Bronchitis pathology

COPD includes chronic bronchitis and emphysema. Chronic bronchitis is defined clinically as a chronic productive cough for at least 3 months in each of two consecutive years in a patient in whom other causes have been excluded.1 Emphysema is defined pathologically as the presence of permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis.1 The major risk factor for both conditions is cigarette smoking, and many patients share characteristics of each condition. Therefore, new consensus guidelines have moved away from using these subsets and instead focus on chronic airflow limitation. 

Continued lung injury from inhalation of particulates, whatever their source, size, or composition, produces inflammation (alveolitis, bronchitis), and perhaps eventually fibrosis, a pathological reaction that distorts the architecture of the airways (Lippman et al., 1971). Lung function is compro-... 

The efficiency of mucociliary transport depends on the force of kinociUary motion and the viscosity of bronchial mucus. Both factors can be altered pathologically (e.g., in smoker s cough, bronchitis) or can be adversely affected by drugs (atropine, antihistamines). 

Although there are only four herbs in the formula, they fit the pathological change of the syndrome perfectly. In clinical practice, this formula is very effective for treating acute bronchitis, pneumonia and asthma. 

As indicated previously, bronchospasm is often present in COPD—that is, in chronic bronchitis and emphysema.121 Chronic bronchitis is a clinical diagnosis applied to a long-standing inflammation of the bronchial tree. Emphysema is a pathologic condition marked by the destruction of alveolar walls and enlargement of the terminal air spaces. 

Probably the vanadium compound to which people are most likely to be exposed is vanadium pentoxide, V205. Exposure normally occurs via the respiratory route, and the pulmonary system is the most likely to suffer from vanadium toxicity. Bronchitis and bronchial pneumonia are the most common pathological effects of exposure skin and eye irritation may also occur. Severe exposure can also adversely affect the gastrointestinal tract, kidneys, and nervous system. 

Pulse rate declined initially, but doubled over the normal rate after 10 h. Animals that died had pulmonary edema. Other clinical effects included ocular irritation, sneezing, salivation, retching, vomiting, general excitement, dyspnea, respiratory distress. Pathologic examination revealed necrosis of the epithelial lining of the respiratory tract, pneumonia, bronchitis, bronchiolitis, and fibrosis. 

Because acute bronchitis is primarily a self-limiting illness and rarely a cause of death, few data are available to describe the pathology. In general, infection of the trachea and bronchi yields... 

What are the main differences in the pathology of asthma and bronchitis ... 

Chronic bronchitis (CB), chronic pulmonary emphysema (CPE) and chronic bronchial asthma (CBA) are common diseases. The concurrence in individual patients of CB and CPE is frequent and of CBA and CB is not unusual. In the United States, the incidence of CB with or without CPE is about 15-30% of all adults (1 ). The estimates for CBA are around 3% ( ). These diseases account for a significant proportion of the morbidity and mortality from all causes. Preventive measures and the use of therapeutic modalities aimed at reversing the pathologic change would be expected to have a significant impact in decreasing the incidence of disability and premature death. 

Comparable findings have been noted in experimental bronchitis produced in rats exposed by inhalation to sulfur dioxide ( ). In that setting, the progression of the pathology is noxious inhalant, inflammatory cellular response, hypersecretion, and lastly, lymphocytic accumulations with or without bacterial pneumonitis. Comparable studies in man do not exist. Consequently there is still controversy relative to the initial pathology in human bronchitis which must occur at a stage before it can be called "chronic". 

Hers, J.F.PH. The pathology of chronic relapsing mucopurulent bronchitis with and without bronchiectasis. In "Bronchitis", edited by N.G.M.Orie and H.J.Sluiter, Charles C.Thomas, Royal Vangorcum, Assen, Netherlands, (1961) 149. 

Consequently, hypertrophy of the carotid bodies has to be expected under all pathological conditions that are accompanied by hypoxia, such as cyanotic congenital heart disease, emphysema and chronic bronchitis, but the ultrastructure of carotid bodies from human beings has been found to be normal when compared to the fine structure of carotid bodies from experimental animals (Bock et al. 1970, SimArszky and Lapis 1970). 

In normal conditions, secretion production is small and voluntary coughing is unproductive. However, when disease is present (such as in acute bronchitis), the molecular components change, production increases considerably, and sputum is formed from mucus, inflammatory cells, cell debris, and bacteria. Disruption of normal secretion or mucociliary clearance impairs pulmonary function and lung defense and increases risk of infection (14). However, it is not clear whether hypersecretion is only a marker of inflammation or a cause of pathological changes. There is even some evidence that stasis of mucus protects against inhaled material (15). 

Stasis of mucus in the airways may contribute to bronchial obstruction in patients with chronic bronchitis and also in patients experiencing an acute asthmatic episode. Mucus retention can cause pathological changes in the lungs and is thought to contribute to the... 

---