Asthma vs. COPD Overview

Asthma vs. COPD

• Asthma is triggered by viruses, allergies, while COPD is triggered by smoking and pollutants.
• Asthma is more common in young ages/adults, while COPD is more frequent in older individuals.
• Asthma has associated pathologies such as rhinitis, conjunctivitis, and dermatitis while COPD does not.
• COPD is genetically linked, Asthma is not.
• Asthma inflammatory cells are eosinophils, COPD inflammatory cells are neutrophils.
• Asthma obstructions are reversible while COPD obstructions are not.
• Asthma responds to glucocorticoids by inflammation reduction, COPD responses can vary.

COPD Treatment

• Stopping smoking slows the progression of the disease.
• Patients should be immunized against influenza and Pneumococcus.
• Initial treatment involves long-acting bronchodilators.
• Patients with high blood eosinophil counts (>300 cells per μL) should be treated with ICS combined with LABA.
• Advanced COPD requires long-term oxygen therapy at home.

COPD Acute Exacerbations Treatment

• Inhaled oxygen is administered in a concentration.
• Blood gases and tissue oxygen saturation should be monitored.
• Broad-spectrum antibiotics such as ceftaroline are used if an infection is present.
• Inhaled bronchodilators are used for symptom management.
• Inhaled steroids improve quality of life.
• A systemically active glucocorticoid such as IV hydrocortisone or oral prednisolone is also administered, although efficacy is modest.

Antiasthmatic Drugs

• Cysteinyl Leukotriene Receptor Antagonists:
  • Act on leukotriene receptors CysLT1 and CysLT2.
  • Decrease acute reactions to aspirin in sensitive patients.
  • Inhibit exercise-induced asthma.
  • Used as an add-on therapy to inhaled corticosteroids and long-acting β2 agonists.
• Biologic Therapy:
  • Anti-IgE: Omalizumab, a humanized monoclonal antibody that binds to human immunoglobulin E.
  • IL-5 Antagonists: Mepolizumab and reslizumab, monoclonal antibodies that inhibit IL-5 signaling and reduce eosinophil production.
  • IL-4/IL-13 Antagonist: Dupilumab, binds to the alpha subunit of the IL-4 receptor and suppresses type 2 inflammation biomarkers.
  • Thymic Stromal Lymphoprotein (TSLP) Antagonist: Tezepelumab, a cytokine that mediates the immune system and structural cells of the airway.

Asthma Treatment Steps

• Step 1: Short-acting bronchodilator alone (SABA or SAMA)
• Step 2: Add a regular inhaled corticosteroid (ICS)
• Step 3: Add a long-acting bronchodilator (LABA or LAMA)
• Step 4: Consider theophylline or leukotriene antagonists (e.g., montelukast).
• Step 5: Add a regular oral corticosteroid (e.g., prednisolone).
• Consider Biologic treatment

Severe Acute Asthma (Status Asthmaticus)

• A medical emergency requiring hospitalization.
• Treatment includes:
  • Oxygen
  • Nebulized salbutamol
  • IV hydrocortisone
  • Oral prednisolone
• Additional measures may include:
  • Nebulized ipratropium
  • IV salbutamol
  • Aminophylline
  • Antibiotics if bacterial infection is present.
• Monitoring of PEFR or FEV1, arterial blood gases, and oxygen saturation is crucial.

Allergic Emergencies

• Anaphylaxis and angio-oedema are emergencies involving acute airways obstruction.
• Adrenaline is potentially life-saving and can be administered IM or IV.
• Patients at risk of acute anaphylaxis may self-administer IM adrenaline using a spring-loaded syringe.
• Oxygen, antihistamine treatment (chlorphenamine), and glucocorticoids are also indicated.

Chronic Obstructive Pulmonary Disease (COPD)

• Third leading cause of death worldwide, causing 3.23 million deaths in 2019.
• Cigarette smoking is the main cause.
• Air pollution may contribute to the etiology.
• Clinical features:
  • Initial attacks of morning cough during winter.
  • Chronic cough with intermittent exacerbations.
  • Progressive breathlessness.
  • Pulmonary hypertension as a late complication, leading to heart failure (cor pulmonale).
  • Exacerbations may be complicated by respiratory failure requiring hospitalization and intensive care.

COPD Pathogenesis

• Fibrosis of small airways, leading to obstruction.
• Destruction of alveoli and elastin fibers in the lung parenchyma, hallmark of emphysema.
• Emphysema causes respiratory failure by impairing gas transfer.
• Chronic inflammation (bronchitis) in small airways and lung parenchyma, characterized by increased macrophages, neutrophils, and T lymphocytes.