XIII - The Lung Flashcards
Loss of lung volume cause by inadequate expansion of airspaces, resulting in shunting of inadequately oxygenated blood from pulmonary arteries into veins.
Atelectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 480
Atelectasis which occurs when an obstruction prevents air from reaching distal airways.
Resorption atelectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 480
Atelectasis usually associated with accumulation of fluid, blood, or air within the pleural cavity, which mechanically collapse the adjacent lung.
Compression atelectasis (aka passive or relaxation 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.
Contraction or cicatricial atelectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 481
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

Acute Respiratory Distress Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 482
Diffuse pulmonary disease characterized by limitation of airflow, usually resulting from an increase in resistance caused by partial or complete obstruction atvany level.
Obstructive pulmonary 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.
Restrictive lung disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483
Lung volumes in obstructive lung disease:FEV1FVCFEV1:FVC ratio
FEV1 - decreasedFVC - normal / increasedFEV1:FVC ratio - decreased. SEE SLIDE 13.2. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483

Lung volumes in restrictive lung diseaseFEV1FVCFEV1:FVC ratio
FEV1 - normal/decreasedFVC - decreasedFEV1:FVC ratio - near normal. SEE SLIDE 13.2. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483

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.

Emphysema(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.
Centriacinar (centrilobular) 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.
Panacinar (panlobular) emphysema. SEE SLIDE 13.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 485

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.
Distal acinar (paraseptal) emphysema. SEE SLIDE 13.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 486

Barrel-chested, dyspneic, prolonged expiration, sits forward in a hunched-over position, adequate oxygenation of oxygen. “Pink puffers”.
COPD predominantly emphysema(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”.
COPD predominantly 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 bronchitis(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.
Chronic bronchiolitis (small airway disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
Most important underlying risk factor for chronic bronchitis.
Cigarette smoking(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

Asthma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
Collections of crystalloids made up of eosinophil proteins.
Charcot-Leyden crystals. SEE SLIDE 13.5. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 492

Whorls of shed epithelium found in mucus plugs.
Curschmann spirals. SEE SLIDE 13.5. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 492

Thick, tenacious mucus plugs with Curshmann spirals and Charcot-Leyden crystals are found histologically in this disease. SEE SLIDE 13.5.

Asthma(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 470
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.

Bronchiectasis(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 471





















