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Part 1 book “Pulmonary pathology - An atlas and text” has contents: Normal cytology and histology, artifacts and age-related changes, malignant neoplasms, benign neoplasms, pulmonary histiocytic proliferations, benign and borderline lymphoid proliferations, granulomatous diseases,… and other contents.
Pulmonary Pathology An Atlas and Text THIRD EDITION Editor-in-Chief Philip T Cagle, MD Professor, Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas Associate Editors Timothy C Allen, MD, JD Professor and Chair, Department of Pathology, University of Mississippi Medical Center, Jackson, Mississippi Mary Beth Beasley, MD Professor, Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York Alain Borczuk, MD Professor of Pathology, Department of Pathology, NewYork-Presbyterian Hospital/Weill Cornell Medical Center, New York, New York Yasmeen M Butt, MD Assistant Professor, Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas Sanja Dacic, MD, PhD Professor of Pathology, Department of Pathology, University of Pittsburgh, Staff Pathologist, Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Aliya N Husain, MD Professor, Department of Pathology, University of Chicago, Chicago, Illinois Brandon T Larsen, MD, PhD Assistant Professor, Department of Laboratory Medicine and Pathology, Mayo Clinic School of Medicine, Senior Associate Consultant, Department of Laboratory Medicine and Pathology, Mayo Clinic Arizona, Scottsdale, Arizona Ross A Miller, MD Assistant Professor, Pathologist, Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas Mari Mino-Kenudson, MD Associate Professor, Department of Pathology, Harvard Medical School, Director, Pulmonary Pathology Service, Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts Sergio Pina-Oviedo, MD Assistant Professor, Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas Kirtee Raparia, MD Associate Pathologist, Department of Pathology, Kaiser Permanente Santa Clara Medical Center, Santa Clara, California Natasha Rekhtman, MD, PhD Associate Attending Pathologist, Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York Anja C Roden, MD Associate Professor, Consultant, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota Sinchita Roy-Chowdhuri, MD, PhD Assistant Professor, Department of Pathology, University of Texas MD Anderson Cancer Cente r, Hou st on, Te xas Lynette M Sholl, MD Associate Pathologist, Department of Pathology, Brigham and Women’s Faulkner Hospital, Boston, Massachusetts Maxwell L Smith, MD Associate Professor, Department of Laboratory Medicine and Pathology, Mayo Clinic School of Medicine, Consultant, Department of Laboratory Medicine and Pathology, Mayo Clinic Arizona, Scottsdale, Arizona Table of Contents Cover image Title page Copyright Dedication Contributing Authors Preface to the Third Edition Preface to the First Edition Acknowledgments Section 1 Normal Cytology and Histology Sinchita Roy-Chowdhuri Chapter Bronchus Chapter Bronchioles and Alveolar Ducts Chapter Blood Vessels and Lymphatics Chapter Alveoli Chapter Pleura Chapter Normal Cytology of the Lung and Pleura Section 2 Artifacts and Age-Related Changes Sinchita RoyChowdhuri Chapter Procedural and Laboratory Artifacts Chapter Reactive Changes, Nonspecific Findings, and Age-Related Changes Chapter Noncellular Structures Section 3 Malignant Neoplasms Mari Mino-Kenudson, Sergio PinaOviedo, Sanja Dacic, Timothy C Allen, Ross A Miller, Philip T Cagle Chapter 10 Adenocarcinoma Part 1. Lepidic Adenocarcinoma Part 2. Acinar Adenocarcinoma Part 3. Papillary Adenocarcinoma Part 4. Micropapillary Adenocarcinoma Part 5. Solid Adenocarcinoma Part 6. Invasive Mucinous Adenocarcinoma Part 7. Colloid Adenocarcinoma Part 8. Fetal Adenocarcinoma Part 9. Enteric Adenocarcinoma Part 10. Signet Ring and Clear Cell Features Chapter 11 Squamous-Cell Carcinoma Part 1. Keratinizing Squamous-Cell Carcinoma Part 2. Nonkeratinizing Squamous-Cell Carcinoma Part 3. Basaloid Squamous-Cell Carcinoma Chapter 12 Adenosquamous Carcinoma Chapter 13 Large-Cell Carcinoma Chapter 14 Neuroendocrine Carcinomas Part 1. Small-Cell Carcinoma Part 2. Carcinoid Tumor Part 3. Atypical Carcinoid Tumor Part 4. Large-Cell Neuroendocrine Carcinoma Chapter 15 Sarcomatoid Carcinomas Part 1. Carcinosarcoma Part 2. Pulmonary Blastoma Part 3. Pleomorphic Carcinoma Chapter 16 Salivary Gland–Type Cancers Part 1. Adenoid Cystic Carcinoma Part 2. Mucoepidermoid Carcinoma Part 3. Epithelial–Myoepithelial Carcinoma Chapter 17 Lymphoepithelioma-Like Carcinoma Chapter 18 NUT Carcinoma Chapter 19 Primary Pulmonary Sarcomas Part 1. Inflammatory Myofibroblastic Tumor Part 2. Pleuropulmonary Blastoma Part 3. Epithelioid Hemangioendothelioma Part 4. Kaposi Sarcoma Part 5. Synovial Sarcoma Part 6. Malignant Solitary Fibrous Tumor Part 7. Intimal Sarcoma Part 8. SMARCA4-Deficient Thoracic Sarcoma Part 9. Primary Pulmonary Myxoid Sarcoma with EWSR1CREB1 Translocation Chapter 20 Secondary Pulmonary Sarcomas Part 1. Leiomyosarcoma Part 2. Angiosarcoma Part 3. Osteosarcoma Part 4. Chondrosarcoma Part 5. Liposarcoma Part 6. Malignant Peripheral Nerve Sheath Tumor Part 7. Rhabdomyosarcoma Part 8. Undifferentiated Soft Tissue Sarcoma Part 9. Ewing Sarcoma Chapter 21 Other Pulmonary Sarcomas Part 1. Alveolar Soft Part Sarcoma Part 2. Clear Cell Sarcoma Part 3. Desmoplastic Small Round Cell Tumor Part 4. Extrarenal Rhabdoid Tumor Part 5. Chordoma Part 6. Extraskeletal Myxoid Chondrosarcoma Chapter 22 Pulmonary B-Cell Lymphomas Part 1. Primary and Secondary Lung Involvement Subpart 1.1 Extranodal Marginal Zone Lymphoma (MZL) of the Mucosa-Associated Lymphoid Tissue (MALT Lymphoma) Subpart 1.2 Diffuse Large B-Cell Lymphoma (DLBCL) Subpart 1.3 Lymphomatoid Granulomatosis (LyG) Part 2. Systemic B-Cell Lymphomas with Secondary Lung Involvement Subpart 2.1 Small B-Cell Lymphomas Subpart 2.2 Other B-Cell Lymphomas Chapter 23 Pulmonary Classical Hodgkin Lymphoma Chapter 24 Pulmonary T-Cell Lymphomas Part 1. Peripheral T-cell Lymphoma, NOS Part 2. Systemic T-cell Lymphomas with Secondary Lung Involvement Subpart 2.1 Pulmonary (Visceral) Involvement by Mycosis Fungoides/Sézary Syndrome Subpart 2.2 Pulmonary Anaplastic Large-Cell Lymphoma (ALCL) Chapter 25 Pulmonary Plasma Cell Neoplasms and Related Conditions Part 1. Primary Pulmonary Plasma Cell Neoplasms Part 2. Systemic Plasma Cell Neoplasm with Secondary Lung Involvement Chapter 26 Other Systemic Hematolymphoid Neoplasms with Secondary Lung Involvement Part 1. Acute Leukemia or Myeloproliferative Neoplasms Subpart 1.1 Acute Leukemia Subpart 1.2 Myeloproliferative Neoplasms Chapter 27 Other Neoplasms of the Lung 10 Figure 78.1 Gross image of bronchiectasis showing dilated segmental bronchi and surrounding parenchymal fibrosis 805 Figure 78.2 A large dilated cystic space lined by ciliated respiratory epithelium and containing mucin with admixed acute inflammatory cells Surrounding fibrosis can be seen 806 CHAPTER 79 Middle Lobe Syndrome Ross A Miller Timothy C Allen The right middle lobe and lingula tend to have reduced collateral ventilation compared with other areas of the lung; the bronchi feeding the right middle lobe and lingula are relatively long and narrow and have a sharp take off from the bronchial tree If there is surrounding lymphadenopathy and/or a mass-forming process, extraluminal compression or intraluminal obstruction can potentially occur and result in middle lobe syndrome Findings include those expected from a postobstructive pathologic process and include atelectasis, infections, organizing pneumonia, lipid pneumonia, and the development of bronchiectasis Middle lobe syndrome is most often seen in adults When it does occur in children, it is often seen in asthmatic patients and spontaneous recovery has been described Lady Windermere syndrome is a classically described rare form of middle lobe syndrome occurring in seemingly healthy middle-aged to elderly women Mycobacterium avium complex has been isolated in these patients and there seems to be a correlation with intentional, long-term, cough suppression Histologic Features ◾ Bronchiectasis, bronchiolectasis, variable inflammation ◾ Organizing pneumonia is often seen; abscess formation can occur ◾ The presence of granulomas and/or granulomatous inflammation may suggest a mycobacterial or fungal infection; one should meticulously look for possible fungal or acid-fast organisms with s peci a l s tai ns at hi ghmagni fi cat i on and corr elate wi t h cul tur es 807 (if available) Figure 79.1 Middle lobe syndrome low-power view shows multiple dilated bronchi with surrounding fibrosis and collapsed lung parenchyma 808 Figure 79.2 Postobstructive pneumonia consists of collapsed lung with intra-alveolar lipid-filled macrophages mixed with neutrophils and interstitial acute and chronic inflammation 809 CHAPTER 80 Tracheobronchopathia Osteochondroplastica Ross A Miller Roberto Barrios∗ Tracheobronchopathia osteochondroplastica (TBO) is an extremely rare condition of unknown etiology causing bronchial obstruction and recurrent pneumonia Numerous nodules composed of bone and cartilage involve the submucosa of the tracheobronchial tree, sparring the membranous portion of the trachea The overlying epithelium can have squamous metaplastic change and/or show areas of erosion/ulceration The condition is typically seen in adult patients and tends to affect males more often than females Usually, the condition is incidentally detected by a chest x-ray or during bronchoscopy; some patients may have nonspecific symptoms such as dyspnea or hemoptysis Bronchoscopic biopsy is typically diagnostic where multiple submucosal 2- to 5-mm nodules are seen involving the tracheobronchial tree The nodules tend to have a propensity for the lower two-thirds of the trachea and often a communication between the nodules and the trachea and/or bronchial cartilage can be found Histologic Features ◾ Tracheal and bronchial submucosal nodules are composed of bone andcar ti l age; the no dul es te nd to be sit ua t ed bet w ee epithelium and normal cartilage ◾ Overlying epithelium can have erosion/ulceration or metaplasia change 810 ◾ Some bone marrow elements can be seen in areas of bone formation ◾ The bone and cartilage is cytologic benign Figure 80.1 Low-power view showing the round areas of ossification partially covered by columnar epithelium Tracheal cartilage plate can also be seen 811 Figure 80.2 High-power view of an area of ossification between the epithelium and the tracheal glands ∗ The author would like to acknowledge the work of Dr Barrios, who contributed to the previous edition 812 CHAPTER 81 Asthma Ross A Miller Philip T Cagle Asthma can occur from a variety of allergic and nonallergic stimuli Regardless of the inciting stimulus, the symptomatology results from increased airway irritability, resulting in acute or episodic airway narrowing The airway narrowing can resolve spontaneously; however, many patients require some type of pharmacologic intervention Various conditions, including eosinophilic esophagitis and Churg–Strauss syndrome, are associated with the condition Cytologic Features ◾ Findings are not specific for asthma; however, abundant mucus, eosinophils and Charcot–Leyden crystals, Creola bodies, and Curschmann’s spirals can be seen Histologic Features ◾ Bronchial and bronchiolar smooth muscle hyperplasia ◾ Bronchial mucus gland hyperplasia ◾ Goblet-cell metaplasia ◾ Mixed inflammation of the bronchial wall typically with abundant eosinophils can be seen ◾ Basement membrane thickening and abundant mucous or mucin plugs in bronchi 813 Figure 81.1 A bronchiole with focal goblet-cell metaplasia and surrounding smooth muscle hyperplasia A mixed inflammatory infiltrate is seen within the wall, and numerous eosinophils are present 814 Figure 81.2 Focal goblet-cell metaplasia is seen along with numerous eosinophils 815 CHAPTER 82 Allergic Bronchopulmonary Aspergillosis Ross A Miller Allergic bronchopulmonary aspergillosis (ABPA) occurs when the bronchial tree becomes colonized with Aspergillus species or other fungal organisms in susceptible individuals ABPA is a hypersensitivity reaction to colonizing fungal elements rather than an invasive fungal infectious process The token finding is the presence of “allergic mucin,” which is characterized by mucin admixed with numerous eosinophils and eosinophil cytoplasmic granular material, similar to the allergic mucin seen in fungal hypersensitivity processes that can occur in the sinuses Occasionally, calcium oxalate crystals can even be seen Special stains for fungal elements can help identify fungal elements within the mucin; however, many times definitive organisms are not seen as they are often fragmented and degenerated or may not be in the plane of section examined Patients affected are typically asthmatics or those who have some other lung pathologic process (cystic fibrosis, etc.) Additional findings that often occur and are associated with ABPA include mucoid impaction, bronchocentric granuloma formation, eosinophilic pneumonias, and even bronchiectasis The presence of these other findings depends on the severity of disease and associated comorbid conditions Histologic Features 816 ◾ Mucus with large numbers of eosinophils; many of the eosinophils are shrunken; degranulation and Charcot–Leyden crystals can be seen ◾ Sometimes calcium oxalate crystals will be present ◾ Occasionally, fungal elements can be identified in the mucus Special stains can be helpful ◾ Desquamated epithelial cells and mixed inflammatory cells can be seen ◾ The bronchi often show findings compatible with asthma ◾ Mucoid impaction, bronchocentric granulomas, eosinophilic pneumonia, and even bronchiectasis can be seen Figure 82.1 ABPA shows mucus containing a dense eosinophilic infiltrate and occasional fungal hyphae 817 Figure 82.2 Higher power image showing eosinophils and scattered Charcot–Leyden crystals within a background of mucus 818 Figure 82.3 Gomori methenamine silver stain showing acute branching hyphae consistent with Aspergillus sp and a Charcot–Leyden crystal Figure 82.4 Underlying bronchiolar mucosa showing features of asthma, including a dense chronic inflammatory infiltrate rich in eosinophils, a thickened basement membrane, and smooth muscle hyperplasia 819 ... Part 9. Candida Part 10 . Phaeohyphomycosis Chapter 12 4 Parasites Part 1. Strongyloides Part 2. Dirofilaria Part 3. Toxoplasma Part 4. Acanthamoeba Part 5. Paragonimus Part 6. Schistosoma 19 Part. .. the Transplanted Lung Chapter 13 2 Other Lung Transplant–Related Pathology Chapter 13 3 Posttransplant Lymphoproliferative Disorders Chapter 13 4 Lung Pathology in Transplantation of Other Organs... Cataloging-in-Publication Data Names: Cagle, Philip T., editor Title: Pulmonary pathology : an atlas and text/ editor-in-chief, Philip T Cagle ; associate editors, Timothy Craig Allen [and 15 others]