1 Pathology Week 13: the Lung Ver.2
Pathology week 13: the Lung ver.2 Atelectasis - either incomplete expansion of the lungs (neonatal) or collapse of previously inflated lung, producing areas of relatively airless pulmonary parenchyma - reduces oxygenation, predisposes to infection - reversible except if caused by contraction o acquired either: resorption atelectasis (obstruction airway, resorption trapped oxygen) • mucus plugging eg asthma, bronchitis, bronchiectasis, post op, FBs • mediastinum shifts towards affected lung compression atelectasis • effusion, pneumothorax, haemothorax, peritonitis – basal atelectasis • mediastinum shift away from affected lung contraction atelectasis • when local or general fibrotic changes in lung prevent full expansion Acute Lung Injury - a spectrum of pulmonary lesions (endothelial and epithelial) - initiated by many factors - susceptibility my be heritable - mediators include cytokines, oxidants, growth factors (incl TNF, IL1, IL6, IL10, TGFβ) - may manifest as congestion, oedema, surfactant disruption, atelectasis - may progress to ARDS or acute interstitial pneumonia Pulmonary Oedema - most common haemodynamic mechanism: ↑ hydrostatic pressure in LVF - heavy, wet lungs – initially basal due to greater hydrostatic pressure - alveolar capillaries engorged, intra-alveolar granular pink precipitate, alveolar microhaemorrhages and haemosiderin-laden macrophages (“heart failure” cells ) - longstanding LVF – many haemosiderin-laden macrophages, fibrosis, thickening alveolar walls – lungs firm and brown (brown induration) Oedema caused
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