R-1

In this close view of the surface of the lung, the normal visceral pleura appears delicate, glistening, thin and transparent. Note the delicate interlobular septae outlining the parenchyma into secondary lobules, the structural sub-unit of the lung, each of which is about 2 cm in greatest dimension. The large vascular lumina in the interlobular septae represent veins, and the smaller lumina in the septae represent lymphatics. Within each secondary lobule, the parenchyma is homogeneous.

R-2

This schematic diagram of the secondary lobule demonstrates its pyramidal shape, with the base butting against or directed towards the visceral pleura and apex pointing towards the hilus. The fibrous interlobular septae contain both lymphatics and veins. Terminal bronchioles and accompanying branches of the small muscular pulmonary artery enter into the apex of the secondary lobules.

R-3

To review the organization of the structural and functional sub-units of the lung, the secondary pulmonary lobules begin with the terminal or the non-respiratory bronchioles, whereas the functional sub-units of the lung, the acini, begin with the respiratory bronchioles.

R-4

The bundles of smooth muscle are wrapped in a band-like fashion around the bronchial wall, much as one would wrap a rubber band around a pencil. The wrapping is important in understanding the severe narrowing and constriction that can occur subsequent to stimulation of these smooth muscle bundles.

R-6

This slide shows the outer structure of the alveolar walls. The alveolar space is at the top. The alveolar wall contains only 4 cell types. Two of the four are alveolar lining epithelial cells. The Type 1 alveolar lining cell is quite thin and attenuated, contains few alveolar cells, covers better than 80% of the surface area, and is known as the membranous pneumocyte. Type 2 alveolar lining cell is cuboidal, has microvilli along its plasmalemma membrane and contains numerous cytoplasmic organelles. It is also known as the granular pneumocyte. The Type 2 cell produces surfactant. The third type of cell found in the alveolar wall is the alveolar capillary endothelial cell. The fourth is the interstitial cell, the cell of origin of collagen and elastin, the supporting connective tissue elements within the alveolar wall.

R-8

Under light microscopy at high magnification, a close view of bronchiolar epithelial lining cells reveals that interspersed between the columnar ciliated cells are taller non-ciliated cells, the Clara cells.

R-9

Each human lung has approximately one hundred and fifty million alveoli. Thus, in both human lungs there are approximately three hundred million alveoli. The total surface area of the normal adult alveoli approaches seventy square meters, approximate dimension of a tennis court. This large surface area permits extremely efficient gas exchanges. This slide shows the scanning electron micrograph of the alveolar surface. Note the interalveolar communication called the pores of Kohn. Some of the larger holes are called fenestra. The size of the holes and fenestra increases with age. These interalveolar communications presumably assist in the equalization of pressure. They are also present in pathological processes for the flow of exudate from one alveolus to another.

R-10

This shows the bronchiolar epithelium with ciliated columnar cells attached to a pink basement membrane. The lining is pseudostratified. Interspersed with columnar lining cells are mucous secreting goblet cells (non-ciliated cells).

R-13

This slide shows a high power view of alveolar lining epithelial cells, Type 2 pneumocyte, which are extremely prominent and hyperplastic. Alveolar edema is noted with presence of red cells.

R-14

This slide shows the necrosis and disappearance of Type 2 pneumocytes and the formation of hyaline membranes.

R-15

This slide shows some of the advanced changes and the effects on the architecture of the lung of a shock lung phenomena (ARDS) in a patient who has been kept alive by artificial ventilation. Note the widening of the interstitium and organization of the hyaline membranes along the alveolar walls, with an increased connective tissue activity within the interstitium. Necrosis and desquamation into the alveolar space is evident.

R-16

This slide shows an additional change that occurs in the advanced changes of shock lung of the adult respiratory distress syndrome; namely, response of the alveolar injury by the development of type II pneumocyte hyprerplasia. This change, of course, reduces the ability of the lung to function as a gas exchange organ.

R-17

This slide shows a complete revision of the architecture of the lung and disorganization. The lining epithelium is irregular and changed into metaplastic squamous epitheliums. There is a mild interstitial infiltrate of lymphocytes and plasma cells. Both immature and mature connective tissue and smooth muscle cell hyperplasia is evident. This is an end stage lung.

R-18

This slide shows a thromboembolus lodged in a major branch of the pulmonary artery. Note the size and extension of the embolus with the hemorrhagic changes in the lung parenchyma in the lower left hand corner.

R-19

In the cut surface of an inflated and fixed right lung, note that the dependent portion of the lower lobe shows a recent massive hemorrhage. Upon close inspection, one can see a laminated discolored brown-black thromboembolism within the branch of the pulmonary artery leading to this portion of the lower lobe. The dependent portion of the lung is the usual location of pulmonary thromboemboli and subsequent infarction, because this area of the lung receives most of the blood flow from the pulmonary artery.

R-20

This is a photomicrograph of an area of incipient infarction. Note the alveolar hemorrhagic and capillary enlargement. The alveolar outlines are still visible through the hemorrhagic area and appear still viable.

R-21

These small capillaries within a thromboembolus undergoing recanalization are filled with erythrocytes. The bronchial lumen is above, and the columnar ciliated bronchial epithelial lining is clearly seen.

R-24

These are more progressive changes within the small muscular artery in sustained pulmonary hypertension. In addition to the hypertrophy of the smooth muscle of the media, there is marked fibrointimal proliferation with narrowing of the lumen of the vessel. These changes in the small muscular pulmonary arteries reflect the pulmonary hemodynamics, and such changes as we see here indicate prolonged and sustained pulmonary hypertension that might be expected, for instance, in an interventricular septal defect.

R-27

The basic physiology of chronic obstructive lung disease is illustrated in this schematic drawing. Bronchiolar plugging, loss of elastic recoil, and destruction of peribronchiolar supporting tissues (alveolar) are all involved. The process is most often initiated by cigarette smoking.

R-28

This is a close-up view of centrilobular emphysema. The study of pathology of pulmonary emphysema is facilitated by inflation and fixation of lungs and macroscopic examination and photography of the cut surfaces. This particular specimen has been photographed under water. Emphysema has twofold anatomic definition. First, there is hyperinflation of the terminal airways, particularly the alveolar; and second, there is a destruction of alveolar walls. Notice the punched out dark pigmented lesions in the central area of this cut surface of inflated and fixed human lungs. These represent the earliest finding in destructive changes of centrilobular emphysema. The term centrilobular implies that these destructive lesions are occurring in the central portion of the secondary lobule, the structural sub-unit of the lung.

R-30

This photograph shows the most important complication of centrilobular emphysema. There is a development of bullae; large areas of destructive change of emphysema greater than 2 cm in diameter. It usually occurs in the upper portion of the upper lobe and is subpleural. Note at the right top corner the subpleural bullae in the upper lobe and the delicate vascular remnants traversing from one side with the bulla to the opposite wall. In contrast to the bulla, a bleb is a dissection of air within the visceral pleura and is entirely different.

R-31

This a whole mount of a section of inflated and fixed lung. it shows extensive panlobular emphysema, the second major type of pulmonary emphysema. The dilatation and destruction of alveoli is equally distributed throughout the secondary lobules. Panlobular emphysema does not select out the central portion of the secondary lobule for the early changes. This picture shows what might be seen in a section of the lung from a homozygous A1 antitrypsin deficient individual.

R-32

This shows panlobular emphysema and as mentioned previously, it is distributed throughout the secondary lobule.

R-35

Shows diagrammatically the effects of chronic obstructive pulmonary disease.

R-36

This is a demonstration of obstruction of segmental and sub-segmental bronchi by mucous. The luminae are filled with glistening grey-white mucous.

R-37

This is a closer view of smaller peripheral airways obstructed by mucopurulent debris. You can locate the small obstructive airways by noting the intimate association with adjacent branches of the pulmonary arteries.

R-38

This slide shows the changes of small peripheral airways in chronic obstructive pulmonary disease associated with irritation from cigarette smoke and causing the metaplasia of the bronchial lining. This bronchiole is lined up almost entirely by goblet cells.

R-40

Subsequent to acute bronchiolitis with incomplete resolution, there is an organization of material within the lumen. Such organization and fibrosis may lead to fibrosing or obliterative bronchiolitis, as seen here. There is abundant fibrosis tissue and chronic inflammatory reaction largely obstructing the lumen of the bronchiole.

R-41

This is the microscopic appearance of chronic bronchitis, the bronchial lumen at left. To the right is a cartilage plate and intervening lamina propria. Here it is readily apparent that almost all lamina propria is occupied by bronchial glands that show hypertrophy and hyperplasia - increase in size and number.

R-42

This is a picture of saccular bronchiectasis purulent material filling the greatly dilated bronchi just beneath the visceral pleural surface.

R-43

Another close view shows dilated bronchi filled with green mucopurulent debris located just beneath the visceral pleural surface. Bronchiectasis, for the pathologist, is a gross diagnosis. It can be readily appreciated on the cut surface of the inflated fixed lungs.

R-44

This is a photomicrograph of a chronic bronchitis and bronchiolitis. Note the infolding of the epithelial lining and chronic inflammatory cell infiltrate.

R-45

The cylindrical bronchiectasis seen in this slide is readily apparent, and one notes transverse spiralling of the bronchial mucosa within the dilated bronchus. Under normal conditions, the bronchi taper as they progress peripherally, whereas in bronchiectasis one notes markedly dilated bronchi in the peripheral portion of the lung just beneath the covering visceral pleura. Chronic bronchiectasis occurs most frequently in the lower lobes of the lung.

R-46

This slide shows a severe saccular bronchiectasis in the lower lobes. Majority of the smaller bronchi supplying the surviving lung tissue are totally destroyed. A variable, but in places extensive, amount of damage occurs to the peribronchial tissue, which are destroyed and replaced by fibrous tissue. The lobe is often of a normal size. There is little or no pleural thickening. The lung outside the dilated bronchi is often normal and well aerated. The walls of the sacs are often multiple and are composed of fibrous granulation tissue, beyond which lies often compressed and chronically inflamed alveolar tissue. The inner surface of the sac is sequentially lined with metaplastic squamous epithelium or with cuboidal epithelium. If severe inflammatory changes are present, the surfaces become extensively ulcerated and the lumen is filled with pus. The elastic muscle and cartilaginous components are often totally destroyed. The wall of the sac is thus sometimes composed entirely of extrabronchial tissue and lies outside the original plane of the bronchial walls. This form of bronchiectasis is the outcome of an acute destructive form of bronchitis and bronchiolitis in which the damage occurs early in the disease.

R-47

This slide shows the AP chest film on a 39-year-old female with bronchopneumonia. The left lung is extensively involved, especially in the lower portions. The involvement of the right lung is patchy. The main pathology is that of air space disease with consolidation in an irregular fashion. Both the upper and the lower lobes are involved on the left side. The left costophrenic angle is blunted. There is a possibility of a small pleural effusion. There are fluffy irregular densities in the parenchyma in the right side.

R-48

This is a cut surface of the right lung showing much more extensive involvement than the chest x-ray would reveal. Clear-cut abscess formation is seen in patchy distribution along with areas of consolidation. Shaggy walled cavity is seen about the centre of the right upper lobe.

R-49

This shows an area of early exudative stage with pulmonary edema. The alveolar walls are intact. Significant acute inflammation is evident. The pink granular material represents edema into the alveolar spaces.

R-50

This shows more advanced stage of cellular and fluid exudation. The alveolar walls are still intact and are recognizable. There is an acute inflammatory cell infiltrate and hemorrhage into the alveolar spaces.

R-51

This slide shows an area of alveolar destruction and breakdown. The inflammatory exudate is composed of acute inflammatory cells, consisting mostly of neutrophils. Some congestion the capillaries of the alveolar walls and edema in the spaces is still present. Eventually, this leads to abscess formation, which was seen in image Resp. K 48.

R-52

This slide shows the severity of tracheobronchitis in this patient. The mucosa is covered with a whitish-yellowish exudate. It is grossly hyperemic. Focally, it is ulcerated.

R-53

This slide shows external surface of the lungs. The upper lobe shows anthracotic pigmentation in the pleural surface. The lower lobe shows bulging and reddish discoloration. Macroscopically, lobar pneumonia is divided into stages of edema, red hepatization, grey hepatization, and a stage of resolution.

R-54

This shows a photomicrograph of the lung in advanced stage of lobar pneumonia. Note that the alveolar architecture is retained. The alveolar spaces are filled with both edema fluid (right lower corner). This is perhaps the first stage of lobar pneumonia. The neutrophilic granulocytes are occupying the alveolar spaces. The unique feature to recognize here is that the alveolar walls remain intact. Recall that in bronchopneumonia there was a destruction of alveolar septae.

R-55

This slide shows a cross surface of the right lung, as well as portions of the visceral pleura. In general, viral pneumonia of the lungs may vary enormously in appearance, depending on the severity and extent of disease. They are usually heavy, bulky and plum colored. Often there are areas of subpleural petechial hemorrhages, as can be seen in this picture on the left side under the subpleural surface. The changes are usually most severe in the lower lobes. The cut surfaces exude blood stained fluid from both bronchi and the lung parenchyma. The septal tissue are extremely edematous.

R-56

This slide shows a picture of viral pneumonitis with the presence of lymphocytic infiltrate in the interstitium, a slight widening of the interstitium, the presence of hyaline membranes, as well as capillary congestion and some exudation of red cells.

R-57

This slide shows, in addition to the interstitial pneumonitis, areas of superimposed focal or patchy bronchopneumonia with the presence of granulocytic infiltrate in the alveolar spaces.

R-58

This slide shows a high power photomicrograph of a viral interstitial pneumonia with superimposed acute component. There is destruction of the alveolar and bronchial cells. In addition to the lymphocytic infiltrate in the interstitium, a large number of neutrophils can be visualized in the alveolar spaces along with capillary congestions. Three large cells infected with cytomegalovirus can be seen. The cell in the centre is the best developed example of internuclear inclusion with perinuclear halo and abundant cytoplasm.

R-59

This slide shows photomicrographs of a giant cell pneumonia. One cause of giant cell pneumonia is measles. Characteristic responses of the whole cell to virus infections are found in the respiratory epithelium at all levels. The changes have been described in cells lining the alveoli. The cytoplasm of 10 to 100 adjacent epithelial cells first becomes eosinophilic and later the cell wall disappears, resulting in the formation of giant cells. The nuclei condense and clump into large masses. Intracytoplasmic inclusions may also be found in individual hyperplastic bronchiolar or alveolar epithelial cells.

R-60

This slide shows the gross photograph of a cut surface of the lung with secondary or progressive pulmonary tuberculosis. There is widespread disease in the form of necrotizing pneumonitis in the upper lobe. Multiple areas of white and cheese-like caseous necrosis are seen. In areas where the process is severe, breakdown in cavitation can be seen as a result of an extreme degree of caseous necrosis. (Fibrocaseating bronchopneumonia).

R-61

In miliary tuberculosis as this photograph shows, the organisms are spread within the blood stream. The deposition is found particularly within organs of the reticuloendothelial system, such as liver, spleen, bone marrow, lymph nodes, and, of course, the lungs. The size of foci are quite small, about the size of millet seeds, thus explaining the name miliary tuberculosis. Note the cut surface of this lung with hundreds of millets throughout.

R-62

This is a photomicrograph of miliary tuberculosis showing caseating granulomas which are discrete. Note that the surrounding parenchyma is relatively intact.

R-63

This cut surface of the lung shows sufficient destructive change with collapse and condensation of the lung parenchyma. Tuberculosis almost always heals with certain (anatomical) sequelae, such as bronchiectasis and/or thrombosis of the pulmonary artery bed.

R-64

This slide shows the staining of tubercle bacilli with fluorescent auramine stain.

R-66

Following aspiration of gastric contents, there is usually a marked disarray of normal architecture. The bronchus of such a lung shows the necrosis of the mucosa, and debris partly fills the lumen. Here is evidence of an aspiration that speaks for itself. A high power microphotograph shows aspiration of vegetable particles found within the bronchiole of a nursing home patient.

R-67

This is a high power photomicrograph of an exogenous lipoid pneumonia. Note the lipid filled macrophages in the bronchial epithelium and the adjacent alveoli. Minor inflammatory reaction is present in this case. There are a variety of causes of inhalational lipoid pneumonia. The condition is most often found in debilitated or wasted patients. It is also found in elderly people with disorders such as Parkinson's disease, severe vascular disorders, and rheumatoid arthritis.

R-68

This slide shows the presence of Aspergillus fungus in the lung. The fungus derives its name from the shape of the fruiting head which resembles the brush used for sprinkling holy water (aspergillum). The hyphae are branched and swell at intervals to form fruiting heads, from which branch shoots known as conidiophores. The principle types of pulmonary aspergillosis include: (1) surface saprophytic infections; (2) nonsuppurative necrotizing infections; (3) suppurative and diffuse pneumonic infections; and (4) granulomatous lesions.

R-69

This slide shows an X-ray picture of Coccidioidomycosis of the lungs. Most commonly, this occurs as an opportunistic infection in patients whose immunologic state is depressed. The infection is divided into three stages: (1) primary; (2) intermediate or pulmonary; and (3) disseminated. The result of a primary chronic infection is the presence of a healed cavity which remains as a permanent thin-walled cystic space lined by a fine layer of scar tissue. Unlike tuberculous cavities, they provide no source of infection and danger to others, though hemorrhage may occur from their walls and rupture of the pleura may cause pneumothorax. The spreading infection which occurs as a complication of this in the very young and very old follows a granulomatous pattern. This closely simulates tuberculosis and tuberculous lymphadenitis. Pathologically, the lesion is granulomatous and the diagnosis depends on the identification of cells of Cocidioides immitis.

R-70

This slide shows the spherule development of C. immitus. Note the acute inflammatory reaction. This section is taken from the edge of a lung abscess cavity aerated from a bronchus.

R-72

This slide shows Pneumocystis pneumonia. Pneumocystis pneumonia is an infection caused by the presence of pneumocystis carinii in the lungs. This organism is at present considered to be a protozoan. This pneumonia occurs mainly in malignant lymphoproliferative disease or follows iatrogenically-produced immunosuppression for the purpose of renal or other forms of tissue transplantation. Radiologic changes in the lung appear early and precede clinical evidence of lung disease, and they consist of irregular areas of opacity in both lung fields. Occasionally, the course of illness may be very rapid, and in such cases other opportunistic infections, including cytomegalovirus disease and fungus infections, are often complicating factors. Microscopically, there is a chronic interstitial pneumonia and many of the alveoli are lined by cuboidal or flattened epithelium. Many of the alveolar ducts and alveoli become distended and filled with characteristic foamy and amorphous contents, including usually a few macrophages. The interstitial infiltrate consists of lymphocytes, large numbers of plasma cells, and macrophages, but fibrosis is absent at first. The foamy intra-alveolar contents consists of honeycomb or very fine-walled cystic spaces which stain faintly by the PAS method.

R-73

The cysts of Pneumocystis carinii are best demonstrated by the silver stain. They measure up to 4.0 micrometers in diameter and are mostly spherical but some are crescentic. They may only be present in some alveoli and are usually most abundant in the center of the alveolar exudate. The accurate diagnosis of pneumocystis pneumonia at the earliest opportunity is of the greatest importance so that treatment can be started. The most reliable and informative procedure is the open lung biopsy, which despite the seriousness of the illness, can be undertaken in most patients.

R-74

This slide shows a close-up of the right upper lobe radiographically from a case of sarcoidosis. Note the reticulo-nodular diffuse interstitial pattern with prominent hilum. Approximately in the centre of the view there is a vague suggestion of honeycomb appearance of the lung parenchyma.

R-75

This slide shows the pleural surface from a case of pulmonary sarcoidosis. The surface shows multiple discrete as well as coalescent nodules with pale areas.

R-76

This slide shows the presence microscopically of non-caseating granulomas with giant cells and fibrosis. Sarcoid lesions are found throughout the interstitial tissues of the lung, including the peribronchial, the perivascular, subpleural and alveolar interstitial tissue. In chronic cases, the nodules become increasingly fibrosed and much of the lung is transformed into dense collagenous fibrous tissue.

R-79

This is a lung whole mount gross picture of anthracosis, which is a form of pneumoconiosis caused by the inhalation of atmospheric soot particles. In the past, the black pigment has usually been regarded as soot or coal dust particles, but it has been shown that the pigment may contain iron and traces of silica, in addition to recognizable particles of coal dust.

R-81

This shows the microscopic appearance of silicosis, under polarized light demonstrating the white dots or small needles, which are the silica particles. Silicosis is a disease that follows the inhalation of minute particles of silica. Silica and silicates are the most common constituents of the earth's crust, and dust containing them constitutes an occupational hazard in mining and innumerable industrial processes. In most forms of pneumoconiosis, the dust particles tend to aggregate in those parts of alveoli which are most fixed; that is, adjacent to vessels, septa, and the alveoli beneath the pleura, and in those alveoli arising from respiratory bronchioles. The affected alveoli and the parent air passages undergo mural thickening due to proliferation of alveolar phagocytes and alveolar epithelial cells. The silicotic nodule consists of layers of hyaline collagenous tissue in which fibers are mostly layered down concentrically.

R-82

This slide shows an intra-alveolar collection of asbestos bodies (ferruginous). The asbestos bodies in the lungs first appear as brown or black pointed fibers, up to 60 micrometers in length, many showing rounded drumstick ends due to their protein covering. Later, horizontal clefts appear across the body of the fiber, dividing it into fragments, until finally the whole fiber disintegrates and disappears. The asbestos bodies stain positively with Prussian blue because of the presence of iron.

R-89

Coned radiograph of the left upper lobe region shows a dense band of atelectasis of about 2 cm in width lying in the first intercostal space extending towards the periphery. In its medial portion, there is a rounded homogenous dense opacity of 2 cm in size overlying the area. There is no evidence of calcification or cavitation. On a closer view of the supraclavicular area, there is also another area of a rounded dense opacity of 1 cm in size. Though the atelectasis can be caused by inflammatory or neoplastic diseases, the presence of two rounded opacities makes a neoplasm (metastatic carcinoma) more likely.

R-90

This slide shows a photograph of the lobectomy specimen from the case. In the centre of the picture there is a bronchus which is markedly thickened and occluded. The band of atelectasis is noted again to the periphery. This was a primary squamous cell carcinoma. In the top portion of the slide, there is an additional neoplasm. The solidification of the lung in that area appears much larger than was visible on the x-ray. This later proved to be a second primary and an adenocarcinoma of the lung.

R-91

This slide shows a microscopy of a squamous cell carcinoma of bronchogenic origin. The cells are large. The nuclear cytoplasmic ratio is markedly increased. Majority of the cells are identifiable as squamous cells with eosinophilic cytoplasm.

R-92

This slide shows the microscopy of the second tumor, an adenocarcinoma at the apex of the lung. The cells are vacuolated and lining fibrovascular cores and exhibit what might be called an adenopapillary pattern.

R-93

This slide shows a rather unusual picture of squamous cell carcinoma spreading and growing from one alveolus into another.

R-94

This slide shows a gross photograph of endobronchial tumor growing on the mucosa of a large bronchus. Note the velvety appearance and loss of ridges in the area of the tumor.

R-95

This slide shows the spread of the tumor in the adjacent lung parenchyma from a major bronchus. Note the fibrosis and constriction of the left bronchial tree. This is the cause of atelectasis or bronchopneumonia distal to the occlusive neoplasm.

R-97

This photograph shows a small cell anaplastic carcinoma. Note the cells are present in nests surrounded by a delicate connective tissue septae. The cells are more or less uniform, except in one portion of the slide where they show spindle pattern. The nuclei are hyperchromatic and the cells have scanty cytoplasms. The general resemblance is to a lymphocyte.

R-98

This slide shows the mixed carcinoma of the lung. A clear-cut keratinizing squamous cell carcinoma is identifiable in a connective tissue stroma as well as a small cell anaplastic carcinoma of the lung. Note that both these tumors are smoking related.

R-99

This slide shows a low power view of a bronchiolaralveolar cell carcinoma of the lung. Note that the architecture resembles normal lung parenchyma with open alveolar spaces. The cells lining the alveolar walls are better shown in the next slide.

R-100

The cells of bronchiloalveolar carcinoma are cuboidal or low columnar with large nuclei. These vessels may or may not produce mucin. The x-ray appearance of these resembles a pneumonic process rather than a neoplastic process. The majority of these tumors remain within the thoracic cavity for long periods of time.

R-101

This is a chest radiograph, PA view. There is a rounded, homogenous dense opacity of 2 cm in size in the left lower zone partly overlying the anterior end of 4th rib. There is no evidence of calcification or cavitation seen. Rest of the lung fields, hila and bony cage are normal. The possibility of primary or metastatic carcinoma is the main consideration.

R-103

This slide shows a characteristic large cell undifferentiated carcinoma of the lung. Note that the tumor is solid without any mucin content.

R-104

This slide shows a pulmonary hamartoma which is composed mainly of cartilaginous tissue with a small piece of the lung parenchyma attached to it. This is a surgical specimen. The term hamartoma describes certain tumors that result from a localized error in development of normal organs. These tumors are non-invasive and vary in size from less than 1 cm to 6 cm in diameter. The surface is lobulated, smooth and usually formed by nodules of cartilage or dense fibrous tissue. Microscopically, the tumor reproduces any of the components of the bronchial tissue, including areas of fibro-cartilage which often calcify, metaplastic bone, collections of lymphocytes, and numerous cleft-like spaces lined in part by cuboidal epithelium and in part by ciliated epithelium.

R-105

This slide shows a tumor under the bronchial epithelium. It is made up of small, round uniform cells with scanty cytoplasm. It is a non-invasive, well encapsulated tumor. In the past, it was customary to divide this tumor into a variety of bronchial adenomas. The current terminology precludes the term adenoma. This variety is a bronchial carcinoid, and the cell of origin is the Kulchitsky cell. Bronchial carcinoids are equally distributed between both lungs. The majority of these tumors assume two distinct forms and grow as either a bronchial polyp or as infiltrating growth or iceberg tumor. Microscopically, the stroma is often extremely vascular and may undergo hyaline change, calcification, or even ossification.

R-106

This slide shows a photomicrograph of a bronchial carcinoid. Note the acino-papillary pattern with vascular cores. Note the size of the cells and the uniformity of these cells.

R-107

This slide shows a classification of bronchogenic carcinoma, the incidence, histology, sex predominance, location, smoking relation, growth rate, metastatic frequency and resectability of these tumors.

R-111

This is a chest radiograph, PA view. There is diffuse interstitial shadowing involving both the lung fields. The linear pattern of the shadowing is particularly striking in the right lung. This appearance may be caused by the thickening of the intercommunicating lymphatics. There are also a few subpleural peripheral septal lines in the right base. Both the hilar shadows are slightly prominent and hazy. Heart is of normal size and shape. There is no demonstrable pleural effusion. This type of interstitial shadowing may be seen in various disease processes, particularly occupational disease like pneumoconiosis, acute left ventricular failure. Lymphangitis carcinomatosis should be considered in the differential diagnosis.

R-112

This slide shows a photograph of an open lung biopsy from the previous case of "lymphangitis carcinomatosa." The term "lymphangitis carcinomatosa" is a misnomer as illustrated on this slide. The tumor is a clear cell carcinoma and is present in blood vessels. The correct terminology for this type of metastasis with a snowstorm pattern is "pulmonary embolic carcinomatosis."

R-113

This slide shows trophoblastic tumor with development of giant cells. Note the amount of red cells. These tumors are extremely hemorrhagic. This is a slide of a metastatic choriocarcinoma from the testes in a male.

R-114

This slide shows a pleural biopsy from a case of metastatic carcinoma of the breast to the pleura with the presence of pleural effusion. Note the islands of neoplastic cells with angulated nuclei and attempt in some areas for formation of glands or tubules. Note the strong desmoplastic reaction.

R-115

A low-power view of a small bronchiole. Note the hypertrophied muscle layer and adjacent inflammation. The lumen is plugged by pale blue staining mucus. This slide is from a 40 y.o. male who died in status asthmaticus.

R-116

A closer view of the same bronchiole again demonstrates the hypertrophied muscle. Note that the mucus contains desquamated cells (from the bronchiolar lung epithelium).