1,721,100 research outputs found
Airway pathology in asthma
No full textAbstract
This review focuses on the major cellular and structural changes present in the airways and lung parenchyma in asthma in comparison with chronic obstructive pulmonary disease (COPD) in an attempt to underline the possible mechanisms contributing to airflow limitation in these two diseases. Both asthma and COPD are characterized by a thickening of the airway wall and by the presence of an inflammatory process, but the inflammatory cells infiltrating the airway wall differ between the two diseases. In asthma, the most striking feature is the eosinophilic infiltration, whereas, in COPD, it is the CD8 T-lymphocytic infiltration of the airway wall. In the lung parenchyma, both diseases are characterized by an inflammatory process, whereas destruction and fibrosis of the alveolar walls occur in COPD but not in asthma. These cellular and structural changes may contribute to the development of airflow limitation (that characterizes both asthma and chronic obstructive pulmonary disease) by inducing either an increase in resistance or a decrease in driving pressure
Why does airway obstruction persist in asthma due to low-molecular-weight agents? A pathologist's view
No full textAbstract
The pathology of occupational asthma, which is similar to that of nonoccupational asthma, is characterized by airway infiltration of eosinophils, mast cells, and T-lymphocytes associated with thickening of the subepithelial reticular basement membrane. Since occupational asthma is caused by exposure to a sensitizing agent present in the working environment, it might be expected that cessation of occupational exposure leads to complete recovery from the disease. Unfortunately, this fa orable prognosis is observed in only a small percentage of patients with occupational asthma; in most of them, symptoms and bronchial hyperresponsiveness persist, although often at a decreased level. The few longitudinal studies performed on airway pathology in subjects with occupational asthma have shown that, after cessation of exposure to the sensitizing agent, some of the pathologic alterations (such as the subepithelial collagen deposition) improve, whereas others (such as the airway eosinophilia) persist. This latter finding suggests a role for eosinophils in the persistence of symptoms and bronchial hyperresponsiveness in the majority of asthmatic subjects even several months after removal from exposure
Attuali conoscenze su patogenesi e anatomia patologica della broncopneumopatia cronica ostruttiva
No full textStructural basis for airflow limitation in chronic obstructive pulmonary disease
No full textAbstract
The airflow limitation that characterises chronic obstructive pulmonary disease (COPD) has two main components: an increased resistance, which is due to airway obstruction, and a loss of the elastic recoil pressure of the lung, which is due to parenchymal destruction. Although it has long been known that the major site of increased resistance in COPD is the peripheral airways, recent studies have shown that central airways are involved in the disease as well. The purpose of this review is to describe the major structural and cellular changes present in peripheral airways, central airways and lung parenchyma of patients with COPD, and to underline the possible mechanisms contributing to airflow limitation in these subjects
Pathophysiology of the small airways in chronic obstructive pulmonary disease.
No full textAbstract
Chronic obstructive pulmonary disease (COPD) is characterized by a persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. From a pathological point of view, COPD is characterized by two distinct and frequently coexisting aspects: small airway abnormalities and parenchymal destruction (or emphysema). When pathological changes are localized in lung parenchyma, they will contribute to airflow limitation by reducing the elastic recoil of the lung through parenchymal destruction, as well as by reducing the elastic load applied to the airways through destruction of alveolar attachments. Conversely, when pathological changes involve the small airways, they will contribute to airflow limitation by narrowing and obliterating the lumen and by actively constricting the airways, therefore increasing the resistance. In this article we will review the structural abnormalities in small airways and their relationship with the disordered pulmonary function in COPD, in the attempt to disentangle the mechanisms contributing to the development and progression of airflow limitation in smokers. We will start by describing the normal structure of the small airways, and then observe the main pathological alterations that accumulate in this site and how they parallel pulmonary function derangement
Pathogenesis and pathology of COPD
No full textAbstract
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation. Since flow is the result of a driving pressure that promotes flow and of an opposing resistance that contradicts it, the reduction in flow observed in COPD has two main components: increased resistance, which is due to airway obstruction, and a loss of the elastic recoil pressure of the lung, which is due to parenchymal destruction. Although it has long been known that the major site of increased resistance in COPD is the peripheral airways, recent studies have shown that central airways are involved in the disease as well. The purpose of this review is to describe the major structural and cellular changes present in peripheral airways, central airways and lung parenchyma of patients with COPD, and to underline the possible mechanisms contributing to airflow limitation in these subjects
The laws of attraction: chemokines, neutrophils and eosinophils in severe exacerbations of asthma
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