DOCSLIB.ORG

Acute Pancreatitis, Non-Alcoholic Fatty Pancreas Disease, and Pancreatic Cancer

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Acute Pancreatitis, Non-Alcoholic Fatty Pancreas Disease, and Pancreatic Cancer JOP. J Pancreas (Online) 2017 Sep 29; 18(5):365-368. REVIEW ARTICLE The Burden of Systemic Adiposity on Pancreatic Disease: Acute Pancreatitis, Non-Alcoholic Fatty Pancreas Disease, and Pancreatic Cancer Ahmad Malli, Feng Li, Darwin L Conwell, Zobeida Cruz-Monserrate, Hisham Hussan, Somashekar G Krishna Division of Gastroenterology, Hepatology and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA ABSTRACT Obesity is a global epidemic as recognized by the World Health Organization. Obesity and its related comorbid conditions were recognized to have an important role in a multitude of acute, chronic, and critical illnesses including acute pancreatitis, nonalcoholic fatty pancreas disease, and pancreatic cancer. This review summarizes the impact of adiposity on a spectrum of pancreatic diseases. INTRODUCTION and even higher mortality in the setting of AP based on multiple reports [8, 9, 10, 11, 12]. Despite the rising incidence Obesity is a global epidemic as recognized by the World of AP over the past two decades, there has been a decrease Health Organization [1]. One third of the world’s population in its overall mortality rate without any obvious decrement is either overweight or obese, and it has doubled over the in the mortality rate among patients with concomitant AP past two decades with an alarming 70% increase in the and morbid obesity [12, 13]. Several prediction models and prevalence of morbid obesity from year 2000 to 2010 [2, risk scores were proposed to anticipate the severity and 3, 4]. Obesity and its related comorbid conditions were prognosis of patient with AP; however, their clinical utility recognized to have an important role in a multitude of is variable, not completely understood, and didn’t take acute, chronic, and critical pancreatic illnesses including obesity as a major contributor into consideration despite the acute pancreatitis, non-alcoholic fatty pancreas disease, aforementioned association [14]. and pancreatic cancer. Obesity was initially reported as an independent Obesity and Acute Pancreatitis predictor of respiratory failure in patients with severe Acute Pancreatitis (AP) is one of the most common AP based on two reports in the early 1990’s [15, 16]. gastrointestinal-related causes of inpatient hospitalizations and health care expenditure (annual cost of 2.6 billion previous reports [17]. Published data prior to year 2000 dollars), with a sizeable mortality rate of 3-5% [5]. There didn’tMore recentdemonstrate data also an independentconfirmed and association substantiated between the continues to be a steady increase in the prevalence of obesity and mortality from AP; however, multiple large inpatient admissions for AP overtime and this attracted prospective studies and meta-analyses over the past two attention to better understanding of this disease process [4, decades showed that obesity (Body Mass Index [BMI]) is 6]. AP typically resolves in the majority of patients without an independent predictor of severity and mortality from AP further complications; however, 20% of patients progress based on multiple risk score assessments [17, 18, 19]. This into severe AP (local and systemic complications), and was also supported by population-based studies [12, 20]. sustain a very high mortality rate up to 30% in the setting of Obesity in the form of excess subcutaneous tissue was also persistent multi-organ failure [7]. Obesity is associated with reported as an important predictor of post-ERCP pancreatitis the development of multiple complications, worse outcomes, based on a recent large retrospective study [21]. Multiple theories were proposed to understand the link Received February 16th, 2017 - Accepted July 29th, 2017 between obesity and AP. Those include 1) toxic effects of Keywords Obesity; Obesity, Morbid; Pancreatic Neoplasms; Pancreatitis the intra-pancreatic fat content, 2) toxic effect of the peri- Abbreviations NAFPD non-alcoholic fatty pancreas disease pancreatic (visceral) fat content, and 3) the overall burden Correspondence Somashekar G Krishna 395 W. 12th Avenue, Suite 262 of obesity on other organ systems. Division of Gastroenterology, Hepatology and Nutrition Columbus, Ohio, USA The intra-pancreatic fat content was shown to Tel +614-293-6255 be proportional to BMI with E-mail [email protected] unsaturated fat content [22, 23, 24]. This intra-pancreatic specific predilection to JOP. Journal of the Pancreas - http://pancreas.imedpub.com/ - Vol. 18 No. 5 – Sep 2017. [ISSN 1590-8577] 365 JOP. J Pancreas (Online) 2017 Sep 29; 18(5):365-368. fat, and more so, the abdominal visceral fat are both Pancreatic steatosis with superimposed acute metabolically active and produce multiple adipokines pancreatitis has also been shown to intensify the and cytokines (Adiponectin, Leptin, TNF a, Interleukin-6, monocyte chemotactic protein-1, macrophage IL-1b, and damage in the setting of obesity [23, 28]; however, there is myeloperoxidase); which through adipocytokine imbalance inflammatory cascade and cause more severe parenchymal state [25, 26], act as a substrate for lipolysis with further pancreatitis.insufficient evidence to suggest an association of NAFPD necrosiscould initiate in the settingand maintain of necrotizing a low pancreatitis pro-inflammatory spectrum with the development of chronic inflammation or chronic Obesity and Pancreatic Cancer through the release of unsaturated fatty acids, [27] help Obesity and high BMI have been proposed as risk surrounding organs, and cause a direct toxic effect on thespread pancreatic the inflammation parenchyma in [23, AP 28]across. Peri-pancreatic visceral fat fatto data about the strength of the association between lipolysis can also result in multisystem injury independent BMIfactors and for pancreaticpancreatic cancercancer. risk;Despite more earlier recent conflicting robust of the development of pancreatic necrosis via the role of prospective and case-control studies highlighted and unsaturated fatty acids [29]. Overall, visceral obesity is strengthened this association [40, 41, 42]. Obesity is now positively correlated with morbidity and mortality among multiple studies [30, 31, 32]. adenocarcinoma. Obesity was shown to increase the incidencerecognized of as pancreatic a significant cancer risk by factor 10-14% for pancreatic for each 5 kg/mductal2 Although most previous reports have focused on central incremental increase in BMI based on a systematic analysis obesity as the main predictor, a recent retrospective study of prospective observational studies [40, 41]. Obese found that excess subcutaneous fat (rather than visceral individuals were also shown to have an approximately obesity) is an important predictor of post ERCP pancreatitis 20% greater risk of developing pancreatic adenocarcinoma compared to normal weight controls based on a pooled the intra-pancreatic and para-pancreatic fat; obesity could analysis from the pancreatic cancer cohort consortium also[21]. predisposeIn addition to thesevere inflammatory AP by reducing hypothesis the pancreatic driven by [42]. Obesity increases the odds of surgical complications microcirculation and causing subsequent ischemic injury. Abdominal visceral obesity also decreases the inspiratory cancer surgical candidates, and ultimately increases capacity due to the restriction of diaphragmatic movement. mortalityand development from pancreatic of pancreatic cancer fistulas surgery among [43, 44] pancreatic. This leads to increased physiologic pulmonary arterio- venous shunting and further hypoxemia with oxygen increase the activity of KRas oncogene [45], increase insulin response, and ultimately increases the rate of multi-organ levelsObesity and insulin-likeas an inflammatory growth factor-1 trigger, with is believedsubsequent to failuredeficits, and further death cellular [8]. Overall, damage, the hyperactive precise mechanisms inflammatory are increase in cellular proliferation, and increase the burden still unclear and this is a material for further investigation. of systemic oxidative stress in mice [43]. Obesity and Non-Alcoholic Fatty Pancreas Disease 5-lipooxygenase (5-LO) and 5-LO activating protein is preferentially and abundantly more present in adipocytes Non-Alcoholic Fatty Pancreas Disease (NAFPD) was and adipose tissue of obese rats compared to their lean counterparts [46] with accumulating evidence about the obesity among other less common predisposing factors role of 5-LO in the growth of pancreatic tumors. Other withfirst describeda variable inprevalence 1933. It isamong associated different with studies aging anddue theories include the role of immune dysfunction from to differences in nomenclature and absence of unifying diagnostic criteria. NAFPD has a reported prevalence of and dysregulation of lipid-regulating proteins in obese 16-35% among an adult Asian population [33, 34, 35] . individuals.the excessive Leptin, production which of ispro-inflammatory fairly more abundant cytokines in It is usually detected incidentally by cross sectional peripheral tissues of obese individuals, has also been abdominal imaging. Believed to develop due to obesity and implicated in the facilitation of pancreatic cancer invasion subsequent pancreatic fat accumulation in the setting of through increasing the matrix metalloproteinase (MMP- metabolic syndrome, and it has been reported to a much 13) activity [47]. lesser extent among non-obese individuals. Extra- and intra lobular pancreatic fat was also The proposed mechanism of pancreatic fat correlated with pancreatic
Load more

Recommended publications
  • Impact of HIV on Gastroenterology/Hepatology
    Core Curriculum: Impact of HIV on Gastroenterology/Hepatology AshutoshAshutosh Barve,Barve, M.D.,M.D., Ph.D.Ph.D. Gastroenterology/HepatologyGastroenterology/Hepatology FellowFellow UniversityUniversityUniversity ofofof LouisvilleLouisville Louisville Case 4848 yearyear oldold manman presentspresents withwith aa historyhistory ofof :: dysphagiadysphagia odynophagiaodynophagia weightweight lossloss EGDEGD waswas donedone toto evaluateevaluate thethe problemproblem University of Louisville Case – EGD Report ExtensivelyExtensively scarredscarred esophagealesophageal mucosamucosa withwith mucosalmucosal bridging.bridging. DistalDistal esophagealesophageal nodulesnodules withwithUniversity superficialsuperficial ulcerationulceration of Louisville Case – Esophageal Nodule Biopsy InflammatoryInflammatory lesionlesion withwith ulceratedulcerated mucosamucosa SpecialSpecial stainsstains forfor fungifungi revealreveal nonnon-- septateseptate branchingbranching hyphaehyphae consistentconsistent withwith MUCORMUCOR University of Louisville Case TheThe patientpatient waswas HIVHIV positivepositive !!!! University of Louisville HAART (Highly Active Anti Retroviral Therapy) HIV/AIDS Before HAART After HAART University of Louisville HIV/AIDS BeforeBefore HAARTHAART AfterAfter HAARTHAART ImmuneImmune dysfunctiondysfunction ImmuneImmune reconstitutionreconstitution OpportunisticOpportunistic InfectionsInfections ManagementManagement ofof chronicchronic ¾ Prevention diseasesdiseases e.g.e.g. HepatitisHepatitis CC ¾ Management CirrhosisCirrhosis NeoplasmsNeoplasms
    [Show full text]
  • Steatosis in Hepatitis C: What Does It Mean? Tarik Asselah, MD, Nathalie Boyer, MD, and Patrick Marcellin, MD*
    Steatosis in Hepatitis C: What Does It Mean? Tarik Asselah, MD, Nathalie Boyer, MD, and Patrick Marcellin, MD* Address Steatosis *Service d’Hépatologie, Hôpital Beaujon, Mechanisms of steatosis 100 Boulevard du Général Leclerc, Clichy 92110, France. Hepatic steatosis develops in the setting of multiple E-mail: [email protected] clinical conditions, including obesity, diabetes mellitus, Current Hepatitis Reports 2003, 2:137–144 alcohol abuse, protein malnutrition, total parenteral Current Science Inc. ISSN 1540-3416 Copyright © 2003 by Current Science Inc. nutrition, acute starvation, drug therapy (eg, corticosteroid, amiodarone, perhexiline, estrogens, methotrexate), and carbohydrate overload [1–4,5••]. Hepatitis C and nonalcoholic fatty liver disease (NAFLD) are In the fed state, dietary triglycerides are processed by the both common causes of liver disease. Thus, it is not surprising enterocyte into chylomicrons, which are secreted into the that they can coexist in the same individual. The prevalence of lymph. The chylomicrons are hydrolyzed into fatty acids by steatosis in patients with chronic hepatitis C differs between lipoprotein lipase. These free fatty acids are transported to the studies, probably reflecting population differences in known liver, stored in adipose tissue, or used as energy sources by risk factors for steatosis, namely overweight, diabetes, and muscles. Free fatty acids are also supplied to the liver in the dyslipidemia. The pathogenic significance of steatosis likely form of chylomicron remnants, which are then hydrolyzed by differs according to its origin, metabolic (NAFLD or non- hepatic triglyceride lipase. During fasting, the fatty acids sup- alcoholic steatohepatitis) or virus related (due to hepatitis C plied to the liver are derived from hydrolysis (mediated by a virus genotype 3).
    [Show full text]
  • In Colorectal Cancer
    Article Evaluation of Adjuvant Chemotherapy-Associated Steatosis (CAS) in Colorectal Cancer Michelle C. M. Lee 1,2 , Jacob J. Kachura 3, Paraskevi A. Vlachou 1,2, Raissa Dzulynsky 1, Amy Di Tomaso 3, Haider Samawi 1,2, Nancy Baxter 1,2 and Christine Brezden-Masley 1,3,4,* 1 St. Michael’s Hospital, 30 Bond St, Toronto, ON M5B 1W8, Canada; [email protected] (M.C.M.L.); [email protected] (P.A.V.); [email protected] (R.D.); [email protected] (H.S.); [email protected] (N.B.) 2 Medical Sciences Building, 1 King’s College Circle, University of Toronto, Toronto, ON M5S 1A8, Canada 3 Mount Sinai Hospital, 1284-600 University Avenue, Toronto, ON M5G 1X5, Canada; [email protected] (J.J.K.); [email protected] (A.D.T.) 4 Lunenfeld-Tanenbaum Research Institute, 600 University Ave, Toronto, ON M5G 1X5, Canada * Correspondence: [email protected]; Tel.: +416-586-8605; Fax: +416-586-8659 Abstract: Chemotherapy-associated steatosis is poorly understood in the context of colorectal can- cer. In this study, Stage II–III colorectal cancer patients were retrospectively selected to evaluate the frequency of chemotherapy-associated steatosis and to determine whether patients on statins throughout adjuvant chemotherapy develop chemotherapy-associated steatosis at a lower frequency. Baseline and incident steatosis for up to one year from chemotherapy start date was assessed based on radiology. Of 269 patients, 76 (28.3%) had steatosis at baseline. Of the remaining 193 cases, patients receiving adjuvant chemotherapy (n = 135) had 1.57 (95% confidence interval [CI], 0.89 to 2.79) times the adjusted risk of developing steatosis compared to patients not receiving chemotherapy (n = 58).
    [Show full text]
  • Symmetrical Peripheral Gangrene Associated with Low Output Cardiac Failure
    Tower Health Scholar Commons @ Tower Health Reading Hospital Internal Medicine Residency Internal Medicine Residency 7-17-2019 Symmetrical Peripheral Gangrene Associated with Low Output Cardiac Failure. Sijan Basnet Reading Hospital-Tower Health Priya Rajagopalan Thomas Jefferson University Hospital Rashmi Dhital Reading Hospital-Tower Health Ataul Qureshi Thomas Jefferson University Hospital Follow this and additional works at: http://scholarcommons.towerhealth.org/ gme_int_med_resident_program_read Part of the Cardiology Commons Recommended Citation Basnet, S., Rajagopalan, P., Dhital, R., & Qureshi, A. (2019). Symmetrical Peripheral Gangrene Associated with Low Output Cardiac Failure.. Medicina (Kaunas, Lithuania), 55 (7) https://doi.org/10.3390/ medicina55070383. This Article is brought to you for free and open access by the Internal Medicine Residency at Scholar Commons @ Tower Health. It has been accepted for inclusion in Reading Hospital Internal Medicine Residency by an authorized administrator of Scholar Commons @ Tower Health. For more information, please contact [email protected]. medicina Case Report Symmetrical Peripheral Gangrene Associated with y Low Output Cardiac Failure Sijan Basnet 1,* , Priya Rajagopalan 2, Rashmi Dhital 1 and Ataul Qureshi 2 1 Department of Medicine, Reading Hospital and Medical Center, West Reading, PA 19611, USA 2 Thomas Jefferson University Hospital, 1025 Walnut Street, Philadelphia, PA 19107, USA * Correspondence: [email protected]; Tel.: +484-628-8255 The abstract was accepted for poster presentation at “Heart Failure Society of America 2018 Annual y Meeting” and was published in Journal of Cardiac Failure. Received: 15 January 2019; Accepted: 15 July 2019; Published: 17 July 2019 Abstract: Symmetrical peripheral gangrene (SPG) is a rare entity characterized by ischemic changes of the distal extremities with maintained vascular integrity.
    [Show full text]
  • Non - Alcoholic Fatty Liver Disease
    NON - ALCOHOLIC FATTY LIVER DISEASE Author: Nicolene Naidu Bachelor of Biological Science (Cellular Biology), Bachelor of Medical Science (Medical Microbiology) (Honours) Non - Alcoholic Fatty Liver Disease (termed NAFLD for short) is a condition characterized by the significant accumulation of lipids in the hepatocytes of the liver parenchyma. While non - alcoholic fatty liver disease and alcoholic liver disease are pathologically similar, unlike alcoholic liver disease, non - alcoholic fatty liver disease occurs in patients who do not have a history of excessive alcohol intake. Another term closely related to NAFLD but more histologically and clinically specific is Non - Alcoholic Steatohepatitis(NASH). It was coined by Ludwig et al in 1980 and is characterised by a fatty liver accompanied by inflammation and hepatocyte injury (“Ballooning”). Fibrosis may or may not be present. It should be noted that the histological appearance of non – alcoholic steatohepatitis is identical to that of alcoholic liver disease. Distinction between the two is based on the amount of alcohol intake. Non - alcoholic fatty liver disease is the loose term used to describe a wide spectrum of liver damage ranging from hepatic steatosis (simple benign fatty liver), non - alcoholic steatohepatitis, chronic fibrosis and cirrhosis (P Angulo, 2002). Figure 1: Showing a drawing of the various stages of liver damage, including a normal liver; fatty liver in which deposits of fat cause liver enlargement; liver fibrosis in which scar tissueforms and more liver cell injury occurs and cirrhosis in which scar tissue makes the liver hard and unable to work properly.(www.liverfoundation.org). 1 Pseudo-alcoholic liver disease, non - alcoholic Laennec’s disease, alcohol-like hepatitis, diabetic hepatitis and steatonecrosis are among the terms that have been used to refer to non – alcoholic fatty liver disease (Shethet al, 1997).
    [Show full text]
  • 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).
    [Show full text]
  • Non-Cancerous Breast Conditions Fibrosis and Simple Cysts in The
    cancer.org | 1.800.227.2345 Non-cancerous Breast Conditions ● Fibrosis and Simple Cysts ● Ductal or Lobular Hyperplasia ● Lobular Carcinoma in Situ (LCIS) ● Adenosis ● Fibroadenomas ● Phyllodes Tumors ● Intraductal Papillomas ● Granular Cell Tumors ● Fat Necrosis and Oil Cysts ● Mastitis ● Duct Ectasia ● Other Non-cancerous Breast Conditions Fibrosis and Simple Cysts in the Breast Many breast lumps turn out to be caused by fibrosis and/or cysts, which are non- cancerous (benign) changes in breast tissue that many women get at some time in their lives. These changes are sometimes called fibrocystic changes, and used to be called fibrocystic disease. 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 Fibrosis and cysts are most common in women of child-bearing age, but they can affect women of any age. They may be found in different parts of the breast and in both breasts at the same time. Fibrosis Fibrosis refers to a large amount of fibrous tissue, the same tissue that ligaments and scar tissue are made of. Areas of fibrosis feel rubbery, firm, or hard to the touch. Cysts Cysts are fluid-filled, round or oval sacs within the breasts. They are often felt as a round, movable lump, which might also be tender to the touch. They are most often found in women in their 40s, but they can occur in women of any age. Monthly hormone changes often cause cysts to get bigger and become painful and sometimes more noticeable just before the menstrual period. Cysts begin when fluid starts to build up inside the breast glands. Microcysts (tiny, microscopic cysts) are too small to feel and are found only when tissue is looked at under a microscope.
    [Show full text]
  • Official Proceedings
    Scientific Session Awards Abstracts presented at the Society’s annual meeting will be considered for the following awards: • The George Peters Award recognizes the best presentation by a breast fellow. In addition to a plaque, the winner receives $1,000. The winner is selected by the Society’s Publications Committee. The award was established in 2004 by the Society to honor Dr. George N. Peters, who was instrumental in bringing together the Susan G. Komen Breast Cancer Foundation, The American Society of Breast Surgeons, the American Society of Breast Disease, and the Society of Surgical Oncology to develop educational objectives for breast fellowships. The educational objectives were first used to award Komen Interdisciplinary Breast Fellowships. Subsequently the curriculum was used for the breast fellowship credentialing process that has led to the development of a nationwide matching program for breast fellowships. • The Scientific Presentation Award recognizes an outstanding presentation by a resident, fellow, or trainee. The winner of this award is also determined by the Publications Committee. In addition to a plaque, the winner receives $500. • All presenters are eligible for the Scientific Impact Award. The recipient of the award, selected by audience vote, is honored with a plaque. All awards are supported by The American Society of Breast Surgeons Foundation. The American Society of Breast Surgeons 2 2017 Official Proceedings Publications Committee Chair Judy C. Boughey, MD Members Charles Balch, MD Sarah Blair, MD Katherina Zabicki Calvillo, MD Suzanne Brooks Coopey, MD Emilia Diego, MD Jill Dietz, MD Mahmoud El-Tamer, MD Mehra Golshan, MD E. Shelley Hwang, MD Susan Kesmodel, MD Brigid Killelea, MD Michael Koretz, MD Henry Kuerer, MD, PhD Swati A.
    [Show full text]
  • Genital Necrotizing Fasciitis: Fournier's Gangrene
    DERMATOLOGY ISSN 2473-4799 http://dx.doi.org/10.17140/DRMTOJ-1-109 Open Journal Case Report Genital Necrotizing Fasciitis: Fournier's * Corresponding author Gangrene Sara Yáñez Madriñán, PhD Department of Obstetrics and Gynecology Service University Hospital of Santiago de Manuel Macía Cortiñas, PhD; Maite Peña Fernández, PhD; Susana González López, * Compostela PhD; Sara Yáñez Madriñán, PhD Corunna, Spain Tel. 650927231 E-mail: [email protected] Department of Obstetrics and Gynecology Service, University Hospital of Santiago de Com- postela, Corunna, Spain Volume 1 : Issue 2 Article Ref. #: 1000DRMTOJ1109 ABSTRACT Article History Necrotizing fasciitis is characterized by a rapidly progressive infectious disease affecting skin Received: January 30th, 2016 and soft tissue, usually accompanied by severe systemic toxicity. In fact, it is considered the Accepted: May 18th, 2016 most serious expression of soft tissue infection, by its rapid destruction and tissue necrosis, Published: May 18th, 2016 reaching more than 30% of patients checkered shock and organ failure. In recent years, its incidence is reported at 1: 100,000. This entity in the case of perineal and genital tract Citation involvement, it is called Fournier’s gangrene. In the specialty of Obstetrics and Gynecology is Cortiñas MM, Fernández MP, López a rare infectious complication. SG, Madriñán SY. Genital necrotizing fasciitis: fournier's gangrene. Derma- INTRODUCTION tol Open J. 2016; 1(2): 30-34. doi: 10.17140/DRMTOJ-1-109 Necrotizing fasciitis is a term that describes a disease condition of rapidly spreading infection, usually located in fascial planes of connective tissue necrosis. Fascial planes are bands of connective tissue tha surround muscles, nerves and blood vessels.
    [Show full text]
  • Testing for Non-Alcoholic Fatty Liver Disease
    Visual summary Testing for non-alcoholic fatty liver disease The term “Non-alcoholic fatty liver disease” (NAFLD) encompasses a spectrum of pathologic conditions, ranging from non-alcoholic fatty liver (NAFL) to steatohepatitis (NASH), fibrosis, and cirrhosis. This flow diagram offers a pragmatic approach to the diagnosis and monitoring of NAFLD in asymptomatic adult patients. Recommended amounts are less than Abnormal Alcohol consumption 14 units for both men liver function within recommended and women, spread tests amounts over a week, with + 2–3 alcohol-free days every week History and Red flags: Consider admission Drug-induced liver injury examination or urgent referral Consider referral to hepatology if patient has a history of drug exposure, such as: Consider alternative diagnoses Suspected malignancy Ascites such as effects of medication, infection, or nutritional Jaundice Encephalopathy Sepsis Valproic acid Oestrogens Tamoxifen Valproic acid problems. Evidence of disordered clotting Haematemesis Tetracycline Amiodarone Perhexiline maleate Valproic acid ALT or ALP very high (5x upper limit of normal) Methotrexate 4,4’-diethylaminoethoxyhexesterol Valproic acid Persistently low albumin or platelets Rapid deterioration Chloroquine L-asparaginase Corticosteroids Non-invasive liver screen (NILS) Refer to Hepatology if NILS Consider non-hepatic Liver tests yield positive results for: causes for raised ALT: Blood tests ultrasound Immunoglobulins raised Hepatitis B or C Thyroid diseases High ferritin and high transferrin saturation Coeliac disease Undertaking a liver biopsy is a risky, potentially painful procedure. Non-invasive techniques can be Autoimmune liver screen (Primary biliary cholangitis) Muscle diseases, such as used to assess the presence of both hepatic Low caeruloplasmin Low alpha 1 anti-trypsin protein polymyositis, heavy exercise steatosis and fibrosis.
    [Show full text]
  • Fat Necrosis
    Fat necrosis This leaflet tells you about fat necrosis. It explains what fat necrosis is, how it’s diagnosed and what will happen if it needs to be followed up or treated. Benign breast conditions information provided by Breast Cancer Care Breast Cancer Care doesn’t just support people when they’ve been diagnosed with breast cancer. We also highlight the importance of early detection and provide up-to-date, expert information on breast conditions and breast health. If you have a question about breast health or breast cancer you can call us free on 0808 800 6000 or visit breastcancercare.org.uk We hope you find this information useful. If you’d like to help ensure we’re there for other people when they need us visit breastcancercare.org.uk/donate Central Office Breast Cancer Care Chester House 1–3 Brixton Road London SW9 6DE Phone: 0345 092 0800 Email: [email protected] Call our Helpline on 0808 800 6000 What is fat necrosis? Fat necrosis is a benign (not cancer) condition and does not increase your risk of developing breast cancer. It can occur anywhere in the breast and can affect women of any age. Men can also get fat necrosis, but this is very rare. Breasts are made up of lobules (milk-producing glands) and ducts (tubes that carry milk to the nipple). These are surrounded by glandular, fibrous and fatty tissue. Sometimes a lump can form if an area of the fatty breast tissue is damaged. This is called fat necrosis (necrosis is a medical term used to describe damaged or dead tissue).
    [Show full text]
  • CELL INJURY Lecture 3
    CELL INJURY Lecture 3 َ{ عَّلَم ْ ِٕ النَسَانَمَا لْم يَْعَلْم } Objectives: ● Understand the causes of and pathologic changes occurring in fatty change (steatosis), accumulations of exogenous and endogenous pigments (carbon, silica, iron, melanin, bilirubin and lipofuscin). ● Understand the causes of and differences between dystrophic and metastatic calcifications. Color Index: Girl’s Slides Important Male’s Notes Female’s Notes 1 Extra information Substance accumulate inside the cell in large Intracellular amounts and cause problems in the cell and the Accumulation: organ it’s called intracellular accumulation. The substance may accumulate in either the cytoplasm or nucleus. And can be: An abnormal A substance that’s substance not present A pigment: it can be always present in normal in the cell normally. an endogenous or an cell but has accumulated exogenous. excess e.g. water, lipids, glycogen, protein, carbohydrates It can be: Endogenous (from Exogenous (from outside inside the body) e.g. a the body) e.g. a mineral or product of abnormal component of bacteria. synthesis or metabolism. ExamplesExamples of of substances substance thatthat accumulateaccumulate in in excess excess in in the the cell: cell: A) water: abnormal accumulation of water in the cells is called hydropic change (cellular swelling). It’s an early sign of cellular degeneration in response to injury (note: it’s due to the failure of energy-dependent ion pump on the plasma membrane ⟶ leading to loss of normal ion & fluid homeostasis). B) Lipids: all major classes of lipids can accumulate in cells: • Accumulation of triglycerides ⟶ steatosis (Fatty change) • Accumulation of cholesterol ⟶ seen in the Atherosclerosis.
    [Show full text]