R. section Labs

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    Alveoli with macrophage, edema
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    alveolar macrophages with cytoplasmic anthracotic pigment (dust cells).
  3. What is a bronchopulmonary segment?
    A bronchopulmonary segment is a subunit of a lung lobe served by a third generation bronchus
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    Heavy, wet lung secondary to acute exudative phase of diffuse alveolar damage (DAD). Scattered small foci of hemorrhage frequently accompany the DAD due to the extensive microvascular injury.
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    Hyaline membranes are rare to absent during the first day following lung injury, then rapidly increase to peak at approximately day 3-5.
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    Micro of lung demonstrating the changes of the exudative phase of diffuse alveolar damage (DAD). Hyaline membranes are prominent.
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    Bilateral fluffy infiltrates reflect the alveolar filling with high protein edema fluid.
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    Lung weight is significantly increased and the lung has a solid, almost meaty appearance in some areas reflecting the consolidative result of organizing DAD. Other areas demonstrate small cysts that are formed as a result of the lung damage.
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    Organizing diffuse alveolar damage. Alveolar spaces are largely filled with debris, inflammatory cells and fibroblasts.
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    Micro of organizing diffuse alveolar damage (DAD). Alveolus in center of field is rimmed by hyperplastic type II pneumocytes attempting to repair the damaged alveolar epithelial surface.
  11. Question: What are hyaline membranes?
    Answer: By light microscopy, hyaline membranes are homogenous eosinophilic structures that are arranged in a layer along the alveolar septa. However, by electron microscopy, hyaline membranes are a heterogenous mix of debris from necrotic cells, proteinaceous material and a small amount of fibrin. Hyaline membranes generally appear 24-48 hours after the onset of the protein-rich pulmonary edema of DAD and are most prominent 3-4 days after injury. They begin to disappear about 1 week after injury as the organizing/proliferative phase of DAD begins.
  12. Question: What is the significance of the type II pneumocyte hyperplasia?
    Answer: While more numerous than type I pneumocytes, type II pneumocytes cover only a small fraction of the alveolar surface (< 5%). Type I pneumocytes are not generally capable of cell division, hence, when large numbers of type I cells are damaged and sloughed as in DAD, it is the type II cells that are responsible for the epithelial repair of the alveolar surface. Several days to a week after the onset of the exudative phase of DAD, the proliferation of type II cells begins. This finding bridges the acute/exudative and the organizing/proliferative stages of DAD. The proliferating II cells reline the denuded epithelial basement membranes and differentiate into type I cells.
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    Arrow points to a large pulmonary artery which has been almost totally obliterated by an organizing white-tan, older pulmonary embolus.
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    Wedge shaped hemorrhagic defect of recent pulmonary embolus with infarction.
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    Marked medial thickening of pulmonary arteries with compression of the vascular lumen. (due to increased pulmonary pressure secondary to PE
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    Recanalization of the occluded artery produces multiple smaller vessels within the original artery.
  17. Question: What are the causes of pulmonary hypertension?
    Answer: There are numerous causes of pulmonary hypertension. In newborn infants, pulmonary hypertension can result from increased pulmonary blood flow (atrial and ventricular septal defects, patent ductus arteriosus) and in adults, from mitral stenosis, left ventricular failure, multiple pulmonary thromboemboli, chronic hypoxia, emphysema, interstitial fibrosis and pulmonary veno-occlusive disease. In addition, some cases of pulmonary hypertension are idiopathic. In general, increased pulmonary blood flow, chronic venous congestion, obstruction of major arteries, hypoxia or destruction of the pulmonary capillary bed can lead to pulmonary hypertension.
  18. Question: What is the likely cause of the vascular changes (medial hypertrophy and subendothelial fibrosis) in the patient with thromboembolitic disease?
    The numerous recent and organized thromboemboli suggests that recurrent embolization of the pulmonary vascular bed is responsible for the development of pulmonary hypertension. The numerous thromboemboli result in a marked increase in pulmonary vascular resistance leading to an increase in pulmonary arterial blood pressure.
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    Two areas of bronchopneumonia. There are multiple similar areas scattered throughout the lung. Sagittal cut of lung with multiple, slightly raised gray-white foci of bronchopneumonia scattered throughout the lung.
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    Numerous pmn's fill alveolar spaces in acute bronchopneumonia
  21. What is the gross anatomic difference between bronchopneumonia (lobular pneumonia) and lobar pneumonia?
    Bronchopneumonia is a patchy suppurative inflammatory process which is distributed along the bronchioles giving this process a "lobular" pattern. Bronchopneumonia is more often multilobar and frequently bilateral and basal because of the tendency for secretions and fluids to gravitate into the lower lobes. Lobar pneumonia is a suppurative inflammatory process involving a large portion of a lobe or an entire lobe.
  22. What organisms are commonly associated with lobar pneumonia?
    Streptococcus pneumoniae (pneumococcus) is the most common cause of community acquired lobar pneumonia. Occasionally other bacteria may cause this entity, especially Klebsiella pneumoniae and Staphylococcus aureus.
  23. Which patients are at risk for developing pneumocystis pneumonia?Image Upload 16
    Pneumonia due to Pneumocystis carinii is a problem in malnourished infants or immunosuppressed patients. Prior to the institution of routine prophylaxis it was the leading cause of respiratory failure in patients with acquired immune deficiency syndrome. The organisms grow within pulmonary alveoli where they can be identified in three developmental stages: cysts, sporozoites and trophozoites. The cysts are cup shaped, round or crescent shaped structures containing up to 8 sporozoites. When sporozoites are released from ruptured cysts, they develop into mature cysts and repeat the cycle. Infection with a second opportunistic and/or infectious agent (Candida, Cytomegalovirus, Aspergillus, Mycobacteria, Legionella pneumophilia or Streptococcus pneumoniae) is common in patients with AIDS and Pneumocystis pneumonia. Pneumocystis carinii is not a virulent organism and generally does not cause disease in healthy individuals who are not immunosuppressed. While once thought to be a parasite, Pneumocystis is now thought to be a fungus.

    PHOTO: Pneumocystis cyst stains darkly with silver (GMS) stain. There are multiple similar cysts within the single alveolus depicted in this photo.
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    Centrilobular (centriacinar) emphysema due to smoking. Note upper zonal prominence.

    • *In contrast panacinar will affect the lower lobes predominately
    • ** Distal Acinar emphysema will also affet the upper lung zone (but will have a subpleural location, and often see the subpleural blebs)
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    Under the microscope, the destructive nature of the emphysematous process can be seen as only "threads" of fibrovascular tissue remain in the abnormally enlarged airspaces.
  26. What is the definition of emphysema?
    Emphysema is defined as permanent, abnormal enlargement of any part or all of the acinus accompanied by destruction of respiratory tissue without significant fibrosis. Note that the enlargement must be permanent, so hyperinflation due to an asthma attack would not qualify as emphysema. The enlargement is abnormal such that the enlargement of alveolar ducts normally seen with aging does not meet the definition of emphysema. Lastly, the definition includes destruction - so the hyperinflation in the contralateral lung seen following pneumonectomy does not meet the criteria for emphysema, even though the residual lung frequently demonstrates permanently enlarged (hyperinflated) acini.
  27. What are the four patterns of acinar involvement in emphysema?
    Emphysema has been classified into four major patterns of acinar involvement; however, many cases exhibit mixed patterns. In centriacinar (proximal acinar) emphysema, the respiratory bronchioles, which are located in the proximal portion of the acinus, are abnormally enlarged and destroyed. In panacinar emphysema, the enlargement and destruction involves the acinus more or less uniformly. In distal acinar emphysema (paraseptal emphysema), alveolar ducts are predominantly affected. In irregularemphysema, there is irregular enlargement and destruction of the acinus.
  28. What patterns of emphysema are associated with chronic airflow obstruction (chronic obstructive pulmonary disease)?
    Proximal acinar (centrilobular/centriacinar) emphysema and panacinar (panlobular) emphysema may be associated with the clinical findings of chronic airflow limitation. Irregular emphysema and distal acinar emphysema are generally not associated with chronic airflow limitation.
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    Slice of lung demonstrating severe bronchiectasis throughout lung in patient with CF
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    triking bronchiectasis with peribronchial and peribronchiolar fibrosis is present. The respiratory epithelium is focally eroded and there is squamous metaplasia. The lumens of airways are focally filled with mucus, leukocytes and necrotic epithelium. There is focal intraalveolar hemorrhage associated with areas of abscess formation and organizing pneumonia.

    Arrow points to inflammatory debris within airway lumen.
  31. What is thought to cause the changes in lung parenchyma in patients with cystic fibrosis?
    The changes in the lungs of patients with cystic fibrosis are secondary to the viscid mucus that results in defective mucociliary clearance, mucus plugs and consequent recurrent infections and inflammation of the bronchial and bronchiolar airways. The resulting peribronchial fibrosis presumably puts traction on weakened conducting airways which causes dilation. Ultimately bronchiectasis, cystic change and fibrosis characterize the gross appearance of the lungs.
  32. What are the two most common organisms responsible for lung infection in cystic fibrosis?
    Staphylococcus aureus and Pseudomonas aeruginosa are the two most common organisms.
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    This is an example of more fully developed bronchiectasis. Ectatic bronchi are distended beyond the confines of the bronchial cartilages with associated attenuation of bronchial smooth muscle bundles. Inspissated mucus is present in distended remodeled air spaces. There is confluent fibrosis with chronic inflammation.

    Destroyed lung parenchyma, distal to an area of obstruction, with honeycomb change, mucostasis and fibrosis.
  34. What are the causes of bronchiectasis and how does the distribution of bronchiectasis vary with the etiology?
    Postinfective`adenovirus, measles, pertussis, tb, staph, intralobar sequestration Bronchial obstructionforeign bodies, tumors, mucous plugs. Irritants - ammonia Aspiration - heroin addicts. Hereditary abnormalities - cystic fibrosis, ciliary dyskinesia. Congenital anomalies - congenital bronchiectasis. Immunologic abnormalities - hypogammaglobulinemia, defective pmn's, macrophages.
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    End stage lung due to UIP. Note small shrunken size of the lung, prominent interstitial fibrosis and zones of honeycomb change.

    Cut sections showed areas of fibrosis, honeycomb change and consolidation more prominent basally and peripherally.
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    The variably sized cystic spaces represent honeycomb lung. These are revised, distorted airspaces lined by bronchiolar epithelium and fibrous tissue. No air exchange takes place in the honeycomb zones.
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    Sections show diffuse interstitial fibrosis with alveolar septa widened by dense fibrosis and mild chronic inflammatory cell infiltrates.
  38. What is the cause of this patient’s lung disease? (interstitial fibrosis)
    The histologic changes are those of end-stage chronic interstitial pneumonitis. The etiology of this process is now impossible to ascertain because of the diffuse scarring. In many cases, the cause of chronic interstitial lung disease is unknown and these cases are usually grouped together as Usual Interstitial Pneumonia (UIP) (Idiopathic Pulmonary Fibrosis). There are several different types of chronic interstitial lung disease including hypersensitivity pneumonitis, usual interstitial pneumonia and interstitial lung disease associated with collagen vascular diseases that can result in an end-stage honeycomb lung. Treatment with chemotherapeutic agents, infections with virus or mycoplasma, exposure to asbestos and prolonged hypersensitivity pneumonitis (mold, animal proteins) can lead to interstitial fibrosis.The prognosis of some forms of interstitial lung disease is not good although it depends upon the specific type of interstitial disease. Most patients with usual interstitial pneumonia have a survival of only four to five years after initial diagnosis. Hypersensitivity pneumonitis is associated with a good prognosis if the offending agent can be identified and avoided. The hallmarks of hypersensitivity pneumonitis include a respiratory bronchiolitis with associated chronic interstitial inflammation including granulomatous inflammation and/or loose aggregates of epithelioid macrophages.
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    View of diaphragm from above demonstrating ivory colored, firm pleural plaques (arrows) associated with exposure to respirable asbestos.
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    Ferruginous body with thin, clear core of asbestos (asbestos body)
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    Malignant mesothelioma of pleura. This pleural based tumor encases the lung and extends along the fissures to involve the hilar structures.
  42. What is asbestosis?
    Asbestosis is asbestos-induced interstitial pulmonary fibrosis
  43. What is the significance of the bilateral pleural plaques noted by chest x-ray and at postmortem?
    Bilateral lower zonal parietal pleural plaques serve as markers of asbestos exposure, in fact, they are the most common manifestation of this exposure. Although there are other rare causes of similar pleural plaques, bilateral symmetrical plaques are most often associated with exposure to respirable asbestos. Plaques are distinct from malignant mesothelioma and there is no evidence of a transition between the two, although they may coexist.
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    Note the prominence of the right hilar outline due to the hilar squamous cell carcinoma.
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    Opened bronchus cuffed by squamous cell carcinoma.
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    Lobules of infiltrating squamous cell carcinoma. Arrow points to a prominent zone of squamous differentiation (squamous pearl/keratinization)
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    Intercellular bridges and/or keratinization by light microscopy are the features of squamous cell carcinoma of the lung.
  48. s the incidence of squamous cell carcinoma related to cigarette smoking?
    Yes. There is a strong association between smoking and squamous carcinoma. All 4 major types of lung carcinoma are associated with smoking; however, squamous carcinoma and small cell carcinoma are strongly associated with a smoking history while adenocarcinoma and large cell undifferentiated carcinoma have definite, although weaker, associations with smoking.
  49. What is the distribution of squamous cell carcinomas within the lung?
    The majority of squamous and small cell bronchogenic carcinomas arise in the central portions of the lung, commonly in association with the main, segmental, or subsegmental bronchi. However, approximately one-third of squamous carcinomas arise in the periphery of the lung. The majority of adenocarcinomas arise in the periphery of the lung.
  50. What are some of the more common symptoms of patients presenting with lung cancer?
    Weight loss, cough, dyspnea, weakness, chest pain, and hemoptysis are some of the more common presenting complaints. Occasionally, a patient will present with symptoms in another body site due to metastatic disease even before the primary lung tumor is identified.
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    Most carcinoid tumors (80%) are centrally located and associated with a bronchus (lobar, segmental or subsegmental).
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    Microscopic appearance of carcinoid tumor. With special stains or electron microscopy numerous neurosecretory granules can be identified within the cytoplasm of the tumor cells.

    The cells of the tumor are remarkably uniform with abundant pink cytoplasm and often centrally located nuclei. Some areas of the tumor are formed by solid sheets of tumor cells growing in a mosaic pattern with numerous capillaries.
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    Carcinoid tumor

    The cells of the tumor are remarkably uniform with abundant pink cytoplasm and often centrally located nuclei. Some areas of the tumor are formed by solid sheets of tumor cells growing in a mosaic pattern with numerous capillaries.
  54. Do bronchial carcinoids produce bioactive peptides?
    Bronchial carcinoids have been shown to produce and release serotonin. However, the association of carcinoid syndrome with a bronchial carcinoid is rare. A number of other bioactive peptides have been shown to be released from bronchial carcinoids including: ACTH, insulin, pancreatic polypeptide and gastrin releasing peptide.
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    Note the accentuation of the interlobular septa and bronchovascular bundles. These structures are richly enmeshed with the lymphatics. In lymphangitic metastatic carcinoma the lymphatics are filled with tumor, accentuating the septa and bronchovascular bundles.

    The mediastinal and hilar lymph nodes are partially replaced with tumor. The pleural surfaces exhibit a lace-like pattern of tumor filling the subpleural lymphatic spaces. Many of the pulmonary arteries are partially filled with metastatic tumor and thrombus. The bronchovascular bundles are grossly thickened due to tumor infiltration.
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    Metastatic carcinoma

    Vascular invasion by tumor is the most prominent finding. Numerous pulmonary arteries are filled with clot and tumor. Some of the small, tumor-filled, thin walled endothelial lined channels in the bronchovascular bundles probably represent lymphatic invasion. The peribronchial tissue is rich in lymphatics - this explains why transbronchial biopsy has such high yields in diseases that are distributed along lymphatics, such as metastatic malignancies, sarcoidosis, tuberculosis and others.
  57. How do tumors generally metastasize to the lungs? What are the more common clinical presentations of metastatic lung disease?
    Metastatic tumors generally reach the lungs via a lymphatic route and/or a hematogenous route. Unusually, tumor is hypothesized to spread along airspaces such as in unusual cases of bronchioloalveolar carcinoma (a variant of adenocarcinoma).
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    This is the most common pattern of metastatic tumor involving the lung - multiple, predominantly peripheral tumor masses.
  59. How do you differentiate a primary adenocarcinoma from a metastatic adenocarcinoma?
    Sometimes with great difficulty! The distinction between a solitary primary adenocarcinoma of the lung in a patient with a history of a previous adenocarcinoma can be very difficult since histologic features of adenocarcinomas are similar from different anatomic sites and the incidence of new primary carcinomas in patients with a known diagnosis of carcinoma is high (i.e., you can’t assume a new pulmonary nodule in a patient with cancer is the same cancer). A pathologist can compare the histologic features of a patient’s previous adenocarcinoma with the histologic features of the new solitary pulmonary adenocarcinoma in an attempt to decide if a tumor is metastasis from a previous known primary. Also, immunohistochemical stains can sometimes help in deciding if a tumor is a metastasis. The presence of multiple tumor nodules in the lung suggests an adenocarcinoma in the lung is a metastasis.
  60. Are there benign tumors of the lung? If so, what is the most common benign tumor of the lung?
    Yes. The hamartoma is the most common benign tumor of the lung in adults.
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    Well demarcated lobulated hamartoma readily shells out from lung parenchyma. Hamartoma is the most common benign tumor of the adult lung
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R. section Labs
R. section Labs