The Lungs

Figure 5.1

Normal lungs, gross

The external surfaces in radiologic orientation show upper, middle, and lower lobes on the right and upper and lower lobes on the left (right lung at left of left panel ). In the right panel the cross-section of normal right lung shows minimal (darker) posterior and inferior congestion. There is minimal anthracotic pigment from dusts in the air breathed in, scavenged by pulmonary macrophages, and transferred to pleural lymphatics to make them appear as streaks of grayish black discoloration.

Figure 5.2

Normal lungs, radiographs

These upright chest radiographs reveal the normal posterior to anterior (PA) (left panel) and lateral (right panel) projection appearance of the lungs in a normal adult man. The darker air density represents the aerated lung parenchyma, with soft tissue and bone of the chest wall and hilum brighter. The normal PA heart shadow is approximately the width of the left lung.

Figure 5.3

Normal lung, gross

The smooth, glistening pleural surface of a lung is shown here. This patient had marked pulmonary edema, which increased the amount of fluid in the lymphatics (↑) that run between lung lobules, outlined here by the white markings that are the lymphatic channels. Anthracotic pigmentation derived from inhaled carbonaceous dusts is also carried by the lymphatics to the pleural surfaces and to hilar lymph nodes. Small amounts of anthracotic pigment are present in nearly every adult lung (but not this patient who lived in a rural setting). Smokers have more anthracosis.

Figure 5.4

Normal lung, CT image

This chest CT scan in “bone window” reveals the normal appearance of the right ( ) and left (×) lungs—essentially black from air density—in a normal man. Contrast material in the bloodstream gives the right (▪) and left (□) chambers of the heart and the aorta (✚) a bright appearance. Bone of the vertebral body and ribs also appears bright. Soft tissues are shades of gray. The anterior to posterior (AP) diameter is normal.

Figure 5.5

Normal adult lung, microscopic

The delicate alveolar walls of the lung have attenuated cytoplasm of the alveolar type I epithelial cells that cannot easily be distinguished from the endothelial cells of the capillaries present within the alveolar walls. These thin alveolar walls enable efficient gas diffusion and exchange so that the alveolar-arterial (A-a) oxygen gradient is typically less than 15 mm Hg in young, healthy individuals, although the A-a gradient may increase to greater than 20 mm Hg in elderly individuals. Occasional alveolar macrophages ( ) clearing debris can be found within the alveolar lumens. The type II pneumocytes (▲) are rounded and produce surfactant that reduces surface tension to increase lung compliance and help to keep the alveoli expanded.

Figure 5.6

Atelectasis, gross

This right lung ( ) is collapsed (atelectatic) because blood filled the pleural cavity (hemothorax) after chest wall trauma. Residual dark red blood remains following removal at autopsy. Such a compression atelectasis can also result from filling the potential pleural space of the chest with air (pneumothorax), transudate (hydrothorax), lymph (chylothorax), or purulent exudate (empyema). The collapsed lung is not aerated, creating a ventilation/perfusion (V/Q) mismatch, acting as a shunt similar to a cardiac right-to-left shunt that bypasses the lungs, with blood gas parameters from collapsed lung approaching the mixed venous blood entering the right heart.

Figure 5.7

Atelectasis, x-ray

This chest radiograph reveals a right tension pneumothorax with expansion of the right chest cavity and displacement of the heart to the left. A pneumothorax occurs with a penetrating chest injury, inflammation with rupture of a bronchus to the pleura, rupture of an emphysematous bulla, or barotrauma from positive-pressure mechanical ventilation. The escape of air into the pleural space eliminates the negative pressure of the thoracic cavity and collapses the lung. With “tension” pneumothorax there is shifting the mediastinum because a ball-valve air leak is increasing the amount of air (here in the right chest cavity). A chest tube can be placed to reexpand the lung. In contrast, a resorption atelectasis from airway obstruction and resorption of air in distal lung parenchyma leads to collapse with a shift of the mediastinum toward the involved lung.

Figure 5.8

Atelectasis, CT image

This chest CT scan in bone window shows a large right pleural effusion (▪) and a smaller left pleural effusion (□). These pleural effusions (dark gray fluid density) resulted from right heart failure (here as a consequence of rheumatic mitral stenosis with chronic pulmonary congestion and subsequent pulmonary hypertension). Note the enlargement of the right atrium (♦). This large effusion has produced bilateral atelectasis of the lower lobes, characterized by a small, dense crescent of light gray nonaerated lung tissue in the region of the effusion on each side (▲).

Figures 5.9 and 5.10

Pulmonary edema, x-rays

Pulmonary passive congestion from left heart failure (cardiogenic edema) increases interstitial markings, and edema fluid spills into alveoli, creating infiltrates. This PA chest radiograph (left panel) shows pulmonary congestion and edema throughout all lung fields. The pulmonary veins are prominent from distension near the hilum. The left heart border is prominent because of left atrial enlargement. This patient had mitral stenosis. The PA chest radiograph (right panel) shows extensive congestion and edema throughout all lung fields from severe congestive heart failure from cardiomyopathy, and the edema obscures the cardiac silhouette and diaphragmatic leaves.

Figures 5.11 and 5.12

Pulmonary edema, microscopic

The alveoli (left panel) are filled with a smooth to slightly floccular pink material (♦) characteristic of pulmonary edema. Capillaries within alveolar walls are congested, filled with many red blood cells (RBCs). Pulmonary congestion with edema is common in patients with heart failure (with elevated B-type natriuretic peptide) and in areas of inflammation of the lung. More marked pulmonary congestion (right panel) with dilated capillaries and leakage of blood into alveolar spaces, leading to the appearance of hemosiderin-laden macrophages (“heart failure cells”) containing brown cytoplasmic hemosiderin granules (←) from breakdown of RBCs.

Figure 5.13

Diffuse alveolar damage, gross

This lung is virtually airless, diffusely firm, and rubbery with a glistening appearance on cut section. Clinically, this is known as acute respiratory distress syndrome (ARDS). Diffuse alveolar damage (DAD) is a form of acute restrictive lung disease resulting from capillary wall endothelial injury from multiple causes, including pulmonary infections, sepsis, inhaled noxious gases, microangiopathic hemolytic anemias, trauma, oxygen toxicity, aspiration, fat embolism, or opiate overdose. DAD causes severe hypoxemia. The lung diffusing capacity for carbon monoxide (D lco ) is reduced. Diseases that affect the alveolar walls (DAD or emphysema) or the pulmonary capillary bed (thromboembolism or vasculitis) decrease the D lco .

Figure 5.14

Diffuse alveolar damage, CT image

This chest CT scan in “lung window” making soft tissues brighter reveals extensive bright patchy bilateral ground-glass opacifications of the lung parenchyma consistent with diffuse alveolar damage (DAD). The acute phase of DAD can develop within hours of capillary injury, with increased vascular permeability and leakage of interstitial fluid into alveoli, forming diffuse “ground-glass” infiltrates. The exuded blood proteins can form hyaline membranes. Injury to type II pneumocytes diminishes surfactant production and reduces lung compliance. Release of interleukin-1 (IL-1), IL-8, and tumor necrosis factor (TNF) promotes neutrophil chemotaxis and activation that further potentiates parenchymal injury.

Figure 5.15

Diffuse alveolar damage, microscopic

At low magnification (right panel) all alveoli are filled with fibrin-rich (pink) edema fluid along with few inflammatory cells (noncardiogenic edema with alveolar injury) from damage to endothelial and epithelial cells. At medium magnification (left panel) the alveolar walls are congested with red blood cells and expanded from inflammation with acute diffuse alveolar damage (DAD), a form of acute lung injury (ALI). Oxygenation is impaired from reduced alveolar ventilation and from diffusion block. ALI and DAD may be part of multiorgan failure.

Figure 5.16

Diffuse alveolar damage, microscopic

Diffuse alveolar damage (DAD) is the final common pathway for various severe lung injuries. In early DAD, pink hyaline membranes ( ) line the alveoli. Later in the first week after lung injury, the hyaline membranes resolve, and macrophage proliferation occurs. If the patient survives more than a week, interstitial inflammation and fibrosis become increasingly prominent, and lung compliance decreases further. There are ventilation/perfusion (V/Q) mismatches. High oxygen tension is needed to treat the hypoxia resulting from DAD, and oxygen toxicity from this therapy exacerbates DAD.

Figure 5.17

Pulmonary centrilobular emphysema, gross

The two major types of emphysema are centrilobular (centriacinar) and panlobular (panacinar). The former involves primarily the upper lobes, as shown here, whereas the latter involves all lung fields, particularly the bases. The central lobular loss of lung tissue with intense black anthracotic pigmentation (←) is apparent as “dirty holes.” In contrast to increased risk for lung cancer, which diminishes when a smoker stops smoking, the lung tissue loss with emphysema is permanent. Centriacinar emphysema initially involves loss of the respiratory bronchioles in the proximal portion of the acinus, with sparing of distal alveoli, and this type is most typical for cigarette smokers.

Figure 5.18

Pulmonary emphysema, radiograph

This PA chest radiograph shows increased interstitial markings with an irregular architecture, and increase in total lung volume with bilateral flattening (↓) of the diaphragmatic leaves, consistent with centrilobular emphysema. The diaphragmatic flattening reduces the efficiency of muscular contraction and lung excursion, increasing the work of breathing. As the severity of emphysema increases, affected individuals begin to use accessory muscles of respiration, such as intercostal muscles and sternocleidomastoids. Affected individuals may also exhibit “pursed lip” breathing to increase central airway pressure to keep distal airways from collapsing as a consequence of the increased lung compliance. Most of the increase in total lung capacity seen with emphysema results from an increase in residual volume.

Figure 5.19

Pulmonary hypertension, CT image

This chest CT scan in “lung window” reveals prominence of bright vascular parenchymal lung markings (▼) from pulmonary hypertension. There are also darker parenchymal lucencies (▲) consistent with a pattern of centriacinar emphysema. The AP diameter of the chest is increased, as a consequence of increased total lung volume, mainly the result of increased residual volume. When the pulmonary vascular bed is reduced, here from loss of lung tissue, then pulmonary arterial pressures increase.

Figures 5.20 and 5.21

Pulmonary panacinar emphysema, gross and chest x-ray

Panacinar emphysema occurs with loss of all portions of the acinus from the respiratory bronchiole to the alveoli. This pattern is typical for α 1 -antitrypsin deficiency. The bullae seen here are most prominent in the lower lobe (→) on the left . The typical chest radiographic appearance of panlobular emphysema, with increased lung volume, worst (darkest) areas in lower lobes, and diaphragmatic flattening, is shown on the right .

Figure 5.22

Distal acinar (paraseptal) emphysema, gross

This more localized form of emphysema can follow focal scarring of the peripheral lung parenchyma with injury from infections and pollutants, including cigarette smoke. Because this process is focal, pulmonary function is not seriously affected, but the peripheral location of the bullae, which can be 2 cm in size or more, along septa may lead to rupture into the pleural space, causing spontaneous pneumothorax. This is most likely to occur in young adults, with sudden onset of dyspnea. Two small bullae (→↓) are seen here just beneath the pleural surface.

Figure 5.23

Distal acinar (paraseptal) emphysema, CT image

The two small foci (◄▲) are subpleural in upper lung. There is slight thickening of the walls of the darkly attenuated emphysematous spaces in these foci. The lucencies within them are <1 cm in size. A lucency 1 cm or larger is called a subpleural bleb and if >2 cm may be termed a bulla. Abnormalities with pulmonary function testing may be absent or minimal. Remaining lung tissue appears normal here, but in some cases interstitial disease may also be present.

Figure 5.24

Pulmonary emphysema, microscopic

There is loss of distal airspaces: bronchioles, alveolar ducts, and alveoli. The remaining airspaces become dilated as shown here; overall, there is less surface area for gas exchange. Emphysema leads to loss of lung parenchyma, loss of elastic recoil with increased lung compliance, and increased pulmonary residual volume with increased total lung capacity. There is decreased diaphragmatic excursion and increased use of accessory muscles for breathing. Over time, with reduced ventilation and air trapping, the partial pressure of arterial oxygen (Pa o 2 ) decreases, the partial pressure of carbon dioxide (Pa co 2 ) increases, and respiratory acidosis ensues, with renal compensation.

Figure 5.25

Interstitial emphysema, gross

Air leaking from the lung has produced clear bubbles (♦) of gas within subcutaneous adipose tissue of the chest wall, as shown here with pale red skeletal muscle at the top. Entrance of air into the connective tissue of the lung, mediastinum, or subcutaneous tissue produces interstitial emphysema . The term pulmonary interstitial emphysema is used when air leaks within the lung into peribronchovascular sheaths, interlobular septa, and visceral pleura. Trauma and mechanical ventilation are risk factors for this condition.

Figure 5.26

Interstitial emphysema, CT image

Note the decreased attenuation (→) of the subcutaneous fat on the right and anterior regions, essentially the same density as the posterior lung (♦) in this upper abdominal CT scan. An air leak from the lungs following trauma, particularly with tension pneumothorax, or around a chest tube, or positive pressure ventilation, may produce dissection of air into soft tissues. On examination with subcutaneous emphysema there can be crepitus. It looks worse than it feels. If air dissects into the mediastinum or around large airways, pulmonary function can be compromised.

Figure 5.27

Chronic bronchitis, microscopic

Note increased numbers of chronic inflammatory cells (♦) in the submucosal region. Chronic bronchitis does not have characteristic pathologic findings but is defined clinically as a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years. Most patients are smokers, but inhaled air pollutants can exacerbate chronic bronchitis. Often, there is parenchymal destruction with features of emphysema as well, and there is often overlap between pulmonary emphysema and chronic bronchitis, with patients having elements of both. Secondary infections are common and worsen pulmonary function further.

Figure 5.28

Chronic bronchitis, microscopic

In the wall of this large bronchus is cartilage (♦) and the bronchial wall is expanded from increased size of mucus-secreting glands ( ) along with chronic inflammatory cell infiltrates (□) to expand the bronchial wall and promote airway obstruction. At the right, above the respiratory epithelium, is increased mucus (✚) in the airway. In this form of COPD patients adapt to hypoventilation with decreased oxygenation and hypercarbia, (without use of accessory muscles increasing caloric demand with weight loss but maintenance of oxygenation with pure emphysema), they appear to be cyanotic with weight gain from peripheral edema.

Figure 5.29

Bronchial asthma, gross

These are the hyperinflated lungs of a patient who died with status asthmaticus. The two major clinical forms of asthma can overlap and symptomatically present similarly. With atopic (extrinsic) asthma, there is typically an association with atopy (allergies) mediated by type I hypersensitivity; asthmatic attacks are precipitated by contact with inhaled allergens. This form occurs most often in childhood. In nonatopic (intrinsic) asthma, more likely to occur in adults with hyperreactive airways, asthmatic attacks are precipitated by a variety of stimuli such as respiratory infections and exposure to cold, exercise, stress, inhaled irritants, and drugs such as aspirin.

Figure 5.30

Bronchial asthma, gross

This cast of the bronchial tree is formed from inspissated mucous secretions and was coughed up during an acute asthmatic attack. The outpouring of mucus from hypertrophied bronchial submucosal glands, bronchoconstriction, and dehydration all contribute to the formation of mucous plugs that can block airways in asthmatic patients, exacerbating airflow obstruction. The result is sudden, severe dyspnea with wheezing and hypoxemia. A severe attack, known as status asthmaticus, can be life threatening.

Figure 5.31

Bronchial asthma, microscopic

Between the bronchial cartilage (♦) on the right and the bronchial lumen (▪) filled with mucus on the left is a submucosa widened by smooth muscle hypertrophy ( ), edema, and an inflammatory infiltrate with many eosinophils. These are changes of bronchial asthma, more specifically, atopic asthma from type I hypersensitivity to allergens. Sensitization to inhaled allergens promotes a subtype 2 helper T-cell (T H 2) immune response with release of interleukin-4 (IL-4) and IL-5 promoting B-cell IgE production and eosinophil infiltration and activation. The peripheral blood eosinophil count and/or sputum eosinophils can be increased.

Figure 5.32

Bronchial asthma, microscopic

Numerous eosinophils in sputum are prominent from their bright-red cytoplasmic granules in this case of bronchial asthma. In the early phase of an acute atopic asthmatic attack, there is cross-linking by allergens of IgE bound to mast cells, causing degranulation with release of biogenic amines and cytokines producing an immediate response in minutes with bronchoconstriction, edema, and mucous production. A late phase develops over hours from activation of the arachidonic acid pathway producing cytokines such as leukotrienes promoting further leukocyte infiltration with continued edema and mucous production.

Figure 5.33

Bronchial asthma, microscopic

Sputum analysis with an acute asthmatic episode may reveal Charcot-Leiden crystals (▲) derived from breakdown of eosinophil granules. Pharmacologic therapies used emergently to treat asthma include short-acting β-adrenergic agonists, such as albuterol, and longer-acting agents such as salmeterol. Theophylline, a methylxanthine, promotes bronchodilation by increasing cyclic adenosine monophosphate (cAMP), whereas anticholinergics, such as tiotropium, also enhance bronchodilation. Long-term asthma control includes use of inhaled glucocorticoids, leukotriene inhibitors such as zileuton, receptor antagonists such as montelukast, and mast cell–stabilizing agents like cromolyn sodium.

Figure 5.34

Bronchiectasis, gross

This focal area of dilated bronchi (↓) is typical of a less common form of obstructive lung disease. Bronchiectasis tends to be a localized process associated with diseases such as pulmonary neoplasms and aspirated foreign bodies that block a portion of the airways, leading to obstruction with distal airway distention mediated by ongoing inflammation and airway destruction. Widespread bronchiectasis is more typical in patients with cystic fibrosis, who have recurrent infections and obstruction of airways by mucous plugs throughout the lungs. A rare cause is primary ciliary dyskinesia in respiratory epithelium, seen with Kartagener syndrome.

Figure 5.35

Bronchiectasis, chest radiograph

This bronchogram shows saccular bronchiectasis involving the right lower lobe. The bright contrast material fills dilated bronchi, giving them an irregular saccular outline. Bronchiectasis occurs with ongoing obstruction and/or infection with inflammation and destruction of bronchi so that there is permanent bronchial dilation. When these dilated bronchi are present, the patient is predisposed to recurrent infections because of stasis in these airways. Copious purulent sputum production with cough is a common clinical manifestation. There is risk for sepsis and dissemination of the infection elsewhere. In cases of severe, widespread bronchiectasis, cor pulmonale can occur.

Figure 5.36

Bronchiectasis, microscopic

This dilated bronchus has an irregular outline in which the mucosa and bronchial wall are not seen clearly because of the necrotizing inflammation (▪) with tissue destruction. Bronchiectasis is not a specific disease, but a consequence of another disease process that promotes airway obstruction and inflammation that eventually dilates airways out to peripheral lung. Innate immune defenses provided by normal structure and function are compromised, and recurrent infection ensues.

Figure 5.37

Idiopathic pulmonary fibrosis, radiograph

The increased brighter interstitial markings in all lung fields are a consequence of idiopathic pulmonary fibrosis. Affected patients have continuing loss of lung volumes; pulmonary function studies show reduced forced vital capacity (FVC) and forced expiratory volume at 1 second (FEV 1 ). Because both are reduced, the FVC/FEV 1 ratio generally remains unchanged. These reductions are typically proportional with restrictive lung diseases such as idiopathic pulmonary fibrosis. This disease is probably mediated by an abnormal inflammatory response to alveolar wall injury. Patients may survive weeks to years, depending on the severity, with eventual end-stage honeycomb fibrosis. Treatment with tyrosine kinase inhibitors suppressing fibrogenesis may slow disease progression.

Figure 5.38

Idiopathic pulmonary fibrosis, CT image

This chest CT scan in “lung window” mode shows very prominent bright interstitial markings most prominent in the posterior lung bases. There are also smaller darker lucent areas that represent honeycomb change, a characteristic feature of usual interstitial pneumonitis (UIP), a descriptive term for an idiopathic and progressive restrictive lung disease that can affect middle-aged individuals with progressive dyspnea, persistent nonproductive cough, and hypoxemia. Patients develop pulmonary hypertension and cor pulmonale as a result. A gain of function mutation of MUC5B encoding a mucin precursor protein providing airway mucus for innate defense may play a role in idiopathic pulmonary fibrosis.

Figure 5.39

Honeycomb change, gross

Regardless of the etiology for restrictive lung diseases, many of them eventually lead to extensive pulmonary interstitial fibrosis. The gross appearance shown here in a patient with organizing diffuse alveolar damage is known as “honeycomb lung” because of the appearance of the irregular residual small dilated airspaces between bands of dense fibrous interstitial connective tissue. The lung compliance is markedly diminished so that patients receiving mechanical ventilation require increasing positive end-expiratory pressure (PEEP), predisposing them to airway rupture and development of interstitial emphysema.

Figure 5.40

Honeycomb change, microscopic

There is dense fibrous connective tissue (♦) surrounding residual airspaces filled with proteinaceous fluid. These remaining airspaces have become dilated and lined by metaplastic bronchiolar epithelium as seen here. The extent of the fibrosis determines the severity of disease, which is marked by progressively worsening dyspnea. The maladaptive repair process of injured lung that produces fibroblast proliferation and collagen deposition is progressive over time. This leads to a marked diffusion block to gas exchange. Lung volumes including vital capacity and residual volume become diminished.

Figure 5.41

Ferruginous bodies, microscopic

The etiology for interstitial lung disease is apparent here as asbestosis. The inhaled long, thin object known as an asbestos fiber becomes coated with iron and calcium, then is called a ferruginous body, several of which are seen here with a Prussian blue iron stain. Ingestion of these fibers by macrophages sets off a fibrogenic response through release of cytokine growth factors that promote continued collagen deposition by fibroblasts. Some houses, business locations, and ships still contain construction materials with asbestos, particularly insulation, so care must be taken to prevent inhalation of asbestos fibers when doing remodeling or reconstruction.

Figure 5.42

Pneumoconiosis, radiograph

This PA chest radiograph shows interstitial fibrosis with irregular bright infiltrates. There is a right pleural plaque (▲) with brighter calcification. Significant exposure to asbestos fibers in inhaled dusts has occurred. The fibers are phagocytized by macrophages, which secrete cytokines such as transforming growth factor-β, which can activate fibroblasts that produce collagenous fibrosis that increases over time, and damaged tissues can undergo dystrophic calcification. The amount of dust inhaled and the length of exposure determine the severity of disease. Patients may remain asymptomatic for years until progressive massive fibrosis reduces pulmonary vital capacity.

Figure 5.43

Pleural fibrous plaques, gross

Seen here on the pleural aspects of the diaphragmatic leaves are multiple tan-white pleural plaques (→) typical for pneumoconioses and of asbestosis in particular. Chronic inflammation induced by the inhaled dust particles results in fibrogenesis. Asbestosis also increases the risk for bronchogenic carcinoma, particularly in smokers.

Figure 5.44

Pleural fibrous plaque, microscopic

This thick fibrous pleural plaque is composed of dense laminated layers of collagen that give a pink appearance with hematoxylin and eosin (H&E) staining and a white to tan appearance grossly. Adjacent lung tissue is seen below (♦). Progressive pulmonary fibrosis leads to restrictive lung disease. Reduction in pulmonary vasculature leads to pulmonary hypertension and cor pulmonale with subsequent right-sided congestive heart failure manifested by peripheral dependent edema, hepatic congestion, and body cavity effusions.

Figure 5.45

Coal worker’s pneumoconiosis, microscopic

Anthracotic pigment deposition in the lung is common but ordinarily is not fibrogenic because the amount of inhaled carbonaceous dusts from environmental air pollution is not large. Smokers have more anthracotic pigmentation because of tobacco smoke tar but still do not have significant disease from the carbonaceous pigment. Massive amounts of inhaled particles (as in “black lung disease” in coal miners), elicit a fibrogenic response to produce coal worker’s pneumoconiosis with the coal macule seen here, accompanied by progressive massive fibrosis. There is increased risk for tuberculosis and lung cancer.

Figure 5.46

Silicosis, microscopic

The most common pneumoconiosis is silicosis. There is an interstitial pattern of disease with eventual development of larger silicotic nodules (♦) that can become confluent. The silicotic nodules shown here are composed mainly of bundles of interlacing pale pink collagen, and there is a surrounding modest chronic inflammatory reaction. More exposure to inhaled silica and an increasing length of exposure determine the amount of silicotic nodule formation and the extent of restrictive lung disease, which is progressive and irreversible. Silicosis increases the risk for lung carcinoma. Impaired macrophage function increases the risk for mycobacterial infections.

Figure 5.47

Pneumoconiosis, radiograph

This chest radiograph shows so many bright, irregularly shaped silicotic nodules, mainly in the upper lung fields, that they have become confluent (progressive massive fibrosis) and have resulted in severe restrictive lung disease. This patient became severely dyspneic. All lung volumes are diminished on spirometry. Occupations such as mining and construction with dust exposure but without proper respiratory protection put workers at risk for pneumoconiosis. Silicates compose more than 90% of rock forming the earth’s crust.

Figure 5.48

Silica crystals, microscopic

By polarized light microscopy, bright white polarizable crystals of varying sizes are shown here within a silicotic nodule. The silica crystals that are inhaled and reach the alveoli are ingested by macrophages, which secrete cytokines to induce a predominantly fibrogenic response. Because the inorganic matrix of the crystals is never completely digested, this process continues indefinitely and is made worse by repeated exposure to dusts containing silicates. The result is the production of many scattered nodular foci of collagen deposition in the lung (silicotic nodules) and eventual restrictive lung disease leading to cor pulmonale.

Figure 5.49

Eosinophilic granuloma, microscopic

Bilateral pulmonary nodules averaging 0.1 to 0.5 cm in size can occur with eosinophilic granuloma, an inflammatory process including a mixture of inflammatory cells with lymphocytes, plasma cells, macrophages, fibroblasts, and even some eosinophils. These interstitial lesions appear in a bronchovascular distribution, often causing nonproductive cough and dyspnea. Greater than 90% of cases occur in smokers, and the collection of Langerhans cells driving this disease may be a response to cigarette smoke. Lesions may stabilize or regress with smoking cessation.

Figure 5.50

Eosinophilic granuloma, microscopic

This form of Langerhans cell histiocytosis (a more disseminated form in young children is called Letterer-Siwe disease) is characterized by presence of round to oval CD1a-positive dendritic cells (antigen-presenting cells related to macrophages) that contains characteristic rod-shaped HX bodies (Birbeck granules) by electron microscopy. Note the prominent eosinophils with bright red cytoplasmic granules. Late findings include bronchial wall destruction, cavitation, and stellate scar formation.

Figure 5.51

Sarcoidosis, CT image

This idiopathic granulomatous disease can affect many organs. An abnormal response to unknown antigen(s) drives this process. Lymph node involvement is present in 100% of cases, and the hilar lymph nodes are most often involved. This chest CT scan with the “bone window” setting shows prominent hilar lymphadenopathy (♦) in a middle-aged woman with sarcoidosis. Patients often have fever, nonproductive cough, dyspnea, chest pain, night sweats, and weight loss. Other organs may be involved.

Figure 5.52

Sarcoidosis, radiograph

In addition to increased interstitial markings, this chest radiograph displays prominent hilar lymphadenopathy from noncaseating granulomatous inflammation (◀) from sarcoidosis. Key cytokines driving granuloma formation including tumor necrosis factor-α and transforming growth factor-β. Patients may have a benign course with minimal pulmonary disease that often resolves with corticosteroid therapy. Some patients have a relapsing and remitting course. Approximately one-fifth of patients, typically those in whom pulmonary parenchymal involvement is greater than lymph node involvement, go on to develop progressive restrictive lung disease.

Figure 5.53

Sarcoidosis, microscopic

Interstitial granulomas can accumulate to produce restrictive lung disease. The granulomas tend to have a bronchovascular distribution. The small sarcoid granulomas shown here are noncaseating, but larger granulomas may have central caseation. The granulomatous inflammation is characterized by collections of epithelioid macrophages, Langhans giant cells, lymphocytes (particularly CD4 cells), and fibroblasts. The CD4 cells participate in a subtype 1 helper T-cell (T H 1) immune response. Not seen here are inclusions within the giant cells, such as asteroid bodies and Schaumann bodies.

Dec 29, 2020 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on The Lungs

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