Essentials of Gross Pathology

Table of contents :
Copyright ©
Preface
Contributors List
Acknowledgments
Contents
1. Fixation 1
2. Museum Preparation Techniques 4
4. Heart 11
5. Lymph Node and Spleen 21
6. Respiratory System 31
7. Head and Neck 54
8. Gastrointestinal Tract 76
9. Liver, Pancreas and Gallbladder 103
10.Urinary Tract 121
13.Breast 211
Orbit
Index 283

Citation preview

Essentials of

Gross Pathqlogy >

•

Chief Editor

Ila Tyagi Editor

fad Abhijit Das

,

i

V * CBS

CBS Publishers & Distributors Pvt Ltd

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imm

Essentials of

Gross

Essentials of

Gross Pathology Chief Editor

Ila Tyagi DNB Associate Professor, Department of Pathology North Delhi Municipal Corporation (NDMC) Medical College and Hindu Rao Hospital (HRH) Delhi

Editor Abhijit Das MD Senior Resident NDMC Medical College and HRH, Delhi

Associate Editors

Namrata Nargotra

Srishti Gupta

MD

Senior Resident NDMC Medical College and HRH, Delhi

Head, Department of Pathology NDMC Medical College and HRH, Delhi

Ritu Arora

Dipti Kalita

MD

Senior Resident NDMC Medical College and HRH, Delhi

MD

MD

Consultant Pathologist, Batra Hospital and Medical Research Centre, Delhi

CBS

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Foreword Gross pathology, a vital part of histopathology, is absolutely necessary in the curriculum of MBBS undergraduates, pathology residents and paramedical students. There is a lacuna in the availability of books which specifically focus on gross features and differential diagnoses of pathological specimens commonly asked in the exams. One has to go through multiple books to gather all the information, which is not only a time consuming task but also adds to a lot of confusion due to discrepancy in different books. This book entitled Essentials of Gross Pathology authored by Dr Ila Tyagi, Dr Namrata Nargotra, Dr Dipti Kalita, Dr Abhijit Das, Dr Srishti Gupta and Dr Ritu Arora is a unique publication. It is no exaggeration when I say that this book is an "all-in-one" practical gross pathology book as it covers all aspects of histopathology specimens for undergraduate's practical examination. It is a one stop source of in-depth and detailed information on the subject written in a very lucid, concise and bullet point form. I am sure this book will be of immense benefit to one and all working in this field . It is my privilege and honor to be invited to contribute the foreword for this comprehensive practical book on gross pathology. I can imagine the hard work put in by the authors preparing this book . I congratulate all of them and specially Dr . Ila Tyagi for initiating such a venture, leading the team, her untiring efforts and her valuable contributions to the subject. I wish all the authors the very best in their future endeavors! Lastly, I thank CBS Publishing House Ltd., New Delhi, for håving readily agreed to publish the book. I know they are second to none in the publication of a series of medical books of value.

Puja Sakhuja Professor and Head Department of Pathology Govind Ballabh Pant Institute of Postgraduate Medical Education and Research, New Delhi-110002

Preface Gross pathology refers to macroscopic manifestation of diseases in organs, tissues and body cavities. Grossing is the first step in surgical pathology and extremely important for correct interpretation and diagnosis. Though several good books on pathology are available for students' consumption, there is a paucity of books on gross pathology. This book serves as a practical guide for the undergraduate museum in all the aspects of gross pathology, i.e. reception of the specimen, fixation, gross examination and dissection, and differential diagnosis and techniques of mounting of the specimens. It includes basic introduction to grossing techniques, a discussion of typical specimen types and a strategic approach to the specimen along with schematic pictures illustrating the same progressing through each organ system. The chapters have been organized in the following fashion. Each chapter begins with a brief review of the normal anatomy of an organ followed by its grossing techniques. We then discuss the salient gross features of important specimens that frequently occur in undergraduate examinations. The chapter ends with a discussion on differential diagnosis focusing predominantly on gross pathology. There are numerous gross pictures and schematic diagrams to illustrate the normal anatomy, grossing techniques and pathology. This book is unique for three reasons. Firstly, it is based on gross pathology—a very crucial aspect of histopathology. Secondly, it provides an accurate and quick description of surgical and autopsy specimens that is easy to digest for students. Lastly, it offers differential diagnosis of important specimens commonly asked in examinations. This book has been compiled after extensive research of current examination trends based on our discussions and continuous interactions with students and faculty alike. In our constant endeavor to keep this book current with examination trends, all suggestions for further improvement are welcomed . We sincerely hope that this book will be of immense help to undergraduate students in their practicals and viva voce examinations.

Editors

Contributors List Ila Tyagi DNB (Institute of Pathology, ICMR Delhi) Associate Professor, Department of Pathology North Delhi Municipal Corporation (NDMC) Medical College and Hindu Rao Hospital, Delhi

Namrata Nargotra

MD (AFMC Pune)

Head, Department of Pathology NDMC Medical College and HRH, Delhi

Srishti Gupta

MD (Army hospital, R &R Delhi)

Senior Resident NDMC Medical College and HRH, Delhi

Ritu Arora MD (GMC Amritsao Senior Resident NDMC Medical College and HRH, Delhi Abhijit Das MD (AIIMS Deihi) Senior Resident NDMC Medical College and HRH, Delhi

Dipti Kalita

MD (AMC Dibrugarh)

Consultant Pathologist, Batra Hospital and Medical Research Centre, Delhi

Acknowledgments We extend our sincere thanks to a number of people without whom this book would not have become a reality. We take this opportunity to thank Mr PK Gupta (Commissioner, MCD) and Mr Pankaj Kumar Singh (Additional, Commissioner, MCD) who are the backbone of the newly formed NDMC Medical College. Our special thanks to Mr Mayank Sharma (former Additional Commissioner, MCD), who played a major role in the formation of this medical college. We also thank our Medical Superintendent Dr KL Khurana for encouraging us and providing us with necessary support at all times. We thank and acknowledge the Dean of our college, Dr Rani Kumar, for her constant encouragement and support. She inspired us to write this book on gross pathology and has been the guiding light in our endeavor. We are greatly indebted to our teacher, mentor and guide Prof Rajbala Yadav . With her vast experience in the field of pathology, she has provided her expert insight to this work . We also thank the other faculty members of our department Dr. Sompal Singh, Dr Manupriya Nain, Dr Jyotsna Nigam and Dr Ruchi Rathore for their support . Our special thanks and acknowledgement to Dr Dinesh Negi, CMO Administration, NDMC Medical College for his constant encouragement and invaluable ideas which have enthused us to strive to do better . This acknowledgement wouldnT be complete without thanking faculty members of other colleges who helped us immensely at all times of need and have been a source of constructive suggestions. For her constant support and encouragement we would like to thank Dr Leela Pant, Medical Suprintendent, Kasturba Hospital (former Head, Department of Pathology, Hindu Rao Hospital) Our special thanks to Dr Vinay Kamal, Director Professor Pathology, MAMC for his constant encourgement, guidance and constructive suggestions. We are greatly indebted to Dr Puja Sakhuja, Head of the Department, Pathology, GB Pant Institute of Postgraduate Medical Education and Research ( GIPMER ), New Delhi for readily helping us and graciously providing us with gross photographs of gastrointestinal and neuropathology specimens. We also thank other faculty members of GIPMER, Prof KR Saran, Prof Vinita Batra and Dr Kaushik Majumdar for their support. We wholeheartedly thank Dr Sunita Saxena, Director and Dr Usha Agarwal, Additional Director, National Institute of Pathology ( NIOP) for helping us. We are greatly indebted to Dr Surider Paul HOD, Government Medical College, Amritsar for supporting us. Constant inspiration and support from Dr Nidhi Verma, Dr Prerna Arora, Dr Meeta Singh (MAMC), Dr Monika Matlani, Dr Meetu Agarwal (Safdarjung Hospital), Dr Fouzia Siraj, Dr Harpreet Walia ( NIOP) and Dr Kavita Gaur (GIPMER ) kept us going through the course of this book . We acknowledge and thank and our residents Dr Gaurav Jain, Dr . Mansi Chandana, Dr.Garima, Dr.Ruchi, Dr Meenal, Dr Alek, Dr Meenakshi, Dr Ranjeet and Dr Varun, Dr Shakti, Dr Pinkey, Dr Anshu, Dr Malini, Dr Swapna, Dr Amul and Dr Shilpi for their help and support . We wholeheartedly thank CBS Publishers and Distributors specially Mr YN Arjuna (Senior Vice-President Publishing, Editoriai and Publicity) for his immense support, encouragement and invaluable guidance for this project and his team Ms Ritu Chawla ( AGM Production ), Neeraj Prasad (Graphic artist) with his untiring efforts on drawings, Ms Jyoti Kaur ( DTP Operator ) for excellent formatting, Mr Kshirod Sahoo ( Proof -reader ) for his excellent work and Mr Sunil Dutt for helping us come out with this book . We sincerely thank the backbone of support-our technical staff Mrs Shakti Kalani, Mr Sukhvinder, Mr Ravi, Mr Aman and Mr Nitish who helped us in setting up the Pathology Museum and mounting. No work is complete without the unending support, patience, constant encouragement of a loving family member . So we thank our family members ( Dr Anand Tyagi, Gen. Sarin, Dr Rajeev Bhagat, Dr Kunjahari Medhi, Mrs Kankana Roy Das and Mr Tarun Aggrawal) for being there with us at times of need . Above all we thank Almighty for the divine blessings without which no work can ever reach completion.

—

Editors

I

Contents

Foreword by Puja Sakhuja

Preface Contributors list

v vii ix

1 . Fixation

1

2. Museum Preparation Techniques

4

3. General Approach to Grossing of Surgical Specimen

8

4. Heart

11

5. Lymph Node and Spleen

21

6. Respiratory System

31

7. Head and Neck

54

8. Gastrointestinal Tract

76

9. Liver, Pancreas and Gallbladder

103

lO. Urinary Tract

121

1 l . Male Genital Tract

151

12. Female Genital Tract

172

13. Breast

211

14. Bones and Joints

220

15. Soft Tissues

249

16. Central Nervous System

266

17 . Eye and the Orbit

279

Index

283

C

APTER

r1>M Usually ear1y Any age (35 yr) adulthood (28) Usually easy to Diagnostic RS Present cells find Mononuclear RS var1ants L&H (popcorn cells) Mononuclear cells Lacunar cells cells RS cells IHC of neoplastlc CD20+, CD45+, EMA+ RS cells CD15+, CD15+, C030+ CD15+, C030+ cells CD1~. co~. EBVC030+, 40% EBV+ usually EBV70% EBV+

1.5-6% M>F Older age (51 ), HIV Infected Individuals Usually easy to find

Background

Scanty lymphocytes, atyplcal hlstlocytes, fibrosis Poor

Incidence Age and Sex

Prognosis

5% Usually young and mk:ldle age (35 yr) Rare/absent

depletion

Prollferatlon of small lymphocytes, nodular pattern of growth Chronic relapslng, may transform Into large Beall NHL

5% M>F Sllghtly older (43 yr) Rare

Prollferatlng lymphocytes, a few hlstlocytes Excellent

Lymphoid nodules, collagen bands Very good

Mixed lnflltrate

good

Mononuclear cells RS cells CD15+, CD30+ most EBV+

Box 5.3 Cl888ical Hodgkin Lymphoma Nodular scl6rosis classics/ Hodgkin lymphoma • Nodular growth pattern with broad birefringent collagen bands surrounding at least one nodule. • In addition to the classic Reed-Sternberg cell (arrow), characteristic lacunar type of RS are present. These cells have abundant clear cytoplasm, muHilobulated nuclei with distinctive perioellular halo. These cells appear lacunar due to the shrinkage of cytOplasm in formalin-fixed tissue (absent in tissues fixed in B-5 or Zenker). • Syncytial variant: prominent aggregates of lacunar cells.

Mixsd C6/lularity classical Hodgkin lymphoma • Effaced lymph node arohitecture. • Classic Reed-Sternberg cells (which tend to be numerous) and atypical mononuclear cells are admixed with in a variable inflammatory background (eosinophils, histiocytes, neutrophils, plasma cells). • Focal necrosis may be present, but fibrosis should be minimal or absent. Lymphocyts-rich classical Hodgkin lymphoma • Two growth patterns: nodular (common) and diffuse (rare). • Characterized by the presence of Reed-Sternberg cells scattered against a nodular (most commonly) or diffuse background largely composed of small lymphocytes. • Background is devoid of eosinophils, neutrophils and necrosis or fibrosis not seen. Lymphocyts-dspletsd classical Hodgkin lymphoma • In this type of HD, the lymph node is depleted of lymphocytes. There are two variants of lymphocyte-depletion HD.

T-cell Lymphoma

Mantle cell lymphoma and DLBCL represent intermediate grade B-cell lymphoma. High grade B-cell lymphoma include Burkitt lymphoma and precursor B-lymphoblastic leukemia/ lymphoma.

Mature T-cell and natural killer cell malignancies are rare, accounting for only 10-12% of all NHL, usually more aggressive than B cell lymphoma. The most common subtypes are peripheral T cell lymphoma and anaplastic large cell lymphoma.

m

Essentials of Grou Pathology

Salient Gross Features Gross features of non Hodgkin lymphoma are shown in Fig. 5.3a, b. The nodes are enlarged and show a homogeneous tan cut surface. Microscopic Features

Microscopic features of chronic lymphocytic leukemia are given in Box 5.4.

BoxS.4 Chranlc Lymphocytlc LeukmnlalSmall Lymphocytlc Lymphoma • The architecture of the node is massively and monotonously effaced by a population of small round lymphocytes with cfumped chromatin, inconspicuous nucleoli, barely visible cytoplasm, and scanty mitotic activity. • Pseudofollicular pattern with rounded, illdefined. paler areas may be present. • Infiltrate may extend through capsule and involve surrounding soft tissue. • Pseudofollicles (proliferation centers) contain prolymphocytes, paraimmunoblasts, and mitotic figures. • Richter syndrome is transformation from B-CLL or other low grade B cell lymphoproliferative disorder to a pleomorphic lymphoma, such as diffuse large Cilll lymphoma; appears to be due to transfonnatlon of previously well differentiated tumor Cillls. • Positive stains are CDS, CD19, CD23, CD20(weak) staining and llght chain restrlctfon. Follicular lymphoma

• The architecture of the node ls effaced by folllcular or nodular pattern of growth. These neoplastlc nodules containing small cleaved cells without nucleon (cemrocytes) and larger noncleaved Cillls wtth moderate cytoplasm, open chromatin and multiple nucleoli (centroblasts). • Minimal or no apoptotic cells or tingible body macrophages. • Attenuated or absem mantle zones. • Often is interfollicular involvemem or capsular infiltration. lmmunophenotype-CD19, CD20, CD22, CD79a, BCL-6, BCL-2, CD10.

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c~'r #' ~ :ti.ri\~ r~;,,_._ • ~~~:J~~~7:· ~'ft(tJ ~-·~l"' 6

Fig. &.3a, b: Non-Hodgkin lymphoma: The nodes are enlarged and show a homogeneous tan cut surface (arrows).

Differences between Hodgkin and non-Hodgkin lymphoma are shown in Table 5.3. Lymph Node Metastasis Lymph nodes are common sites of metastatic disease. Nodal metastases are common with carcinoma, melanoma or germ cell tumors; rare with CNS tumors and sarcoma (except for angiosarcoma, clear cell

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sarcoma, epithelioid sarcoma, MFH, rhabdomyosarcoma or synovial sarcoma). Lymphomas and melanoma must be ruled out. Special stains such as reticulin, mucin stains and immwtohistochemical studies are particularly helpful. A panel of antibodies should be employed, preferably including at least antibodies to cytokeratin, CD45RB (LCA), and ~100 protein.

Lymph Node and Spleen Tabla 5.3: Differences between Hodgkin and Non-Hodgkin lymphomas Hodgkin lymphoma

Non-Hodgkin lymphoma (Fig. 5.3)

More often localized to a single axial group of nodes (cervical, mediastinal, para-aortic) Orderly spread by contiguity Mesenteric nodes and Waldeyer ring rarely involved Involvement of extranodal sites, such as the spleen, liver, or bone marrow, is less common Constitutional symptoms common Spillover to blood is rare

More frequent involvement of multiple peripheral nodes

Salient Gross Features Gross features of lymph node metastasis are shown in Fig. 5.4. Single or multiple randomly distributed tumor nodules. Microscopic Features Microscopic features of lymph node metastasis are given in Box 5.5.

SPLEEN CongesHve Splenomegaly

Results from systemic causes like right heart failure or local causes (i.e., cirrhosis). Portal hypertension produces enlargement of spleen (i.e., congestive splenomegaly) [Note: Spleen weighs up to ~500 gm, normally < 150 gm]. Clinically, it presents as mild to moderate enlargement of spleen. Initially may be symptomless, whereas massive spleen may lead to dragging sensation.

Noncontiguous spread Waldeyer ring and mesenteric nodes commonly involved Extranodal presentation common Constitutional symptoms uncommon May spread to blood

Box 5.5 Lymph Node Metastasis

F6Stur68 favoring lymphoma Lymphomas are more likely multifocaJ with diffuse penetration of vessel wall, minimal necrosis, no nesting, not limited to sinuses, not limited to intravascular invasion; differentiate based on special stains/immunostains CD45/LCA. pan-keratin, S100, touch preparations (clumping favors carcinoma), EM for epithelial features. Features favortng carcinoma Carcinomas usually have cohesive tumor cells, sinus involvement, clear1y defined margins with lymphoid tissue; may resemble Hodgkin lymphoma due to prominent nucleoli and mixed inflammatory infiltrate.

Salient Gross Features Gross features of congestive splenomegaly are shown in Fig. 5.5. • Spleen is enlarged, heavy, firm and tense. • Splenic capsule is thickened and fibrotic. • Cut surface shows gray tan and meaty appearance. Microscopic Features Fig. 6.'= Metastatic lymph node: Image shows single grayish-white metastottc tumor deposit.

Microscopic features of congestive splenomegaly are given in Box 5.6.

m

Essentials of Grou Pathology

Fig. 5.5: Congestive splenomegcly: Image shows enlarged spleen with thickened and flbrollc capsule. Box 5.6 Congestive Splenomegaly • Marked dllatatlon of the veins and sinuses, fibrosis of the red pulp, and accumulation of hemoslderfn-contalnlng macrophages. • Iron and calcium containing ftbrotlc nodules (Gamna-Gandy bodies) (arrow) secondary to hemorrhage. • Lymphoid follicles are inconspicuous.

Fig. S.6a, b: Splenlc rupture (arrow).

Microscopic Features

Microscopic features of ruptured spleen are given in Box.5.7. Amytoldosls Spleen

Ruptured Spleen

The most common cause of laceration spleen is blwtt trauma. Trauma can be direct and indirect. Nontraumatic rupture occurs in an enlarged spleen, seen in acute infections (pneumonia, septicemia and acute endocarditis). Spontaneous rupture may also occur due to chronic malaria, infectious mononucleosis, typhoid fever, splenic abscess, thalassemia and leukemia.

Salient Gross Features Gross features of ruptured spleen are shown in Fig. 5.6 1. Grossly the capsule is tense and ruptured. 2. Laceration is present. 3. Cut surface shows hemorrhage and necrosis.

Amyloidosis spleen is seen in two patterns, namely sago spleen and lardaceous spleen. 1. Sago spleen: Amyloid deposits are largely limited to splenic follicles, producing tapioca- like granules on gross. 2. Lardaceous spleen: Amyloid deposition is in the walls of splenic sinus and in connective tissue framework in red pulp, giving a map like pattern. • • •

•

Box 5.7 Ruptured Spleen Usually small capsular tear, often in the superior pole arid/ orhllum. A neutrophlllc lnftltrate below capsular tear and along the edges of the tear. Foci of lntraparenchymal hemorrhage are often presem. Lymphoid hyperplasia with prominent marglnal zone commonly seen.

Lymph Node and Spleen Salient Gross Fea'/ures Gross features of amyloidosis spleen are shown in Fig. 5.7 1. Spleen may be normal sized, moderate to markedly enlarged. 2. Cut surface shows pale, waxy and translucent surface.

Microscopic Features Microscopic features of amyloidosis spleen are given in Box5.8.

GROSSING LYMPH NODE

Lymph Node Biopsy Lymph node biopsies are commonly done for: 1. Diagnosis of lymphoma. 2. Evaluation of metastasis. 3. Diagnosis of inf-ectious disease.

Gross Procedure 1. If lymph node is received in fresh state cut 2-3 mm slices perpendicular to its long axis and a. If infectious disease is suspected send small amount of tissue for culture. b. If hematolymphoid malignancy is suspected submit tissue for flow cytometry, cytogenetics and molecular genetics. 2. Make touch imprint smears by gently touching the cut surface on alcohol cleaned glass slid~fix in methanol and stain one with Wright Giemsa stain and other with hematoxylin and eosin stain. 3. Place one of the slices in fixative and kept for histopathological examination. 4. If lymph node is received in fixative cut2-3 mm slices and submit.

Gross Description 1. Fixed or fresh when received. 2. Condition of the capsule. 3. Appearance of the cut surface. Fig. 5.7: Gross teatres of omyloldosls spleen.

Box 5.8 Amyloidoeie Spleen

Sections for Histology 1. Cross-section of node including part of capsule. 2. If the objective of dissection is to rule out metastasis and if the tumor is grossly visible, a section that includes tumor is sufficient. If not, the lymph node is sectioned in 2-3 mm slices and all the slices are submitted. 3. One cassette should be used for one lymph node unless colored ink is used to distinguish different lymph nodes.

SPLEEN

Splenectomy specimen: Splenectomy is the removal of the entire spleen after ligating the splenic artery and vein. Gross Procedure 1. Spleen should be received in the laboratory fresh and immediately after excision.

m

Essentials of Grou Pathology

2. Weigh and measure the specimen. 3. Examine the capsule-intact or lacerated, tense or wrinkled. 4. Examine the hilum for lymph nodes. 5. Cut the spleen using a long sharp blade in any plane into thin slices. 6. Examine the cut surfaces for appearance of red pulp and white pulp and any lesion. a. Expansion of red pulp gives cut surface a diffuse red appearance. b. Expansion of white pulp gives rise to white nodules in a red background. c. H nodules are present, document the number of descrete nodules. 7. If the lymph node has been removed for hematopoieti.c malignancy and nodules is found a. First prepare four to five touch smears and next submit fresh tissue for irnmunophenotyping, cytogenetics and molecular genetics. b. Submit representative sections from nodules for light microscopy. 8. H storage disease is suspected tissue should be fixed in gluterald.ehyde for electron microscopy.

9. If infectious pathology is suspected fresh tissue should be sent for culture.

Gross DescrlpHon 1. Weight and dimensions of the specimen. 2. Cut surface: Appearance of white pulp and red pulp, nodule, fibrosis, hemorrhage, necrosis. 3. Capsule: Intact or tom. 4. Presence of intraparenchymal hemorrhage.

Sections for Histology 1. H weight is normal and gross appearance is normal: 2.

3. 4.

5.

submit eight sections from different areas. H the spleen. is enlarged but appears uninvolved (no focal lesion present): Submit eight sections plus one extra section for every 50 g weight. For traumatic rupture of spleen, submit two to four sections of the splenic parenchyma. H nodules are present, at least one section representing each type and one section that includes splenic capsule. In case of incidental splenectomy, one to two section is adequate if spleen appears grossly normal.

C

APTER

Respiratory System

ANATOMY PATHOLOGY Lungs

Silicosis Asbestosis Lung Tumours Squamous Cell Carcinoma Adenocarcinoma Small Cell carcinoma Bronchial Carcinoid Lung Metastasis Pleura Benign Mesothelioma Malignant Mesothelioma

Pneumonia Lobar Pneumonia Bronchopneumonia (Lobular pneumonia) Emphysema Bronchiectasis Tuberculosis of Lung Sarcoidosis of Lung Lung Abscess (Pulmonary Abscess) Pneumoconioses Coal Worker's Pneumoconiosis (CWP)

GROSSING

ANATOMY

PATHOLOGY

LUNGS

LUNGS

Respiratory system is an outgrowth from ventral wall of the foregut, developmentally. Trachea gives rise to 2 main bronchi-left and right. Left bronchus (Fig. 6.1) divides into 2 lobar bronchi and.right bronchus into three lobar bronchi, thus giving rise to two lobes on the left and three lobes on the right. Right main bronchus (Fig. 6.1) is more vertical, so aspirated foreign materials enter into right lung more than left. Progressive branching of bronchi forms bronchioles which differ from bronchiby lack of cartilage and submucosal glands. Further branching of bronchioles leads to terminal bronchioles which measure 10/10 hpf, larger cells with vesicular, coarse or fine chromatin, visible nucleoli and less intense neuroendocrine markers positivity. c

.__- - -Spherical, polypoid mass projecting into bronchial lumen

Circumscribed, yellow tan mass with intact mucosa

Fig. 6. t6ci-c: Gross picture shows a spherical polypoid tumor with intact bronchial mucosa arising from major bronchus and projecting Into the bronchial lumen (arrow). Cut surface shows clrC\lmscrlbed grey-white areas with areas of hemorrhage.

m • • • •

Essentials of Grou Pathology

Box 8.14 Bronchial carcinoid Uniform cuboidal cells may be arranged in aggregates, trabewlae or cord like pattern, separated by fine fibrous septa. Neoplastic cells have centrally placed oval nuclei, abundant amount finely granular cytoplasm. Mitosis and necrosis seen rarely. IHC: NSE, chromogranin, synaptophysin, NF.

carcinomas and sarcomas from various sites can metastasize to lungs vie hematogenous or lymphatic routes or by direct extension. Most common carcinomas th.at metastasize to lwtgs are carcinomas of bowel, breast, thyroid, kidney, pancreas and liver. Other noncarcinomatous tumors include osteosarcoma, neuroblastoma, melanoma, Wilm.s' tumors, lymphomas and leukaemias.

Salient Gross Features Gross features of lung metastasis are shown in Fig. 6.17. • Hematogenous metastasis is more common in peripheral part of lung. • It shows single or multiple nodular discrete lesions, which appear radiologically as cannon-ball

secondaries. • Lymphatic metastases are confined to peribronchiolar or perivascular locations. • Cut sections of lesions are grey-white. Some lesions may show areas of hemorrhage and necrosis. • Small cell lung carcinoma (SCLC): Extensive mitosis >10/10 hpf, fine chromatin, indistinct nucleoli, nuclear moulding. • Intestinal or pancreatic carcinoid: TIF-1 negative, while 90% of pulmonary carcinoids are TIF-1 positive. • Adenocarcinomas: More atypia, more mucin production, less neuroendoaine markers positivity.

Lung Metastasis

Lung metastasis or secondary tumors are more common as compared to primary tumors of lung. Both

Microscopic Features

Microscopic features of lung metastasis of lung are given in Box 6.15.

PLEURA Mesothelioma is a rare tumor arising from mesothelial lining of serous cavities, mostly in pleural cavity and rarely in peritoneal and pericardia! cavities. Pleural mesothelioma is of two types-benign (solitary) and malignant (diffuse).

;-----'"'.:!,.__- Multiple, discrete, grey-white nodular tumor deposits

Fig. 6. I 7a-c: Cut surface e:xhlblts multfple grey-white discrete metastattc tumor deposits of variable sizes.

Respiratory System Box 6.15 Lung Meta8ta8ie

• Histomorphology is similar to the primary tumors of the respective souroes, from where tumors metastasize to lungs. • Most common sources are carcinomas of intestine, thyroid, breast, kidney, liver, osteosarcoma, neuroblastoma, Wilms tumor, lymphoma and melanoma.

Box 6.1

e Benign Meeothelioma

• Increased collagen and reticulin fibers with collagen are arranged in whirling pattem with interspersed fibroblasts. • Tumours may show clefts of in variable sizes lined by mesothelial cells.

Microscopic Features Microscopic features of benign (solitary) mesothelioma of lung are given in Box 6.16.

Benign (Solitary) Mesothelloma

Benign pleural mesothelioma is also known as pleural fibroma. It is an asymptomatic incidental finding, not related to asbestos exposure. Surgical removal is generally curative.

Salient Gross Features • Shows solitary, circumscribed, small firm mass, measuring 25 lymphocytes/100 gastric foveolar cells). Collagen°'-!• gastrHls: Increased thickness of subeplthellal collagenous plate (>15 µm) with lymphocytic gastritis.

Microscopic Features

Microscopic features of menetrier disease and gastric polyp are given in Boxes 8.6 and 8.7 respectively. Mallgnant Lesion

Adenocarcinoma of Stomach Adenocarcinoma is the most common malignancy of stomach. They are common in low socioeconomic groups, individuals with multifocal mucosa! atrophy and intestinal metaplasia. It can be classified into two types based on histology-intestinal and diffuse infiltrative types. They are often discovered at advanced stages presenting with anorexia, weight loss, altered bowel habits and anemia. Two important prognostic indicators of gastric cancer are depth of invasion, lymph nodal and distant metastasis at the time of diagnosis.

GastrolntesHnal Tract

a

b

Fig. 8.&a, b: Stomach shaped mass of heir. Box 8.8 Menetrler Disease (Hypertrophlc gastropathy) GroBS: Mainly involves body and fundus, sparing antrum. Gastric wall is markedly thickened. Gastric mucosa shows enlarged and cerebriform rugae. Histoptdhology: Foveolar hyperplasia with atrophy of fundic glands, elongated and tortuous superficial pits, at places dilated pits may extend through muscularis mucosae. Muscularis mucosae shows hyperplasia and extends upwards between glands. Box 8.7 Gastric Polyp Hyperplaatlc polyp: Branched and elongated foveolar pits in background of Inflamed and edematous lamlna proprla, may show surface ulceratlon or regenerative glands or granulation tissue. Fundlc gland polyp: Composed of dilated and small glands with parietal and chief cell lining. Inflammatory fibroid polyp: Arises from submucosal as granulation tissue reaction comprising of mixed inflammation, fibroblasts and capillary proliferation. lmmunohistochemistry: CD34, vimentin (positive), CK. CD117 (negative), it harbors PDGFR·a. mutation.

Virch.ow's node is the supraclavi.cular sentinel lymph node, where gastric carcinoma metastasis may first be detected. Sister Mary Joseph nodules are subcutaneous nodules at periumbilical region, resulting from metastatic deposits of gastric cancer. Intestinal Type

It develops from precursor lesions like flat dysplasia and ad.enomas. Mean age of presentation is 55 years with M:F ratio of 2:1. It expands centripetally into the gastric lumen and wall and has a better prognosis. Microscopically, it is characterised by tubular and acinar pattern of growth of tumor cells in the stomach wall. Diffuse Gastric Cancer

Diffuse gastric cancer has no identifiable precursor lesions. There is equal gender preponderance. It occurs in younger patients and has a poor prognosis. Microscopically, it is characterised by signet ring cells infiltrating the stomach wall. Salient Gross Features

Gross features of adenocarcinoma of stomach are shown in Fig. 8.6 1. Adenocarcinoma usually involves gastric antrum. 2. Lesser curvature involved more than greater curvature. 3. Intestinal type: Presents as bulky tumor with exophytic mass or an ulcerated tumor. 4. Diffuse type: Presents as an infiltrative tumor. Usually there is no mass, but stomach wall is stiff (desmoplastic reaction) which is a diagnostic clue. Rugae are flattened diffusely and wall is thickened leading to leather bottle appearance or linitis plastica.

m

Essentials of Grou Pathology

Ulcerated tumor and ----:::a~...-.~ heaped up margin curvature

• Fig. 8.6a-e: Adenocarclnoma of stomach. Images show grey white exophyHc growth protruding Into the lumen (black arrow). (Fig. 8.6a-d: Courie$y: GIPMER).

Microscopic Features Microscopic features of adenocarcinoma of stomach are given in Box 8.8. Differential Diagnosis • Benign ulcer (Table 8.3).

Note: No gross feature can reliably distinguish benign from malignant ulcer. SMALL AND LARGE INTESTINES Small and large intestines make up majority of the GI tract. They are sites of many diseases. Colon is the most common site of GI neoplasia in Western populations.

GastrolntesHnal Tract Box 8.8 Adenocarclnoma Stomach • Many histological classifications, according to WHOpapillary, tubular, mucinous, signet ring type. Most commonly used Lauren's classification-intestinal type and diffuse type. • Intestinal type forms glands with dysplastic epithelial lining, whereas diffuse type shows mucin filled signet ring oell (red arrow) infiltration with intense desmoplastic response. • IHC: CK (positive), PAS, Alcian blue, mucicarmine (mucin stain in signet ring cells, also positive in mucinophages, Alcian blue shows dark blue globoid in goblet cells, PAS shows magenta color in foveolar cells).

Infarction can be of two types-mucosal/mural and trans.mural infarct. Causes of intestinal ischemia are given in Box 8.9. Gross features of gangrene intestine are shown in Fig. 8.7. Mucosal and mural infarction 1. Affected segment is dark red or purple due to luminal hemorrhage. 2. Lacks hemorrhage and exudation on serosal aspect. 3. Mucosa may be ulcerated. 4. Bowel wall is thickened.

TransmUl'al infarction 1. Spleztic flexure is the commonest site. 2. There is sharp dem.arcation between normal and ischemic bowel in arterial occlusion. 3. Infarction is of hemorrhagic type (red infarct) and bowel is intensely congested purple-red in color. 4. Blood-tinged mucus or frank blood fills the lumen and the wall becomes edematous, thickened and rubbery along with purulent exudates and fibrin deposition over the serosal surface. 5. Perforation may be noted in muscularis propria. Necrosis is death of a group of cells, often accompanied by an inflammatory infiltrate. It is a result of three factors, namely (a) denaturation of intracellular proteins, (b) enzymatic digestion of lethally injured cells, (c) loss of membrane integrity. On the basis of etiology and morphology, following types of necrosis are identified-t-E·2-~ ulcer

d

Fig. 8. t2a-d: Intestinal segmerm with ulcerated mucosa with perforation (red arrow). The ulcers are transverse (black arrow) and covered with yellow white coseous material. The wall ls thickened (o-c). Diagrammatic dlfferenttatton between tubercular and typhoid Intestinal ulcers (d). (Fig. 8.12a and b: Courtesy: GIPMER)

GastrolntesHnal Tract

Hyperplastic cecal tuberculosis • There is wall thickening of terminal ileum, cecum and ascending colon. • Mucosal ulceration is noted along with serosal adhesions. Microscopic Features Microscopic features of intestinal tuberclosis are given in Box 8.15. Dlfferenffal Diagnosis 1. Crohn's disease (Table 8.6) 2. Enteric fever (Table 8.7) Ulcerative Colitis mcerative colitis is a severe ulcerating inflammatory disease, limited to colon and rectum. It involves only mucosa and submucosa. It is caused by a combination of defects in host interaction with intestinal microbiota, intestinal epithelial dysfunction and aberrant mucosal immune responses. tncerative colitis is a relapsing disorder, characterised by bloody diarrhoea with stringy, mucoid material, lower abdominal pain and cramps, temporarily relieved by d.efaecation. Depending upon the segment involved, the nomenclature is as follows: • Pancolitis: Disease of entire colon. • Left-sided disease: Rectum; ascending colon, transverse colon. • Ulcerative proctitis: Rectal involvement. Box 8.15 Intestinal Tuberculoeia • Caseating epilhelioid cell granulomas with Langhans' giant cells (arrow) in all layers of intestine. • Muscle layers may show variable fibrosis. • Sloughed out mucosa! surface with areas of ulceration.

Table 8.8: Differences between intestinal tuberculosis and Crohn's disease Features

Intestinal tubsrcu/osis Crohn's disease

Ulcers Creeping fat Cobblestone appearance Multiple segments

Transverse Absent Absent

Longitudinal usually Present Present

Usually less than 4

Multiple

Tabla 8.7: Differences between lntestlnal tubarculosls and enteric f&ver Features

Intestinal tuben:ulosls

Enterlc fever

Ulcers Ulcer colour

Transverse Yellow-white due to caseation Common

Along the bowel axis Black due to sloughed appearance Seldom occurs

Rbrotic stenosis

• Ulcerative proctosignwiditis: Rectum, sigmoid colon involvement.

• Backwash ileitis: Mild mucosa! inflammation of distal ileum in severe pancolitis. Salient Gross Features Gross features of ulcerative colitis are shown in Fig. 8.13. 1. Ulcerative colitis always involves rectum and extends in continuous fashion to involve colon. 2. Colonic mucosa.is red, granular or can have extensive broad based ulcers. 3. tncers are aligned along the long axis of colon. 4. Mucosa is studded with characteristic pseudopolyps (these are isolated islands of regenerating mucosa bulging into lumen. Tip of the polyps may fuse to form mucosal bridges). 5. Mucosa is atrophied in chronic cases. Serosal surface is unremarkable (Note: No mural thickening, no stricture formation). 6. Toxic megacolon and colonic dilation (when inflammatory process damages muscularis propria and disturbs neuromuscular function). Microscopic Features Microscopic features of ulcerative collites and giardiasis are given in Boxes 8.16 and 8.17 respectively. Microscopic features of colonic adenoma are given in BoxS.18. Differential Diagnosis Crohn's disease is given in Table 8.8.

m

Essentials of Grou Pathology

-~"""'-'>-Red ,

granular colonic mucosa

• ~~r--Pseudopolyps (regenerative mucosa)

Fig. 8. t 3a-c: Thin and flaccid bowel wall. The mucosa Is granular and arythamatous. Pseudopolyp$ (arrow) are seen. (Courtesy: GIPMER)

• • • • •

Box 8.16 Ulceratlve Colltls Crypt abacua: Neutrophlllc accumulation In the crypts. Lamina propria shows marked congestion and hemorThages. Intestinal lining show mucodepletion with diminution of goblet cells. Mucosal ulceration with crypt branching and distortion. Some of the crypts show regenerative changes.

Box 8.17 Giardini• Organisms mostly found along luminal border inducing mucosa! inflammatory infiltrate of variable degrae. Pear shaped organism with equal size of enterocyle nudei, trophozoite has two identical nuclei, known as monkey face.

GastrolntesHnal Tract Box 8.18 Colonlc Adenorna Adenoma may be tubular, villous or tubulovillus.

Tubular adenorna: Tubular glands with dysplastic lining. Lining cells have hyperchromatic stratified nuclei with mitotic figures. Villoue adenoma: Papillary fronds with dysplastic lining and central lamina propria.

Table 8.8: Differences between ulcerative colitis and Crohn's disease Feature

Utcetattve co1ms

Ctohn's dlssase

Distribution

Diffuse, cantlnous

Depth of Involvement Mucosa! appearance Bowel wall Creeping mesenterlc fat Stricture Fistula Fissuring Heal Involvement

Mucosa, submucosa Irregular ulcers, friable, atrophy Thin Absent

Focal (skip), segmental Transmural Cobblestonlng Thlcksned or normal Common --•1-~-

Usually absent Usually absent Usually absent 75% tumor). • Defined margin with pushing border. • No glandular or ductal components. • High grade nuclear features. • Prominent lymphoplasmacytic response. • IHC: CK5/6 (positive), ER, PR, Her2-neu (negative), EGFR (positive).

Differential diagnosis infiltrating duct carcinoma • Does not show syncytial pattern. • Lacks lymphocytic infiltration. • Has infiltrative borders unlike medullary carcinoma (pushing borders). D. Mucinous carcinoma Differential diagnosis-Mucocele like tumor • It consists of cysts lined by benign epithelial cells. These cysts have mucin. • Tumor cells are not seen to float in the mucin.

Table 13.1 lmmunohlstochemlcal profiles In breast lesions IDC ILC Triple negative breast carcinoma Medullary carcinoma Muclnous/collold carcinoma Tubular carcinoma Papillary carcinoma Metaplastic carcinoma

ER, PR(+ In low grade), Her2-neu (-more In high grade) ER, PR (variable), Her2-neu (+ in 30% cases), E-cadherin (-), mucicannine, alcian blue and PAS(+ lntracytoplasmlc sialomucln of signet ring cells) ER, PR, Her2-neu (-), CK 5/6, EGFR, SMA, p63 (+in most basal like phenotypic tumor) ER, PR (- in 90% cases), Her2-neu (-), CK 5/6, EGFR (+) PAS(+ mucln), CK7 (+),CK 20 (-),ER, PR (variable), neuroendocrine marker positive (when Neuroendocrine differentiation) EMA, ER(+), S100, SMA (-as no myoepithellal cells) S100, Calponin, SMA, p63 (-to focal+), ER, PR(+), Her2-neu, CK 5/6 (-),CEA(+ in 85% cases) [note: benign papllloma lesions CEA negative] CK, EMA (+ epithelial and focal mesenchymal), vimentin, EGFR (+), p63 (+ mesenchymal), ER, PR, Her2-neu (-)

Breast

a Fig. 13.~-c: Cut surface of sarcoma breast. The tumor Is 111-deflned, gray-white. fleshy with lnflltratllle margins (arrow). Hemorrhagic foci are noted.

E. Tubular carcinoma

Differencial diagnosis-Sclaosing adenosis Has to be differentiated histomorphologically. The lobular architecture is maintained in tubular carcinoma. Tubules are lined by myoepithelial cells.

• Cut surface shows fleshy grey white, ill-defined friable spongy and hemorrhagic mass with infiltrative margins. • Hematogeneous spread to the lung is commonly seen. • Lymph node metastases is rare.

sarcoma Brean

Microscopic Features

Sarcomas are mesenchymal tumor and include angiosarcoma, rhabdomyosarcoma, liposarcoma, leiomyosarcoma, chondrosarcoma and osteosarcoma.

Microscopic features of sarcoma breast are shown in

Salient Gross Features

Gross features of sarcoma breast are shown in Fig.13.4. • Sarcomas usually present as bulky palpable masses.

Box 13.5 Sarcoma breast

Box 13.7. lmmwtohistochemical profiles in breast lesions are given in Table 13.1.

GROSSING BREAST We commonly re1.5 cm. • Central nidus is soft, friable and red in color, it may be yellow, granular and gritty if calcified. • Cortical bone may be thin or destroyed. • It may show hemorrhagic areas and cyst formation within nidus, leading to secondary aneurysmal cyst formation.

Microscopic Features Microscopic features of osteoblastoma are shown in Box 14.4. Differential Diagnosis

• Osteoid osteoma: Severe pain, less than 1 cm, periphery shows fibrovascular rim, nidus shows zonal pattern with central mineralization, no progressive growth. • Giant cell tumor: Long bone epiphysis, rare in vertebrae, larger giant cells with more nuclei, mononuclear stromal cells. • Aneurysm.al bone cyst: May have similar clinical presentation and radiographic findings. • Osteoblastk osteosarcoma: Radiograph shows poorly circumscribed with cortical destruction, periosteal reactive bone formation, permeative

• Osteosarcoma: Lacks fibrovascular stroma and osteoblast:ic rimming. • Stresss fracture: Zonal pattern with central more mature and dense bone and peripheral woven bone. Osteoblastoma

Osteoblastoma mostly occurs in 2nd and 3rd decades of life with M:F ratio of 3:1. Most conunon sites are vertebrae, sacrum followed by mandible, craniofacial bone and bone of extremities. It is typically

a -...___

b

Fig. 14.Sci, b: Gross picture shows on intmmedullary rumor with thinned out cortex. Tumor exhibits areas of hemorrhage and cystic changes (arrow).

Bones and Joints Box 14.4 Osteoblastoma • Irregular interlacing network of osteoid with prominent osteblastic rimming and associated with variable mineralization. • Fibrovascular septa separating osteoid contains multinucleated osteoclast like giant cells. • May show secondary aneurysmal cystic change. • Osteoblast may show abundant mitotic activity but no atypical forms. Osteoblast may show epithelioid features (when epithelioid osteoblast exceeds>75% of osteoblast population known as aggressive osteoblastoma). • Rarely bizarre multinucleated giant cells without mitotic activity seen, known as pseudomalignant osteoblastoma.

growth pattern, stroma sarcomatoid showing atypia and mitosis, sheets of aypical osteoblasts. Osteosarcoma Osteosarcoma is the most common primary malignant bone tumor that produces bone matrix, i.e. osteoid. It comprises 20% of primary bone cancers. It has bimodal age distribution with M:F ratio of 1.6:1. About 75% of

a

osteosarcomas occur below 20 yrs of age, while 25% are seen in elderly, in setting of Paget disease of bone, bone infarcts or prior irradiation. It originates from metaphyseal regions of lone bones of extremities (50% around knee joint, others: flat bones of pelvis, upper end humerus, jaw bones, etc.). Mostly it arises in medullary cavity (can be intracortical or surface origin). Frequently it is a primary, solitary, intramedullary tumor arising in metaphysis of long bone. Clinically it presents with painful, progressive enlarging mass (Note: Fracture may be the first symptom). Radiograph shows a large, destructive, mixed lytic and blastic mass with infiltrative margins. Tumor breaks through cortex, lifts periosteum, causing a triangular shadow between cortex and raised periosteum known as Codman triangle (characteristic, but not diagnostic of osteosarcoma). Treatment is multimodality approach including chemotherapy and limb salvaging surgery. Conventional lntramedullary Osteosarcoma Conventional osteosarcoma shows a bimodal age distribution, mostly occurring in 2nd decade with a second small peak in patients older than 50 years of age. Hereditary retinoblastoma patients are at an increased risk of developing osteosarcoma. Most common sites are distal femur, proximal tibia and proximal humerus. Patients typically present with short term mild, intermittent pain. Some cases may show elevated level of serum alkaline phosphatase. Imaging shows a large lytic or sclerotic or mixed lytic-sclerotic in medullary bone of metaphysis lesion that may extend through cortex producing a soft tissue mass. Salient Gross Features

Gross features of conventional intramedullary osteosarcoma are shown in Fig. 14.6.

b

Fig. 14.6a, b: Distal femur shows an lntramedullary. metaphyseal grey white tumor extending through cortex Into adjoining soft tissue. Cut surface of the tumor is fleshy, grey white showing foci of hemorrhage (arrow).

Essentials of Gross Pathology

• Resected specimen shows a medullary metaphyseal mass that generally penetrates through cortex and invades into soft tissue. • It may show skip lesions in which normal marrow separates the tumor islands. • Cut sections exhibit a heterogenous variable mass depending on stromal components. • Ossified areas are firm, yellowish white and chondroid areas are lobulated, light grey and translucent. • Osteoblastic areas are firm and gritty. Fibroblastic areas are fleshy and soft in consistency. • Tumor may contain large areas of hemorrhage, necrosis and cystic changes. Microscopic Features

Microscopic features of conventional intramedullary osteosarcoma are shown in Box 14.5. Differential Diagnosis

• Fracture callus: No atypia or mitosis, cartilage with enchondral ossification. • Osteomyelitis: Radiography mimics osteosarcoma, differentiated histologically.

Box 14.5 Conventlonal lntramedullary Osteosarcoma • Malinant spindle cells with tumor osteoid production. • May have osteoblastic, chondroblastic, fibroblastic or malignant fibrous histiocytoma like differentiation. • Tumour osteoid represented by eosinophilic amorphous fibrillary process or lace like pattern surrounded by malignant tumor cells. • Brisk mitotic activity with some atypical forms. • May have large number of osteoclast-like giant cells known as giant cell rich osteosarcoma. • Areas of necrosis seen.

• Osteoblastoma: Lacks atypical mitosis, lacks infiltrative growth pattern. • Giant cell tumor: Affects skeletally mature bone, epiphyseal, extends towards articular cartilage, mononuclear stromal cells without atypia. • Chondrosarcoma: - Low grade chondrosarcoma with areas of ossification: Not contain high grade cartilaginous component. - Dedifferentiated chondrosarcoma: Retains low grade chondrosarcomatous foci. - Clear cell chondrosarcoma: Epiphyseal location and clear cells. • Malignant fibrous histiocytoma: Older patients, lacks tumor osteoid. • Small cell tumors (Ewing sarcoma, lymphoma, mesenchymal chondrosarcoma): - Ewing sarcoma: No tumor osteoid, CD 99 positivity. - Lymphoma: No osteoid, LCA (leucocyte common antigen) positivity. - Mesenchymal chondrosarcoma: No osteoid, SlOO positivity. • Metastatic carcinoma: Prostate and breast cancers may show osteoblastic reaction, immunohistochemistry helps to differentiate (prostate PSA, AMACR; Breast-ER, PR, Her2Neu, GCDFP-15). Telangiectatic Osteosarcoma

Telangiectatic osteosarcoma occurs in 2nd decade with M:F ratio of 2:1. It accounts for4% of all osteosarcomas. Most common sites are distal femur, proximal tibia and proximal humerus. Radiography shows a lytic lesion in metaphysic with infiltrative destructive margin. Salient Gross Features

Gross features of telangiectatic osteosarcoma are shown in Fig. 14.7. • It shows a hemorrhagic mass. • Cut sections show multi.cystic and necrotic areas. • No fleshy areas or sarcoma-like areas are seen. Microscopic Features

Microscopic features of telangiectatic osteosarcoma are shown in Box 14.6. Differential Diagnosis

• Aneurysmal bone cyst Stroma lacks cytologic atypia and atypical mitosis, may contain reactive bone with atypical osteoblast. • Conventional osteosarcoma: Not purely lytic, may contain foci of telangiectatic areas.

Bones and Joints

Multicystic and hemorrhagic necrotic mass showing metaphyseal lytic lesion

a Fig. 14.7a, b: Distal end of femur shows a large hemonhoglc tumor with cortfcol destructton (arrow). Cut surface Is mulHcY511c and necroHc.

• • • •

Box 14.8 Telanglectatlc Osteoaarcoma Numerous cystlike spaoes resembling aneurysmal bone cysts. Septa of cysts contain malignant stromaJ cells admixed with mullinudeated giant cells. Mitosis including atypical forms seen. Tumor osteoid found focally in a lacelike pattern.

Parosteal Osteosarcoma Parosteal osteosarcoma occurs in 3rd decade with female predominance (M:F=l:l.5). Three forth cases are seen in distal posterior femur, followed by tibia. Clinically it presents as painless mass of long duration. Radiography shows radiodense, bosselated, mushroom-shaped mass on bony surface. In long standing case it may encircle bone. String sign is a lucent zone between tumor and cortex.

Salient Gross Features Gross features of parosteal osteosarcoma are shown in Fig.14.8. • Well ossified.mass attached tocorticalsurfaceofbone. • Some may show cartilaginous cap that may show foci of high grade sarcomatous region or undifferentiated areas. Microscopic Features

Microscopic features of parosteal osteosarcoma are shown in Box 14.7.

Rg. 14.aa, b: Posterior aspect of distal femur shows a grey white mass with cartflaglnous cap (arrow) attached to cortfcal surface.

Differential Diagnosis

• Osteochondroma: Medullary space contains adipose tissue or hematopoietic tissue. • Myositis ossificans: Maturation towards lamellar bone, marked adipose tissue begins at periphery and ext:ends centrally at proliferative process, which is reverse in parosteal osteosarcoma.

Essentials of Gross Pathology Box 14.7 Parosteal Osteosarcoma • Parallel arrays of tumur osteoid separated by hypocellular fibrotic stroma with minimal cytological atypia. • Islands of cartilaginous tissue with minimal atypia. • No periosteal new bone formation.

parosteal osteosarcoma age groups. It is seen in diaphysis and metaphysic of tibia and femur. Patients present with pain, swelling for less than one year duration. Radiography shows a surface radiolucent tumor with speculated calcification, perpendicular to long axis of bone. Salient Gross Features

Gross features of periosteal osteosarcoma are shown in Fig. 14.9. • It shows a lobulated mass having cartilaginous

appearance over bone surface. • It may show cortical erosion, but does not extend to medullary cavity. Microscopic Features

Microscopic features of periosteal osteosarcoma are shown in Box 14.8. Differential Diagnosis

• High grade surface osteosarcoma: Lacks low grade areas. • Periosteal osteosarcoma: Abundant cartilage, periosteal reaction, high grade osseous part. Periostea/ Osteosarcoma

Periosteal osteosarcoma occurs in 2nd and 3rd decades with male predominance (M:F=l.7:1). Patients are older than conventional osteosarcoma and younger than

• Periosteal chondroma: Smaller, well defined, benign chondroid tissue, no malignant osteoid. • Periosteal chondrosarcoma: Low grade, radiography shows popcorn calcification, no tumor osteoid. • Parosteal osteosarcoma: Low grade malignant fi.broosseous tumor without chondroid differentiation, imaging is more radiodense. • Conventional intramedullary osteosarcoma: High grade tumor, medullary lesion.

Fig. 14.9a, b: Dlaphysls of femur shows a grey white surface tumor (arrow) with cortlcal erosion. Medullary cavity Is not Involved by tumor.

Bones and Joints Box 14.8 Perlosteal Osteosarcoma • Lobulated chondromatous tissue with high grade nuclear features separated by high grade sarcomatous spindle cell component. • Mallgnant osteoid. • May have periosteal bone formation with cortical destruction.

• High grade surface osteosarcoma: Osteoid part is pleomorphic and high grade, lacks cartilaginous differentiation. High Grade Surface Osteosarcoma High grade surface osteosarcoma occurs in 3rd and 4th decades with MF ratio of 3:1. Most common sites are distal and mid femur, proximal humerus and fibula. Patients present with pain and swelling. Radiography is like periosteal osteosarcoma except mineralization that is like conventional osteosarcoma (i.e. fluffy, cumulus cloudy appearance). Note: Perpendicular calcification to long axis of bone in periosteal osteosarcoma.

• Parosteal osteosarcoma: Lacks high grade anaplastic features. • Conventional intramedullary osteosarcoma: Significant medullary involvement. Low Grade Central Osteosarcoma Low grade central osteosarcoma occurs in 3rd and 4th decades with equal sex distribution. Patients give history of pain without swelling for many years. Most common sites are mid and distal femur, proximal and mid tibia. Radiography shows a large intramedullary poorly demarcated mass that either is sclerotic or shows trabeculations. Generally no periosteal reaction is seen Salient Gross Features

Gross features of low grade central osteosarcoma are shown in Fig. 14.10.

Sallent Gross Features

• Large, lobulated surface mass that may be soft to firm. • May be hemorrhagic. • Rarely it involves medullary component. Microscopic Features

Microscopic features of high grade surface osteosarcoma are shown in Box 14.9. Differential Diagnosis

• Dedifferentiated parosteal osteosarcoma: Residual low grade malignant fibroblastic stromal part.

a

Box 14.9 High Grade Surface Osteosarcoma • Histology as conventional osteosarcoma. • Usually no medullary involvement.

b Fig. 14. lDa, b: Middle part of femur shows a medullary grey white firm to fleshy tumor {arrow) with cortical destruction. Interface between tumour and uninvolved bone is indistinct.

Essentials of Gross Pathology

• Tumor shows a gritty grey medullary mass that may contain fibrous and fleshy areas. • Some tumors show cortical destruction. • It may extend along the length of bone with poor demarcation between tumor and uninvolved medullary bone. Microscopic Features

Microscopic features of low grade central osteosarcoma are shown in Box 14.10. Box 14.10 Low Grade Central Osteosarcoma • Histology similar to parosteal osteosarcoma, intramedullary fibre-osseous process (i.e. irregular bony trabeculae) separated by fibrous spindle cell stroma. • Stromal spindle cells with minimal atypia and infrequent mitosis. • Rare chondroid foci.

incidental finding. It stops growing when growth plate closes.

Salient Gross Features Gross features of osteochondroma are shown in Fig. 14.11. • Osteochondroma produces a sessile or mushroom shaped protrusion from host bone. • Size varies from 1 to 20 cm. • Cap is composed of benign hyaline cartilage of varying thickness (2 cm), increase cellularity, nuclear atypia, multinucleation, mitotic activity, fibroblastic stroma in medullary cavity instead of fat and hematopoietic tissue, cartilaginous cap shows low grade malignant chondrocytes without enchondral ossification. • Parosteal osteosarcoma: Continuity with medullary cavity of parent bone not present, attached to surface of parent bone. Enchondromo

Enchondroma affects all age groups, mostly between 2nd to 5th decades. It occurs predominantly in appendicular skeleton, mainly bones of hands and feet. Box 14.11 Osteochondroma • Hyaline cartilaginous cap with evenly distributed chondrocytes. • Junction of cap and bone show enchondral ossification. • Chondrocytes may show mild atypia and pleomorphism. • Note: Features to be looked for to exclude malignancysignificant chondrocytic atypia, high mitotic activity, clinical features of malignany, i.e. pain, rapidly enlarging tumor >6 cm, radiographic signs (irregular thickened cartilaginous cap, permeation of periostium into soft tissue and bony destruction).

Generally these tumors are asymptomatic, identified incidentally. Pain may be the presenting feature in association with pathological fracture or trauma to bone. Radiography shows well defined, lucent medullary mass. Salient Gross Features

• Curretage specimens comprises of fragments of blue gray, transluscent, glistening cartilage with focal areas of calcification. • Resected specimen shows a medullary mass. Cut sections show a lobulated, cartilaginous tumor tissue with peripheral irregular margins. • Focal calcified areas appear as yellowish white. Microscopic Features

Microscopic features of enchondroma are shown in Box 14.12. Differential Diagnosis

• Prominent costochondral cartilage: Clinically mimic enchondroma, benign chondrocytes with orderly arrangements. • Fibrous dysplasia with chondroid differentiation: Imaging reveals diaphyseal lesion, fibro-osseous elements present. • Low grade chondrosarcoma: Painful, radiography shows cortical destruction, thickening and soft tissue mass, increased cellularity and binucleate chondrocytes, marrow permeation, prominent myxoid features, increased proliferative activity. Periosteal Chondroma

Periosteal chondroma occurs in 2nd and 3rd decades of life with a M:F ratio of 2:1. Proximal humerus, proximal and distal femur and hand bones are most commonly affected. These are generally asymptomatic, mostly found incidentally. Tumors may occasionally be palpable. Radiography shows a periosteal mass with variable mineralization. Salient Gross Features

Gross features of periosteal chondroma are shown in Fig. 14.12.

• • • •

Box 14.12 Enchondroma Lobulated mature hyaline cartilage with low cellularity and bland cytological features. May have rare multinucleated cells. May have calcification and enchondral ossification. Tumors of hands and feats may show higher cellularity.

Essentials of Grou Pathology Chondroblastoma Chondroblastoma occurs mostly in 2nd decade (95% cases between 5 and 25 years of age) with a M:F ratio of 1.5:1. Common sites include distal femur, proximal tibia and proximal humerus. It arises in epiphysis. It generally presents with pain over months to years with associated muscle wasting and arthralgia. Radiography shows a circumscribed, well defined epiphyseal lytic mass with sclerotic rim. Sa/lent Gross Features

a Lobulatea cortical chondroid mass with thin rim of periosteum

Gross features of chondroblastoma are shown in Fig. 14.13.

b

Fig. 14.12a, b: Gross specimen shows a lobulated wbperlosteal grayish pink chondrold mass with foct of calclflcatlon (arrow).

• Subperiosteal, cortical, lobulated chondroid mass with an outer thin rim of periosteum. • Sometimes yellow areas of calcification are present. • Tumor does not extend to medullary cavity. Microscopic Features

Microscopic features of periosteal chondroma are shown in Box 14.13. Differential Diagnosis

• Juxta cortical chondrosan:oma: Extension into soft tissue, cytological atypia and no periosteal new bone at periphery. • Periosteal osteosarcoma: Imaging shows perpendicular feathery calcifications, twnor osteoid and mesenchymal stroma in between lobules of cartilage. Box 14.13 Perioeteal Chondroma • Histology similar to enchondroma. • Junction of tumor and medullary cavity shows a rim of lamellar bone.

b Rg. 14.13a, b: Proximal humefus shows a well defined epiphyseal mass surrounded by sclerottc bone. Cut surface shows a grey white f\Jmor with areas of hemorrhage and cysHc changes (arrow).

Bones and Joints • Curettage specimens show gritty and friable red tissue with yellowish white focal areas of calcifications. • Resected specimen shows a well demarcated epiphyseal mass. Cut sections show grey white areas containing regional calcifications, hemorrhage and cystic changes. • A thin rim of sclerotic bone is seen surrounding tumor mass. • Focal blue grey areas are seen resembling chondroid matrix. Microscopic Features

Microscopic features of chondroblastoma are shown in Box 14.14. Differential Diagnosis

• Chondromyxoid fibroma: Metaphyseal, lack calcification and more prominent myxoid stroma. • Giant cell tumor: Occurs in mature skeleton, stromal cells with groove absent (5100 negative), lacks chondroid matrix and calcification. • Eosinophilic granuloma: Lacks calcification and chondroid matrix. • Aneurysmal bone cyst: 5100 negative while chondroblastoma with secondary aneurysmal bone cyst formation shows stromal 5100 positivity. • Clear cell chondrosarcoma: Older patients, malignant chondrocytes, clear cytoplasm, more heavily calcified than chondroblastoma. • Chondroblastic osteosarcoma: Tumor osteoid present, rarely involves epiphysis.

Mitotic activity is less, if prominent it supports chondrosarcoma. Salient Gross Features

Gross features of chondromyxoid fibroma are shown in Fig. 14.14. • It shows a circumscribed, lobulated, soft, grey white tumor. • Some tumors show hemorrhagic and cystic areas. • Myxoid areas may be seen occasionally. Microscopic Features

Microscopic features of chondromyxoid fibroma are shown in Box 14.15. Differential Diagnosis

• Chondroblastoma: Epiphyseal, chicken wire calcifications (both radiologically and histologically). • Medullary chondrosarcoma: Older patients, predominantly in axial skeleton, poorly circumscribed, calcification present, cortical destruction.

Chondrosarcoma lntramedullary Chondrosarcoma (Conventional) Chondrosarcoma is a malignant tumor of chondroblast.

Chondromyxold Flbroma Chondromyxoid fibroma occurs in 2nd and 3rd decades of life with a M:F ratio of 1.5:1. It predominantly occurs in metaphysis of long bones of lower extremities. Most common sites are distal femur and proximal tibia. Patients usually present with pain of long duration. Radiography shows an eccentric, expansile, lobulated metaphyseal mass, sometimes extending into epiphysis.

a

Box 14.14 Chondroblastoma • Immature stromal cells (chondroblast), multinucleated giant cells, chondroid matrix. • Stromal cells with fried egg appearance (centrally placed round nucleus and abundant eosinophilic cytoplasm), nuclear grooving. • Infrequent mitosis without atypical forms. • Linear calcification surrounding stromal cells giving chicken wire appearance. • May have secondary cystic or myxoid changes.

b Fig. 14.14a, b: Gross picture exhibits a circumscribed, lobulated. greyish brown tumour which on cut surface shows myxoid and cysttc areas (arrow).

Essentials of Gross Pathology Box 14.15 Chondromyxoid Fibroma • Lobulated myxoid area, composed of stellate or spindle cells with hypercellularity at periphery. • Lobules separated by fibrous tissue containing a few multinucleatted giant cells. • May have bizarre cells with pleomorphic hyperchromatic nuclei or cystic changes or foci of necrosis.

Conventional chondrosarcoma is seen in older (rare below 45 years of age) patients with a (M:F) ratio of 1.5:1. It has a predilection for trunk. Pelvis, ribs, proximal femur and proximal humerus can also be affected. Patients complain of dull aching pain at rest that is worsened at night. Radiography shows a radiolucent mass with variable calcification and cortical destruction. Cortical thickening represents extension into Haversian system. Cartilaginous tumors of hands and feet usually behave as benign lesions, while cartilaginous tumors of axial skeleton are usually aggressive. Salient Gross Features Gross features of intramedullary chondrosarcoma (conventional) are shown in Fig. 14.15. • Chondrosarcoma may vary in size from a few centimeters to extremely large tumor with firm consistency. • It shows a nodular mass with blue, grey, glistening and translucent cartilaginous tissue. • Periphery of tumor shows yellowish areas of calcifications. • Tumor may show foci of hemorrhage, necrosis and myxoid degeneration. • Presence of fleshy tissue on cut section represents high grade tumors.

Fig. 14.15: Cut surface of rib shows a lobulated, bluish grey, glistening cartilaginous tu mar with focal areas of hemorrhage and yellowish calcification (arrow).

Microscopic Features

Microscopic features of intramedullary chondrosarcoma (conventional) are shown in Box 14.16. Differential Diagnosis

• Enchondroma: Typically not painful, radiologically intramedullary translucent lesion without cortical destruction. Histology similar to grade 1 chondrosarcoma, however, it shows chondroid lobules separated by normal hematopoietic tissue, whereas chondrosarcoma shows chondroid lobules separated by fibrous tissue. • Fracture callus: Benign chondrocytes, specific clinical and radiological features. • Chondroblastic osteosarcoma: Tumor osteoid present, prominent periosteal reaction, younger age group than chondrosarcoma. Dedifferentiated Chondrosarcoma

Dedifferentiated chondrosarcoma is a rare tumor representing about 10% of all chondrosarcomas. It occurs in older patients with equal sex distribution. Most common sites are femur, pelvis and humerus. Patients present with recent increase in pain and rapidly enlarging mass. Most patients have pathological fracture. Radiography shows two distinct areas-poorly defined lytic areas that exhibit cortical destruction and expansion with soft tissue mass formation and other radiodense areas containing calcification characteristic of chondroid differentiation. Characteristic histology shows abrupt and sharply demarcated transition zone between Box 14.16 lntramedullary Chondrosarcoma • Chondroid matrix with variable cellularity. • Chondrocytes with hyperchromatic nuclei in clusters along with occasional giant cells. • Mitosis present, foci of necrosis.

Bones and Joints chondroid and dedifferentiated components. This tumor has a poor prognosis. Salient Gross Features

Gross features of dedifferentiated chond.rosarcoma are shown in Fig. 14.16. • Tumor shows two different areas - areas of blue, glistening chondroid tissue admixed with well demarcated soft, tan yellow fleshy tissue. • Chondroid areas show yellowish areas of calcifications. • Tan fleshy areas show foci of hemorrhagic and necrotic areas. Microscopic Features

Microscopic features of dedifferentiated chondrosarcoma are shown in Box 14.17. Dlfferenffal Diagnosis

• Malignant fibrous histiocytoma: Lacks cartilaginous components. • Fibrosarcoma: Lacks cartilaginous components. • Mesenchymal chondrosa:rcoma: Younger age group, gradual transition between cartilaginous and dedifferentiated components.

Box 14.17 Dedlfferentlated Chondroaarcoma • Carttlaglnous component as low grade chondrosan::oma. • Sharply demarcated dedlfferentlated part that may have features of malignant fibrous histiocytoma or fibrosarcoma or osteosarcoma or rhabdomyosarcoma or angiosarcoma.

• High grade intramed.ullary chondrosarcoma: May contain spindle cell areas mimicking dedifferentiated part, however th.ere is no abrupt transition between them. • Metastatic sarcoma to bone (leiomyosarcoma, angiosarcoma, rhabdo-myosarcoma): Lacks cartilaginous part. Mesenchymal Chondrosarcoma

Mesenchymal chondrosarcoma is a rare tumor accounting for romatosis/Desmoid Tumor/Musculoaponeurotic Flbromatosis Flbrosarcoma Flbrohlstlocytic Tumor Dermatoflbrosarcoma Protruberans (DFSP) Malignant Fibrous Histiocytoma (MFH) Adlpocytlc Tumours Lipoma Llposarcoma

Capillary Hemangioma Angiosarcoma

Skeletal Mu.cle Tumors Rhabdomyoma Rhabdomyosarcoma (RMS) Neural Tumore Schwannoma/Neurtlemmoma Neuroflbroma Malignant Peripheral Nerve Sheath Tumor {MPNST)

GROSSING

Plantar fibromatosis (Ledderhose disease): It occurs on plantar surface, non-weight bearing area of foot. It is seen both in children and adults.

PATHOLOGY FIBROBLASTIC/MYOFIBROBLASTIC TUMORS

Penile fibromatosis (Peyronie's disease): It is seen on dorsal aspect of penis of adults. Sometimes fibromatoses may be associated with diabetes, cirrhosis and epilepsy.

Superflclal Flbromatosls

Superficial fibromatosis is a tumor like lesion of fibrous tissue, regarded as non-metastasizing fibroblastic tumor. It invades locally and recurs after surgical excision. It presents as a small, slow growing subcutaneous nodule or thickening. There are three types of superficial fibromatoses-palmar, plantar and penile fibromatosis.

Salient Gross Features

Gross features of superficial fibromatosis are shown in Fig. 15.1. • It shows single or multiple firm nodules or scar-like tissue in subcutis. • Cut section is grey white. • Necrosis or hemorrhage is not seen.

Palmar fibromatosis (Dupuytren contracture): It is seen on palmar surface of hands and may result in contracture. It occurs mostly in adults with male predominance and often bilateral in alcoholics. 249

Essentials of Grou Pathology

Microscopic Features Microscopic features of superficial fibromatosis are shown in Box 15.1.

Differential Diagnosis • Calcifying aponeurotic fibroma: Children and adolescents, infiltrative growth pattern, hyalinised nodules with stippled calcification, sometimes with chondroid areas. • Fibroma of tendon sheath: Well circumscribed mass firmly attached to tendon sheath, hypocellular, bland spindle cells separated by hyalinised collagenous stroma. • Fibrosarcoma (infantile and adult types): Infantile fibrosarcoma in dmal tubular eplthellum 141 PSA 46. 148 Psommoma bodies 61. 143. 188, 197. 275, 276 PSAP 46. 148 P$eudocapeulated mo• 143 P$eudoei:>!lhellomatou$ hyperJ)loSlo 187 ~doglondular

1um1na 68 pattem 173 tronsformanon 107 Pseudomallgnont osteoblastoma 225 Pseudomonas 35, 122 Pseudopolyp 85. 89. 101 Pseudosarcomatous tlbromatosls 251 PTEN tumor 178 Pulmonary abse9$$ 39. 40 artery 51 tlbrosl$ 42 scar 46 tuberculosis 50, 88 valve 11 PUNLMP (paplllory urothellol neoplasm of low mallgnant potennal) 146 Pure ock::lum gall$t0n8$ 115 oxalate 139 l)h0$i:>hal$ 139

PurklnJ& tlbl'G$ 11 Purulent so1p1nglt1$ 198 Pyelonephrttls 122 OC\lte 122 cnronlc 124 tuberculou$ pyelonephr1Hs 126 xanthogranulomatous pyelonephrtlls 125 Pyalos:>hlabltb 98 PylOrlc valvea 79 Pyogenk:: Obse9$$ 38 bOOterta 221 osteomyellt1$ 221. 222 Pyramidal IObe 54 Pyrlform fas.so 71 sinus 75 Quadrar& lobe 103 Rodie! scxir 216 Radloff on fibrosis 17 1heropy 179 Radlool neck dlssec:tlon 75 Radleal cVSfe¢10my 145 excb10ns/amputa11on 264 hysterectomy 179 neck dlssect!On (RND) 75 orchlectomy 155, 171 prostatectomlas 168. 169. 170 RadlculOr pain 275 Rapldly progressive glomerulonephrtHs 131 Reactive astrocyto.sls 268 bOne

226

mesothellal hyperplaSla 50 Rectum 172 Red pulp 21. 30

Reed-Sternberg oell 23 Reflux nephrol)Qthy 124 Reglonal l)Qncreatectomy 118 Relnke's spaoe 69 ReJuvenator $Olutl0n s Renal cell carcinoma d'lromophobe RCC 143 clos.s!flcaHon 140 clear cell RCC 141 poplllary RCC 142 Renal odenocarclnoma 140 capsule 148 lnfcre1$ 128 multk::ywflc dYSi:>IOSla 135 pelvl$ 121. 122 scarring 123 s1nu$ 121 stones 125 transplant 132 vein 142. 148 Rentronn shape 136 Respiratory system anatomy 31 g10$Slng 50 pothOlogy 31 R8$plrotory brond'llO!aS 31 eplltlellum 44 $Y$tem 31 R9$toratlon of specimen s Restrictive cordlomyopattly 15, 17 RET prottxincogene 61 Rafe cysladenoma 187 testes 171 Retention polyps 91 Retk::ulln 26 tlbel$ 49 framework 111 stain 106. 197 Retlform Sertoll-l.eydlg cell tumor 189 Retlnoblastoma 279. 281 Retlnocytoma$ 281 Retrol)erttoneol organ 104 Rhabdold cells 274 tumor 145 Rhobdomyoma 261 Rhabdomyosarcoma 26.65.261. 182 RheumaHc fever 12 heart disease 12 Rheumatoid orthrttls 40. 41. 246 s:>neumoconlOSIS 41 Richter $Vndrome 26 Rlac:!Ell thyroldms 63 Right Ol!lal appendage 19 Right coronary ortery 11. 13 Right hemlcolectomy 101 Right-sided C-Olon concer 93 Rockltan~'$ Aschoff $lnu$8$ 114 RokltoMky protuberance 195 $lnus 114 Rol)ey collagen 180 fiber$ 257 Rosenfhal flbers 269 Rosette$ 174. 275 Round cell LPS 258 Ruptured spleen 28 Sego spleen 28. 29 Salvary duct carcinoma 65 Sollvory gland 54 Sollvory gland QClnlc cell carcinoma 68 adenoid cystic carcinoma 67

carcinoma &x pleomorphlc adenoma 65 carcln0$0rcoma 65 mucoepldermold carcinoma 66 i:>leomorphlc adenomo 64 warltlln tumor 66 Solplngectomles 208 Solplngltls 198 Solt and pepper sl)ecldlng 273 Solvaglng surgery 225 Sanderson's polsters 56 Sorcold·llke disorders 39 Sorcoldo11s lung 38 Sarcoma bt'EIO$t 217 Sorcomotold carcinoma 72, 126 pattem 50 Sorcomerlc proteins 15 Satellite 18$10"9 219 nodule 110. 2S4 tumor 148 SaU90ge llke form 85 Scar carcinoma 45. 46 Schaumann bodies 22. 38, 39 Schlller-Duvol bodl9$ 158, 163, 194. 195 Sd'llstosoma hemotoblum lnfecnon 145 Schwannomo 95. 96.. 262. 263, 272 Sclrmou$ 110 growth 116 tumor 110 Scleroslng adenoslS 168. 211. 21 S Scleroslng osteomyelltls of Garre 222 sebaOEIOU$ gland carcinoma 279 Sebaceous cell oorclnoma 280 gland corclnoma 280 Secondary amyloldosls 40 aneurysmal cyst 224 synovtal chondrometos:>laslO 245 tubel'C\llosls of Lung 37 seepage of Ink 9 segmental esophogectomy 98 semnunor vatves 11. 18 semlnol vesicles 170 semlnlferoU$ tubules 152 sem1noma 152.. HxHS8. 161. 163 sepnc Infarcts 12 sequemum 221. 222 serosor tuberol8$ 198 SerOU$

carcinomas 187 ~noflbromo 189 eystodenoma ovary 189 tumors 187 sertoll cell nodule with lntratubular germ call neoi:>10S10 164 serron oells 152. 161 tumorof 162 serum AfP or hCG 157 serum COIOltonln 62 Sex cord strcmol tumors 154, 161. 197 Sharpey$' t1be111 221 Shepherd deformity 237 Slolometaplo$1a 67 Sk::kle cell disease 123 Signet ring appearance 165 carcinoma 258 oell 58. 78. 83 Slllcon dioxide 41 Sllk::0$1$ 40. 41 Slllcottc nOdules 41. 42 Slmple CWP 40

s1mp1e renal cvn 139. 135. 139 Singers' nodule 69 Slnu$ nOde 19 Slpple'$ syndrome 61 Sister Mory Joseph nOdules 81 Sjc)gren syndrome 63 Skeletal muscle tumours rhabdomyomo 260 rhobdomyosorcoma (RMS) 260 Sleeve lobectomy SO Smell cell neoplasms Ewing sarcoma 240 lymphoma 241 Small oell corcrnoma 44, 46. 47, 174 oellGBM 270 eel 1111g corcnomo (SCLC) 45. 48 oell nonkerot1n121ng corcnoma 174 contracted kidney 126 Intestine 76, 77 round cell tumors 240 Smoky/coca colored urine 130 Snoke llke f\Jmour 110 soap bubble os:>l)&Oronce 240 Sodium hydroauls:>hlte s. 6 Soft ttsaue tumou111 gl'O$'$ing 263 pathology 248 Solid yolk soc tumor 192 Solttory ~brous tumor 50. 183, 254. 276 nOdule 57 Space of Dlsse 104. 108 Spermotk:: gronuloma 153 Spermatocyttc semlnoma 156, 157. 160 Sl)ermatogonlO 152 Si:>henO!d wing 276 Spldercells 261 Spino bltlda 159 Splndle cell or pleomorphlc llpoma 257. 258 typeRMS 261 Spleen congestive splenomegaly 27 amyloldosls spleen 27 lordaceous spleen 28 sago spleen 28 ruptured spleen 27 Ss:>lenectomy $p8ch'len 29 Si:>lanlc copeula 27 Splanlc flexure 84. 101 Spoke-wheal appearance 144 appearance 136 spaces 260 Squomooo1umnor Junction 99. 173 SQuamOU$ corclnoma 281 oell carcinoma 44, 45. 71, 174 oell ocrclnoma of cervix 173 lntraeplthellal leslon 175 metoplaSla 67, 174 morulas 179 Stoghorn stone 140 Stophy1ococcU$ 35 OUteU$ 221 Stell ate eels 19, 104. 258 lncluslon 39 renculum 240 soar 110 Sten~n·s duct 55 Step$ of gross exam1not10n dissection 8 gross deect1pnon 9 orientation 8 sompllng9 Stcmoch 76. 78

Essentials of Grou Pathology Storage disease 30 of specimen 7 Strawberry hemangloma 260 stresss fracture 224 string sign 227 S!Tomal nodule 181. 183 Stromal sarcomas 180 Struvlte stone 139 Subcapsula r fibrosis of llver l 07 Subependymal giant cell astrocytoma 267. 269 Subependymoma 271 Subglottic carcinomas 71 tumor 75 Subllngual gland 55 Submandlbular 54, 67 gland 55. 64, 75 tTlangle 55 Submaxlllectomy 74 Subpleural bullae 34 space 42 Subtotal thyroldectomy 73 Superflclal fibromatosiS 249. 251 parottdectomy 74 Supraclavicular sentinel lymph node 81 Supraglottlc laryngectomy 74 tumor 75 Suprascapular fossae 22 Supratentorial tumors 272 Surface paplllomas 187 Surfactant opoproteln 42 Suspensory ligaments of cooper 211 Sustantacular cells 50 SV40 (simian vacuolating virus) 49 SWlss roll method 120 SWyer Jomes syndrome 36 Synaptophysin 48. 50, 62 Syncyttotrophoblast 156, 158 Synovial diSeases pigmented v111onodular synovltls 246 synavial chandromatosis 245 Synovlal chondromatosls 244, 245 chondrosarcoma 245 sarcoma (monophaslc) 26, 144. 253. 264 Taenla coll 77, 101 Tamoxifen 178 Tanycyttc Ependymoma 273 Tapeworm Echlnococcus granulosus l 08 TB empyema 38 T-cell lymphoma 25 T-cell rosettes 23 Telanglectatlc osteosarcoma 227. 243 Temporal artery biopsy 20 Teratocarclnoma 159, 161 Terotoma 159. 160. 195 Terminal bronchlole 31 Testtcular tumors 155 adenomatoid 164 chorlocarclnoma l 59 embrycnal carcinoma 157 gonadoblastoma 164 granuloso cell tumor 163

leydlg cell tumor 161 mixed germ cell tumor 16l semlnoma 155 sertoll cell tumor/ androblastoma 162 spermatocytic seminoma 156 teratomo 160 testieular lymphoma 164 yollc sac tumor 158 Testicular feminization 163 lymphoma 164 tumors 154 Thrombomodulin 148, 261 Thrombotic thrombocytopenic purpura 131 Thyroglobulin 46, 59. 62 Thyrohyold membrane 55 Thyroid capsule 56 cartilage 54. 55 gland 54 malignancy 57 Thyroid chronic lymphocytic thyroiditis 63 follicular adenoma 57 follicular carcinoma 57 medullary carcinoma 60 nodular goitre 56 papillary carcinoma 59 Thyroldlsatton of tubules l 25 Tongue-lilce protrusions 65 Torsion of testis 153, l 54 Total hepatectomy 117 laryngectomy 74 pancreatectomy 118 parotldectomy 74 salpingectomy specimen 209 thyroldectomy 73 vulvectomy specimen 208 Toxic megacolon 89 Toxoplasmosls 131 Trochee 31 Tracheal ring 54 Tracheobronchial Instillation 52 tree 91 Tracheostomy site 75 Tronsformation zone 204 Transitional cell carcinoma 145. 174 cell metaplasla 176 zone 170 Translucent papillary lesions 17 Transmural lnfarctton 83 Transurethral resectton 146, l 69 Traumatic rupture 30, 1l 7 synovitis 246 Trichobezoar 80 Trilateral retinoblastoma 279 Triple phosphate stone 139 Trisomy 13 152 Trlsomy 7 and 17 141 Trophoblastlc hyperplasia 200 of early gestatton 202 Trophoblastlc hyperplasla 201 tissue 199 Tubercular epididymo-orchitis 152 Tuberculosis lung 36 military 38

primary 37 secondary 37 Tuberculous lymphadenltls 21 pyelonephrltts 122. 126, l 27 salplngltls 198 Tube-ovarian abscess 198 Tubular adenoma 91 carcinoma 214. 216. 21 7 necrosis 123 sclerosis 152 Tumor osteold 227 Tunica albugenla 151. 156, 171 vaglnalls 151 TURP 167 Type II endometrlal adenocorclnoma 178 Typhoid fever 28

u shaped depression 125 scar 127 Ulceratlve colitis 89 Ulcerative colltts 84, 85, 89-91 proctltts 89 proctosigmoiditis 89 Unclnate process l 04 Undescended testis 152. 153, 164, 171 Undifferentiated carclnomo 197 endometrlal sarcoma 182 Unicameral bone cyst 243, 244 Unilateral renal dysplasla 133 Universal precautions lo Uremic sponge kidney l 37 Ureteric orifices 150 Urethral meatus 152 Uric acid 139 stone of 139 Urinary bladder 145 Urinary tract anatomy 121 kidney 121 urinary bladder 122 grossing 148 pathology l 22 Urinary bladder 122. l 45. 172 catecholamines 241 Urothelial carcinoma 146, 147 with squamous differentiation 148 Urothellal papllloma l 46 Uterine cornua 206 Uterine leiomyoma 182 Uterus 185. 184 Uterus adenocarclnoma 177 types I and II endometrial 177 adenomyosls uterus l 85 carcinoma endometrium 177 endometrial polyp 176 endometrlal stromal nodule 179 lelomyoma hlstologlcal variants 183 Intramural 182 submucous 182 subserous 182 leiomycsarcoma 184

low grade endometrlol stromal sarcoma 180 undifferentiated endometrial sarcoma 182

V shaped scar l 27 Vaglnal cuff margin 206 Vas deferens 151 Vascular tumours angiosorcoma 259 caplllary hemangloma 259 Vascular sinusoids 103 tumor 260 Ventrlcular cavities 15 compliance 15 hypertrophy 14 septum 19 thickness 11 wall 13 Verocay body 263 Verrucae 12 Verrucous carcinoma 165. 174. 187 Veslcoureteral reflux l 23. 124 Villoglandular structures 178 Villous adenoma 91 edema 201 mucosa 77 VIN of usual type (u-VIN) 187 Vlrchow's node 81 Vltelllne duct 87 Vitreous body 279 Vocal nodule and polyp 71 Volkman's canals 221 Volvulus Intestine 84 von Brunn nests 147 Vulvo 173 condyloma acumlnate 185 squamous cell corcinoma 186 vulval lntraeplthellal neoplasla (VIN) 186 Woldeyer ring 26 Warthln's duct 55 Warthin's tumor 66 Wavy collagen 263 Wavy serpentine nuclei 263 Waxy appearance 107. 129 Wegener granulomatosls 38 Well differentiated llposarcoma 256-258 Whipple's pancreatlcoduodenectomy 118 Whipple's procedure 118 White pulp 30 Whorled cut surface 183 Wllms· tumor/nephroblastomo 144. 145 Wright Glemso stain 29 Xa nthogranulomatous cholecystltls 114

Xanthogranulomatous pyelonephrltls 125, l 26 Yellow-green mucopurulent secretions 35 Yellow-white mottling 45 Yolk soc tumor 158, 163, 194, 195 Zellballen 63 zenker's l Zonal pattern 126. 224