Question | Answer |
extrinsic asthma | type I hypersensitvity response involving IgE bound to mast cells, begins in childhood |
intrinsic asthma | asthma associated with chronic bronchitis, and exercise or cold induced asthma, begins in adult life |
bronchial asthma | episodic dyspnea and wheezing expiration caused by narrowing of the airways, increased sensitivity of air passages to stimuli |
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 |
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 |
centrilobular emphysema | dlilation of respiratory bronchioles; most often upper part of pulmonary lobes |
panacinar emphysema | dilation of entire acinus, distributed unifromly throughout lung; associated with loss of elasticity ( alpha one antitrypsin) |
paraseptal emphysema | dilation invvlving mainly distal part of acinus; tends to localize subjacent to pleura and interlobar septa; associated occasionaly with large subpleural bullae |
irregular emphysema | irregular involvement of aciuns with scarring within the walls of enlarged air spaces; usually a complication of various inflammatory process |
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 |
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 |
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 |
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 |
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 |
asbestosis | leads to diffuse interstitial fibrosis; characterized by ferruginous bodies (prussian blue) |
asbestosis | dense hyalinized fibrocalcific plaques of parietal pleura; predisposition to bronchogenic carcinoma, malignant mesothelioma |
bronchopneumonia | staph aureus. H. influenza, klebsiella; characterized by patchy distribution involving one or more lobes |
lobar pneumonia | strep pneumoniae; characterized by intra-alveolar exudate; may involve an entire lobe |
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) |
lung abscess | frequently caused by staph, pseudomonas, Klebsiella, or proteus; clinically manifest by fever, foul smelling, purulent sputum |
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 |