Asthma Overview and Causes

Asthma

• Asthma is a chronic inflammatory disorder of the airways, causing variable airflow obstruction, bronchial hyperresponsiveness, and airway remodeling. It is often reversible with treatment.

Most Likely Causes

• Inhaled Allergens (Environmental Triggers): Common triggers include dust mites, pollen, pet dander, mold, and cockroach droppings.
• Air Pollutants and Irritants: Exposure to air pollution, tobacco smoke, strong odors, and chemical irritants can trigger asthma.
• Genetic and Environmental Interactions: A genetic predisposition combined with environmental exposure increases asthma risk.
• Respiratory Infections: Viral infections (like RSV and rhinovirus) in childhood can increase asthma risk.

Pathophysiology

• Sensitization and Initial Immune Response: Inhaled allergens are processed by antigen-presenting cells (APCs), like dendritic cells, in the airways. APCs present allergens to naive T-helper cells (Th0), which differentiate into Th2 cells that secrete cytokines. IL-4 stimulates B cells to produce IgE antibodies specific to the allergen. IgE antibodies bind to mast cells, sensitizing them.
• Early Phase Response: Upon re-exposure, mast cells degranulate, releasing histamine, leukotrienes, and prostaglandins. These cause bronchoconstriction, vasodilation, increased vascular permeability (leading to mucus secretion), and airway swelling. This rapidly causes wheezing, shortness of breath, and chest tightness.
• Late Phase Response (4-8 Hours After Initial Exposure): Eosinophils, neutrophils, and basophils are recruited to the inflammation site, along with additional pro-inflammatory cytokines and cytotoxic mediators.

Airway Remodeling

• Chronic Inflammation: Uncontrolled asthma can lead to structural changes in the airways. Smooth muscle hypertrophy, goblet cell hyperplasia, and deposition of extracellular matrix proteins (subepithelial fibrosis) stiffens the airway wall. This makes the airways hyperresponsive to irritants, perpetuating the cycle.

Disease Transmission

• Not transmissible. It is a non-communicable chronic disease.

Risk Factors (Modifiable)

• Allergen Exposure: Exposure to common allergens like pollen, dust mites, animal dander, and mold.
• Air Pollution: Exposure to air pollutants.
• Occupational Exposure: Exposure to chemical irritants and fumes in certain workplaces.
• Respiratory Infections: Viral infections in childhood (e.g., RSV, rhinovirus).
• Smoking: Active and passive smoking in childhood.
• Obesity: Obesity linked to pro-inflammatory mediators from adipose tissue.
• Diet: Diets low in antioxidants, omega-3 fatty acids, and fruits/vegetables could increase risk.

Risk Factors (Non-Modifiable)

• Genetic Factors: Family history of asthma, eczema, and allergic rhinitis.
• Age: Childhood exposure to allergens and infections.
• Sex: Males at greater risk in childhood, females in adulthood.
• Ethnicity: Some studies show higher rates among certain groups.

Clinical Manifestations

• Intermittent Symptoms: Wheezing, shortness of breath, chest tightness, and cough that worsen at night, early morning, or upon exposure to triggers.
• Airway Obstruction: Difficulty exhaling, air trapping in the alveoli, prolonged expiratory phase, and reduced lung capacity.
• Hyperinflation of the Lungs: Dyspnea (shortness of breath), and use of accessory muscles.
• Severe Asthma Exacerbations: Respiratory acidosis due to CO2 retention, potentially life-threatening.