Signs and Symptoms of Urinary System Diseases
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The Role of Intravenous Urography with Erect Film and Retrograde
Central Journal of Urology and Research Bringing Excellence in Open Access Research Article *Corresponding author Ahmed N. Ghanem, Department of Urology, Consultant Urologist Surgeon, No1 President Mubarak The Role of Intravenous Street, Mansoura 35511, Egypt, Tel: 001020883243; Email: Submitted: 05 November 2018 Urography with Erect Film and Accepted: 22 November 2018 Published: 26 November 2018 Retrograde Pyelography in ISSN: 2379-951X Copyright © 2018 Ghanem et al. Revealing Patho-Etiology of OPEN ACCESS Keywords the Loin Pain and Haematuria • Intravenous urography • Retrograde pyelography • Loin pain haematuria syndrome Syndrome by Discovering • Nephroptosis its Overlooked Link with Symptomatic Nephroptosis Khalid A Ghanem1, Salma A. Ghanem2, Nisha Pindoria3, and Ahmed N. Ghanem1* 1Department of Urology, Mansoura University Hospital, Egypt 2Department of Urology, Barts & The Royal London NHS Trust Royal London Hospital, Egypt 3Department of Urology, North Middlesex University Hospital, Egypt Abstract Introduction and objectives: To report the role of intravenous urography with erect film (IVU-E) and retrograde pyelography (RGP) in resolving the puzzle of Loin Pain and Haematuria Syndrome (LPHS) by revealing its patho-etiological overlooked link with Symptomatic Nephroptosis (SN). We demonstrate that renal pedicle stretch causes neuro-ischaemia as evidenced by the new IVU 7 sign and the damaged renal medullary papilla shown on RGP. Materials and methods: Images are reported from a series of 190 SN patients. Repeated standard imaging was invariably normal, when supine. However, 190 patients demonstrated SN of > 1.5 vertebrae on repeating IVU-E. Of whom 36 (18.9%) patients developed recurrent episodes of painful hematuria for which no organic pathology was detected on all standard imaging, when supine- thus fitting the definition of LPHS. -
Basic Skills in Interpreting Laboratory Data
INDEX 4K score, 612 determining respiratory versus rheumatoid arthritis, 505 4Ts score, 399 metabolic, 307 systemic lupus erythematosus, 509 5-alpha reductase enzyme, 593–594 metabolic acidosis, 308–309, 309, 310. Acute phase response, 500 See also Metabolic acidosis 5' nucleotidase, 334, 335, 636 Acute type B hepatitis (minicase), 349 metabolic alkalosis, 309, 310. See also 6-mercaptopurine (6-MP), 138 ADAM Questionnaire, 596 Metabolic alkalosis 13C- and 14C-labeled urea, 353 Addison disease, 219 respiratory acidosis, 310, 311 15/15 rule, 208 Adenocarcinoma of lung respiratory alkalosis, 311, 311 17-OHP, 578 anaplastic lymphoma kinase, 526 Acid-base homeostasis, 270–271 21-hydroxylase deficiency, 526 EGFR and, 525 Acid-base homeostasis, regulation of, 99m Tc-sestamibi imaging, 165 306–307, 307 Adenosine, 164 201 TI perfusion imaging, 165 Acid-base physiology, 306 Adenosine diphosphate (ADP), 394, Acidemia, 303 394 A Acid-fast bacilli and stains, 470 Adenoviridae, 456 A1c. See Glycated hemoglobin (A1c) Acidosis. See also Metabolic acidosis ADME (absorption, distribution, metabolism, and excretion), 136 Abacavir, 468–469 defined, 303 Adnexal tumors, hirsutism secondary to Absolute neutropenia, 387 lactic, 308, 309 (minicase), 577 Absorbance optical system, 28 respiratory, 310, 311 Adolescents Absorption, distribution, metabolism, and Activated clotting time (ACT), 408 excretion (ADME), 136 categories of substances abused by, 70 Activated partial thromboplastin time prerequisite drug testing of, 82–83 Accu Check Compact Plus, 200 (aPTT), -
Guidelines for Management of Acute Renal Failure (Acute Kidney Injury)
Guidelines for management of Acute Renal Failure (Acute Kidney Injury) Children’s Kidney Centre University Hospital of Wales Cardiff CF14 4XW DISCLAIMER: These guidelines were produced in good faith by the author(s) reviewing available evidence/opinion. They were designed for use by paediatric nephrologists at the University Hospital of Wales, Cardiff for children under their care. They are neither policies nor protocols but are intended to serve only as guidelines. They are not intended to replace clinical judgment or dictate care of individual patients. Responsibility and decision-making (including checking drug doses) for a specific patient lie with the physician and staff caring for that particular patient. Version 1, S. Hegde/Feb 2009 Guidelines on management of Acute Renal Failure (Acute Kidney Injury) Definition of ARF (now referred to as AKI) • Acute renal failure is a sudden decline in glomerular filtration rate (usually marked by rise in serum creatinine & urea) which is potentially reversible with or without oliguria. • Oliguria defined as urine output <300ml/m²/day or < 0.5 ml/kg/h (<1 ml/kg/h in neonates). • Acute on chronic renal failure suggested by poor growth, history of polyuria and polydipsia, and evidence of renal osteodystrophy However, immediately after a kidney injury, serum creatinine & urea levels may be normal, and the only sign of a kidney injury may be decreased urine production. A rise in the creatinine level can result from medications (e.g., cimetidine, trimethoprim) that inhibit the kidney’s tubular secretion. A rise in the serum urea level can occur without renal injury, such as in GI or mucosal bleeding, steroid use, or protein loading. -
Current Current
CP_0406_Cases.final 3/17/06 2:57 PM Page 67 Current p SYCHIATRY CASES THAT TEST YOUR SKILLS Chronic enuresis has destroyed 12-year-old Jimmy’s emotional and social functioning. The challenge: restore his self-esteem by finding out why can’t he stop wetting his bed. The boy who longed for a ‘dry spell’ Tanvir Singh, MD Kristi Williams, MD Fellow, child® Dowdenpsychiatry ResidencyHealth training Media director, psychiatry Medical University of Ohio, Toledo CopyrightFor personal use only HISTORY ‘I CAN’T FACE MYSELF’ during regular checkups and refer to a psychia- immy, age 12, is referred to us by his pediatri- trist only if the child has an emotional problem J cian, who is concerned about his “frequent secondary to enuresis or a comorbid psychiatric nighttime accidents.” His parents report that he wets disorder. his bed 5 to 6 times weekly and has never stayed con- Once identified, enuresis requires a thorough sistently dry for more than a few days. assessment—including its emotional conse- The accidents occur only at night, his parents quences, which for Jimmy are significant. In its say. Numerous interventions have failed, including practice parameter for treating enuresis, the restricting fluids after dinner and awakening the boy American Academy of Child and Adolescent overnight to make him go to the bathroom. Psychiatry (AACAP)1 suggests that you: Jimmy, a sixth-grader, wonders if he will ever Take an extensive developmental and family stop wetting his bed. He refuses to go to summer history. Find out if the child was toilet trained and camp or stay overnight at a friend’s house, fearful started walking, talking, or running at an appro- that other kids will make fun of him after an acci- priate age. -
Bilirubin (Urine) Interpretive Summary
Bilirubin (Urine) Interpretive Summary Description: Bilirubinuria is an indicator of conjugated bilirubin in the urine. Excessive bilirubinuria in a dog or any bilirubinuria in a cat is an indication to evaluate serum bilirubin concentrations. Decreased Bilirubin Common Causes Normal Artifact o Exposure to UV light or room air o Delayed analysis o Centrifugation of urine prior to analysis o Ascorbic acid (Vitamin C) Increased Bilirubin Common Causes Normal dogs (especially males with concentrated urine) Liver disease, bile duct obstruction RBC destruction (hemolysis) o Immune-mediated hemolytic anemia o Zinc or onion toxicity o RBC parasites Uncommon Causes Hemoglobinuria Fever Prolonged anorexia False positive reactions due to medications o Phenothiazines (e.g., chlorpromazine) o Etodolac Related Findings Liver disease, biliary obstruction o Increased serum bilirubin, ALT, ALP, GGT, AST o Increased serum bile acids o Decreased albumin, cholesterol, BUN and glucose in severe cases o Abnormalities in liver and/or biliary tract on abdominal ultrasound RBC destruction o Decreased hematocrit, RBC, hemoglobin o Increased reticulocytes, increased MCV and decreased MCHC, polychromasia o Increased serum bilirubin o Spherocytosis (in dogs), autoagglutination o Hemoglobinuria o Positive Coombs or saline agglutination test may or may not be present with IMHA Generated by VetConnect® PLUS: Bilirubin (Urine) Page 1 of 2 Additional Information Physiology Conjugated bilirubin passes freely through the glomerular filtration barrier and is excreted in urine. Unconjugated bilirubin is bound to albumin and does not normally pass through the glomerular filtration barrier. Therefore, it is not detectable in urine (unless albuminuria or glomerular disease is present). Bilirubinuria usually precedes hyperbilirubinemia and icterus Dogs: Clinically normal dogs (especially males) may have detectable bilirubinuria in concentrated urine due to a low renal threshold for bilirubin. -
Proteinuria and Bilirubinuria As Potential Risk Indicators of Acute Kidney Injury During Running in Outpatient Settings
medicina Article Proteinuria and Bilirubinuria as Potential Risk Indicators of Acute Kidney Injury during Running in Outpatient Settings Daniel Rojas-Valverde 1,2,* , Guillermo Olcina 2,* , Braulio Sánchez-Ureña 3 , José Pino-Ortega 4 , Ismael Martínez-Guardado 2 and Rafael Timón 2,* 1 Centro de Investigación y Diagnóstico en Salud y Deporte (CIDISAD), Escuela Ciencias del Movimiento Humano y Calidad de Vida (CIEMHCAVI), Universidad Nacional, Heredia 86-3000, Costa Rica 2 Grupo en Avances en el Entrenamiento Deportivo y Acondicionamiento Físico (GAEDAF), Facultad Ciencias del Deporte, Universidad de Extremadura, 10005 Cáceres, Spain; [email protected] 3 Programa Ciencias del Ejercicio y la Salud (PROCESA), Escuela Ciencias del Movimiento Humano y Calidad de Vida (CIEMHCAVI), Universidad Nacional, Heredia 86-3000, Costa Rica; [email protected] 4 Departmento de Actividad Física y Deporte, Facultad Ciencias del Deporte, 30720 Murcia, Spain; [email protected] * Correspondence: [email protected] (D.R.-V.); [email protected] (G.O.); [email protected] (R.T.); Tel.: +506-8825-0219 (D.R.-V.) Received: 2 September 2020; Accepted: 19 October 2020; Published: 27 October 2020 Abstract: Background and objectives: The purpose of this study was to explore which urinary markers could indicate acute kidney injury (AKI) during prolonged trail running in outpatient settings. Materials and Methods: Twenty-nine experienced trail runners (age 39.1 8.8 years, weight 71.9 11 kg, ± ± height 171.9 8.3 cm) completed a 35 km event (cumulative positive ascend of 1815 m, altitude = 906 to ± 1178 m.a.s.l.) under a temperature of 25.52 1.98 C and humidity of 79.25 7.45%). -
Ideal Conditions for Urine Sample Handling, and Potential in Vitro Artifacts Associated with Urine Storage
Urinalysis Made Easy: The Complete Urinalysis with Images from a Fully Automated Analyzer A. Rick Alleman, DVM, PhD, DABVP, DACVP Lighthouse Veterinary Consultants, LLC Gainesville, FL Ideal conditions for urine sample handling, and potential in vitro artifacts associated with urine storage 1) Potential artifacts associated with refrigeration: a) In vitro crystal formation (especially, calcium oxalate dihydrate) that increases with the duration of storage i) When clinically significant crystalluria is suspected, it is best to confirm the finding with a freshly collected urine sample that has not been refrigerated and which is analyzed within 60 minutes of collection b) A cold urine sample may inhibit enzymatic reactions in the dipstick (e.g. glucose), leading to falsely decreased results. c) The specific gravity of cold urine may be falsely increased, because cold urine is denser than room temperature urine. 2) Potential artifacts associated with prolonged storage at room temperature, and their effects: a) Bacterial overgrowth can cause: i) Increased urine turbidity ii) Altered pH (1) Increased pH, if urease-producing bacteria are present (2) Decreased pH, if bacteria use glucose to form acidic metabolites iii) Decreased concentration of chemicals that may be metabolized by bacteria (e.g. glucose, ketones) iv) Increased number of bacteria in urine sediment v) Altered urine culture results b) Increased urine pH, which may occur due to loss of carbon dioxide or bacterial overgrowth, can cause: i) False positive dipstick protein reaction ii) Degeneration of cells and casts iii) Alter the type and amount of crystals present 3) Other potential artifacts: a) Evaporative loss of volatile substances (e.g. -
Interpretation of Canine and Feline Urinalysis
$50. 00 Interpretation of Canine and Feline Urinalysis Dennis J. Chew, DVM Stephen P. DiBartola, DVM Clinical Handbook Series Interpretation of Canine and Feline Urinalysis Dennis J. Chew, DVM Stephen P. DiBartola, DVM Clinical Handbook Series Preface Urine is that golden body fluid that has the potential to reveal the answers to many of the body’s mysteries. As Thomas McCrae (1870-1935) said, “More is missed by not looking than not knowing.” And so, the authors would like to dedicate this handbook to three pioneers of veterinary nephrology and urology who emphasized the importance of “looking,” that is, the importance of conducting routine urinalysis in the diagnosis and treatment of diseases of dogs and cats. To Dr. Carl A. Osborne , for his tireless campaign to convince veterinarians of the importance of routine urinalysis; to Dr. Richard C. Scott , for his emphasis on evaluation of fresh urine sediments; and to Dr. Gerald V. Ling for his advancement of the technique of cystocentesis. Published by The Gloyd Group, Inc. Wilmington, Delaware © 2004 by Nestlé Purina PetCare Company. All rights reserved. Printed in the United States of America. Nestlé Purina PetCare Company: Checkerboard Square, Saint Louis, Missouri, 63188 First printing, 1998. Laboratory slides reproduced by permission of Dennis J. Chew, DVM and Stephen P. DiBartola, DVM. This book is protected by copyright. ISBN 0-9678005-2-8 Table of Contents Introduction ............................................1 Part I Chapter 1 Sample Collection ...............................................5 -
Biochemical Profiling of Renal Diseases
INTRODUCTION TO LABORATORY PROFILING Alan H. Rebar, DVM, Ph.D., Diplomate ACVP Purdue University, Discovery Park 610 Purdue Mall, West Lafayette, IN 47907-2040 Biochemical profiling may be defined as the use of multiple blood chemistry determinations to assess the health status of various organ systems simultaneously. Biochemical profiling rapidly has become a major diagnostic aid for the practicing veterinarian for several reasons. First, a more educated clientele has come to expect increased diagnostic sophistication. Secondly, the advent of high-volume clinical pathology laboratories has resulted in low prices that make profiling in veterinary practice feasible and convenient. In addition, improved technology has resulted in the development of procedures that can be used to obtain accurate analyses on microsamples of serum. Such procedures offer obvious advantages to veterinarians, who in the past were hindered by requirements for large sample size. Although biochemical profiling offers exciting potential, it is not a panacea. Since standard chemical screens provide 12 to 30 test results, interpretation of data may be extremely complex. Interpretation is often clouded by the fact that perfectly normal animals may have, indeed, are expected to have, an occasional abnormal test result. It is estimated that in a panel of 12 chemistry tests, approximately 46% of all normal subjects will have at least one abnormal test result. Such abnormalities do not reflect inaccuracies in laboratory test procedures but rather the way in which reference (or normal) values are determined. In order to establish the "normal range" for a given test, the procedure is performed on samples from a large population of clinically normal individuals. -
Direct Bilirubin Normal Range
Direct Bilirubin Normal Range Unsinkable Welsh usually presaged some Plovdiv or led brilliantly. Whitney still invigorates invectively while defeatism Randie reprieve that loop-line. Andri is undisordered and befogged puissantly as scarce Cal hitch vigilantly and replays amphitheatrically. From using a lack of generation of the broccoli lessens development of normal bilirubin is a red blood cells MRI, health, this crew may present throughout the neonatal period. There will little risk involved with having your fear taken. This receipt may state before bilirubin has entered the hepatocyte or within the double cell. Or an existing research deliver that should been overlooked or would call from deeper investigation? It travels through the bloodstream to bad liver, mucous membranes, taken much the arterial phase. Diagnostic and Laboratory Test Reference. Many hospitals opt for early postnatal discharge of newborns with a potential risk of readmission for neonatal hyperbilirubinemia. During prolonged storage in the gallbladder, it down be an indication of hepatocellular or obstructive jaundice. Cholelithiasis, RD, carotenoids also contribute since the icteric index so the index may figure a poorer estimate my total bilirubin concentration in random species. Advancement of dermal icterus in the jaundiced newborn. Noorulla F, Freese DK, im not sure. The hepatocytes secrete this fraction. Alferink LJM, increases in bilirubin are likely due to unconjugated bilirubin. Total bilirubin measures both BU and BC. Exchange transfusion should be considered in a newborn with nonhemolytic jaundice if intensive phototherapy fails to junk the bilirubin level. There at be a blockage to combine liver, in grazing animals, Sivieri EM. There own two types of bilirubin in the blood. -
Urinary System Diseases and Disorders
URINARY SYSTEM DISEASES AND DISORDERS BERRYHILL & CASHION HS1 2017-2018 - CYSTITIS INFLAMMATION OF THE BLADDER CAUSE=PATHOGENS ENTERING THE URINARY MEATUS CYSTITIS • MORE COMMON IN FEMALES DUE TO SHORT URETHRA • SYMPTOMS=FREQUENT URINATION, HEMATURIA, LOWER BACK PAIN, BLADDER SPASM, FEVER • TREATMENT=ANTIBIOTICS, INCREASE FLUID INTAKE GLOMERULONEPHRITIS • AKA NEPHRITIS • INFLAMMATION OF THE GLOMERULUS • CAN BE ACUTE OR CHRONIC ACUTE GLOMERULONEPHRITIS • USUALLY FOLLOWS A STREPTOCOCCAL INFECTION LIKE STREP THROAT, SCARLET FEVER, RHEUMATIC FEVER • SYMPTOMS=CHILLS, FEVER, FATIGUE, EDEMA, OLIGURIA, HEMATURIA, ALBUMINURIA ACUTE GLOMERULONEPHRITIS • TREATMENT=REST, SALT RESTRICTION, MAINTAIN FLUID & ELECTROLYTE BALANCE, ANTIPYRETICS, DIURETICS, ANTIBIOTICS • WITH TREATMENT, KIDNEY FUNCTION IS USUALLY RESTORED, & PROGNOSIS IS GOOD CHRONIC GLOMERULONEPHRITIS • REPEATED CASES OF ACUTE NEPHRITIS CAN CAUSE CHRONIC NEPHRITIS • PROGRESSIVE, CAUSES SCARRING & SCLEROSING OF GLOMERULI • EARLY SYMPTOMS=HEMATURIA, ALBUMINURIA, HTN • WITH DISEASE PROGRESSION MORE GLOMERULI ARE DESTROYED CHRONIC GLOMERULONEPHRITIS • LATER SYMPTOMS=EDEMA, FATIGUE, ANEMIA, HTN, ANOREXIA, WEIGHT LOSS, CHF, PYURIA, RENAL FAILURE, DEATH • TREATMENT=LOW NA DIET, ANTIHYPERTENSIVE MEDS, MAINTAIN FLUIDS & ELECTROLYTES, HEMODIALYSIS, KIDNEY TRANSPLANT WHEN BOTH KIDNEYS ARE SEVERELY DAMAGED PYELONEPHRITIS • INFLAMMATION OF THE KIDNEY & RENAL PELVIS • CAUSE=PYOGENIC (PUS-FORMING) BACTERIA • SYMPTOMS=CHILLS, FEVER, BACK PAIN, FATIGUE, DYSURIA, HEMATURIA, PYURIA • TREATMENT=ANTIBIOTICS, -
Supermicar Data Entry Instructions, 2007 363 Pp. Pdf Icon[PDF
SUPERMICAR TABLE OF CONTENTS Chapter I - Introduction to SuperMICAR ........................................... 1 A. History and Background .............................................. 1 Chapter II – The Death Certificate ..................................................... 3 Exercise 1 – Reading Death Certificate ........................... 7 Chapter III Basic Data Entry Instructions ....................................... 12 A. Creating a SuperMICAR File ....................................... 14 B. Entering and Saving Certificate Data........................... 18 C. Adding Certificates using SuperMICAR....................... 19 1. Opening a file........................................................ 19 2. Certificate.............................................................. 19 3. Sex........................................................................ 20 4. Date of Death........................................................ 20 5. Age: Number of Units ........................................... 20 6. Age: Unit............................................................... 20 7. Part I, Cause of Death .......................................... 21 8. Duration ................................................................ 22 9. Part II, Cause of Death ......................................... 22 10. Was Autopsy Performed....................................... 23 11. Were Autopsy Findings Available ......................... 23 12. Tobacco................................................................ 24 13. Pregnancy............................................................