Color Atlas of Pathology (Thieme ) - dokument [*.pdf] At a Glance 1 Fundamentals of Pathology 2 2 Cellular Pathology 6 3 Connective Tissue . who helped to make the Color Atlas of Anatomy a success. We are particularly of tissues Color Atlas of A Color Atlas of Forensic Pathology. This is a very practical atlas and guide that provides color photo- graphs of appropriate gross and his- tological patterns of various tumors of the central nervous.
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حصريا تحميل كتاب color atlas of pathology مجاناً PDF اونلاين r nursus nikolaus riede:(Author n nThe pocket is an excellent reference work that presents . Book Reviews. Pathology: A Color Atlas, by Ivan Damjanov and James Linder,. pp, with illus, $, St Louis, Mo, Mosby (telephone: ), Pathology A Color ruthenpress.info - Ebook download as PDF File .pdf), Text File .txt) or read book online.
Its cellular components provide oxygen transport erythrocytes and protective responses to infectious and non-infectious agents lymphoid cells, mononuclear phagocytic cells, granulocytes and supportive tissues. In addition, degenerative changes of erythrocytes, circulatory disturbances and abnormal deposits may occur.
In cachexia the hematopoietic tissue in the bone marrow can be displaced by gelatinous, almost translucent material, the serous atrophy of bone marrow.
Non- infectious agents can induce atrophic changes, either by 'exhaustion' of the response capacity of the tissue or as a direct or indirect effect on the effector cells. High levels of glucocorticoids may cause lymphodepletion in lymphoid tissues.
Filtering of lymph in the lymph nodes with deposition or processing of filtered material may reveal important information. The same applies to the filtering of blood in the spleen.
Reactive Ilyperplasia of hematopoietic tissue can expand into and replace fatty bone marrow. Mostly, the myeloid cell series is involved and the process will result in leukocytosis in the. Because of the close relation between adapiiue reactioitv and inflammatory reaction these two processes are often difficult to distinguish, especially based on gross morphology.
Humoral immune reactivity is evidenced by B-cell hyperplasia with large secondary follicles and many plasma cells in the medullary cords of the lymph nodes, and cellular immunity evidenced by hyperplasia of the paracortical zones lymph nodes or periarterial lymph sheaths PALS, spleen.
Most hyperplastic reactions are non-specific in that they do not reveal the identity of the agent responsible. When characteristic inflammatory changes like suppuration, necrosis or caseation are visible in lymph nodes or spleen, lymphadenitis and splenitis are appropriate terms.
Neoplasms of the hematopoietic system are also relatively common in both companion animals and production animals and are classified according to their histogenetic lineage.
The different types of malignant lymphoma and leukemia are the most frequent hematopoietic tumors. Characterization of tumor cell populations in companion animals is increasingly facilitated by immunohistochemical methods. In several species e. Bone marrow, diaand metaphysis of femur. Red blood forming and yellow fatty bone marrow displaced bygelatinous andtranslucent material traversed bysmall blood vessels.
Atrophy of hematopoietic tissue dueto cachexia. Bone marrow, mid-diaphyseal area of femur. Increased number of immature myeloid cells myeloblasts and megakaryocytoblasts , few normoblasts. Leukocytosis dueto infection.
Adult cat. Nitrate nitrite poisoning. Random, loosely arranged meshwork of delicate fibrin fibrils, after settling out and coagulation of stagnant blood. In a neighboring vessel accumulation of leukocytes as a buffy coat between plasma and red clot. Concentrically arranged, densely packed aggregations of fibrin fibrils, deposited in flowing blood.
The thrombus is attached to the damaged arterial wall,and is covered by a red clot. Pseudomembranous rhinitis. Surface of thrombus covered by endothelium. Formation of newcanals lined byendothelium allowing some blood flow. Many small hemorrhages. Defective hemostasis following immune-mediated destruction of thrombocytes by maternal antibodies in colostrum.
Although primary plug formation by platelets is impaired, coagulation isstill possible, preventing larger hemorrhages. Porcine thrombocytopenia purpura. Newborn piglet. Adrenal gland, sagittalsection.
Extensive cortical hemorrhages dueto consumption of clotting factors and loss of platelets by disseminated intravascular coagulation DIC. Hemorrhages of similarsize may also be due to primary vascular damage e. Escherichia coli endotoxic shock. Glomerular capillaries obstructed by hyaline microthrombi platelets and fibrin , causing oliguria or anuria. Protein casts in Bowman'sspace and mosttubules. Hyaline droplets, due to protein pinocytosis cf.
Acute tubular necrosis often occurs during DIC see Fig. Neville, Douglas D. Damm, Dean K. White, and Charles A. Inasmuch as intraoral roentgenograms are a major diagnostic aid for detecting the pathologic conditions of mineralized structures for example, teeth and jawbone , the authors have interspersed numerous roentgenologic photographs throughout the text. This atlas is organized into chapters that cover a specific anatomic location pathologic changes in the teeth or salivary glands , chapters that review various pathologic changes infection, soft tissue or osseous tumors, chemical or physical injuries , and chapters that address oral manifestations of systemic disease dermatologic or hematopoietic.
Because of the extensive photographs, this text will be valuable to persons new in the field, such as dental or medical students; it will be a motivational source to lead them to more comprehensive and scientifically organized textbooks. Moreover, it presents a "bird's-eye view" of the field of oral diagnosis and oral pathologic conditions. This text will be of limited value to practicing clinicians because a high percentage of oral-facial pathologic entities manifest in many forms; thus, a clinical photograph is seldom pathognomonic for a disease entity.
This relationship is particularly true for soft tissue tumors and oral manifestations of systemic disease. If used clinically, the book tempts clinicians to include or exclude various diagnostic entities on the basis of clinical appearance; thus, I hesitate to recommend it to medical specialists in clinical practice. In summary, this excellent text is a reading and teaching resource for medical and dental students and should be available in all teaching settings.
Eugene E. Keller, D. Pizzo and Catherine M. A disease that is steadily growing because of the increase in incidence of human immunodeficiency virus HIV infection among women of childbearing age, AIDS will afflict an estimated 20, children in the next 5 years. In response to the urgency of this escalating problem, experts from many disciplines have contributed information to this definitive resource. That the entire book was published within 9 months after the chapters were submitted is a tribute to the joint efforts of the contributing authors and the two editors, all of whom are outstanding authorities in the field.
This timeliness makes the book particularly valuable. Those who are involved in the care of HIV-infected youths-infants, children, and adolescents-will find detailed coverage of every aspect of the disease. The book addresses the current magnitude of the AIDS problem, epidemiologic features and transmission, difficulties in diagnosis, natural history, and age-dependent differences in the clinical and laboratory manifestations of HIV infection.
An extensive review ofthe social, ethical, legal, and public policy issues that surround HIV infections is included. Strategies of prevention and education are presented, as are management considerations such as clinical pharmacologic effects, drug development, immunomodulating factors, passive immunizations, and vaccines.
The contributions are accompanied by useful photomicrographs, diagrams, and tables. Every chapter has an extensive bibliography, and references as recent as have been included in many chapters. An ultrastructural and morphometric study of 24 cases. A clinicopathologic study of 67 cases. The undifferentiated carcinoma.. Helquist H. It may begin as squamous cell dysplasia or carcinoma in situ Fig. Heffner DK. A clinicopathologic and immunohistochemical study of 14 cases. Wenig BM: Non-Hodgkin's lymphoma of the sinonasal tract.
Devaney K. Slavin RG: Nasal polyps and sinusitis. A clinicopathologic study of 23 cases. Mod Pathol 9: False cord and ventricle are free of tumor. Gale Net al: Criteria for grading in the Ljubljana classification of epithelial hyperplastic laryngeal lesions.
Invasive carcinomas show variable degrees of keratinization Figs. Laryngectomy specimen showirig recurrent carcinoma of the right vocal cord. Ultrastruct Pathol Vertical section through a supraglottic squamous carcinoma. Troncoso Petal: Neuroendocrine tumors of the nasal cavity.
Mackay B. Such lesions are often aneuploid even though they show some degree of "surface maturation" into keratinized squamous cells. Cardesa A. Vertical section through a carcinoma localized to the true vocal cord. Carcinoma of the larynx is a squamous cell carcinoma in 95 percent of patients. Wenig BM. Sem Ding Pathol Gnepp DR: Sinonasal fibrosarcomas. Michaels L: Benign mucosal tumors of the nose and paranasal sinuses.
Abbondanzo SL: Olfactory neuroblastoma and other round cell lesions of the sinonasal region. Hyams VJ: Hemangiopericytoma-like intranasal tumors. Squamous cell carcinoma of the larynx.
Further Reading Fig. Keratinizing intraepithelial dysplasia of larynx. Tumor cells are surrounded by lymphocytes. Bronchogenic cyst. Tracheoesophageal fistulas. Pulmonary anomalies range from minor variations in the lobar configuration to major developmental defects such as unilateral pulmonary agenesis or hypoplasia Fig.
This resected cyst has a rugged internal surface. So-called intralobar sequestration. Bronchogenic cyst develops from an accessory fetal lung bud that becomes isolated from the rest of the tracheobronchial tree. This posterior midline subpleural cyst was compressing the esophagus. Pulmonary hypoplasia has been identified in 10 percent to 15 percent of all neonatal autopsies and in 50 percent of neonates who have other significant congenital anomalies.
The most important of these conjoined anomalies is tracheoesophageal fistula Diagram Type C malformations account for 85 percent of all cases. It is therefore not surprising that developmental anomalies involving one system are accompanied by abnormalities in the other. Anomalies limited to parts of a lung may remain asymptomatic until adult life. Bronchial anomalies include abnormal branching patterns. The most important of these anomalies are congenital cystic adenomatoid malformation and extralobar bronchopulmonary sequestration or accessory lobe Figs.
Congenital cystic adenomatoid malformation. The interstitium is fibrosed and contains inflammatory cells. Intralobar sequestration. The mass consists of markedly dilated bronchi filled with mucus and surrounded by fibrous tissue.
Pulmonary hypoplasia in a neonate. The lung is composed of cystic bronchi and air spaces. This mass. The wall of the cyst is lined by pseudostratified or tall columnar epithelium resembling the lining of proximal bronchioli or small bronchi. The atelectatic parenchyma appears dark red in contrast to the paler areas of normally aerated lung right upper corner. Neonatal atelectasis. Hyaline membranes are brown due to staining with meconium.
Severe hyaline membrane disease that is treated aggressively may result in development of chronic lung changes known as bronchopulmonary dysplasia Fig. The lungs of such neonates contain amniotic fluid with squamous and inflammatory cells Fig.. Aspiration of infected amniotic fluid by the fetus accounts for 20 percent to 40 percent of early-onset neonatal sepsis and pneumonia. Resorption of hyaline membranes. Histologically it can be divided sequentially into three overlapping phases: Secondary changes such as intraalveolar hemorrhage.
Alveoli are collapsed and the alveolar ducts and respiratory bronchioli are dilated and lined by hyaline membranes. Clinically it presents as neonatal respiratory distress syndrome or hyaline membrane disease.
The lungs show patchy atelectasis Fig. Pulmonary interstitial air.
Neonatal respiratory distress syndrome. Histologically pulmonary alveoli are collapsed and atelectatic. Most neonatal pneumonias are acquired during labor and delivery. Neonatal pneumonia typically is a complication of: Oxygen therapy and mechanical ventilation cause additional changes that cannot be separated from those caused by the disease itself.
The process is dominated by organization of hyaline membranes by granulation tissue. The lungs are consolidated except for a few cystic and slit-like spaces. Bronchopulmonary dysplasia. Air-filled spaces extending the interlobular septa are seen through the pleura. The alveoli contain nucleated squamous cells and scattered inflammatory cells.
Amniotic fluid aspiration with early pneumonia. Lungs are in part consolidated and in part cystic. The alveoli are partially obliterated by ingrown granulation tissue. Bacterial infection presents as lobar or lobular pneumonia also known as bronchopneumonia. The alveolar walls are of normal thickness and do not contain red blood cells.
The lungs appear only focally consolidated. Primary tuberculosis. Bronchopneumonia presents in the form of more circumscribed infiltrates Fig. Without treatment. The entire lung appears consolidated and the parenchyma is bulging on cross section. The infiltrates are peribronchial and appear distinct from the surrounding parenchyma. The alveoli are filled with neutrophils. Lobar pneumonia. These infiltrates are initially composed of neutrophils and are predominantly inside the alveoli Fig.
Pulmonary tuberculosis presents with a spectrum of changes. Histologically all tuberculous lesions contain granulomas Fig. Secondary tuberculosis results in widespread dissemination of mycobacteria and the formation of multiple small nodules miliary tuberculosis. In lobar pneumonia entire lobes of one or both lungs are involved Fig. Pneumonia caused by Staphylococcus aureus may result in massive tissue breakdown Fig. Lobar pneumonia in the stage of gray hepatization.
Similar changes can be caused by fungi such as Histoplasma capsulatum. In severe cases the abundant fibrin cannot be removed and it stimulates the ingrowth of granulation tissue into the alveoli organizing pneumonia Fig. From Woods CL. Necrotizing pneumonia.
The large subpleural abscess contains brownish-yellow pus. The primary lesion appears as a sharply demarcated subpleural nodule. The exudate is accompanied by necrosis of alveolar septa.
Pulmonary tuberculosis. Gutierrez Y: Diagnostic pathology of infectious diseases. Courtesy of Cathy Looby. The surrounding parenchyma appears consolidated and contains scattered smaller whitish-yellow abscesses. The parenchyma and hilar lymph nodes contain numerous. Lung abscess. Granulomas of tuberculosis consist of lymphocytes.
The alveoli contain abundant fibrin. Secondary pulmonary tuberculosis. The bluish material represents bacterial colonies. Organizing pneumonia. The alveoli contain well-developed fibrin-rich hyaline membranes and some edema fluid.
Viral pneumonia caused by the cytomegalovirus CMV. The alveolar septa are widened. The alveoli contain edema fluid. Pneumocystis carinii cysts are seen in silver-impregnated cytologic smear prepared. Typical intranuclear inclusions are seen in desquamated pneumocytes.
Such changes are indistinguishable from other forms of diffuse alveolar damage DAD. Viral infections cause alveolar cell injury. Alveolar cell injury caused by viruses such as influenza or adenovirus produce histologically nonspecific changes.
Pneumocystis carinii pneumonia. CMV inclusions appear as basophilic blue material in the nucleus and the cytoplasm. Viral pneumonia. In most instances the causative virus is not visible except in some infections that are caused by herpes simplex virus 1 HSV. The alveoli contain proteinaceous acellular floccular material. Fungal cysts can be seen in slides impregnated with silver according to Gomori.
Circulatory collapse that occurs in shock and multiple organ failure often is clinically associated with adult respiratory distress syndrome ARDS. Pulmonary infarct.
The main branches of the pulmonary artery are occluded with thromboemboli. Thromboemboli that lodge in peripheral pulmonary arteries cause infarcts. The septa are necrotic and the alveoli contain blood. Diffuse alveolar damage. Infarct is triangular and hemorrhagic. Pulmonary thromboembolism. Chronic heart failure results in brown induration of the lungs. Saddle emboli of the main pulmonary artery and the emboli occluding the major branches of the pulmonary artery usually cause sudden death Fig.
Air spaces contain hyaline membranes. Acute left heart failure results in passive pulmonary congestion and intraalveolar hemorrhage. Pulmonary emboli may involve the main pulmonary artery. Clinically they may cause sudden death. In patients who survive. Pulmonary Emboli Pulmonary thromboembolism is one of the leading causes of death. On gross examination pulmonary infarcts appear red. Ultimately the disease may progress to diffuse pulmonary fibrosis. Medial hypertrophy and muscularization of an arteriole grade I.
Pulmonary infiltration and eosinophilia PIE is a syndrome that could have many causes. Secondary pulmonary hypertension is a consequence of left heart failure. The principal pathologic changes occur in the bronchi and bronchioli. Plexogenic pulmonary arteriopathy. Focal cellular infiltrates composed of lymphocytes and a few plasma cells are less common.
Foreign antigens usually induce a cellmediated reaction in the form of granulomas Fig. Concentric laminar intimal fibroelastosis grade 3. The causes of primary or idiopathic hypertension are not known. Pulmonary hypertension can be classified as primary or secondary.
The most important in this group of diseases are asthma. Fibrinoid degeneration grade 6. Plexiform lesion grade 4. The mucus inthelumen o f thebronchi may contain CharcotLeyden crystals derived from the granules of eosinophils and Curshman spirals.
Necrotizing arteritis grade 6. Pulmonary Hypertension episodes of wheezing and increased resistance to expiratory air flow. Elastica—van Gieson stain. Concentric intimal proliferation grade 2.
The lungs also may be affected by systemic autoi mmune diseases such as systemic lupus erythematosus. Many drugs may induce the same syndrome. In advanced cases buds of organizing fibrovascular tissue Masson bodies fill the respiratory bronchioli and alveolar ducts Fig.
Sjogren syndrome. Congenital heart disease with left-to-right shunting of blood also causes pulmonary hypertension. Other immune-mediated diseases such as Goodpasture syndrome and Churg-Strauss syndrome are less common. Hypersensitivity pneumonia extrinsic allergic alveolitis can be induced by a number of allergens or drugs Fig.
Eosinophilic pneumonia often is found in such cases by lung biopsy Fig. Clinically it may present under several conditions such as farmer's lung. Eosinophilic pneumonia. Curshman spiral. Allergic drug reaction. The lumen contains mucus. Hypersensitivity pneumonia. The bronchiole has a hy erplastic epithelium. The air spaces contain loosely structured granulomas with multinucleated giant cells. The alveolar septa are thickened and infiltrated with mononuclear cells.
The alveoli and thickened septa are infiltrated by eosinophils and lymphocytes. Inflammatory cells are present in variable amounts and often are not prominent.
In later stages of the disease the airways are obliterated by fibroblastic granulation tissue. Charcot-Leyden crystals. The bronchi typically have thickened walls. Centriacinar emphysema most often is found in cigarette smokers and typically shows centriacinar deposition of black pigment anthracosis. In cystic fibrosis. These changes contribute to a variegated " geographic map-like" appearance of tissues in histologic sections.
Other forms of emphysema such as paraseptal or irregular emphysema usually associated with scarring are less important clinically. All forms of emphysema can give rise to pulmonary subpleural bullae.
The involved bronchi and bronchioli are markedly dilated. Chronic bronchitis is defined clinically as chronic lung disease presenting as cough with expectoration and lasting at least three months during two consecutive years.
It occurs in two main forms: Wegener granulomatosis is an immune-mediated disease that involves the upper and lower respiratory tracts and kidneys.
AIDS or cancer therapy. Similar air-filled bullae. The bronchi show histologic signs of chronic inflammation and contain mucus admixed with pus Fig. Emphysema is a permanent loss of pulmonary parenchyma that leads to an enlargement of air space distal to the terminal bronchioles.
The lung lesions may present as pale infarcts or bulky necrotic nodules Fig The enlarged bronchial mucous glands occupy more than 40 percent of the thickness of the wall. A B Fig.. It may occur in several clinical settings such as: Histologic features include vasculitis accompanied by thrombosis and pulmonary infarcts.
Bronchiectasis Bronchiectasis is an irreversible dilatation of bronchi accompanied by an infection of the bronchial wall and obliteration of distal airways.
Wegener granulomatosis. People who are exposed to chronic irritants such as cigarette smoke also suffer from chronic pulmonary infections. The lung parenchyma contains two nodules showing central necrosis. Kartagener syndrome. Chronic Obstructive Pulmonary Disease COPD is a clinical diagnosis that includes two closely related entities that typically cause dyspnea and other respiratory problems in chronic cigarette smokers: Panacinar panlobular emphysema typically is encountered in persons with a i -antitrypsin deficiency.
The section shows areas of vasculitis. Panacinar emphysema. The bronchiole is filled with an exudate composed of neutrophils. Subpleural bullae. Cystic fibrosis. The wall of the bronchus is thickened and inflamed. This lung from a year-old man shows diffuse bronchiectasis. Chronic bronchitis. Also note the pigmentation inside the cystic central spaces. Centriacinar emphysema. Note that the large air spaces are surrounded by a normal alveolar network. The entire pulmonary parenchyma has a delicate cotton candy—like texture.
Larger nodules seen on radiographic examination of the lungs of coal workers with rheumatoid arthritis Caplan lesion show central necrosis surrounded by palisading macrophages that are reminiscent of subcutaneous rheumatoid nodules Fig. Hard metal disease sporadically develops in workers who are employed in industries in which synthetic hard metals are produced or are used in cuttings and fabrication of metal parts.
This lung of a slate worker shows perivascular inflammation and fibrosis. Silicates account for one third of all known mineral species and are ubiquitous.
Silicosis is an inflammatory and fibrotic lung disease that is caused by the inhalation of silica crystals. Inhalation of silicates such as talc or kaolin produces peribronchial and perivascular aggregates of macrophages that are heavily laden with dust and associated with fibrosis Fig. Several clinical and pathologic forms of silicosis are known. Typical lesions. The silicates not evident in this slide could be seen by polarization microscopy. Black pigment is evidence of anthracosis.
B Fig. The lung of a coal worker shows anthracosilicotic lesions more prominent in the upper lobes. The most important pneumoconioses are silicosis. The disease becomes evident within days or weeks after exposure. It is composed of concentrically layered whorled collagen bands.
Polarization microscopy reveals birefringent particulate matter that appears granular. Silica crystals can be seen in these lesions by polarization microscopy. The lungs show grossly visible black pigmentation Fig. The monocular cell infiltrate at the periphery represents a response to nonquartz silicate particles.
Numerous nonfibrous ferruginous bodies that have round or irregularly shaped black cores also are present. Reddish-brown macules composed of hemosiderin-laden macrophages gradually develop in the lungs Fig. Progressive massive fibrosis. Coal workers ' pneumoconiosis is a fibrosing lung disease of coal workers. Multinucleated giant cells are especially prominent in talcosis. Siderosis applies to the deposition of iron oxide in the lungs.
Histologically the lungs show variable degrees of fibrosis accompanied by infiltrates composed of macrophages and giant cells Fig. A Silicatosis is caused by inhalation of particulate nonfibrous silicate minerals in the absence of silica dust. Typical histologic findings include macules primary dust foci. The lung parenchyma contains aggregates of macrophages and multinucleated giant cells. The lungs show increased black pigmentation. Hard metal disease.
Macule consists of fibrous tissue impregnated with carbon particles. Coal workers' pneumoconiosis. The lungs of this iron ore miner contain aggregates of hemosiderin-laden macrophages. The nodule has a variegated appearance and contains zones of necrosis. Caplan lesion in coal workers' pneumoconiosis.
Variable degrees of fibrosis may be found. Nodule represents a stellate heavily pigmented scar. Asbestos bodies found in or adjacent to the walls of fibrotic res- piratory bronchioles are the hallmark of this disease Fig.
The incidence of bronchial carcinoma also is increased after chronic exposure to asbestos. The most serious consequence of asbestos exposure is mesothelioma. Commercial and noncommercial asbestos. Noncaseating granulomas are found in the peribronchiolar parencyma. Berylliosis is a granulomatous lung disease that develops after exposure to aerosolized beryllium particles. Beryllium has been used for the production of lamps. Histologically mesotheliomas may be classified as epithelial. In addition to pulmonary fibrosis.
Asbestosis is a fibrotic lung disease consequent to longterm exposure to all types of asbestos Diagram The lung contains numerous noncaseating granulomas composed of epithelioid macrophages and giant cells. Histologically the disease is indistinguishable from sarcoidosis and presents in the form of noncaseating pulmonary granulomas Fig. This epithelial variant shows a glandulopapillary growth pattern.
Air spaces contain beaded iron-encrusted brown asbestos bodies. Asbestos body. Malignant mesothelioma. White plaques cover the parietal pleura. Fibrosarcomatous mesothelioma is composed of spindle shaped cells. This pleural tumor has invaded the pericardial cavity encasing the heart. Masson bodies in the alveolar ducts appear as oval shaped structures composed of fibroblasts and collagen. Pulmonary alveolar proteinosis is a disease of unknown etiology.
Parts of the lungs become consolidated due to the accumulation of lipid-rich proteinaceous material in the alveoli Fig.
The epithelium of terminal bronchioles proliferates. The symptoms fail to resolve and the lung parenchyma undergoes patchy consolidation Fig.
Chronic idiopathic pulmonary fibrosis begins insidiously and progresses to end-stage lung disease over a variable period. Most cases of so-called usual interstitial pneumonia UIP show this histologic pattern. Idiopathic organizing pneumonia. Microscopic sections show numerous fibroblastic polypoid protrusions Masson bodies obliterating the respiratory bronchioles. The most important of these diseases are listed in Table Microscopic features include prominent fibrosis replacing focally the normal lung parenchyma.
These findings are. Dyspnea and deterioration of pulmonary function is invariably related to a loss of pulmonary parenchyma and pulmonary fibrosis. Masson bodies obliterate the lumen of bronchioli. In this variant the thick-walled alveoli are filled with numerous macrophages Fig.
The remaining air spaces are abnormal. It presents as progressive dyspnea and respiratory insufficiency. The obliterated bronchioli surrounded with consolidated parenchyma impart a micronodular pattern to the cross section of the lung parenchyma. Bronchiolitis obliterans. Some cases. The lungs are firm and fibrotic and the normal areas alternate with foci of scarring Fig. Idiopathic pulmonary fibrosis. Pulmonary alveolar proteinosis. Desquamative interstitial pneumonia. The alveoli are filled with granular.
The alveoli have thick walls and are filled with numerous macrophages. Cross section of the lung shows fibrosis with microcystic dilatation of air spaces. The lung parenchyma has a simplified structure because of a loss of alveoli.
Several microscopic categories are recognized Table Hilar squamous cell carcinoma. Neuroendocrine granules can be seen by electron microscopy. The tumor originates from the main bronchus. Histologically they present as squamous cell. Bronchioloalveolar carcinoma is a form of peripheral adenocarcinoma that grows along the alveolar septa.
The tumor contains areas of necrosis right upper corner. Other primary malignant tumors are less common. Squamous cell carcinoma of the bronchus. Hilar tumors originate from the epithelium of the main bronchi Fig. Peripheral subpleural tumors. The tumor is composed of small blue cells that have elongated or round nuclei.