ARDS is characterized by diffuse alveolar damage, which is a hallmark of the condition. This involves damage to the alveolar-capillary barrier, leading to increased permeability and subsequent pulmonary edema
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The damage results in neutrophilic alveolitis and the deposition of hyaline membranes, which are fibrin-rich deposits along the alveolar walls
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Inflammatory Response:
The syndrome involves a robust inflammatory response, characterized by the activation of inflammatory cells and the release of cytokines. This response is essential for the normal host defense but becomes harmful when excessive and widespread
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Inflammation leads to apoptosis and necrosis of alveolar epithelial and endothelial cells, contributing to increased permeability and alveolar edema
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Coagulation Pathways:
Coagulation pathways are also dysregulated in ARDS, contributing to microvascular thrombosis within the lungs
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Phases of ARDS:
ARDS progresses through several phases:
Exudative Phase: Characterized by edema and inflammation.
Proliferative Phase: Involves repair processes and some degree of resolution.
Fibrotic Phase: May occur in some patients, leading to lung fibrosis and chronic impairment
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Heterogeneity and Phenotypes:
The clinical and biological presentation of ARDS is heterogeneous, with varying degrees of lung and systemic involvement. This variability has led to efforts to identify distinct phenotypes of ARDS, which could improve understanding and treatment strategies
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