Asthma & Bronchiectasis

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Pathophysiology

Summary

Asthma is characterized by hyperreactive airways, featuring reversible, intermittent airway inflammation and obstructive symptoms that trap air in the distal airways. The pathology involves chronic bronchial inflammation primarily with eosinophils, enriched by helper T cells releasing IL-4 and IL-13, as well as smooth muscle hypertrophy, and increased mucus secretion. These changes are generally confined to larger airways, sparing respiratory units. Mucus plugs in bronchi and bronchioles can also occur.

Asthma often manifests through a type I hypersensitivity reaction, initiated by mast cell degranulation due to IgE coating and re-exposure to antigens like animal dander, pollen, dust, and other environmental triggers. This degranulation releases proinflammatory molecules like histamine and leukotrienes, leading to an early phase of acute asthma exacerbation featuring bronchoconstriction, mucus production, and vasodilation in large airways. This is followed by a late phase 4-8 hours later, consisting of inflammation involving eosinophils, neutrophils, and T-cells.

Chronic asthma, caused by recurrent inflammation, results in permanent structural changes to the bronchial wall, known as airway remodeling—which includes bronchial smooth muscle hypertrophy, thickened basement membrane, and hypertrophy of submucosal mucus glands. Other common triggers of asthma include viral infections, second-hand smoke, and air pollutants for non-atopic asthma, as well as aspirin, the most common cause of drug-induced asthma. Symptoms may range from acute dyspnea during exacerbations to chronic cough, particularly nocturnal cough in children. It's also highly associated with a family history of asthma or allergies.

Diagnostic features of asthma include Curschmann spirals (sloughing of bronchial epithelium) and Charcot-Leyden crystals (concretions of eosinophilic proteins) in the sputum. Spirometry often shows a FEV1/FVC ratio <0.7 and FEV1 <80%. In acute exacerbations, initial respiratory alkalosis from hyperventilation can progress to acidosis as the severity increases. Air trapping in acute exacerbations can be seen as hyperinflated lungs on CXR, characterized by a flattened diaphragm & lengthened cardiac silhouette. Severe attacks can lead to pulsus paradoxus.

Bronchiectasis involves permanent dilation of the bronchi and bronchioles, typically caused by chronic recurrent bacterial infections. This pathology is most commonly seen in the lower lobes and is marked by copious sputum production. In the U.S., the leading cause is cystic fibrosis, while tuberculosis is the most common etiology globally. Dysfunctional cilia or tumors causing airway obstruction can also initiate this condition. Bronchiectasis may present as hemoptysis due to parenchymal damage and inflammation.

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FAQs

What distinguishes asthma from emphysema in terms of airway characteristics?

Asthma is marked by hyperreactive airways, chronic bronchial inflammation primarily involving eosinophils, increased mucus secretion, and smooth muscle hypertrophy and hyperactivity. Unlike emphysema, damage to the airways in asthma are intermittent and reversible. The primary obstruction in asthma restricts air from exiting the lungs, leading to air trapping in the distal airways.

What initiates the inflammatory cascade in atopic asthma and how does it progress?

In asthma, exposure to antigens like animal dander, pollen, and dust triggers helper T cells to release interleukins 4 and 13. These interleukins signal B cells to produce IgE antibodies. Upon re-exposure to the antigen, IgE antibodies on mast cells are crosslinked, triggering degranulation. This releases proinflammatory molecules such as histamine, acetylcholine, and leukotrienes, leading to bronchoconstriction, mucus production, and vasodilation in the large airways. A late-phase inflammatory response involving eosinophils, neutrophils, and T cells occurs 4-8 hours after the initial reaction.

What structural changes can occur in the airways due to chronic asthma?

Chronic asthma leads to airway remodeling, which includes bronchial smooth muscle hypertrophy, a thickened basement membrane, and hypertrophy of submucosal mucus glands. These structural changes result from recurrent, chronic inflammation and are generally irreversible, leading to a permanent alteration of the bronchial wall.

What symptoms are associated with asthma and how is it diagnosed clinically?

Common symptoms of asthma include acute dyspnea and a chronic cough (which may be the only symptom in children) that often worsens at night. Diagnostic tests include chest x-rays, where air trapping appears as hyperinflation, and spirometry, which typically shows a FEV1/FVC ratio of less than 0.7 and an FEV1 less than 80% of the expected value.

What is bronchiectasis and what are its primary causes?

Bronchiectasis is characterized by permanent dilation of the bronchi and bronchioles, resulting from recurrent bacterial infections and inflammation that destroy the airway's supporting muscle and elastic tissue. It predominantly affects the lower lobes and is marked by copious sputum production. Common causes include chronic bacterial infections, cystic fibrosis (#1 in U.S), and tuberculosis (#1 worldwide).