotherapy of Asthma Biologics : Medications: Omalizumab (anti- IgE ), Mepolizumab, Reslizumab , Benralizumab (anti-IL-5), Dupilumab (anti-IL-4/IL-13). Mechanism: Target specific pathways in the inflammatory response (e.g., IgE , IL-5, IL-4/IL-13). Use: For severe asthma with specific phenotypes (e.g., allergic or eosinophilic asthma). Combination Inhalers: Medications: Fluticasone/Salmeterol, Budesonide/Formoterol. Use: Combine ICS and LABA for convenience and improved adherence.

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28. 28 Pharmacotherapy of COPD Bronchodilators Short-Acting Beta2-Agonists (SABAs): Medications: Albuterol , Levalbuterol. Mechanism: Relax bronchial smooth muscle. Use: As-needed relief of symptoms. Short-Acting Anticholinergics: Medications: Ipratropium. Mechanism: Block muscarinic receptors, reducing bronchoconstriction. Use: As-needed relief of symptoms. Long-Acting Beta2-Agonists (LABAs): Medications: Salmeterol, Formoterol, Indacaterol. Mechanism: Relax bronchial smooth muscle for extended periods. Use: Maintenance therapy for persistent symptoms.

29. 29 Pharmacotherapy of COPD Long-Acting Anticholinergics (LAMA): Medications: Tiotropium, Aclidinium, Umeclidinium. Mechanism: Prolonged bronchodilation by blocking muscarinic receptors. Use: Maintenance therapy for persistent symptoms. Combination Bronchodilators: Medications: LABA/LAMA combinations such as Indacaterol or Glycopyrronium , Umeclidinium or Vilanterol. Use: More effective for maintenance therapy by targeting different pathways

30. 30 Pharmacotherapy of COPD Anti-Inflammatory Agents Inhaled Corticosteroids (ICS): Medications: Fluticasone, Budesonide. Mechanism: Reduce airway inflammation. Use: Typically used in combination with LABAs for patients with frequent exacerbations; not recommended as monotherapy. Phosphodiesterase-4 Inhibitors: Medications: Roflumilast. Mechanism: Reduce inflammation by inhibiting the breakdown of cyclic AMP. Use: For severe COPD with chronic bronchitis and a history of exacerbations.

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32. 32 Pharmacotherapy of COPD Combination Therapies ICS/LABA: Medications: Fluticasone/Salmeterol, Budesonide/Formoterol. Use: Maintenance therapy for patients with frequent exacerbations. LABA/LAMA: Medications: Indacaterol/ Glycopyrronium , Umeclidinium/Vilanterol. Use: For more effective symptom control. Triple Therapy: Medications: ICS/LABA/LAMA combinations such as Fluticasone/Umeclidinium/Vilanterol. Use: For patients with severe COPD and frequent exacerbations.

33. 33 Pharmacotherapy of COPD Other Treatments Mucolytics : Medications: N-acetylcysteine. Mechanism: Thin mucus to make it easier to cough up. Use: For patients with chronic bronchitis and excessive mucus production. Antibiotics : Use: For treating acute exacerbations caused by bacterial infections. Oxygen Therapy: Use: For patients with severe hypoxemia to maintain adequate oxygen levels. Vaccinations : Medications: Influenza and pneumococcal vaccines. Use: Prevent respiratory infections that can exacerbate COPD.

34. 34 References: Global Initiative for Asthma. (2023). Global strategy for asthma management and prevention. Retrieved from https://ginasthma.org/gina-reports/ Global Initiative for Chronic Obstructive Lung Disease. (2023). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Retrieved from https://goldcopd.org/gold-reports/ National Asthma Education and Prevention Program. (2007, updated 2020). Expert panel report 3 (EPR-3): Guidelines for the diagnosis and management of asthma. National Heart, Lung, and Blood Institute. Retrieved from https://www.nhlbi.nih.gov/health-topics/guidelines-for-diagnosis-management-of-asthma Mosenifar , Z. (2023). Asthma medication. Medscape. Retrieved from https://emedicine.medscape.com/article/296301-overview Mosenifar , Z. (2023). Chronic obstructive pulmonary disease (COPD) medication. Medscape. Retrieved from https://emedicine.medscape.com/article/297664-medication Kumar, V., Abbas, A. K., & Aster, J. C. (2021). Robbins and Cotran pathologic basis of disease (10th ed.). Elsevier. Bourdin, A., Burgel , P. R., Chanez , P., Garcia, G., Perez, T., Roche, N., & Tillie- Leblond , I. (2022). Recent advances in COPD: Pathophysiology, diagnosis and treatment. Respiratory Medicine and Research, 81, Article 100007. https://doi.org/10.1016/j.resmer.2022.100007

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