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lung pathology

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Question
Answer
extrinsic asthma   type I hypersensitvity response involving IgE bound to mast cells, begins in childhood  
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intrinsic asthma   asthma associated with chronic bronchitis, and exercise or cold induced asthma, begins in adult life  
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bronchial asthma   episodic dyspnea and wheezing expiration caused by narrowing of the airways, increased sensitivity of air passages to stimuli  
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bronchial athma   bronchial smooth muscle hypertrophy, hyperplasia of goblet cells, thickening'hyalinization of basement membrane, proliferation of eosinophils; complicated by superimposed infection, chronic bronchitis, and pulmonary emphysema  
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chronic bronchitis   productive cough over 3 months in 2 years, linked to cigarette smoking, air pollution, infection, hyperplasia of mucus-secreting submucousal glands, may lead to cor pulmonale  
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centrilobular emphysema   dlilation of respiratory bronchioles; most often upper part of pulmonary lobes  
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panacinar emphysema   dilation of entire acinus, distributed unifromly throughout lung; associated with loss of elasticity ( alpha one antitrypsin)  
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paraseptal emphysema   dilation invvlving mainly distal part of acinus; tends to localize subjacent to pleura and interlobar septa; associated occasionaly with large subpleural bullae  
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irregular emphysema   irregular involvement of aciuns with scarring within the walls of enlarged air spaces; usually a complication of various inflammatory process  
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bronchiectasis   permanent abnormal bronchial dilation; predisposed by chronic sinusitis; most often involves lwer lobes of both lungs; characterized by copious purulent sputum, hemoptysis, and recurrent pulmonary infection that may lead to lung abcess  
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ARDS   produced by diffuse alveolar damage with increase in alveolar capillary permeability, causing leakage of protein rich fluid into alveoli; marked by formation of intra-alveolar hyaline membrane composed of fibrin and cellular debris  
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simple coal worker pneumoconiosis   marked by coal macules around bronchioles formed by ingestion of coal dust particles by macrophages; most cases is incosequential and prodcues no disability  
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progressive massive fibrosis   marked by fibrotic nodules filled with necrotic black fluid; can result in bronchiectasis, pulmonary HTN or death from respiratory failure or right sided heart failure  
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silicosis   marked by silicotic nodules that enlarge and eventually obstruct the airways and blood vessels; increases susceptibility to TB; damage to macrophages intiates inflammatory respnse mediated by lysosomal enzymes and various chemical mediators  
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asbestosis   leads to diffuse interstitial fibrosis; characterized by ferruginous bodies (prussian blue)  
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asbestosis   dense hyalinized fibrocalcific plaques of parietal pleura; predisposition to bronchogenic carcinoma, malignant mesothelioma  
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bronchopneumonia   staph aureus. H. influenza, klebsiella; characterized by patchy distribution involving one or more lobes  
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lobar pneumonia   strep pneumoniae; characterized by intra-alveolar exudate; may involve an entire lobe  
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lung abscess   localized area of suppuration within parenchma, usually resulting form bronchial obstruction or spiration of gastric contents; seen especially in pateints predisposed to aspiration (LOC, EtOH)  
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lung abscess   frequently caused by staph, pseudomonas, Klebsiella, or proteus; clinically manifest by fever, foul smelling, purulent sputum  
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squamous cell carcinoma   central location; appears as a hilar mass and frequently results in cavitation; clearly linked to smoking; may be marked by inappropriate parathyroid hormone like activity with resultant hyperclacemia  
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