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Review Article Alcohol Induced Liver Disease
J Clin Pathol: first published as 10.1136/jcp.37.7.721 on 1 July 1984. Downloaded from J Clin Pathol 1984;37:721-733 Review article Alcohol induced liver disease KA FLEMING, JO'D McGEE From the University of Oxford, Nuffield Department ofPathology, John Radcliffe Hospital, Oxford OX3 9DU, England SUMMARY Alcohol induces a variety of changes in the liver: fatty change, hepatitis, fibrosis, and cirrhosis. The histopathological appearances of these conditions are discussed, with special atten- tion to differential diagnosis. Many forms of alcoholic liver disease are associated with Mallory body formation and fibrosis. Mallory bodies are formed, at least in part, from intermediate filaments. Associated changes in intermediate filament organisation in alcoholic liver disease also occur. Their significance in the pathogenesis of hepatocyte death may be related to abnormalities in messenger RNA function. The mechanisms underlying hepatic fibrogenesis are also discussed. Although alcohol has many effects on the liver, all formed after some period of alcohol abstinence, except cirrhosis are potentially reversible on cessa- alcohol related changes may not be seen. Accord- tion of alcohol ingestion. Cirrhosis is irreversible ingly, we shall consider the morphological changes and usually ultimately fatal. It is therefore important associated with alcohol abuse under the headings in to determine what factors are responsible for Table 1. development of alcohol induced cirrhosis, especially In the second part, the pathogenesis of alcohol since only 17-30% of all alcoholics become' cirrho- induced liver disease will be discussed, but this will tic.' This is of some urgency now, since there has deal only with the induction of alcoholic hepatitis, been an explosive increase in alcohol consumption fibrosis, and cirrhosis-that is, chronic alcoholic http://jcp.bmj.com/ in the Western World, particularly affecting young liver disease-and not with fatty change, for two people, resulting in a dramatic increase in the inci- reasons. -
Fructose Diets on the Liver of Male Albino Rat and the Proposed Underlying Mechanisms S.M
Folia Morphol. Vol. 78, No. 1, pp. 124–136 DOI: 10.5603/FM.a2018.0063 O R I G I N A L A R T I C L E Copyright © 2019 Via Medica ISSN 0015–5659 journals.viamedica.pl The differential effects of high-fat and high- -fructose diets on the liver of male albino rat and the proposed underlying mechanisms S.M. Zaki1, 2, S.A. Fattah1, D.S. Hassan1 1Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Cairo, Egypt 2Fakeeh College for Medical Sciences, Jeddah, Saudi Arabia [Received: 23 May 2108; Accepted: 26 June 2018] Background: The Western-style diet is characterised by the high intake of energy- -dense foods. Consumption of either high-fructose diet or saturated fat resulted in the development of metabolic syndrome. Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Many researchers studied the effect of high-fat diet (HFD), high-fructose diet (HFruD) and high-fructose high-fat diet (HFHF) on the liver. The missing data are the comparison effect of these groups i.e. are effects of the HFHF diet on the liver more pronounced? So, this study was designed to compare the metabolic and histopathological effect of the HFD, HFruD, and HFHF on the liver. The proposed underlying mechanisms involved in these changes were also studied. Materials and methods: Twenty four rats were divided into four groups: con- trol, HFD, HFruD, and HFHF. Food was offered for 6 weeks. Biochemical, light microscopic, immunohistochemical (Inducible nitric oxide synthase [iNOS] and alpha-smooth muscle actin [α-SMA]), real-time polymerase chain reaction (gene expression of TNF-α, interleukin-6, Bax, BCL-2, and caspase 3), histomorphometric analysis and oxidative/antioxidative markers (thiobarbituric acid reactive substances [TBARS], malondialdehyde [MDA]/glutathione [GSH] and superoxide dismutase [SOD]) were done. -
Eponyms in Digestive System Pathology
Panacea Journal of Medical Sciences 2020;10(2):58–67 Content available at: https://www.ipinnovative.com/open-access-journals Panacea Journal of Medical Sciences Journal homepage: www.ipinnovative.com Review Article Eponyms in digestive system pathology Ahmad Al Malki1, Hassan Al Solami2, Khalid Al Aboud3,*, Wafa Al Joaid3, Saleha Al Asmary4 1Dept. of Surgery, King Faisal Hospital, Makkah, Saudi Arabia 2Dept. of Gastroenterology, King Faisal Hospital, Makkah, Saudi Arabia 3Dept. of Public Health, King Faisal Hospital, Makkah, Saudi Arabia 4Nursing College, King Saud University, Riyadh, Saudi Arabia ARTICLEINFO ABSTRACT Article history: Eponyms are known type of medical terminology. This mini-review provide highlights on some of the Received 04-05-2020 eponyms of the digestive system pathology. Accepted 06-05-2020 Available online 26-08-2020 © 2020 Published by Innovative Publication. This is an open access article under the CC BY-NC license (https://creativecommons.org/licenses/by-nc/4.0/) Keywords: Diseases Eponyms Gastroenterology 1. Introduction An eponym is a person, place, or thing after whom or which someone or something is named. There are several anatomical and pathological eponyms in the digestive systems. 1–4 We have reviewed selected eponyms of the digestive system pathology, and present it in a tabulation form in table.1. 5–41 The remarks surrounding the terms and eponyms in the digestive system are no different from those encountered in medicine in general. We are not interested to mention these are remarks, as these have been discussed extentensively in the medical literature. However, we list few examples. Some of the eponyms are no longer in use. -
Special Activities
59th Annual International Conference of the Wildlife Disease Association Abstracts & Program May 30 - June 4, 2010 Puerto Iguazú Misiones, Argentina Iguazú, Argentina. 59th Annual International Conference of the Wildlife Disease Association WDA 2010 OFFICERS AND COUNCIL MEMBERS OFFICERS President…………………………….…………………...………..………..Lynn Creekmore Vice-President………………………………...…………………..….Dolores Gavier-Widén Treasurer………………………………………..……..……….….……..…….Laurie Baeten Secretary……………………………………………..………..……………….…Pauline Nol Past President…………………………………………………..………Charles van Riper III COUNCIL MEMBERS AT LARGE Thierry Work Samantha Gibbs Wayne Boardman Christine Kreuder Johnson Kristin Mansfield Colin Gillin STUDENT COUNCIL MEMBER Terra Kelly SECTION CHAIRS Australasian Section…………………………..……………………….......Jenny McLelland European Section……………………..………………………………..……….….Paul Duff Nordic Section………………………..………………………………..………….Erik Ågren Wildlife Veterinarian Section……..…………………………………..…………Colin Gillin JOURNAL EDITOR Jim Mills NEWSLETTER EDITOR Jenny Powers WEBSITE EDITOR Bridget Schuler BUSINESS MANAGER Kay Rose EXECUTIVE MANAGER Ed Addison ii Iguazú, Argentina. 59th Annual International Conference of the Wildlife Disease Association ORGANIZING COMMITTEE Executive President and Press, media and On-site Volunteers Conference Chair publicity Judy Uhart Marcela Uhart Miguel Saggese Marcela Orozco Carlos Sanchez Maria Palamar General Secretary and Flavia Miranda Program Chair Registrations Elizabeth Chang Reissig Pablo Beldomenico Management Patricia Mendoza Hebe Ferreyra -
The Morphology of Cirrhosis' Recommendations on Definition, Nomenclature, and Classification by a Working Group Sponsored by the World Health Organization
J Clin Pathol: first published as 10.1136/jcp.31.5.395 on 1 May 1978. Downloaded from Journal of Clinical Pathology, 1978, 31, 395-414 The morphology of cirrhosis' Recommendations on definition, nomenclature, and classification by a working group sponsored by the World Health Organization P. P. ANTHONY, K. G. ISHAK, N. C. NAYAK, H. E. POULSEN, P. J. SCHEUER, AND L. H. SOBIN From the Bland-Sutton Institute ofPathology, Middlesex Hospital Medical School, London, the Armed Forces Institute ofPathology, Washington, the All India Institute ofMedical Sciences, New Delhi, Hvidovre Hospital, University of Copenhagen, The Royal Free Hospital School ofMedicine, London, and the Cancer Unit of the World Health Organization, Geneva SUMMARY This memorandum provides guidelines on the definition, nomenclature, and classification of cirrhosis, chronic hepatitis, and hepatic fibrosis. These are considered according to morphological characteristics and aetiology. It is hoped that this system will serve as a standard for diagnostic, research, and epidemiological purposes. The relationship of cirrhosis to liver cell carcinoma is briefly discussed and the possible morphological markers of an increased risk of malignancy are defined. The aim of this paper is to provide guidelines for the morphological terms but, in spite of many attempts, pathologist on the definition, nomenclature, and no single definition exists that does not require classification of hepatic cirrhosis and related con- further elaboration or qualification. The essential ditions. The many systems of classification in current features are considered to be parenchymal necrosis, http://jcp.bmj.com/ use (Table 1) hinder rather than help comparisons of regeneration, and diffuse fibrosis, resulting in dis- published data and the evaluation of relationships organisation of the lobular architecture throughout between cirrhosis and liver cancer. -
Histopathologic Diagnosis of Chronic Viral Hepatitis
Marmara Medical Journal 2016; 29 (Special issue 1): 18-28 DOI: 10.5472/MMJsi.2901.05 REVIEW / DERLEME Histopathologic diagnosis of chronic viral hepatitis Kronik viral hepatitin histopatolojik tanısı Çiğdem ATAİZİ ÇELİKEL ABSTRACT ÖZ Morphological evaluation of the liver continues to play a central Kronik viral hepatit tanısı, derecelendirme ve evreleme açısından, role for the diagnosis, grading and staging of chronic viral hepatitis. karaciğerin morfolojik değerlendirmesi önem taşır. Tanımsal The defining morphology is necroinflammation, that is hepatocyte morfoloji hepatosit hasarı ve inflamasyon ile karakterize injury and inflammation. Hepatocyte injury is usually irreversible, nekroinflamasyondur. Hepatosit hasarı, apoptoz ve/veya nekroz and presents as apoptosis and/or necrosis. Mononuclear cell şeklinde olup, genellikle geri dönüşümsüzdür. Portal alanda infiltration of the portal tracts, that is usually accompanied by mononükleer hücre infiltrasyonuna, çoğu zaman periportal periportal (interface) and lobular inflammation is typical. Continued (interfaz) ve lobüler inflamasyon eşlik eder. İnterfazda periportal necroinflammatory activity at the limiting plate destroying hepatositlerde süregelen hasar fibrogenezi tetikler ve siroz periportal parenchyma initiates fibrogenesis leading to cirrhosis. gelişebilir. Tamir dokusunun parçalanması, bozulan vaskülatürün Fibrosis can be reversible with fragmentation of scar tissue, organizasyonu ve hepatosit rejenerasyonu ile fibrozis/siroz resolving vascular derangements and parenchymal regeneration. -
A Novel Splice Site Indel Alteration in the EIF2AK3 Gene Is Responsible For
Sümegi et al. BMC Medical Genetics (2020) 21:61 https://doi.org/10.1186/s12881-020-0985-6 RESEARCH ARTICLE Open Access A novel splice site indel alteration in the EIF2AK3 gene is responsible for the first cases of Wolcott-Rallison syndrome in Hungary Andrea Sümegi1, Zoltán Hendrik2, Tamás Gáll1, Enikő Felszeghy3, Katalin Szakszon3, Péter Antal-Szalmás4, Lívia Beke2, Ágnes Papp3, Gábor Méhes2, József Balla1,5 and György Balla1,3* Abstract Background: Wolcott-Rallison Syndrome (WRS) is a rare autosomal recessive disease that is the most common cause of neonatal diabetes in consanguineous families. WRS is caused by various genetic alterations of the Eukaryotic Translation Initiation Factor 2-Alpha Kinase 3 (EIF2AK3) gene. Methods: Genetic analysis of a consanguineous family where two children were diagnosed with WRS was performed by Sanger sequencing. The altered protein was investigated by in vitro cloning, expression and immunohistochemistry. Results: The first cases in Hungary, − two patients in one family, where the parents were fourth-degree cousins - showed the typical clinical features of WRS: early onset diabetes mellitus with hyperglycemia, growth retardation, infection-induced multiple organ failure. The genetic background of the disease was a novel alteration in the EIF2AK3 gene involving the splice site of exon 11– intron 11–12 boundary: g.53051_53062delinsTG. According to cDNA sequencing this created a new splice site and resulted in a frameshift and the development of an early termination codon at amino acid position 633 (p.Pro627AspfsTer7). Based on in vitro cloning and expression studies, the truncated protein was functionally inactive. Immunohistochemistry revealed that the intact protein was absent in the islets of pancreas, furthermore insulin expressing cells were also dramatically diminished. -
Chronic-Binge Model of Alcoholic Hepatitis in Long Evans Rats
Ashdin Publishing Journal of Drug and Alcohol Research ASHDIN Vol. 3 (2014), Article ID 235837, 10 pages publishing doi:10.4303/jdar/235837 Research Article Chronic-Binge Model of Alcoholic Hepatitis in Long Evans Rats Teresa Ramirez,1 Ming Tong,2 and Suzanne M. de la Monte3 1Division of Gastroenterology and Liver Research Center, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI 02903, USA 2Department of Medicine, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI 02903, USA 3Departments of Medicine, Pathology, Neurology, and Neurosurgery, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI 02903, USA Address correspondence to Suzanne M. de la Monte, suzanne delamonte [email protected] Received 22 November 2013; Revised 8 May 2014; Accepted 2 June 2014 Copyright © 2014 Teresa Ramirez et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background. Alcoholic hepatitis (AH) is largely a liver disease (ALD) that culminates in cirrhosis and liver histopathologic diagnosis that is based upon the presence of failure [26]. The major cause of ALD is heavy drinking over significant inflammation, hepatocellular lipid accumulation, ballooned prolonged periods [37]. degeneration of hepatocytes, and Mallory-Denk bodies. Underlying biochemical and molecular abnormalities -
Methodical Instruction for Lectures
Ministry of Public Health of Ukraine Ukrainian Medical Stomatological Academy Approved at the meeting of the department Infection diseases and epidemiology «28» August 2019 protocol № 1 from «28» August 2019 the Head of the Department _________ Koval T.I. Methodical Instruction for lectures Study discipline Infectious diseases and epidemiology Module № Infectious diseases and epidemiology Topic Acute respiratory viral infections. Clinical characteristics and prevention of influenza. Course 4 Faculty Stomatological Number of teaching hours: 2 Poltava -2019 1. Scientific and methodological substantiation of the topic. Infectious diseases today remain extremely relevant. In the past decades, previously unknown infections — HIV infection, Lyme disease, campylobacteriosis, SARS, and others — have spread, and the achieved reduction in the incidence of diphtheria and measles has not been maintained. There is an increase in the incidence of viral hepatitis, acute intestinal infectious diseases, tuberculosis among the population of Ukraine and other countries. The clinical manifestations of infectious diseases can be different, often atypical, can lead to hospitalization of the patient in a medical institution of any profile. The ability to recognize infectious pathology, correctly conduct differential diagnosis, prescribe appropriate treatment, ensure that the necessary preventive measures are taken that are necessary for a doctor of any specialty. In our country, the classification of infectious diseases, academician L.V. Gromashevsky, has become most widespread. The classification is based on the principle of the predominant localization of the pathogen in the body, which is due to a certain transmission mechanism. One of the most important components in the treatment of patients for infectious diseases is inpatient treatment. Infectious Diseases Hospital is a special medical institution, which has a number of structural and functional units in order to ensure effective treatment, examination and isolation of patients. -
Table I. Genodermatoses with Known Gene Defects 92 Pulkkinen
92 Pulkkinen, Ringpfeil, and Uitto JAM ACAD DERMATOL JULY 2002 Table I. Genodermatoses with known gene defects Reference Disease Mutated gene* Affected protein/function No.† Epidermal fragility disorders DEB COL7A1 Type VII collagen 6 Junctional EB LAMA3, LAMB3, ␣3, 3, and ␥2 chains of laminin 5, 6 LAMC2, COL17A1 type XVII collagen EB with pyloric atresia ITGA6, ITGB4 ␣64 Integrin 6 EB with muscular dystrophy PLEC1 Plectin 6 EB simplex KRT5, KRT14 Keratins 5 and 14 46 Ectodermal dysplasia with skin fragility PKP1 Plakophilin 1 47 Hailey-Hailey disease ATP2C1 ATP-dependent calcium transporter 13 Keratinization disorders Epidermolytic hyperkeratosis KRT1, KRT10 Keratins 1 and 10 46 Ichthyosis hystrix KRT1 Keratin 1 48 Epidermolytic PPK KRT9 Keratin 9 46 Nonepidermolytic PPK KRT1, KRT16 Keratins 1 and 16 46 Ichthyosis bullosa of Siemens KRT2e Keratin 2e 46 Pachyonychia congenita, types 1 and 2 KRT6a, KRT6b, KRT16, Keratins 6a, 6b, 16, and 17 46 KRT17 White sponge naevus KRT4, KRT13 Keratins 4 and 13 46 X-linked recessive ichthyosis STS Steroid sulfatase 49 Lamellar ichthyosis TGM1 Transglutaminase 1 50 Mutilating keratoderma with ichthyosis LOR Loricrin 10 Vohwinkel’s syndrome GJB2 Connexin 26 12 PPK with deafness GJB2 Connexin 26 12 Erythrokeratodermia variabilis GJB3, GJB4 Connexins 31 and 30.3 12 Darier disease ATP2A2 ATP-dependent calcium 14 transporter Striate PPK DSP, DSG1 Desmoplakin, desmoglein 1 51, 52 Conradi-Hu¨nermann-Happle syndrome EBP Delta 8-delta 7 sterol isomerase 53 (emopamil binding protein) Mal de Meleda ARS SLURP-1 -
Viral Hepatitis (I)
Viral Hepatitis (I) Luigi Terracciano Department of Pathology University Hospital Basel Basel, 19. 04. 2016 Definition Hepatitis means inflammation of the liver characterized by a variable combination of : • mononuclear inflammation (lymphocytes and plasma cells) • hepatocellular necrosis/apoptosis • hepatocellular regeneration Viral Hepatitis Unless otherwise specified, the term "viral hepatitis" is reserved for infection of the liver caused by a group of viruses having a particular affinity for the liver Systemic viral infections that can involve the liver include: 1.infectious mononucleosis (Epstein-Barr virus), which may cause a mild hepatitis during the acute phase; 2.cytomegalovirus, particularly in the newborn or immunosuppressed patient; 3.yellow fever, which has been a major and serious cause of hepatitis in tropical countries. Hepatotropic viruses cause overlapping patterns of disease Viral Hepatitis The Hepatitis Viruses Hepatitis A Virus Hepatitis B Virus Hepatitis C Virus Hepatitis D Virus Hepatitis E Agent Icosahedral capsid, Enveloped dsDNA Enveloped ssRNA Enveloped ssRNA Unenveloped ssRNA ssRNA Transmission Fecal-oral Parenteral; close contact Parenteral; close contact Parenteral; Waterborne close contact Incubation Period 2-6 wk 4-26 wk 2-26 wk 4-7 wk 2-8 wk Carrier state None 0.1-1.0% of blood donors 0.2-1.0% of blood donors. 1-10% in drug addicts Unknown in U.S. and Western worldi in U.S and Western world and hemophiliacs 1-2% of blood donors Chronic hepatitis None 5-10% of >50% <5% coinfection, None / Very rare acute -
Keyword Associations
Bare Minimum Keyword Associations USMLE & COMLEX Review Northwestern Medical Review [email protected] Northwestern Medical Review PO Box 22174 Lansing, Michigan 48909 www.northwesternmedicalreview.com Copyright © 2015 Northwestern Medical Review eBookit.com and Northwestern Medical Review Second Edition ISBN 978-0-9960-9340-1 All rights reserved. Written, published, and printed in the United States of America. No part of this book may be used, reproduced, or transmitted in any form or by any means, electronic or mechanical without written permission from its author or Northwestern Medical Review. All photos adapted from fotolia.com Northwestern Medical Review claims no rights to USMLE or COMLEX USMLE ® National Board of Medical Examiners COMLEX ® National Board of Osteopathic Medical Examiners This book is adapted from the first chapter of Primary Care for the USMLE and COMLEX by Northwestern Medical Review. The full book version is primarily intended to accompany online or live review courses from Northwestern Medical Review. How to use this book This book is adapted from the first chapter of Northwestern Medical Review’s Primary Care for the USMLE and COMLEX book. It contains exceptionally high-yield material found on board exams. The mini-chapters are divided into sections containing commonly tested concepts with keywords that should immediately come to mind while you’re taking your exam. In the back of the book are two additional sections: a Test Your Knowledge section containing questions and answers with explanations from our follow-along lecture workbooks and NMR Question Bank, and a Sample Mnemonics section containing examples of memorable mnemonics from our course material.