XIII - The Lung Flashcards
(145 cards)
Atelectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 480
Loss of lung volume cause by inadequate expansion of airspaces, resulting in shunting of inadequately oxygenated blood from pulmonary arteries into veins.
Resorption atelectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 480
Atelectasis which occurs when an obstruction prevents air from reaching distal airways.
Compression atelectasis (aka passive or relaxation atelectasis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 481
Atelectasis usually associated with accumulation of fluid, blood, or air within the pleural cavity, which mechanically collapse the adjacent lung.
Contraction or cicatricial atelectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 481
Atelectasis which occurs when either local or generalized fibrotic changes in the lung or pleura hamper expansion and increase elastic recoil during expiration.
Acute Respiratory Distress Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 482
Lungs are dark red, firm, airless and heavy. There is capillary congestion, necrosis of alveolar epithelial cells, interstitial and intra-alveolar edema and hemorrhage and neutrophils in capillaries. Hyaline membrane is also characteristic, lining the alveolar ducts. SEE SLIDE 13.1
Obstructive pulmonary disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483
Diffuse pulmonary disease characterized by limitation of airflow, usually resulting from an increase in resistance caused by partial or complete obstruction atvany level.
Restrictive lung disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483
Diffuse pulmonary disease characterized by reduced expansion of lung parenchyma accompanied by decreased total lung capacity.
FEV1 - decreasedFVC - normal / increasedFEV1:FVC ratio - decreased. SEE SLIDE 13.2. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483
Lung volumes in obstructive lung disease:FEV1FVCFEV1:FVC ratio
FEV1 - normal/decreasedFVC - decreasedFEV1:FVC ratio - near normal. SEE SLIDE 13.2. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483
Lung volumes in restrictive lung diseaseFEV1FVCFEV1:FVC ratio
Emphysema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 485
Characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls without obvious fibrosis. There is thinning of the alveolar walls and loss of elastic tissue. SEE SLIDE 13.3.
Centriacinar (centrilobular) Emphysema. SEE SLIDE 13.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 485
Type of emphysema involving the central or proximal parts of the acini, formed by respiratory bronchioles, while distal parts are spared. Lungs deep pink and less voluminous, affecting the upper 2/3 of the lungs. Occurs in smokers.
Panacinar (panlobular) emphysema. SEE SLIDE 13.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 485
Type of emphysema wherein the acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal alveoli. Occurs more commonly in the lower lung zones. Occurs in a-antitrypsin deficiency.
Distal acinar (paraseptal) emphysema. SEE SLIDE 13.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 486
Type of emphysema wherein only the distal part is primarily involved. Lesion is adjacent to the pleura along the lobular connective tissue septa and at the lobe margins. More severe at the upper half of the lungs, forming bullae.
COPD predominantly emphysema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
Barrel-chested, dyspneic, prolonged expiration, sits forward in a hunched-over position, adequate oxygenation of oxygen. “Pink puffers”.
COPD predominantly chronic bronchitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
History of recurrent infections with purulent sputum, less prominent dyspnea and respiratory drive, becomes hypoxic and are pften cyanotic and obese. “Blue bloaters”.
Chronic bronchitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
Defined as persistent productive cough for at least 3 consecutive months in at least 2 consecutive years.
Chronic bronchitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
Mucosal lining of the larger airways is usually hyperemic and swollen with edema fluid, often covered by a layer of mucinous or mucopurulent secretions. Trachea and bronchi have enlarged mucus-secreting glands.
Chronic bronchiolitis (small airway disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
Characterized by goblet cell metaplasia, mucus plugging, inflammation and fibrosis, and sometimes complete obliteration of the lumen due to fibrosis.
Cigarette smoking(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
Most important underlying risk factor for chronic bronchitis.
Asthma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
Triad of 1.intermittent and reversible airway obstruction2.chronic bronchial inflammation with eosinophils3.bronchial smooth muscle cell hypertrophy and hyperreactivity SEE SLIDE 13.7
Charcot-Leyden crystals. SEE SLIDE 13.5. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 492
Collections of crystalloids made up of eosinophil proteins.
Curschmann spirals. SEE SLIDE 13.5. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 492
Whorls of shed epithelium found in mucus plugs.
Asthma(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 470
Thick, tenacious mucus plugs with Curshmann spirals and Charcot-Leyden crystals are found histologically in this disease. SEE SLIDE 13.5.
Bronchiectasis(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 471
Permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic supporting tissue, resulting from chronic necrotizing infections. There is intense acute and chronic inflammatory exudate within the walls, with mixed flora often cultured. There is also peribronchiolar fibrosis in chronic cases. SEE SLIDE 13.6.