ARDS is due to a defect
Ans. d. Endothelial cells The alveolar capillary membrane is formed by two separate barriers: Microvascular endothelium and Alveolar epithelium. In ARDS the integrity of this barrier is compromised by either endothelial or epithelial injury or, more commonly, both." ARDS is a clinical syndrome associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most commonly associated with ARDS is DAD, which is characterized by a diffuse inflammation of lung parenchyma. The triggering insult to the parenchyma usually results in an initial release of cytokines and other inflammatory mediators secreted by local epithelial and endothelial cells."-http://en.wikipedia.otg/wiki/Acute_respiratory_ distress syndrome "The intimal lining of all blood vessels is a single layer of functionally and structurally heterogeneous endothelial cells depending on organ and vascular bed location. Pulmonary microvascular endothelium is a metabolically active organ essential for maintaining adequate pulmonary and systemic cardiovascular homeostasis. Noxious stimuli compromise pulmonary endothelial functional and structural integrity leading to noncardiogenic pulmonary edema and parenchymal inflammation. Thus, pulmonary endothelium has a key role in the development of acute lung injury (ALI) and its most severe form, the acute respiratory distress syndrome (ARDS). "- Curr Opin Crit Care 14:22-30 Acute Respiratory Distress Syndrome Pathogenesis: The alveolar capillary membrane is formed by two separate barriers: Microvascular endothelium Alveolar epithelium. In ARDS the integrity of this barrier is compromised by either endothelial or epithelial injury or, more commonly, both. Markers of endothelial injury and activation such as endothelin and von Willebrand factor can be detected at high levels in the serum of patients with ARDS. The acute consequences of damage to the alveolar capillary membrane include increased vascular permeability and alveolar flooding, loss of diffusion capacity, and widespread surfactant abnormalities caused by damage to type II pneumocytesQ Endothelial injury also triggers the formation of microthrombi that add the insult of ischemic injury. Hyaline membranes so characteristic of ALI/ARDS result from inspissation of protein rich edema fluid that entraps debris of dead alveolar epithelial cellsQ.
Type 1 pneumocytes
Type 2 pneumocytes
Clara cells
Endothelial cells