Pituitary Tumors Early Detection, Diagnosis, and Staging Detection and Diagnosis
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GH/IGF-1 Abnormalities and Muscle Impairment: from Basic Research to Clinical Practice
International Journal of Molecular Sciences Review GH/IGF-1 Abnormalities and Muscle Impairment: From Basic Research to Clinical Practice Betina Biagetti * and Rafael Simó * Diabetes and Metabolism Research Unit, Vall d’Hebron Research Institute and CIBERDEM (ISCIII), Universidad Autónoma de Barcelona, 08193 Bellaterra, Spain * Correspondence: [email protected] (B.B.); [email protected] (R.S.); Tel.: +34-934894172 (B.B.); +34-934894172 (R.S.) Abstract: The impairment of skeletal muscle function is one of the most debilitating least understood co-morbidity that accompanies acromegaly (ACRO). Despite being one of the major determinants of these patients’ poor quality of life, there is limited evidence related to the underlying mechanisms and treatment options. Although growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels are associated, albeit not indisputable, with the presence and severity of ACRO myopathies the precise effects attributed to increased GH or IGF-1 levels are still unclear. Yet, cell lines and animal models can help us bridge these gaps. This review aims to describe the evidence regarding the role of GH and IGF-1 in muscle anabolism, from the basic to the clinical setting with special emphasis on ACRO. We also pinpoint future perspectives and research lines that should be considered for improving our knowledge in the field. Keywords: acromegaly; myopathy; review; growth hormone; IGF-1 1. Introduction Acromegaly (ACRO) is a rare chronic disfiguring and multisystem disease due to Citation: Biagetti, B.; Simó, R. non-suppressible growth hormone (GH) over-secretion, commonly caused by a pituitary GH/IGF-1 Abnormalities and Muscle tumour [1]. -
Endocrine Pathology (537-577)
LABORATORY INVESTIGATION THE BASIC AND TRANSLATIONAL PATHOLOGY RESEARCH JOURNAL LI VOLUME 99 | SUPPLEMENT 1 | MARCH 2019 2019 ABSTRACTS ENDOCRINE PATHOLOGY (537-577) MARCH 16-21, 2019 PLATF OR M & 2 01 9 ABSTRACTS P OSTER PRESENTATI ONS EDUCATI ON C O M MITTEE Jason L. Hornick , C h air Ja mes R. Cook R h o n d a K. Y a nti s s, Chair, Abstract Revie w Board S ar a h M. Dr y and Assign ment Co m mittee Willi a m C. F a q ui n Laura W. La mps , Chair, C ME Subco m mittee C ar ol F. F ar v er St e v e n D. Billi n g s , Interactive Microscopy Subco m mittee Y uri F e d ori w Shree G. Shar ma , Infor matics Subco m mittee Meera R. Ha meed R aj a R. S e et h al a , Short Course Coordinator Mi c h ell e S. Hir s c h Il a n W ei nr e b , Subco m mittee for Unique Live Course Offerings Laksh mi Priya Kunju D a vi d B. K a mi n s k y ( Ex- Of ici o) A n n a M ari e M ulli g a n Aleodor ( Doru) Andea Ri s h P ai Zubair Baloch Vi nita Parkas h Olca Bast urk A nil P ar w a ni Gregory R. Bean , Pat h ol o gist-i n- Trai ni n g D e e p a P atil D a ni el J. -
1-Anatomy of the Pituitary Gland
Color Code Important Anatomy of Pituitary Gland Doctors Notes Notes/Extra explanation Please view our Editing File before studying this lecture to check for any changes. Objectives At the end of the lecture, students should be able to: ✓ Describe the position of the pituitary gland. ✓ List the structures related to the pituitary gland. ✓ Differentiate between the lobes of the gland. ✓ Describe the blood supply of pituitary gland & the hypophyseal portal system. الغدة النخامية Pituitary Gland (also called Hypophysis Cerebri) o It is referred to as the master of endocrine glands. o It is a small oval structure 1 cm in diameter. o It doubles its size during pregnancy. lactation ,(الحمل) pregnancy ,(الحيض) A women experiences changes in her hormone levels during menstruation But only the pituitary gland will only increase in size during pregnancy .(سن اليأس) and menopause ,(الرضاعة) X-RAY SKULL: LATERAL VIEW SAGITTAL SECTION OF HEAD & NECK Extra Pituitary Gland Position o It lies in the middle cranial fossa. o It is well protected in sella turcica* (hypophyseal fossa) of body of sphenoid o It lies between optic chiasma (anteriorly) & mamillary bodies** (posteriorly). Clinical point: *سرج الحصان Anterior to the pituitary gland is the optic chiasm, so if there was a tumor in the pituitary gland or it was ** Part of hypothalamus enlarged this could press on the chiasm and disrupt the patients vision (loss of temporal field). Extra Pictures The purple part is the sphenoid bone Hypophyseal fossa Pituitary Gland The relations are important Important Relations • SUPERIOR: Diaphragma sellae: A fold of dura mater covers the pituitary gland & has an opening for passage of infundibulum (pituitary stalk) connecting the gland to hypothalamus. -
MDM2 Gene Polymorphisms May Be Associated with Tumor
in vivo 31 : 357-363 (2017) doi:10.21873/invivo.11067 The Role of p16 and MDM2 Gene Polymorphisms in Prolactinoma: MDM2 Gene Polymorphisms May Be Associated with Tumor Shrinkage SEDA TURGUT 1, MUZAFFER ILHAN 2, SAIME TURAN 3, OZCAN KARAMAN 2, ILHAN YAYLIM 3, OZLEM KUCUKHUSEYIN 3 and ERTUGRUL TASAN 2 Departments of 1Internal Medicine, and 2Endocrinology and Metabolism, Bezmialem Vakif University, Istanbul, Turkey; 3Department of Molecular Medicine, The Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey → Abstract. Aim: Prolactinomas are thought to arise from genotype (TT+GG) of MDM2 SNP309T G was clonal expansion of a single mutated cell which is subjected significantly higher than in heterozygous genotype (TG) to growth stimuli of several permissive factors, although the carriers (odds ratio(OR)=0.18, 95% confidence pathogenetic mechanisms underlying tumorigenesis remain interval(CI)=0.06-0.58; p=0.003). Conclusion: This study unclear. The present study aimed to investigate the role of showed that p16 and MDM2 polymorphisms do not play a → → p16 (540C G and 580C T) and mouse double minute 2 decisive role in tumorigenesis, but some genotypes of these → (MDM2) (SNP309T G) gene polymorphisms in polymorphisms might be associated with follow-up tumorigenesis and characteristics of prolactinoma. Patients characteristics of prolactinoma. and Methods: A total of 74 patients with prolactinoma and 100 age- and gender-matched healthy individuals were Prolactinoma is the most frequent type of functional pituitary enrolled in the study. Serum prolactin levels were measured tumor, with an estimated prevalence of approximately 45 by enzyme-linked immunosorbent assay (ELISA). p16 and cases per 100,000 population in adults (1). -
Glossary of Pediatric Endocrine Terms
Glossary of Pediatric Endocrine Terms Adrenal Glands: Triangle-shaped glands located on top of each kidney that are responsible for the regulation of stress response by producing hormones such as cortisol and adrenaline. Adrenal Crisis: A life-threatening condition that results when there is not enough cortisol (stress hormone) in the body. This may present with nausea, vomiting, abdominal pain, severely low blood pressure, and loss of consciousness. Adrenocorticotropin (ACTH): A hormone produced by the anterior pituitary gland that triggers the adrenal gland to produce cortisol, the stress hormone. Anterior Pituitary: The front of the pituitary gland that secretes growth hormone, gonadotropins, thyroid stimulating hormone, prolactin, adrenocorticotropin hormone. Antidiuretic Hormone: A hormone secreted by the posterior pituitary that controls how much water is excreted by the kidneys (water balance). Bone Age Study: An X-ray of the left hand and wrist to assess a child’s skeletal age. It is often used to evaluate disorders of puberty and growth. Congenital Adrenal Hyperplasia: A group of disorders which impair the adrenal steroid synthesis pathway. This causes the body makes too many androgens. Sometimes the body does not make enough cortisol and aldosterone. Constitutional Delay of Growth and Puberty: A normal variant of growth in which children grow at a slower rate and begin puberty later than their peers. They may appear short until they have catch up growth. They usually end up at a normal adult height. A diagnosis of constitutional delay of growth and puberty is often referred to as being a “late bloomer.” Cortisol: The “stress hormone”, which is produced by the adrenal glands. -
Synchronous Morphologically Distinct Craniopharyngioma and Pituitary
orders & is T D h e n r Bhatoe et al., Brain Disord Ther 2016, 5:1 i a a p r y B Brain Disorders & Therapy DOI: 10.4172/2168-975X.1000207 ISSN: 2168-975X Case Report Open Access Synchronous Morphologically Distinct Craniopharyngioma and Pituitary Adenoma: A Rare Collision Entity Harjinder S Bhatoe*, Prabal Deb and Sudip Kumar Sengupta Institute of Neuroscience, Max Super Speciality Hospital, New Delhi, India Abstract While pituitary tumors and craniopharyngiomas share a common lineage, their simultaneous occurrence is distinctly rare. We present one such patient, an adult male with two distinct tumors, that were excised by two different approaches. Relevant literature is briefly reviewed. Keywords: Brain tumor; Collision tumor; Craniopharyngioma; Pituitary tumor Introduction Simultaneous occurrence of morphological distinct, discreet intracranial tumors sharing the same cell lineage is a rarity. Pituitary tumors and craniopharyngiomas share a common lineage. Simultaneous occurrence of these two tumors in the same patient is rare and has been reported only nine times so far (Table 1). While pituitary tumours are centred in the sella, craniopharyngiomas may occur anywhere from the pituitary gland to the third ventricle. Association of intra-third ventricular craniopharyngioma and growth hormone- Figure 1: Contrast MRI (T1-weighted sagittal) showing intra-third-ventricular secreting pituitary macroadenoma as two distinct, unconnected tumors craniopharyngioma and pituitary adenoma. occurring synchronously has not been reported so far. Case Report A 35-year-old male was admitted with six-month-history of generalized headache, gradual loss of vision and intermittent generalized tonic clonic seizures. Clinically, he had acromegaly and optic atrophy with no perception of light. -
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. -
Clinical Radiation Oncology Review
Clinical Radiation Oncology Review Daniel M. Trifiletti University of Virginia Disclaimer: The following is meant to serve as a brief review of information in preparation for board examinations in Radiation Oncology and allow for an open-access, printable, updatable resource for trainees. Recommendations are briefly summarized, vary by institution, and there may be errors. NCCN guidelines are taken from 2014 and may be out-dated. This should be taken into consideration when reading. 1 Table of Contents 1) Pediatrics 6) Gastrointestinal a) Rhabdomyosarcoma a) Esophageal Cancer b) Ewings Sarcoma b) Gastric Cancer c) Wilms Tumor c) Pancreatic Cancer d) Neuroblastoma d) Hepatocellular Carcinoma e) Retinoblastoma e) Colorectal cancer f) Medulloblastoma f) Anal Cancer g) Epndymoma h) Germ cell, Non-Germ cell tumors, Pineal tumors 7) Genitourinary i) Craniopharyngioma a) Prostate Cancer j) Brainstem Glioma i) Low Risk Prostate Cancer & Brachytherapy ii) Intermediate/High Risk Prostate Cancer 2) Central Nervous System iii) Adjuvant/Salvage & Metastatic Prostate Cancer a) Low Grade Glioma b) Bladder Cancer b) High Grade Glioma c) Renal Cell Cancer c) Primary CNS lymphoma d) Urethral Cancer d) Meningioma e) Testicular Cancer e) Pituitary Tumor f) Penile Cancer 3) Head and Neck 8) Gynecologic a) Ocular Melanoma a) Cervical Cancer b) Nasopharyngeal Cancer b) Endometrial Cancer c) Paranasal Sinus Cancer c) Uterine Sarcoma d) Oral Cavity Cancer d) Vulvar Cancer e) Oropharyngeal Cancer e) Vaginal Cancer f) Salivary Gland Cancer f) Ovarian Cancer & Fallopian -
Hypothalamus and Pituitary Gland Development in the Common Snapping Turtle, Chelydra Serpentina, and Disruption with Atrazine Exposure
University of North Dakota UND Scholarly Commons Theses and Dissertations Theses, Dissertations, and Senior Projects January 2016 Hypothalamus And Pituitary Gland Development In The ommonC Snapping Turtle, Chelydra Serpentina, And Disruption With Atrazine Exposure Kathryn Lee Gruchalla Russart Follow this and additional works at: https://commons.und.edu/theses Recommended Citation Russart, Kathryn Lee Gruchalla, "Hypothalamus And Pituitary Gland Development In The ommonC Snapping Turtle, Chelydra Serpentina, And Disruption With Atrazine Exposure" (2016). Theses and Dissertations. 2069. https://commons.und.edu/theses/2069 This Dissertation is brought to you for free and open access by the Theses, Dissertations, and Senior Projects at UND Scholarly Commons. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of UND Scholarly Commons. For more information, please contact [email protected]. HYPOTHALAMUS AND PITUITARY GLAND DEVELOPMENT IN THE COMMON SNAPPING TURTLE, CHELYDRA SERPENTINA, AND DISRUPTION WITH ATRAZINE EXPOSURE by Kathryn Lee Gruchalla Russart Bachelor of Science, Minnesota State University, Mankato, 2006 A Dissertation Submitted to the Graduate Faculty of the University of North Dakota in partial fulfillment of the requirements for the degree of Doctor of Philosophy Grand Forks, North Dakota August 2016 Copyright 2016 Kathryn Russart ii iii PERMISSION Title Hypothalamus and Pituitary Gland Development in the Common Snapping Turtle, Chelydra serpentina, and Disruption with Atrazine Exposure Department Biology Degree Doctor of Philosophy In presenting this dissertation in partial fulfillment of the requirements for a graduate degree from the University of North Dakota, I agree that the library of this University shall make it freely available for inspection. -
Incidental Pituitary Adenomas
Neurosurg Focus 31 (6):E18, 2011 Incidental pituitary adenomas WALAVAN SIVAKUMAR, M.D.,1 ROUKOZ CHAMOUN, M.D.,1 VINH NGUYEN, M.D.,2 AND WILLIAM T. COULdwELL, M.D., PH.D.1 Departments of 1Neurosurgery and 2Radiology, University of Utah, Salt Lake City, Utah Object. Pituitary incidentalomas are a common finding with a poorly understood natural history. Over the last few decades, numerous studies have sought to decipher the optimal evaluation and treatment of these lesions. This paper aims to elucidate the current evidence regarding their prevalence, natural history, evaluation, and management. Methods. A search of articles on PubMed (National Library of Medicine) and reference lists of all relevant ar- ticles was conducted to identify all studies pertaining to the incidence, natural history, workup, treatment, and follow- up of incidental pituitary and sellar lesions, nonfunctioning pituitary adenomas, and incidentalomas. Results. The reported prevalence of pituitary incidentalomas has increased significantly in recent years. A com- plete history, physical, and endocrinological workup with formal visual field testing in the event of optic apparatus involvement constitutes the basics of the initial evaluation. Although data regarding the natural history of pituitary incidentalomas remain sparse, they seem to suggest that progression to pituitary apoplexy (0.6/100 patient-years), visual field deficits (0.6/100 patient-years), and endocrine dysfunction (0.8/100 patient-years) remains low. In larger lesions, apoplexy risk may be higher. Conclusions. While the majority of pituitary incidentalomas can be managed conservatively, involvement of the optic apparatus, endocrine dysfunction, ophthalmological symptoms, and progressive increase in size represent the main indications for surgery. -
Pituitary Disease Handbook for Patients Disclaimer This Is General Information Developed by the Ottawa Hospital
The Ottawa Hospital Divisions of Endocrinology and Metabolism and Neurosurgery Pituitary Disease Handbook for Patients Disclaimer This is general information developed by The Ottawa Hospital. It is not intended to replace the advice of a qualified health-care provider. Please consult your health-care provider who will be able to determine the appropriateness of the information for your specific situation. Prepared by Monika Pantalone, NP Advanced Practice Nurse for Neurosurgery With guidance from Dr. Charles Agbi, Dr. Erin Keely, Dr. Janine Malcolm and The Ottawa Hospital pituitary patient advisors P1166 (10/2014) Printed at The Ottawa Hospital Outline This handbook is designed to help people who have pituitary tumours better understand their disease. It contains information to help people with pituitary tumours discuss their care with health care providers. This booklet provides: 1) An overview of what pituitary tumours are and how they are grouped 2) An explanation of how pituitary tumours are investigated 3) A description of available treatments for pituitary tumours What is the Pituitary Gland? The pituitary gland is a pea size organ located just behind the bridge of the nose at the base of the brain, in a bony pouch called the “sella turcica.” It sits just below the nerves to the eyes (the optic chiasm). The pituitary gland is divided into two main portions: the larger anterior pituitary (at the front) and the smaller posterior pituitary (at the back). Each of these portions has different functions, producing different types of hormones. Optic Pituitary Hypothalamus tumor chiasm Pituitary stalk Anterior Sphenoid pituitary gland sinus Posterior pituitary gland Sella Picture provided by turcica pituitary.ucla.edu 1 The pituitary gland is known as the “master gland” because it helps to control the secretion of various hormones from a number of other glands including the thyroid gland, adrenal glands, testes and ovaries.