obstructive lung disorders are characterised by blockage of airflow through the airways. Obstruction may be chronic.
This is usually a secondary bacterial infection of the bronchi, preceded by a common cold or influenza, and may also complicate measles and whooping cough in children. Viral infection depresses normal defence mechanisms, allowing pathogenic bacteria already present in the respiratory tract to multiply. Downward spread of infection may lead to bronchiolitis and/or bronchopneumonia, especially in children and in debilitated or older adults.
This common disorder becomes increasingly debilitating as it progresses. Chronic bronchitis is defined clinically when an individual has had a cough with sputum for 3 months in 2 successive years. It is a progressive inflammatory disease resulting from prolonged irritation of the bronchial epithelium, often worsened by damp or cold conditions. It is often a consequence of cigarette smoking but can also follow episodes of acute bronchitis (often caused by Haemophilus influenza or Streptococcus pneumonia) and
chronic exposure to airborne irritants such as urban fog, vehicular exhaust fumes or industrial pollutants. It develops mostly in middle-aged men who are chronic heavy smokers and may have a familial predisposition. Acute exacerbations are common, and often associated with infection. The changes occurring in the bronchi are described here.
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Increased size and number of mucus glands
The increased volume of mucus may block small airways and overwhelm the ciliary escalator, leading to reduced clearance, a persistent cough and infection.
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Oedema and other inflammatory changes
These cause swelling of the airway wall, narrowing the passageway and obstructing airflow.
Reduction in number and function of ciliated cells
Ciliated epithelium is progressively destroyed and replaced by a different type of epithelium with no cilia. This may precede neoplastic (cancerous) change. As ciliary efficiency is reduced, the problem of mucus accumulation is worsened,
further increasing the risk of infection.
Fibrosis of the airways
Inflammatory changes lead to fibrosis and stiffening of airway walls, further reducing airflow.
This is worse with physical exertion and increases the work of breathing. Ventilation of the lungs becomes severely impaired, causing breathlessness and leading to hypoxia, pulmonary hypertension and right-sided heart failure. As respiratory failure develops, arterial blood PO is reduced (hypoxaemia) and is accompanied by a rise in arterial blood PCO2
(hypercapnia). When the condition becomes
more severe, the respiratory centre in the medulla responds to rather than to hypercapnia. In the later stages, the inflammatory changes begin to affect the smallest bronchioles and the alveoli themselves, and emphysema develops (see next section). The term chronic obstructive
pulmonary disease (COPD) is sometimes used to describe this situation.
Asthma is a common inflammatory disease of the airways associated with episodes of reversible over-reactivity of the airways smooth muscle. The mucous embrane and muscle layers of the bronchi and bronchioles become thickened and the mucous glands enlarge, reducing airflow in the lower respiratory tract. The walls swell and thicken with inflammatory exudate and an inflUx of inflammatory cells, especially eosinophils. During an asthmatic attack, spasmodic contraction of bronchiolar muscle (bronchospasm) constricts the airways and there is excessive secretion of thick, sticky mucus, which further narrows the airway. Only partial expiration is achieved, so the lungs become hyperinflated and there is severe dyspnoea and wheezing. The duration of attacks usually varies from a few minutes to hours. In severe acute attacks the bronchi may be obstructed by mucus plugs, blocking airflow and leading to acute respiratory failure, hypoxia and possibly death. Non-specific factors that may precipitate asthma attacks include cold air, cigarette smoking, air pollution, upper respiratory tract infection, emotional stress and strenuous exercise.There are two clinical categories of asthma, which generally give rise to identical symptoms and are treated in the same way. Important differences include typical age of onset and the contribution of an element of allergy. Asthma, Whatever the aetiology, can usually be well controlled with inhaled anti-inflammatory and bronchodilator agents, enabling people to live a normal life.
Atopic (childhood-onset, extrinsic) asthma
This occurs in children and young adults who have atopic (type I) hypersensitivity (p. 417) to foreign protein, eg pollen, dust containing mites from carpets, feather pillows, animal dander or fungi. A history of infantile eczema or food allergies is common and there are often close family members with a history of allergy. As in hay fever, antigens (allergens) are inhaled and absorbed by the bronchial mucosa. This stimulates the production of immunoglobulin E (IgE) antibodies, which bind to the surface of mast cells and basophils round the bronchial blood vessels. When the allergen is encountered again, the antigen/ antibody reaction results in the release of histamine and other related substances that stimulate mucus secretion and muscle contraction, narrowing the airways. Attacks tend to become less frequent and less severe with age
Non-atopic (adult-onset, intrinsic) asthma
This type occurs later in adult life and there is no history of childhood allergic reactions. It can be associated with chronic inflammation of the upper respiratory tract, e.g. chronic bronchitis or nasal polyps. Other trigger factors L include exercise and occupational exposure, e.g. inhaled paint fumes. Aspirin triggers an asthmatic reaction in some people. Attacks tend to increase in severity over time and lung damage may be irreversible. Eventually, impaired lung ventilation leads to hypoxia, pulmonary hypertension and right-sided heart failure.
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