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Determining whether multiple carcinomas represent synchronous primaries or intrapulmonary metastases is a difficult topic arrhythmia vs palpitations purchase cheap zestoretic. Because the resected lung tissue is collapsed, pathologists may have more difficulty than radiologists or surgeons identifying small tumors. This is particularly the case with adenocarcinomas with a predominant lepidic component. Multiple tumors are considered synchronous primaries if they are of different histological cell types. Multiple tumors of similar histological appearance should only be considered to be synchronous primary tumors if in the opinion of the pathologist, based on features such as differences in morphology, immunohistochemistry and/or molecular studies, or, in the case of squamous cancers, being associated with carcinoma in situ, they represent differing subtypes of the same histopathological cell type. Such cases should also have no evidence of mediastinal nodal metastases or of nodal metastases within a common nodal drainage. These circumstances are most commonly encountered when dealing with lepidic-pattern adenocarcinomas (see Chapter 27). The highest T category and stage of disease should be assigned and the multiplicity or the number of tumors should be indicated in parenthesis. Careful palpation during surgery and by the pathologist of the resected specimen is therefore required to screen for the presence of additional tumor nodules. Only nodules discovered for the first time at pathological examination are classified as additional nodules. However, oncologists have not found it useful, preferring to continue with the "limited" versus "extensive" classification. However, many issues remain unresolved including the validity of this system for typical versus atypical carcinoid tumors, the validity of staging multicentric carcinoid tumors, the validity of size cut-offs in the determination of T value, and the prognostic significance of thoracic lymph node metastases. The designation R1 (microscopic incomplete resection) is assigned when there is microscopic evidence of residual disease at either the resection margins or lymph node margins feature extracapsular extension. The designation R2 (macroscopic incomplete resection) is assigned if macroscopic evidence of residual disease is identified at the resection margins, at the edge of lymph nodes with extracapsular extension or if either involved lymph nodes, pleural or pericardial nodules were not resected at surgery. Cases where there is no macroscopic or microscopic evidence of residual disease but nodal assessment has been based on less than the number of nodes/stations recommended for complete resection and/or the highest mediastinal node removed/sampled is positive qualify for this designation. Effect of formalin fixation on tumor size determination in stage I non-small cell lung cancer. Effect of number of lymph nodes sampled on outcome in patients with stage I non-small-cell lung cancer. Which is the better prognostic factor for resected non-small cell lung cancer: the number of metastatic lymph nodes or the currently used nodal stage classification The impact of stage and cell type on the prognosis of pulmonary neuroendocrine tumors. International Association for the Study of Lung Cancer Staging Handbook in Thoracic Oncology. Impact of positive pleural lavage cytology on survival in patients having lung resection for non-small-cell lung cancer: an international individual patient data meta-analysis. It may be helpful as a supplement to morphology in classifying primary lung tumours. This subclassification is increasingly important, as emerging therapeutic options demand increasing diagnostic exactitude. The technique is also invaluable in deciding whether a tumor, particularly an adenocarcinoma, is a pulmonary primary or arises from an extra-pulmonary site. If metastatic, immunohistochemical stains can also often determine the primary site. Since the exact conditions of tissue fixation, antigen retrieval and staining vary between laboratories, diagnostic laboratories do not exactly reproduce the conditions of the published studies. Deciding whether a tumor shows positive staining also has an element of subjectivity. Cut-off levels vary between studies and often involve a combination of staining intensity and proportion of cells stained, for which there is no universally agreed scoring system. Some antibodies, when applied to some tumors, have given rise to hundreds of reported cases with consistent results.

Electron microscopy Electron microscopy has not been described for pulmonary chondroma connexin 43 arrhythmia order zestoretic cheap. Radiographic findings Pulmonary chondromas are well-circumscribed tumors with socalled "popcorn" calcification on X-ray. Differential diagnosis the primary differential diagnosis of pulmonary chondroma is pulmonary hamartoma. Unlike pulmonary chondroma, the latter contains varying amounts of fat and has cleft-like spaces of entrapped lung epithelium. Unlike pulmonary chondromas, pulmonary hamartomas typically lack a thin fibrous pseudocapsule, and significant osseous metaplasia or calcification. Malignant histological features and a clinicoradiological history of chondrosarcoma at another site will assist in determining the diagnosis. Prognosis and natural history Surgery is typically curative for pulmonary chondromas. As with other tumors, centrally located primary pulmonary chondrosarcomas may elicit symptoms earlier, and with more severity, than peripheral tumors. Very rarely, poorly differentiated and dedifferentiated primary pulmonary chondrosarcomas have been reported. Sarcomatoid mesothelioma with chondrosarcomatous foci might be confused with primary pulmonary chondrosarcoma. Von Recklinghausen disease is a predisposing factor and perhaps for this reason neurofibroma is the most common nerve sheath tumor. Morphology, immunohistochemistry and ultrastructural studies are identical to soft tissue counterparts. The differential diagnosis for benign lesions includes intrapulmonary solitary fibrous tumor while malignancies should be separated from metastatic lesions as well as other rare sarcomas. Benign lesions amenable to surgical resection are cured, while malignant tumors are often treated with surgery, chemotherapy and radiation therapy. This minute schwannoma demonstrates the origin of primary pulmonary nerve sheath tumors. However, the ages range from approximately 10 to 60 years of age, with a mean of approximately 45 years. Macroscopic pathology Most granular cell tumors of the lung arise as polypoid 2 to 3 cm endobronchial masses. Granular cell tumors of the lung generally arise from the bronchial wall and there is variable infiltration of this structure and underlying lung parenchyma. Tumors may exhibit ulceration of overlying bronchial mucosa, especially if the tumor is pedunculated. Radiographically demonstrated infiltrative tumor may suggest a preoperative diagnosis of malignancy. Very rarely, granular cell tumor of the lung will radiographically present as a peripheral coin lesion. Increased tumor size, multiple endobronchial tumors and extrapulmonary tumor involvement do not affect benignity. The tumor border 1241 Chapter 33: Mesenchymal and miscellaneous neoplasms may be "pushing" or infiltrative. Metastasis, necrosis, inflammation and hemorrhage are not characteristics of pulmonary granular cell tumor. If one or two of the criteria, excluding focal pleomorphism, were present, this warranted the diagnosis of atypical granular cell tumor. Granular cell carcinomas defined as malignant showed a high rate of metastases and short survival. Occasionally adenocarcinomas may exhibit finely granular cytoplasm, but nuclear atypia, necrosis and mitoses are not characteristics of pulmonary granular cell tumor. Especially in the case of peripheral tumors, multiple tumors, or tumors exhibiting significant atypia, hemorrhage or necrosis, metastatic granular cell tumor from a non-pulmonary site must be considered in the differential diagnosis. Histiocytic reactive conditions, such as malakoplakia and mycobacterial infections, may superficially resemble pulmonary granular cell tumor. These conditions do not exhibit a monotonous sheet of cells, and typically have an associated variable, mixed inflammatory infiltrate.

Predominantly necrotic carcinoma may only have viable tumor cells on alveolar walls pulse pressure graph buy zestoretic 17.5 mg otc. The "alveolar filling" pattern aptly describes tumor cells filling airspaces without destroying alveolar septa. This microscopic field is from the edge of the carcinoma and features a host immune response. Cytology Squamous cell carcinoma is readily diagnosable on a variety of sample types ranging from sputum secretions to percutaneous needle aspirates (Table 4). Rapid and accurate diagnoses can be rendered regardless of whether a tumor is bronchoscopically visualized. Keratinizing squamous carcinoma usually exfoliates as single cells, so one should not diagnose this tumor type unless single cells are seen. In some cases the cytoplasm obscures karyolytic nuclei producing so-called "ghost cells". Malignant pearls differ from benign counterparts in that the former are usually smaller with greater amounts of cytoplasmic keratinization. Also, only poorly differentiated carcinomas demonstrate bizarre shapes or abnormal nucleoli. Tumor cells vary in size but thick cytoplasm is apparent (Papanicolaou preparation). Cells vary in size and shape but all are significantly larger than background inflammatory cells (Papanicolaou preparation). This nonkeratinizing carcinoma has less cytoplasm than most keratinizing variants. The presence of occasional keratinizing cells, probably derived from the shedding surface cells, aid in tumor classification. This sheet-like arrangement of tumor cells has ample cytoplasm and variable-sized nuclei. Oral cavity, esophagus and upper respiratory tract carcinomas can be diagnosed in exfoliative samples, while metastases from the uterine cervix and urinary bladder, to name a few, may rarely initially present as pulmonary disease. Clinical correlation serves one far better than even judicious use of immunohistochemical stains. Papillary architecture but no cellular detail may be seen in fine-needle aspirates. Gene expression profiling is positioned to solve this common clinical dilemma (see below). Cells have short filopodial processes that interdigitate with processes of adjacent tumor cells. The sulfhydryl-rich membrane-coating granules deposit along the inner surface of the cell membrane prior to cell death and should not be confused with surfactant granules. Tumor cells penetrate lung parenchyma along the epithelial side of the alveolar basal lamina and extend small pseudopods through that basal lamina. Non-neoplastic alveolar epithelial cells are detached from the basal lamina or are overgrown by tumor cells but not destroyed. Aberrant methylation of CpG islands in the promoter region of tumor suppressor genes is perhaps the most common mechanism for inactivating cancer-related genes in non-small cell lung cancer. However, tumor cavitation rather than squamous histology may be the risk for severe pulmonary hemorrhage associated with bevacizumab. Overdiagnosing carcinoma on cytological and biopsy specimens is particularly perilous and one should correlate the morphological findings with clinical and radiographic information in all cases. Reactive squamous atypia as well as metaplastic mucosa are recognized findings in diffuse alveolar damage, pulmonary infections, infarcts, and in individuals treated for malignancy with chemotherapy and/or radiation therapy. The cytological hallmarks of reactive atypia include bizarre nuclei with preserved nuclear/cytoplasmic ratios. Recognizing the underlying pathology, such as an infarct or diffuse alveolar damage, as well as extension of metaplastic epithelium through the canals of Lambert into alveolar spaces, suggests the correct diagnosis. While squamous cell papillomas lack malignant cytology and stromal invasion, pulmonary involvement with laryngotracheal papillomatosis can be extremely difficult to distinguish from carcinoma. Papillomas may fill airspaces and elicit a pseudodesmoplastic stromal response, yet only carcinoma destroys underlying lung and infiltrates in small irregular nests and single cells. Entrapped benign glandular cells or pseudogland formations should not be mistaken for adenosquamous carcinoma.

Rudner Drug-induced lung disease represents one of the more challenging areas of pulmonary medicine from both a clinical and pathological standpoint blood pressure medication hair growth buy discount zestoretic 17.5 mg on line. Over 300 agents are associated with adverse pulmonary reactions and the list is continually expanding. Anaphylaxis, bronchospasm and pulmonary edema are examples of such acute reactions. Subacute reactions occur days to weeks following administration and chronic reactions manifest months to years after initiation of a particular drug. Complicating the picture are drug reactions presenting as an acute lung disease in patients who have taken a drug for years. Further confounding the picture, a patient may have multiple factors which could potentially contribute to the development of pulmonary disease. Radiographic findings similarly tend to reflect the wide range of histological findings associated with drug toxicity and are typically not specific by themselves. However, since elevated levels have not been observed in infectious pneumonia, aspergillosis, asthma, idiopathic eosinophilic pneumonia or organizing pneumonia, this test may be of some value. Criteria for diagnosis of a pulmonary drug reaction include correct identification of the drug in question, exclusion of other primary or secondary lung diseases, an appropriate temporal relationship, a characteristic reaction pattern to a specific drug, and remission of symptoms with removal of drug. Confirmation would ideally include recurrence of symptoms with rechallenge but in reality this is seldom done. In other clinical situations, where the association is less clear cut or the patient has other potential diagnostic considerations, biopsy may be performed. First, he/she should identify the histological pattern of disease, which may exclude other diagnoses. For example, eosinophilic pneumonia in a patient with suspected toxicity, related to sulfasalazine, and lacking other potential causes of eosinophilic pneumonia supports a clinical diagnosis of drug toxicity. The second major role of the pathologist is to exclude other potential causes of lung disease, especially infections. As with most diffuse lung diseases, a wedge biopsy or large tissue sample provides the most information with regard to classification of the histological pattern of disease. It is essential the pathologist remembers a small biopsy may not be representative. Drug-induced pulmonary disease in the broadest sense also includes secondary infections and malignancies, which are covered elsewhere in the text. Histological patterns associated with drug toxicity Drug-induced lung disease is not characterized by a single or specific histological pattern of lung disease. A single drug may be associated with multiple different microscopic patterns of pulmonary disease. Additionally, retrospective review of the literature is complicated by the use of outdated or inappropriate nomenclature. Table 1 summarizes the most common histological patterns of disease and the associated drugs. Additionally, some drug toxicities have been associated with a presentation of radiographic nodules, mimicking malignancy. While some of these reactions represent nodular foci of organizing pneumonia or granulomas, unique findings, such as those discussed in the section on amiodarone, also occur. As the list of drugs with pulmonary reactions is constantly expanding, the reader is referred to the excellent website Pleural disease associated with drug toxicity, while less frequently encountered than parenchymal, will also be discussed. Drug reactions associated with selected drugs of frequent clinical inquiry will follow. Pathogenesis of drug-induced pulmonary disease the mechanism of drug-induced pulmonary injury is poorly understood. Most therapeutic drugs reach the lungs through the bloodstream via intravenous or enteric intake, although some may be administered by inhalation. Several theories have been suggested regarding the development of pulmonary toxicity. First, a drug may cause direct injury to pneumocytes or capillary endothelium resulting in release of cytokines and recruitment of inflammatory cells.

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