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Hyperplasia (Growth Factors
Adaptations Robbins Basic Pathology Robbins Basic Pathology Robbins Basic Pathology Coagulation Robbins Basic Pathology Robbins Basic Pathology Homeostasis • Maintenance of a steady state Adaptations • Reversible functional and structural responses to physiologic stress and some pathogenic stimuli • New altered “steady state” is achieved Adaptive responses • Hypertrophy • Altered demand (muscle . hyper = above, more activity) . trophe = nourishment, food • Altered stimulation • Hyperplasia (growth factors, . plastein = (v.) to form, to shape; hormones) (n.) growth, development • Altered nutrition • Dysplasia (including gas exchange) . dys = bad or disordered • Metaplasia . meta = change or beyond • Hypoplasia . hypo = below, less • Atrophy, Aplasia, Agenesis . a = without . nourishment, form, begining Robbins Basic Pathology Cell death, the end result of progressive cell injury, is one of the most crucial events in the evolution of disease in any tissue or organ. It results from diverse causes, including ischemia (reduced blood flow), infection, and toxins. Cell death is also a normal and essential process in embryogenesis, the development of organs, and the maintenance of homeostasis. Two principal pathways of cell death, necrosis and apoptosis. Nutrient deprivation triggers an adaptive cellular response called autophagy that may also culminate in cell death. Adaptations • Hypertrophy • Hyperplasia • Atrophy • Metaplasia HYPERTROPHY Hypertrophy refers to an increase in the size of cells, resulting in an increase in the size of the organ No new cells, just larger cells. The increased size of the cells is due to the synthesis of more structural components of the cells usually proteins. Cells capable of division may respond to stress by undergoing both hyperrtophy and hyperplasia Non-dividing cell increased tissue mass is due to hypertrophy. -
World Journal of Pharmaceutical and Life Sciences
wjpls, 2017, Vol. 3, Issue 8, 66-68 Review Article ISSN 2454-2229 Farman . World Journal of Pharmaceutical World Journal and Lifeof Pharmaceutical Sciences and Life Sciences WJPLS www.wjpls.org SJIF Impact Factor: 4.223 ONE TOO MANY- POLYORCHIDISM A RARE CASE REPORT AND REVIEW OF LITERATURE Dr. Farman Ali* India. *Corresponding Author: Dr. Farman Ali India. Email ID: [email protected], Article Received on 12/08/2017 Article Revised on 03/09/2017 Article Accepted on 24/09/2017 ABSTRACT Polyorchidism is the incidence of more than two testicles in a male. It is a rare congenital anomaly involving the abnormal division of the genital ridge longitudinally or transversely, mainly occurring in the scrotum. Triorchidism(presence of 3 testes) is the most common occurrence of this condition. They mostly occur on the left side. There have been only 140-200 pathological cases that are published in world journal literature, out of which only a few cases have been reported in India. A rare case was reported of a 20 year old man with polyorchidism presenting with an inguinal hernia, describing the clinical features, it's surgical findings and a review of the literature. The most common sites are: Scrotal(66%), inguinal(25%), and abdominal(9%). This condition is mostly asymptomatic but may commonly present with features like maldescent(40%), hernia(30%), torsion(15%), hydrocoele(9%) and malignancy(6%). Spermatogenesis may be normal only in 50% of cases. If symptoms present, they may be scrotal pain, swelling and infertility. High accuracy of pre-operative ultrasound evaluation of scrotal mass differentiates this benign entity from ominous abnormalities and prevents unnecessary surgical exploration of sonographically normal, uncomplicated and orthotopic supernumerary testes. -
Massachusetts Birth Defects 2002-2003
Massachusetts Birth Defects 2002-2003 Massachusetts Birth Defects Monitoring Program Bureau of Family Health and Nutrition Massachusetts Department of Public Health January 2008 Massachusetts Birth Defects 2002-2003 Deval L. Patrick, Governor Timothy P. Murray, Lieutenant Governor JudyAnn Bigby, MD, Secretary, Executive Office of Health and Human Services John Auerbach, Commissioner, Massachusetts Department of Public Health Sally Fogerty, Director, Bureau of Family Health and Nutrition Marlene Anderka, Director, Massachusetts Center for Birth Defects Research and Prevention Linda Casey, Administrative Director, Massachusetts Center for Birth Defects Research and Prevention Cathleen Higgins, Birth Defects Surveillance Coordinator Massachusetts Department of Public Health 617-624-5510 January 2008 Acknowledgements This report was prepared by the staff of the Massachusetts Center for Birth Defects Research and Prevention (MCBDRP) including: Marlene Anderka, Linda Baptiste, Elizabeth Bingay, Joe Burgio, Linda Casey, Xiangmei Gu, Cathleen Higgins, Angela Lin, Rebecca Lovering, and Na Wang. Data in this report have been collected through the efforts of the field staff of the MCBDRP including: Roberta Aucoin, Dorothy Cichonski, Daniel Sexton, Marie-Noel Westgate and Susan Winship. We would like to acknowledge the following individuals for their time and commitment to supporting our efforts in improving the MCBDRP. Lewis Holmes, MD, Massachusetts General Hospital Carol Louik, ScD, Slone Epidemiology Center, Boston University Allen Mitchell, -
Acquired Tumors Arising from Congenital Hypertrophy of the Retinal Pigment Epithelium
CLINICAL SCIENCES Acquired Tumors Arising From Congenital Hypertrophy of the Retinal Pigment Epithelium Jerry A. Shields, MD; Carol L. Shields, MD; Arun D. Singh, MD Background: Congenital hypertrophy of the retinal lacunae in all 5 patients. The CHRPE ranged in basal di- pigment epithelium (CHRPE) is widely recognized to ameter from 333mmto13311 mm. The size of the el- be a flat, stationary condition. Although it can show evated lesion ranged from 23232mmto83834 mm. minimal increase in diameter, it has not been known to The nodular component in all cases was supplied and spawn nodular tumor that is evident ophthalmoscopi- drained by slightly prominent, nontortuous retinal blood cally. vessels. Yellow retinal exudation occurred adjacent to the nodule in all 5 patients and 1 patient developed a second- Objectives: To report 5 cases of CHRPE that gave rise ary retinal detachment. Two tumors that showed progres- to an elevated lesion and to describe the clinical features sive enlargement, increasing exudation, and progressive of these unusual nodules. visual loss were treated with iodine 125–labeled plaque brachytherapy, resulting in deceased tumor size but no im- Methods: Retrospective medical record review. provement in the visual acuity. Results: Of 5 patients with a nodular lesion arising from Conclusions: Congenital hypertrophy of the retinal pig- CHRPE, there were 4 women and 1 man, 4 whites and 1 ment epithelium can spawn a nodular growth that slowly black. Three patients were followed up for typical CHRPE enlarges, attains a retinal blood supply, and causes exuda- for longer than 10 years before the tumor developed; 2 pa- tiveretinopathyandchroniccystoidmacularedema.Although tients were recognized to have CHRPE and the elevated no histopathologic evidence is yet available, we believe that tumor concurrently. -
A Rare Case of Polyorchidism in a Cat with Four Intra&
Reprod Dom Anim doi: 10.1111/rda.12461 ISSN 0936–6768 Short Communication A Rare Case of Polyorchidism in a Cat with Four Intra-abdominal Testes J Roca-Ferrer, E Rodrıguez, GA Ramırez, C Moragas and M Sala Centre Veterinari Bonavista, Cornella de Llobregat, Catalonia, Spain Contents Polyorchidism, the presence of more than two testes, Polyorchidism is a rare congenital anomaly defined as the is an uncommon congenital anomaly both in human presence of more than two histologically proven testes. We and veterinary medicine. The first reports of polyorchi- report a case of a 9-month-old European cat with four intra- dism in veterinary medicine were concerned with the abdominal testes. The diagnosis was performed by means of finding of supernumerary testes in horses as incidental ultrasonography, intra-operative examination and histological events during castration (Earnshaw 1959) while in confirmation. The case reported here presents an extremely humans the first case was reported during a routine rare anomaly, as no previous studies in veterinary medicine have reported the presence of four testes. This case suggests autopsy in 1670 (Bergholz and Wenke 2009). The that supernumerary testes should be included as differential number of cases reported in the literature is very low. diagnoses for intra-abdominal masses. In veterinary medicine, five cases have been published up to now, as illustrated in Table 1. In human medicine, 140 cases have been reported (Bergholz and Wenke Introduction 2009). In both veterinary and human medicine, the most Cryptorchidism, the failure of one or both testes to common case of polyorchidism is the presence of a descend into scrotum, is a common congenital abnor- single supernumerary testis (triorchidism). -
Chapter 1 Cellular Reaction to Injury 3
Schneider_CH01-001-016.qxd 5/1/08 10:52 AM Page 1 chapter Cellular Reaction 1 to Injury I. ADAPTATION TO ENVIRONMENTAL STRESS A. Hypertrophy 1. Hypertrophy is an increase in the size of an organ or tissue due to an increase in the size of cells. 2. Other characteristics include an increase in protein synthesis and an increase in the size or number of intracellular organelles. 3. A cellular adaptation to increased workload results in hypertrophy, as exemplified by the increase in skeletal muscle mass associated with exercise and the enlargement of the left ventricle in hypertensive heart disease. B. Hyperplasia 1. Hyperplasia is an increase in the size of an organ or tissue caused by an increase in the number of cells. 2. It is exemplified by glandular proliferation in the breast during pregnancy. 3. In some cases, hyperplasia occurs together with hypertrophy. During pregnancy, uterine enlargement is caused by both hypertrophy and hyperplasia of the smooth muscle cells in the uterus. C. Aplasia 1. Aplasia is a failure of cell production. 2. During fetal development, aplasia results in agenesis, or absence of an organ due to failure of production. 3. Later in life, it can be caused by permanent loss of precursor cells in proliferative tissues, such as the bone marrow. D. Hypoplasia 1. Hypoplasia is a decrease in cell production that is less extreme than in aplasia. 2. It is seen in the partial lack of growth and maturation of gonadal structures in Turner syndrome and Klinefelter syndrome. E. Atrophy 1. Atrophy is a decrease in the size of an organ or tissue and results from a decrease in the mass of preexisting cells (Figure 1-1). -
Ultrasound of the Scrotum
Ultrasound of scrotum 21.06.2011 12:42 1 EFSUMB – European Course Book Editor: Christoph F. Dietrich Ultrasound of the scrotum Paul S. Sidhu, Boris Brkljacic2, Lorenzo E. Derchi3 2Medical School, University of Zagreb, 3Department of Radiology, University of Genoa Corresponding author: Paul S. Sidhu BSc MBBS MRCP FRCR DTM&H Consultant Radiologist and Senior Lecturer King‟s College London Department of Radiology King‟s College Hospital Denmark Hill London SE5 9RS United Kingdom Tel: ++44 (0) 20 3299 3063 Fax: ++44 (0) 20 3299 3157 E-mail: [email protected] Ultrasound of scrotum 21.06.2011 12:42 2 Content Content ................................................................................................................................................. 2 Introduction .......................................................................................................................................... 3 Sonographic examination technique .................................................................................................... 3 Gross Anatomy..................................................................................................................................... 4 Embryology ...................................................................................................................................... 4 Scrotal sac and testicular anatomy ................................................................................................... 4 Vascular anatomy ............................................................................................................................ -
PATHOPHYSIOLOGY UNIT-1 .Basic Principles of Cell Injury And
B.PHARMACY2nd SEMESTER SUBJECT: PATHOPHYSIOLOGY UNIT-1 .Basic Principles of Cell Injury and Adaptation Cell Injury: Introduction • Cell injury is defined as a variety of stresses a cell encounters as a result of changes in its internal and external environment. • The cellular response to stress may vary and depends upon the following: – The type of cell and tissue involved. – Extent and type of cell injury. ETIOLOGY OF CELL INJURY: 1. Genetic causes • Developmental defects: Errors in morphogenesis • Cytogenetic (Karyotypic) defects: chromosomal abnormalities • Single-gene defects: Mendelian disorders • Multifactorial inheritance disorders. 2. Acquired causes • Hypoxia and ischaemia • Physical agents • Chemical agents and drugs • Microbial agents • Immunologic agents • Nutritional derangements • Aging • Psychogenic diseases • Iatrogenic factors • Idiopathic diseases. 2.1. Oxygen deprivation: HYPOXIA Ischemia (loss of blood supply). Inadequate oxygenation (cardio respiratory failure). Loss of oxygen carrying capacity of the blood (anemia or CO poisoning). 2.2. PHYSICAL AGENTS: Trauma Heat Cold Radiation Electric shock 2.3. CHEMICAL AGENTS AND DRUGS: Endogenous products: urea, glucose Exogenous agents Therapeutic drugs: hormones Nontherapeutic agents: lead or alcohol. 2.4. INFECTIOUS AGENTS: Viruses Rickettsiae Bacteria Fungi Parasites 2.5. Abnormal immunological reactions: The immune process is normally protective but in certain circumstances the reaction may become deranged. Hypersensitivity to various substances can lead to anaphylaxis or to more localized lesions such as asthma. In other circumstances the immune process may act against the body cells – autoimmunity. 2.6. Nutritional imbalances: Protein-calorie deficiencies are the most examples of nutrition deficiencies. Vitamins deficiency. Excess in nutrition are important causes of morbidity and mortality. Excess calories and diet rich in animal fat are now strongly implicated in the development of atherosclerosis. -
Sacrococcygeal Teratoma in the Perinatal Period
754 Postgrad Med J 2000;76:754–759 Postgrad Med J: first published as 10.1136/pgmj.76.902.754 on 1 December 2000. Downloaded from Sacrococcygeal teratoma in the perinatal period R Tuladhar, S K Patole, J S Whitehall Teratomas are formed when germ cell tumours tissues are less commonly identified.12 An ocu- arise from the embryonal compartment. The lar lens present as lentinoids (lens-like cells), as name is derived from the Greek word “teratos” well as a completely formed eye, have been which literally means “monster”. The ending found within sacrococcygeal teratomas.10 11 “-oma” denotes a neoplasm.1 Parizek et al reported a mature teratoma containing the lower half of a human body in Incidence one of fraternal twins.13 Sacrococcygeal teratoma is the most common congenital tumour in the neonate, reported in Size approximately 1/35 000 to 1/40 000 live Size of a sacrococcygeal teratoma (average 8 births.2 Approximately 80% of aVected infants cm, range 1 to 30 cm) does not predict its bio- are female—a 4:1 female to male preponder- logical behaviour.8 Altman et al have defined ance.2 the size of sacrococcygeal teratomas as follows: The first reported case was inscribed on a small, 2 to 5 cm diameter; moderate, 5 to 10 Chaldean cuneiform tablet dated approxi- cm diameter; large, > 10 cm diameter.14 mately 2000 BC.3 In the modern era, the first large series of infants and children with sacro- Site coccygeal teratomas was reported by Gross et The sacrococcygeal region is the most com- al in 1951.4 mon location. -
Somatic Events Modify Hypertrophic Cardiomyopathy Pathology and Link Hypertrophy to Arrhythmia
Somatic events modify hypertrophic cardiomyopathy pathology and link hypertrophy to arrhythmia Cordula M. Wolf*†, Ivan P. G. Moskowitz†‡§¶, Scott Arno‡, Dorothy M. Branco*, Christopher Semsarian‡§ʈ, Scott A. Bernstein**, Michael Peterson‡¶, Michael Maida‡, Gregory E. Morley**, Glenn Fishman**, Charles I. Berul*, Christine E. Seidman‡§††‡‡, and J. G. Seidman‡§†† Departments of *Cardiology and ¶Pathology, Children’s Hospital, Boston, MA 02115; ‡Department of Genetics, Harvard Medical School, Boston, MA 02115; §Howard Hughes Medical Institute, Boston, MA 02115; and **Department of Cardiology, New York University School of Medicine, New York, NY 10010 Contributed by Christine E. Seidman, October 19, 2005 Sarcomere protein gene mutations cause hypertrophic cardiomy- many HCM patients who succumb to ventricular arrhythmias all opathy (HCM), a disease with distinctive histopathology and in- of these risk factors are absent (11–13). creased susceptibility to cardiac arrhythmias and risk for sudden Increased myocardial fibrosis and abnormal myocyte archi- death. Myocyte disarray (disorganized cell–cell contact) and car- tecture are associated with arrhythmia vulnerability in many diac fibrosis, the prototypic but protean features of HCM histopa- cardiovascular diseases (14–16), and these parameters are hy- thology, are presumed triggers for ventricular arrhythmias that pothesized to also increase sudden death risk in HCM (12, 17). precipitate sudden death events. To assess relationships between In support of this suggestion, histopathological studies -
See Anorgasmia Absent Ejaculation: See Anejaculation Adaptive Filter, 6
Index A ultrasonography, 41 Absence of Orgasm: see Anorgasmia Beta-human chorionic gonadotropin, 193 Absent ejaculation: see Anejaculation Blue dot sign, 130 Adaptive filter, 6 Broadband transducer, 2 Addison disease, 328 selection, 5 Adenomatoid tumor, 160 handling, 5 MRI, 174 Broad-spectrum antibiotics, 95 ultrasonography, 174 Bulbourethral glands AdrenoCorticoTropic hormone (ACTH), 236, 285, 328 infection, 93 Adrenogenital syndrome, 328 parasitic, 113 Acute appendicitis, 122 non infection inflammation, 112 Androgen deficiency, 36, 303, 304 insensitivity syndrome, 286 C replacement factors, 210 Calcifications, 313 Androtest, 232 associated with cystic masses, 317 Anejaculation, 13, 36, 37 associated with solid masses, 317 Anorchidism, 34 MRI, 330 Anorgasmia, 37 ultrasonography, 330 Anosmia, 209 extra-testicular, 318 Antisperm antibodies, 211, 213 isolated and macroscopic, 318 Aromatase activity, 210 Carcinoma in situ (CIS), 314 Arteriography, 295 echopattern, 316 Arteriovenous fistula, 82 CEUS: see Contrast-enhanced ultrasonography Asthenospermia, 212 Chlamydia, 88, 211 Azoospermia, 208, 210, 241, 249, 292 Choriocarcinoma, 152, 168 factors regions (AZF), 234, 249 imaging, 168 non-obstructive (NOA), 234, 249–250, 255, 256 Coded transmission, 6 management, 249 Collection of the semen sample, 218 sperm retrival, 251 Colour Doppler Ultrasonography limits, 116 testis histology predominant patterns, 249 Complete Androgen Insensitivity Syndrome (CAIS) , 233 obstructive, 212 Computer Aided Sperm Analysis (CASA system), 219 clinical presentation, 242 Congenital adrenal hyperplasia, 285, 328 imaging, 275 Congenital testicular adrenal rest, 329 management, 242 MRI, 324 treatment options, 242 ultrasonography, 324 Coni vasculosi, 30 Contrast-enhanced ultrasonography: B see also Scrotal -enhanced ultrasonography Bag of worms: see also Varicocele, 144 complex cystic lesions, 348 Banking sperm, 152 contrast agents, 344 Behcet’s disease, 113 high degree testicular torsion, 345 Bell clapper deformity, 49 inflammation, 350 MRI, 163 low degree testicular torsion, 346 M. -
Syndromic Aspects of Testicular Carcinoma
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by University of Groningen University of Groningen Syndromic aspects of testicular carcinoma Lutke-Holzik, MF; Sijmons, RH; Sleijfer, DT; Sonneveld, DJA; Hoekstra-Weebers, JEHM; van Echten-Arends, J; Hoekstra, HJ Published in: Cancer DOI: 10.1002/cncr.11155 IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2003 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Lutke-Holzik, MF., Sijmons, RH., Sleijfer, DT., Sonneveld, DJA., Hoekstra-Weebers, JEHM., van Echten- Arends, J., & Hoekstra, HJ. (2003). Syndromic aspects of testicular carcinoma. Cancer, 97(4), 984-992. https://doi.org/10.1002/cncr.11155 Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. Download date: 12-11-2019 984 Syndromic Aspects of Testicular Carcinoma 1 Martijn F.