In hyaline membrane disease the pathology in the lung consists of –
Correct Answer: Fibrin
Description: PATHOGENESIS. In both neonatal and adult type ARDS, there is damage to alveolocapillary wall triggered by etiologic factors listed above, and the final pathologic consequence of formation of hyaline membrane is also similar. However, how it occurs is different in the neonates than in adults. The sequence of events in the pathogenesis of both neonatal and adult ARDS is schematically illustrated in and is outlined below: Neonatal ARDS. Entry of air into alveoli is essential for formation of hyaline membrane i.e. dead born infants do not develop HMD. i)The basic defect in neonatal ARDS is a deficiency of pulmonary surfactant, normally synthesised by type II alveolar cells. The production of surfactant is normally increased sholy before bih but in prematurity and in neonatal hypoxia from any of the foregoing causes, its synthesis is decreased. The main function of alveolar surfactant being lowering of alveolar surface tension, its deficiency leads to increased alveolar surface tension which in turn causes atelectasis . ii)Atelectasis of the lungs results in hypoventilation, pulmonary hypoperfusion and ischaemic damage to capillary endothelium. iii)This results in ischaemic necrosis of the alveolocapillary wall, exudation of plasma proteins including fibrinogen into the alveoli and eventually formation of hyaline membrane on the alveolar surface containing largely fibrin. Adult ARDS: The mechanism of acute injury by etiologic agents listed above depends upon the imbalance between proinflammatory and anti-inflammatory cytokines: i) Activated pulmonay macrophages release proinflammatory cytokines such as IL8, IL1, and tumour necrosis factor (TNF), while macrophage inhibitory factor (MIF) helps to sustain inflammation in the alveoli. Number of neutrophils in the alveoli is increased in acute injury. Neutrophils on activation release products which cause active tissue injury e.g. proteases, platelet activating factor, oxidants and leukotrienes. ii) Besides the role of cytokines in acute injury, a few fibrogenic cytokines such as transforming growth factor-a (TGF-a) and platelet-derived growth factor (PDGF) play a role in repair process by stimulation of proliferation of fibroblast and collagen. In either case, injury to the capillary endothelium leads to increased vascular permeability while injured pneumocytes, especially type 1, undergo necrosis. The net effect of injury to both capillary endothelium and alveolar epithelium is interstitial and intra-alveolar oedema, congestion, fibrin deposition and formation of hyaline membranes. As a result of coating of the alveoli with hyaline membranes, there is loss of surfactant causing collapse called 'stiff lung'. There is an attempt at regeneration of alveolar cells by proliferation of type II alveolar cells so as to increase the secretion of surfactant
Category:
Pathology
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