Kidney Solid Tumor Rules
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Kidney, Ureter, Urinary Bladder & Urethra
Kidney, Ureter, Urinary bladder & Urethra Red: important. Black: in male|female slides. Gray: notes|extra. Editing file ➢ OBJECTIVES • The microscopic structure of the renal cortex and medulla. • The histology of renal corpuscle, proximal and distal tubules, loop of Henle, and collecting tubules & ducts. • The histological structure of juxtaglomerular apparatus. • The functional structures of the different parts of the kidney. • The microscopic structure of the Renal pelvis and ureter. • The microscopic structure of the urinary bladder and male and female urethra Histology team 437 | Renal block | All lectures ➢ KIDNEY o Cortex: Dark brown and granular. Content of cortex (renal corpuscle, PCT, loop of Henle, DCT, part of collecting tubule) o Medulla: 6-12 pyramid-shape regions (renal pyramids) content of medulla ( collecting duct, loop of Henle, collecting tubule) o The base of pyramid is toward the cortex (cortico-medullary border) o The apex (renal papilla) toward the hilum, it is perforated by 12 openings of the ducts of Bellini (Papillary “collecting” ducts) in region called area cribrosa. o The apex is surrounded by a minor calyx. o 3 or 4 minor calyces join to form 3 or 4 major calyces that form renal pelvis. o Pyramids are separated by cortical columns of Bertin (renal column) ➢ URINIFEROUS TUBULE o It is the functional unit of the kidney. o Is formed of: 1- Nephron. 2-Collecting tubule. o The tubules are densely packed. o The tubules are separated by thin stroma and basal lamina. Histology team 437 | Renal block | All lectures ➢ NEPHRON o There are 2 types of nephrons: a- Cortical nephrons. b- Juxtamedullary nephrons. -
Sarcomatoid Renal Cell Carcinom Atoid Renal Cell Carcinoma
Research Article Sarcomatoid renal cell carcinoma: A case series K Subashree 1*, M Susruthan 2, N Priyathersini 3, Leena Dennis Joseph 4, Sandhya Sundaram 5 1PG Student, 2,3 Assistant Professor, 4,5 Professor, Department of Pathology , Sri Ramachandra Medical College and Research Institute Porur, Chennai-116, Tamil Nadu, INDIA. Email : [email protected] Abstract Introduction: Renal cell carcinoma is the most common form of Renal malignancy. Sarcomatoid renal cell carcinoma represents a high grade dedifferentiation of Renal cell carcinoma. This phenotype can occur in all subtypes of renal cell carcinomas, including clear cell, papillary, chromophob e, and collecting duct carcinoma. Although prognosis in sarcomatoid renal cell carcinoma is known to be extremely poor, little is known about the clinicopathologic information about them. Methods and Methodology: The population of this retrospective study consisted of all patients who underwent surgery for Renal cell carcinoma between January 2010 and February 2013 in the Department of Pathology, Sri Ramachandra university and Research Institute .A total of 64 renal cell carcinoma cases were diagnosed among which 9 had sarcomatoid changes. All 9 cases were reassessed and the diagnosis was confirmed on the basis of morphologic features. Complete baseline and follow -up data were available for analysis for all 9 patients. Conclusion: Present study showed that s arcomatoid changes were seen more commonly in younger age group with male preponderance and ne crosis was a consistent feature. Sarcomatoid areas constitute 1-25% in majority of cases which makes extensive sampling an important measure. Majority of renal cell carcinomas with sarcomatoid changes ha ve a high grade and high stage. -
Non-Wilms Renal Cell Tumors in Children
PEDIATRIC UROLOGIC ONCOLOGY 0094-0143/00 $15.00 + .OO NON-WILMS’ RENAL TUMORS IN CHILDREN Bruce Broecker, MD Renal tumors other than Wilms’ tumor are tastases occur in 40% to 60% of patients with infrequent in childhood. Wilms’ tumors ac- clear cell sarcoma of the kidney, whereas they count for 6% to 7% of childhood cancer, are found in less than 2% of patients with whereas the remaining renal tumors account Wilms’ tumor.**,26 This distinct clinical behav- for less than l%.27The most common non- ior is one of the features that has led to its Wilms‘ tumors are clear cell sarcoma of the designation as a separate tumor. Other clini- kidney, rhabdoid tumor of the kidney (both cal features include a lack of association with formerly considered unfavorable Wilms’ tu- sporadic aniridia or hemihypertrophy. mor variants but now considered separate tu- Clear cell sarcoma of the kidney has not mors), renal cell carcinoma, mesoblastic been reported to occur bilaterally and is not nephroma, and multilocular cystic nephroma. associated with nephroblastomatosis. It has Collectively, these tumors account for less been reported in infancy and adulthood, but than 10% of the primary renal neoplasms in the peak incidence is between 3 and 5 years childhood. of age. It has an aggressive behavior that responds poorly to treatment with vincristine and actinomycin alone, leading to its original CLEAR CELL SARCOMA designation by Beckwith as an unfavorable histology pattern. The addition of doxorubi- Clear cell sarcoma of the kidney is cur- cin in aggressive chemotherapy regimens has rently considered a separate tumor distinct improved outcome. -
Rare Sarcomatoid Carcinoma of the Liver in a Patient with No History of Hepatocellular Carcinoma: a Case Report
Rare sarcomatoid carcinoma of the liver in a patient with no history of hepatocellular carcinoma: a case report Abstract Sarcomatoid carcinoma is a rare malignant tumor of unknown pathogenesis characterized by poorly differentiated carcinoma tissue containing sarcoma-like differentiation of either spindle or giant cell and rarely occurs in the gastrointestinal tract and hepatobiliary-pancreatic system.1 Primary hepatic sarcomatoid carcinoma accounts for only 0.2 % of primary malignant liver tumors, and 1.8% of all surgically resected hepatocellular carcinomas.2 The majority of hepatic sarcomatoid carcinoma cases appear to occur simultaneously with hepatocellular or cholangiocellular carcinoma.3 The preferred treatment for hepatic sarcomatoid carcinoma is surgical resection and the overall prognosis is poor.4 This case depicts a 62-year-old female who underwent initial resection of a cavernous hemangioma in 2010. Seven years after her initial diagnosis, she developed what was initially felt to be local recurrence of the hemangioma but additional diagnostic workup with a liver biopsy confirmed primary hepatic sarcomatoid carcinoma. Keywords Sarcomatoid Carcinoma, Hepatocellular Carcinoma, Primary Hepatic Sarcomatoid Carcinoma Case Report A 62-year-old female with past medical history significant for vegan diet, hypothyroidism, iron deficiency anemia, and cavernous liver hemangioma presented with weight loss and abdominal fullness for approximately one month with two days of acute altered mental status, fatigue, and weakness. Patient had a complicated gastrointestinal history and underwent surgical resection of a cavernous hemangioma in 2010. Six years later, she developed abdominal fullness with right upper quadrant pain and an abdominal ultrasound at that time suggested hemangioma recurrence. In 2017, she underwent laparoscopy with unroofing of the hemangioma, drainage of an old organizing hematoma, removal of debris, and placement of an omental patch. -
Genitourinary PAX8
174A ANNUAL MEETING ABSTRACTS RMC and 19/21 (90%) of CDC cases. In contrast, 31/34 (91%) UUC were negative for Genitourinary PAX8. p63: p63 was positive in 7/12 (58%) RMC and in 3/21 (14%) CDC. Staining was focal in 6/7 RMC and strong in 4/7. Almost all (97%) UUC were p63 positive 767 Histopathologic Features of Bilateral Renal Cell Carcinomas: A (moderate/strong and multifocal/diffuse in 80% of cases). The one p63 negative UUC Study of 24 Cases was a microinvasive high grade tumor and was also negative for PAX8. J Abdelsayed, JY Ro, LD Truong, AG Ayala, SS Shen. The Methodist Hospital and Weill Conclusions: We suggest a binary panel of PAX8 and p63 as an aid in the differential Medical College of Cornell University, Houston, TX. diagnosis of high grade renal sinus epithelial neoplasms. (PAX8+/p63+) profile Background: The incidence of bilateral renal cell carcinoma (bRCC) has been reported supported the dx of RMC with a sensitivity of 58.3% and specificity of 89%. (PAX8+/ to vary from 1.5% to 11%. Clear understanding of the clinicopathologic features of p63-) profile supported the diagnosis of CDC with a sensitivity of 85.7% and a specificity bRCCs including the distinction between synchronous and metachronous tumors has of 89%. Finally (PAX8-/p63+) profile supported the diagnosis of UUC with a sensitivity important implications in patients’ management and follow up. The purpose of this study of 88% and a specificity of 100%. The concomitant expression of p63 and PAX8 in RMC is to summarize the clinicopathologic features of bRCCs and compare them with those seen in our study further suggests an intermediate phenotype between renal tubular and of unilateral renal cell carcinomas (uRCCs). -
Pediatric Abdominal Masses
Pediatric Abdominal Masses Andrew Phelps MD Assistant Professor of Pediatric Radiology UCSF Benioff Children's Hospital No Disclosures Take Home Message All you need to remember are the 5 common masses that shouldn’t go to pathology: 1. Infection 2. Adrenal hemorrhage 3. Renal angiomyolipoma 4. Ovarian torsion 5. Liver hemangioma Keys to (Differential) Diagnosis 1. Location? 2. Age? 3. Cystic? OUTLINE 1. Kidney 2. Adrenal 3. Pelvis 4. Liver OUTLINE 1. Kidney 2. Adrenal 3. Pelvis 4. Liver Renal Tumor Mimic – Any Age Infection (Pyelonephritis) Don’t send to pathology! Renal Tumor Mimic – Any Age Abscess Don’t send to pathology! Peds Renal Tumors Infant: 1) mesoblastic nephroma 2) nephroblastomatosis 3) rhabdoid tumor Child: 1) Wilm's tumor 2) lymphoma 3) angiomyolipoma 4) clear cell sarcoma 5) multilocular cystic nephroma Teen: 1) renal cell carcinoma 2) renal medullary carcinoma Peds Renal Tumors Infant: 1) mesoblastic nephroma 2) nephroblastomatosis 3) rhabdoid tumor Child: 1) Wilm's tumor 2) lymphoma 3) angiomyolipoma 4) clear cell sarcoma 5) multilocular cystic nephroma Teen: 1) renal cell carcinoma 2) renal medullary carcinoma Renal Tumors - Infant 1) mesoblastic nephroma 2) nephroblastomatosis 3) rhabdoid tumor Renal Tumors - Infant 1) mesoblastic nephroma 2) nephroblastomatosis 3) rhabdoid tumor - Most common - Can’t distinguish from congenital Wilms. Renal Tumors - Infant 1) mesoblastic nephroma 2) nephroblastomatosis 3) rhabdoid tumor Look for Multiple biggest or diffuse and masses. ugliest. Renal Tumors - Infant 1) mesoblastic -
A Metanephric Adenoma of the Kidney Associated with Polycythemia: a Case Report
352 ONCOLOGY LETTERS 11: 352-354, 2016 A metanephric adenoma of the kidney associated with polycythemia: A case report PENGFEI WANG, YUAN TIAN, YUEHAI XIAO, YANG ZHANG, FA SUN and KAIFA TANG Department of Urology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China Received January 11, 2015; Accepted September 24, 2015 DOI: 10.3892/ol.2015.3868 Abstract. Metanephric adenoma (MA) of the kidney is a 54-year-old female that presented with MA associated with rare and frequently benign tumor with a favorable prognosis polycythemia. that is often diagnosed following surgical treatment. In the present study, a 54-year-old female patient presented with Case Report complaints of intermittent right-flank pain and anterior abdominal pain occurring over 2 years and sporadic gross A 54-year-old female patient presented to the Affiliated hematuria occurring over 3 months. Ultrasonography and Hospital of Guizhou Medical University (Guiyang, China), computerized tomography imaging revealed a neoplasm with complaints of intermittent right flank pain and ante- lesion localized in the right kidney. Successful open approach rior abdominal pain that occurred over a 2-year period and radical nephrectomy was performed and post-surgical histo- sporadic gross hematuria that occurred over 3 months in pathological examination verified the lesion as a MA of the March 2013. The patient had no other symptoms. Physical kidney. Radical nephrectomy, cryoablation or radiofrequency examination revealed no significant conclusions. Urinalysis may used to treat MA and a selective panel of immunostains, revealed hematuria in the urine culture and a routine including WT1, EMA and AMACR, may be useful for diag- blood examination exhibited a hematocrit (Hct) volume of nosis. -
Familial Adenomatous Polyposis Polymnia Galiatsatos, M.D., F.R.C.P.(C),1 and William D
American Journal of Gastroenterology ISSN 0002-9270 C 2006 by Am. Coll. of Gastroenterology doi: 10.1111/j.1572-0241.2006.00375.x Published by Blackwell Publishing CME Familial Adenomatous Polyposis Polymnia Galiatsatos, M.D., F.R.C.P.(C),1 and William D. Foulkes, M.B., Ph.D.2 1Division of Gastroenterology, Department of Medicine, The Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, Quebec, Canada, and 2Program in Cancer Genetics, Departments of Oncology and Human Genetics, McGill University, Montreal, Quebec, Canada Familial adenomatous polyposis (FAP) is an autosomal-dominant colorectal cancer syndrome, caused by a germline mutation in the adenomatous polyposis coli (APC) gene, on chromosome 5q21. It is characterized by hundreds of adenomatous colorectal polyps, with an almost inevitable progression to colorectal cancer at an average age of 35 to 40 yr. Associated features include upper gastrointestinal tract polyps, congenital hypertrophy of the retinal pigment epithelium, desmoid tumors, and other extracolonic malignancies. Gardner syndrome is more of a historical subdivision of FAP, characterized by osteomas, dental anomalies, epidermal cysts, and soft tissue tumors. Other specified variants include Turcot syndrome (associated with central nervous system malignancies) and hereditary desmoid disease. Several genotype–phenotype correlations have been observed. Attenuated FAP is a phenotypically distinct entity, presenting with fewer than 100 adenomas. Multiple colorectal adenomas can also be caused by mutations in the human MutY homologue (MYH) gene, in an autosomal recessive condition referred to as MYH associated polyposis (MAP). Endoscopic screening of FAP probands and relatives is advocated as early as the ages of 10–12 yr, with the objective of reducing the occurrence of colorectal cancer. -
Familial Adenomatous Polyposis and MUTYH-Associated Polyposis
Corporate Medical Policy Familial Adenomatous Polyposis and MUTYH-Associated Polyposis AHS-M2024 File Name: familial_adenomatous_polyposis_and_mutyh_associated_polyposis Origination: 1/1/2019 Last CAP Review: 8/2021 Next CAP Review: 8/2022 Last Review: 8/2021 Description of Procedure or Service Familial adenomatous polyposis (FAP) is characterized by development of adenomatous polyps and an increased risk of colorectal cancer (CRC) caused by an autosomal dominant mutation in the APC (Adenomatous Polyposis Coli) gene (Kinzler & Vogelstein, 1996). Depending on the location of the mutation in the APC gene FAP can present as the more severe classic FAP (CFAP) with hundreds to thousands of polyps developing in the teenage years associated with a significantly increased risk of CRC, or attenuated FAP (AFAP) with fewer polyps, developing later in life and less risk of CRC (Brosens, Offerhaus, & Giardiello 2015; Spirio et al., 1993). Two other subtypes of FAP include Gardner syndrome, which causes non-cancer tumors of the skin, soft tissues, and bones, and Turcot syndrome, a rare inherited condition in which individuals have a higher risk of adenomatous polyps and colorectal cancer. In classic FAP, the most common type, patients usually develop cancer in one or more polyps as early as age 20, and almost all classic FAP patients have CRC by the age of 40 if their colon has not been removed (American_Cancer_Society, 2020). MUTYH-associated polyposis (MAP) results from an autosomal recessive mutation of both alleles of the MUTYH gene and is characterized by increased risk of CRC with development of adenomatous polyps. This condition, however, may present without these characteristic polyps (M. -
Primary Hepatic Neuroendocrine Carcinoma: Report of Two Cases and Literature Review
The Jackson Laboratory The Mouseion at the JAXlibrary Faculty Research 2018 Faculty Research 3-1-2018 Primary hepatic neuroendocrine carcinoma: report of two cases and literature review. Zi-Ming Zhao The Jackson Laboratory, [email protected] Jin Wang Ugochukwu C Ugwuowo Liming Wang Jeffrey P Townsend Follow this and additional works at: https://mouseion.jax.org/stfb2018 Part of the Life Sciences Commons, and the Medicine and Health Sciences Commons Recommended Citation Zhao, Zi-Ming; Wang, Jin; Ugwuowo, Ugochukwu C; Wang, Liming; and Townsend, Jeffrey P, "Primary hepatic neuroendocrine carcinoma: report of two cases and literature review." (2018). Faculty Research 2018. 71. https://mouseion.jax.org/stfb2018/71 This Article is brought to you for free and open access by the Faculty Research at The ousM eion at the JAXlibrary. It has been accepted for inclusion in Faculty Research 2018 by an authorized administrator of The ousM eion at the JAXlibrary. For more information, please contact [email protected]. Zhao et al. BMC Clinical Pathology (2018) 18:3 https://doi.org/10.1186/s12907-018-0070-7 CASE REPORT Open Access Primary hepatic neuroendocrine carcinoma: report of two cases and literature review Zi-Ming Zhao1,2*† , Jin Wang3,4,5†, Ugochukwu C. Ugwuowo6, Liming Wang4,8* and Jeffrey P. Townsend2,7* Abstract Background: Primary hepatic neuroendocrine carcinoma (PHNEC) is extremely rare. The diagnosis of PHNEC remains challenging—partly due to its rarity, and partly due to its lack of unique clinical features. Available treatment options for PHNEC include surgical resection of the liver tumor(s), radiotherapy, liver transplant, transcatheter arterial chemoembolization (TACE), and administration of somatostatin analogues. -
Your Kidneys and Kidney Cancer
Your Kidneys and Kidney Cancer DID YOU KNOW? Kidney Disease Kidney Cancer Having advanced Having kidney cancer kidney disease or a can increase your risk About 1/3 of kidney cancer kidney transplant can for kidney disease or patients have or will develop increase your risk for kidney failure. kidney disease.2 kidney cancer. TOP Kidney cancer is among the 10 10 most common cancers in both men and women.1 KIDNEYS Your kidneys’ main job is to About 62,000 kidney cancers clean waste and extra water 62,000 occur in the U.S. each year.1 from your blood. Having kidney disease means your kidneys are damaged and cannot do this job well. KIDNEY CANCER Over time, kidney disease can get worse and lead to kidney failure. Once kidneys fail, treatment with dialysis or a Kidney cancer is a disease that kidney transplant is needed starts in the kidneys. It happens to stay alive. when kidney cells grow out of control and form a lump (called a “tumor”). The cancer may stay in your kidneys or spread to other parts of your body. 1 Your Kidneys and Kidney Cancer SYMPTOMS Most people don’t have symptoms in the early stages of kidney disease or kidney cancer. Advanced Kidney Cancer Advanced Kidney Disease Blood in the urine Feeling tired or short of breath Pain on the sides of the mid-back Loss of appetite A lump in the abdomen Dry, itchy skin (stomach area) Trouble thinking clearly Weight loss, night sweats, unexplained fever Frequent urination Swollen feet and ankles, Tiredness puiness around eyes Talk to Your Healthcare Provider About your risk for kidney cancer About your risk for kidney disease CANCER TREATMENTS Some cancer treatments can increase your risk for kidney disease or kidney failure. -
What Is a Gastrointestinal Carcinoid Tumor?
cancer.org | 1.800.227.2345 About Gastrointestinal Carcinoid Tumors Overview and Types If you have been diagnosed with a gastrointestinal carcinoid tumor or are worried about it, you likely have a lot of questions. Learning some basics is a good place to start. ● What Is a Gastrointestinal Carcinoid Tumor? Research and Statistics See the latest estimates for new cases of gastrointestinal carcinoid tumor in the US and what research is currently being done. ● Key Statistics About Gastrointestinal Carcinoid Tumors ● What’s New in Gastrointestinal Carcinoid Tumor Research? What Is a Gastrointestinal Carcinoid Tumor? Gastrointestinal carcinoid tumors are a type of cancer that forms in the lining of the gastrointestinal (GI) tract. Cancer starts when cells begin to grow out of control. To learn more about what cancer is and how it can grow and spread, see What Is Cancer?1 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 To understand gastrointestinal carcinoid tumors, it helps to know about the gastrointestinal system, as well as the neuroendocrine system. The gastrointestinal system The gastrointestinal (GI) system, also known as the digestive system, processes food for energy and rids the body of solid waste. After food is chewed and swallowed, it enters the esophagus. This tube carries food through the neck and chest to the stomach. The esophagus joins the stomachjust beneath the diaphragm (the breathing muscle under the lungs). The stomach is a sac that holds food and begins the digestive process by secreting gastric juice. The food and gastric juices are mixed into a thick fluid, which then empties into the small intestine.