Saunders Comprehensive Review for the NAVLE PDF

This page intentionally left blank Patricia A. Schenck, DVM, PhD Section Chief, Endocrine Diagnostic Section Diagnostic Center for Population and Animal Health Michigan State University Lansing, Michigan 3251 Riverport Lane St. Louis, Missouri 63043 SAUNDERS COMPREHENSIVE REVIEW FOR THE NAVLE® ISBN: 978-1-4160-2926-7 Copyright © 2010 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830 (UK); fax: (+44) 1865 853333; e-mail: [email protected]. You may also com- plete your request on-line via the Elsevier website at http://www.elsevier.com/permissions. Notice Knowledge and best practice in this ﬁeld are constantly changing. As new research and experi- ence broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information pro- vided (i) on procedures featured or (ii) by the manufacturer of each product to be adminis- tered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on his or her own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Author assumes any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher Library of Congress Cataloging-in-Publication Data Schenck, Patricia A. Saunders comprehensive review for the NAVLE / Patricia A. Schenck. p. ; cm. Includes bibliographical references. ISBN 978-1-4160-2926-7 (pbk. : alk. paper) 1. Veterinarians—Licenses—North America—Examinations—Study guides. 2. Veterinary medicine—Examinations, questions, etc. I. Title. II. Title: Comprehensive review for the NAVLE. [DNLM: 1. Veterinary Medicine—Examination Questions. SF 759 S324s 2010] SF759.S34 2010 636.089076—dc22 2009029108 Vice President and Publisher: Linda Duncan Acquisitions Editor: Penny Rudolph Associate Developmental Editor: Lauren Harms Publishing Services Manager: Anitha Raj Design Direction: Jessica Williams Printed in the United States of America Last digit is the print number: 9 8 7 6 5 4 3 2 1 Section Editors Rebecca S. McConnico, DVM, PhD, DACVIM Associate Professor Department of Veterinary Clinical Sciences Louisiana State University Baton Rouge, Louisiana William Raphael BVSc, MS, DABVP (Dairy) Assistant Professor Department of Large Animal Clinical Sciences Michigan State University East Lansing, Michigan v This page intentionally left blank Contributors Laura Jean Armbrust, DVM, DACVR Nickol P. Finch, DVM Associate Professor Clinical Assistant Professor Department of Clinical Sciences Department of Exotics and Wildlife Veterinary Medical Teaching Hospital Washington State University Kansas State University Veterinary Teaching Hospital Manhattan, Kansas Pullman, Washington Valerie A. Chadwick, DVM Daniel L. Grooms DVM, PhD, DACVM Assistant Professor Associate Professor Department of Small Animal Clinical Sciences Department of Large Animal Clinical Sciences Veterinary Teaching Hospital Michigan State University Michigan State University East Lansing, Michigan East Lansing, Michigan J. Jill Heatley, DVM, MS, DABVP(Avian), DACZM Dennis J. Chew, DVM, DACVIM Clinical Associate Professor Professor and Attending Clinician Department of Zoological Medicine Department of Veterinary Clinical Sciences College of Veterinary Medicine College of Veterinary Medicine Texas A&M University The Ohio State University College Station, Texas Columbus, Ohio Roy N. Kirkwood, DVM, PhD, DECAR F. Dunstan Clark, DVM, PhD, DACPV Associate Professor, Swine Production Medicine Assistant Professor Department of Large Animal Clinical Sciences Center of Excellence for Poultry Science Michigan State University University of Arkansas East Lansing, Michigan Fayetteville, Arkansas Sidonie N. Lavergne, DVM, PhD Natalie J. Coffer, BVetMed, MS, DACVIM-LA Assistant Professor Associate Veterinarian College of Veterinary Medicine Apex Veterinary Hospital, Equine P.A. University of Illinois Apex, North Carolina Urbana, Illinois Benjamin J. Darien, DVM, MS Britta S. Leise, MS, DVM, DACVS Associate Professor Clinical Instructor Department of Veterinary Medical Sciences Department of Veterinary Clinical Sciences School of Veterinary Medicine College of Veterinary Medicine University of Wisconsin, Madison The Ohio State University Madison, Wisconsin Columbus, Ohio Yvonne A. Elce, DVM, DACVS Sandra Manfra Marretta, DVM, DACVS, AVDC Assistant Professor Professor Small Animal Surgery and Dentistry Department of Veterinary Clinical Sciences Department of Veterinary Clinical Medicine The Ohio State University College of Veterinary Medicine Columbus, Ohio University of Illinois Urbana, Illinois A. Thomas Evans, DVM, MS, DACVA Professor Emeritus Michigan State University East Lansing, Michigan vii viii Contributors Margaret A. Masterson, DVM, MS, DACVPM Patricia A. Talcott, DVM, PhD Associate Professor Associate Professor Department of Veterinary Preventative Medicine Department of Veterinary Comparative Anatomy, College of Veterinary Medicine Pharmacology and Physiology The Ohio State University Veterinary Diagnostic Toxicologist Columbus, Ohio Washington Animal Disease Diagnostic Lab College of Veterinary Medicine Elizabeth Rustemeyer May, DVM, DACVD Washington State University Assistant Professor of Dermatology Pullman, Washington Department of Veterinary Clinical Sciences Iowa State University Craig A. Thompson, DVM, DACVP Ames, Iowa Clinical Assistant Professor Department of Comparative Pathobiology Michal Mazaki-Tovi, DVM, DECVIM-CA School of Veterinary Medicine Graduate Research Assistant Purdue University Department of Pathobiology and Diagnostic Investigation West Lafayette, Indiana Michigan State University East Lansing, Michigan Wendy M. Townsend, DVM, MS, DACVO Assistant Professor of Comparative Ophthalmology Colin F. Mitchell, BVM&S, DACVS Department of Small Animal Clinical Sciences Assistant Professor Michigan State University Department of Veterinary Clinical Sciences East Lansing, Michigan School of Veterinary Medicine Louisiana State University Lauren A. Trepanier, DVM, PhD, DACVIM, DACVCP Baton Rouge, Louisiana Professor Department of Medical Sciences Jon S. Patterson, DVM, PhD, DACVP University of Wisconsin, Madison Professor Madison, Wisconsin Department of Pathobiology and Diagnostic Investigation Diagnostic Center for Population and Animal Health H. Fred Troutt, VMD, PhD, DACVN Michigan State University Professor East Lansing, Michigan Department of Veterinary Clinical Medicine University of Illinois S. Brent Reimer, DVM, DACVS Urbana, Illinois Staff Surgeon Iowa Veterinary Specialties Katrina R. Viviano, PhD, DVM, DACVIM Des Moines, Iowa Clinical Assistant Professor Department of Medical Sciences Ashley B. Saunders, DVM, DACVIM University of Wisconsin Assistant Professor Madison, Wisconsin Department of Small Animal Clinical Sciences College of Veterinary Medicine Deborah V. Wilson, DVM, BVSc, MS, DACVA Texas A&M University Professor College Station, Texas Department of Large Animal Clinical Sciences Michigan State University Patricia A. Schenck, DVM, PhD East Lansing, Michigan Section Chief, Endocrine Diagnostic Section Diagnostic Center for Population and Animal Health Michigan State University Lansing, Michigan Preface Saunders Comprehensive Review for the NAVLE® is the ﬁrst times. The student may also choose to use questions and only review text for the NAVLE® (North American from only the speciﬁc chapters he or she most needs to Licensing Examination). Passing the NAVLE® is a require- study. The student receives instant feedback as to ment for licensure to practice veterinary medicine in North whether the question was answered correctly or incor- America, and approximately 10% of students who take the rectly. If the student answers correctly the rationale is NAVLE® do not pass it. This comprehensive text, in outline provided; if the student answers incorrectly the correct format for ease of review, will help students prepare for the answer with rationale is provided. NAVLE® by covering the content on each of the major dis- ciplines on which the NAVLE® questions are based. The EXAM MODE companion CD-ROM bound inside the book provides addi- Exam mode is built to emulate the NAVLE® test-taking tional examination preparation by allowing students to experience. The exam contains 360 NAVLE®-style ques- practice their test-taking skills in one of two ways: answer- tions, and the examination is scored; once it is completed ing questions only from the areas they need to study most, or once time runs out, the student can review the exam in or to taking a mock 360-question NAVLE® examination. The its entirety with answers, rationales, and references to rel- content review of the essential topics in veterinary medi- evant chapters. Rationales are provided for correct an- cine in the text and the pool of 1,600 practice questions swer choices. This feature allows students to determine available on the companion CD combine to make Saunders why their answers are correct or incorrect so that they Comprehensive Review for the NAVLE® an invaluable study are able to determine which content areas require further tool for any veterinary medicine student. study. In review mode, a bar graph displays all of the sec- tions of the exam, showing students which sections re- quire further study. Results of the student’s performance REVIEW BOOK may be archived for comparison with results of exams The book contains 59 chapters and is organized into ﬁve taken later. sections: General Disciplines in Veterinary Medicine, Some of the questions on the CD use the case-based Small Animal, Equine, Food Animal, and Exotics. Topics format with relevant radiographs, photos, and patient covered in those sections include hematology, dermatol- histories that students will use to formulate their an- ogy, pharmacology, surgery, preventive medicine, and swers. Answers are provided for every question, and important diseases and disorders. The division of the text rationales are provided for every correct answer by species and the outline format of the content facilitate so that students can evaluate how well they have the student’s review process. Writers are recognized learned the material before they take the real board authorities in their ﬁelds, and much of the content is cul- examination. tivated from Elsevier’s leading veterinary texts. Software Updates Feature The companion CD has a software updating system COMPANION CD-ROM embedded. This system includes an online update The CD bound inside each book contains 1,600 quiz ques- capability to allow the user to download future updates tions in study mode and a 360-question practice exam that or to read messages from the publisher. The CD in- can be taken in exam mode. cludes an option: “Select the Check for Updates button Challenging review questions have been created to to periodically check for updates or messages for this correlate with each chapter of the review book. Answers software. If updates are available, the software will step are accompanied by rationales for increased comprehen- you through the download and installation process. sion. To further emulate the licensing examination, cer- You must be connected to the internet for this feature tain questions include images that the test taker must to work.” consider to be able to answer each question. INTERACTIVE EXAM PRACTICE CD-ROM PRACTICE QUIZ (STUDY MODE) The study mode includes a pool of 1600 multiple-choice A separate interactive exam practice CD is also avail- questions that can be randomized so that the student can able for sale. It offers more than 6,400 review questions use any number of questions an unlimited number of and has a built-in scoring function that allows you to ix x Preface monitor your progress. The test taker can review ques- most topics. After you feel comfortable with your knowl- tions two ways: edge of that material, try to take a 360-question practice Review by speciﬁc topic or species: Practice questions test through Exam Mode on the CD-ROM. When you offer students the ability to take a nearly unlimited num- view your results from the practice test, note the sec- ber of tests, answering as many or as few questions as tions where you missed the most questions. Go back they want at one time. Case-based questions offer stu- and review those sections in the book, then take ques- dents the opportunity to apply concepts learned in tions on the CD from only that section through Study their studies to real-life situations, like they will be Mode. Try taking a practice test again through Exam required to do when they take the NAVLE®, Feedback is Mode and see how your results improve. immediate and includes rationales for correct answers. When you take practice tests, take them in a quiet en- Sample test in blocks of 60 questions with a time limit vironment and make sure you are not interrupted. This of 65 minutes: This ratio of the number of questions will help you prepare best for the board examination to the length of time emulates the actual NAVLE® experience and will give you the most accurate results test-taking experience. for your practice tests. Strong preparation can help de- crease test-day anxiety. It is important to take care of yourself during this cru- STUDY TIPS cial time. Be sure to sleep well, eat a balanced diet, When you are reading Saunders Comprehensive and maintain a routine that includes scheduled blocks Review for the NAVLE®, highlight topics that you feel of study time to prohibit procrastination. you need require additional study. — Patricia A. Schenck When you take a quiz on the companion CD, select ques- tions from the chapters where you have highlighted the Acknowledgments I would like to thank all the staff at Elsevier that worked And thanks to all the four-legged critters in my life that with me from the beginning of this project through the ﬁ- have reminded me why I wanted to be part of this great nal steps, especially Jolynn Gower, Managing Editor; veterinary profession. Penny Rudolph, Publisher; Lauren Harms, Developmental Special acknowledgment is extended to my graduate Editor; Mary Pohlman, Senior Project Manager; and Laura student, Dr. Michal Mazaki-Tovi, for her contributions to Loveall, Senior Project Manager. this project, especially for working on the ﬁgures included This project would not have been possible without the in the text. Thanks also to my friend, Christopher enormous effort and dedication from all the authors who Hamilton, for his proofreading skills and for helping contributed review outlines and questions. me maintain my sanity. I am thankful to all the veterinary students and Finally, I am grateful to my parents for their love and veterinarians I interact with, and continue to learn from, support. every day. —Patricia A. Schenck xi This page intentionally left blank Contents SECTION I GENERAL DISCIPLINES IN Chapter 31 Cardiovascular Disease, 410 VETERINARY MEDICINE Chapter 32 Hematology, 414 Chapter 1 Clinical Pathology: Clinical Chemistry, 1 Chapter 33 Dermatology, 419 Chapter 2 Clinical Pathology: Cytology, 18 Chapter 34 Diagnostic Imaging, 425 Chapter 3 Clinical Pathology: Hematology, 24 Chapter 35 Endocrine Disorders, 429 Chapter 4 Dentistry, 31 Chapter 36 Gastrointestinal Diseases, 435 Chapter 5 Diagnostic Imaging, 40 Chapter 37 Infectious Diseases, 439 Chapter 6 Food Safety, 56 Chapter 38 Nervous System Disorders, 447 Chapter 7 Necropsy Techniques, 65 Chapter 39 Nutrition, 456 Chapter 8 Ophthalmology, 84 Chapter 40 Oncology, 459 Chapter 9 Pharmacology, 94 Chapter 41 Ophthalmology, 465 Chapter 10 Toxicology, 111 Chapter 42 Orthopedic Disorders, 467 Chapter 43 Preventive Medicine, 470 SECTION II SMALL ANIMAL Chapter 44 Reproductive Disorders, 475 Chapter 11 Anesthesia, 155 Chapter 45 Respiratory Disorders, 485 Chapter 12 Cardiovascular Disorders, 165 Chapter 46 Restraint, 493 Chapter 13 Dermatology, 189 Chapter 47 Surgery, 495 Chapter 14 Emergency Medicine, 201 Chapter 48 Urinary Disorders, 539 Chapter 15 Endocrine Disorders, 208 Chapter 16 Gastrointestinal Disorders, 225 SECTION IV FOOD ANIMAL Chapter 17 Hematology, 249 Chapter 49 Bovine Medicine and Management, 543 Chapter 18 Infectious Diseases, 260 Chapter 50 Camelid Medicine and Management, 570 Chapter 19 Nervous System Disorders, 277 Chapter 51 Ovine/Caprine Medicine and Chapter 20 Nutrition, 290 Management, 577 Chapter 21 Oncology, 297 Chapter 52 Swine Medicine and Management, 592 Chapter 22 Orthopedic Disorders, 305 Chapter 53 Poultry Medicine and Management, Chapter 23 Preventive Medicine, 332 599 Chapter 24 Reproductive Disorders, 342 Chapter 25 Respiratory Disorders, 353 SECTION V EXOTICS Chapter 26 Restraint, 365 Chapter 54 Pet Birds, 611 Chapter 27 Soft Tissue Surgery, 368 Chapter 55 Ferrets, 625 Chapter 28 Urinary System Disorders, 384 Chapter 56 Rabbits, 629 Chapter 57 Rodents, 636 SECTION III EQUINE Chapter 58 Reptiles, 642 Chapter 29 Anesthesia, 401 Chapter 59 Zoo Animals, 648 Chapter 30 Behavior, 407 Index 671 xiii This page intentionally left blank SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE Clinical Pathology: Clinical Chemistry 1 CH A P TE R Patricia A. Schenck 2. Better method than endogenous creatinine EVALUATION OF RENAL FUNCTION clearance and approximate inulin clearance I. Blood urea nitrogen (BUN) in dogs A. Decreased glomerular ﬁltration rate (GFR) results C. Single-injection methods for estimation of GFR in increased BUN 1. Post-iohexol clearance B. Affected by urea production in the liver and the a. Give iohexol IV, and collect plasma at rate of excretion by the kidney 2, 3, and 4 hours postiohexol C. Increased dietary protein and gastrointestinal b. Plasma clearance is calculated using the area (GI) bleeding both increase BUN under the plasma concentration vs. time curve II. Creatinine 2. Inulin clearance is considered the gold stan- A. An elevation indicates that less than 25% of the dard for measurement of GFR, but inulin is original functioning renal mass remains not easily measured and is not available at B. A normal serum creatinine concentration does commercial laboratories not exclude the possibility of renal disease V. Urine osmolality C. Young animals have lower serum creatinine A. There is usually a linear relationship between concentrations than do older animals urine osmolality and speciﬁc gravity D. Cachexia often causes lower serum creatinine B. Urine osmolality depends on the number of concentrations osmotically active particles present in urine III. Serum phosphorus concentration C. If urine contains a large amount of larger-molecular- A. An increase in serum phosphorus is not seen until weight solutes such as glucose, mannitol, or radio- more than 85% of nephrons are nonfunctional in graphic contrast agents, the urinary speciﬁc gravity chronic renal diseases will be disproportionately high compared with the B. Tubular reabsorption of phosphorus is regulated osmolality by parathyroid hormone. Renal secondary hyper- VI. Fractional excretion of electrolytes parathyroidism tends to keep the serum phos- A. Sodium phorus concentration within normal limits by 1. Useful in the differentiation of prerenal and excreting more phosphorus into the urine until primary renal azotemia renal disease is advanced 2. In animals with prerenal azotemia and volume C. Serum phosphorus concentrations can be much depletion, there should be sodium conservation higher in immature animals because of bone with a very low fractional excretion of sodium growth 3. In animals with primary renal disease, the frac- IV. Renal clearance (estimation of GFR) tional excretion of sodium should be higher A. Endogenous creatinine clearance determination than normal 1. Collect all urine for 12 or 24 hours (record B. Potassium volume), and determine serum and urine 1. May be useful in the evaluation of chronic renal creatinine concentrations failure patients with hypokalemia to determine 2. Performed when renal disease is suspected but whether the kidneys are contributing to the both BUN and serum creatinine concentrations hypokalemia are normal 2. Varies considerably depending on diet B. Exogenous creatinine clearance C. Phosphorus 1. Creatinine is administered subcutaneously 1. May be useful during treatment of chronic or intravenously (IV); then urine is collected renal failure to determine whether dietary or via catheterization three times at 20-minute drug therapy is effective with a reduction in intervals fractional excretion of phosphorus 1 2 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE 2. Does not offer any advantage in diagnosis of acidosis, respiratory acidosis, or paradoxical chronic renal failure aciduria in metabolic alkalosis with potas- VII. Urinary enzymes sium and chloride depletion A. -glutamyltransferase (GGT) is a membrane- d. Causes of alkaline urine include plant-based bound enzyme speciﬁc for renal tubular damage diets, urine that has been allowed to B. N-acetyl--D-glucosaminidase (NAG) stand open to air at room temperature, 1. Lysosomal enzyme produced by many tissues postprandial alkaline tide, urinary tract but not ﬁltered normally infection (UTI) by urease-positive organ- 2. Increases in urinary NAG are speciﬁc for renal isms, contamination of sample with bacte- tubular damage ria during or after collection, administra- VIII. Urinalysis tion of alkalinizing agents, metabolic A. Physical properties alkalosis, respiratory alkalosis, stress in- 1. Color duction of respiratory alkalosis (cats), and a. Normally colorless to deep amber in color distal renal tubular acidosis (if very concentrated). Deep amber color 2. Protein may also be due to bile pigments a. Trace to 1 protein is normal in urine with b. Red or reddish brown color is due to intact high USG red blood cells (RBCs), hemoglobin, or b. Dipstick methods are more sensitive to myoglobin albumin than globulins c. Dark brown to black is most likely due c. False positives occur in very alkaline urine or to the conversion of hemoglobin to in urine contaminated with benzylalkonium methemoglobin chloride d. Yellow-brown to yellow-green is due to d. Renal proteinuria may result from increased bilirubin glomerular ﬁltration of protein, failure of e. Green color may be due to Pseudomonas tubular reabsorption of protein, tubular infection or to oxidation of bilirubin to secretion of protein, protein leakage from biliverdin damaged tubular cells, or renal parenchy- 2. Appearance mal inﬂammation a. Urine is normally clear in dogs but may be e. Persistent moderate or heavy proteinuria cloudy in about 20% in the absence of urine sediment abnormali- b. Cloudy urine usually contains increased ties suggests glomerular disease cells, crystals, mucus, or casts f. Active sediment with mild to moderate c. Horse urine is typically cloudy because of proteinuria suggests inﬂammatory renal mucus disease or lower urinary tract disease d. Rabbit urine is white and opaque because 3. Glucose of the high concentration of calcium a. Normally not present in dog and cat urine carbonate b. Glucose appears in urine if plasma glucose 3. Odor exceeds approximately 180 mg/dL in the a. The normal odor of urine is due to volatile dog and 300 mg/dL in the cat fatty acids c. Causes of glucosuria include diabetes melli- b. An ammonia odor is due to release of tus (most common), stress or excitement ammonia by urease-producing bacteria (especially in cats), chronically sick cats in 4. Urine speciﬁc gravity (USG) is the weight of the absence of hyperglycemia, renal tubular urine compared to that of distilled water disease, administration of glucose-containing a. USG estimated by dipstrip is NOT accurate. ﬂuids, and severe urethral obstruction in USG should be estimated by refractometry. some cats Make sure the refractometer is temperature 4. Ketones compensated and has different scales for a. Not normally present in dog and cat urine different species b. Inadequate consumption of carbohydrates b. First-morning urine samples typically have or impaired utilization of carbohydrates can the highest urinary concentration lead to ketone production c. Dogs or cats with any detectable dehydration c. Causes of ketonuria include diabetic keto- should elaborate maximally concentrated acidosis (most common), starvation or urine (USG 1.040) prolonged fasting, glycogen storage dis- B. Chemical examination ease, low carbohydrate-high fat diet, and 1. pH persistent hypoglycemia (decreased insulin a. Measurement by pH meter is superior to induces ketone formation) dipstrip methods 5. Bilirubin b. Urine pH varies with diet and acid-base a. Only conjugated bilirubin appears in the balance. Urine pH is usually acidic in urine. A small amount of bilirubin may carnivores and alkaline in herbivores normally be seen in concentrated urine c. Causes of acidic urine include meat diets, samples from normal male dogs. It is not administration of acidifying agents, metabolic normally found in cat urine CHAPTER 1 Clinical Pathology: Clinical Chemistry 3 b. Bilirubin is derived from the breakdown of (3) Clumps or “rafts” are most common heme by the reticuloendothelial system in neoplasia but may occur with c. Bilirubin may appear in the urine prior to inﬂammation the observation of hyperbilirubinemia c. Renal epithelial cells d. Causes of bilirubinuria include hemolysis, (1) Small epithelial cells from the renal liver disease, extrahepatic biliary obstruc- tubules or pelvis tion, fever, and starvation (2) Appearance in urine is never normal 6. Blood and is observed in patients with isch- a. Positive earlier than the observation of emic, nephrotoxic, or degenerative hematuria renal disease b. Dipstick tests do not differentiate from 5. Casts are cylindrical molds of the renal tubules intact RBCs or hemoglobin composed of aggregated protein or cells c. Causes of hemoglobinuria from hemolysis a. Hyaline include transfusion reaction, immune (1) Pure protein precipitates of Tamm- mediated hemolytic anemia, disseminated Horsfall mucoprotein intravascular coagulopathy (DIC), splenic (2) Dissolve rapidly in dilute or alkaline torsion, severe hypophosphatemia, heat urine stroke, zinc toxicity, and phosphofructoki- (3) Have the least pathologic signiﬁcance nase or pyruvate kinase deﬁciency and may form transiently with fever, C. Urinary sediment exercise, or passive congestion to the 1. Sediment preparation kidney a. Perform on fresh urine samples b. Cellular casts b. Centrifuge 5 to 10 mL of urine at 1000 to (1) White cell casts suggest pyelonephritis 1500 rpm for 5 minutes. Stain with but may also be caused by interstitial ne- Sedi-Stain phritis, nephrosis, or glomerulonephritis c. Number of casts is recorded per low-power (2) Red cell casts are fragile and rarely ﬁeld, and cells are recorded per high-power found. They may be noted in acute ﬁeld glomerulonephritis, renal trauma, or 2. RBCs after violent exercise a. Occasional RBCs are normal (3) Hemoglobin casts are casts where the b. Excessive number of RBCs is called hema- hemoglobin color is retained in the cast turia, but origin cannot be determined (4) Renal epithelial casts occur with severe c. Lipid droplets are often confused with tubular injury and suggest acute tubular RBCs, especially in cats necrosis or pyelonephritis (Figure 1-1) d. Causes of hematuria include trauma, (5) Renal fragments are a variant of epithe- urolithiasis, neoplasia, UTIs idiopathic lial casts where portions of the renal feline lower urinary tract disease, chemi- tubules slough into urine. Their appear- cally induced cystitis, systemic diseases ance suggests severe renal injury associated with hemorrhage, renal infarct, (6) Mixed casts contain multiple cell types nephritis, nephrosis, parasites, renal c. Granular casts (Figure 1-2) pelvic hematoma, or genital tract (1) Represent the degeneration of cells or contamination precipitation of ﬁltered plasma proteins 3. White blood cells (WBCs) (2) Fatty casts are a type of granular cast a. Occasional WBCs are normal that may be seen in nephrotic syn- b. Excessive WBCs in urine sediment is called drome or diabetes mellitus pyuria and indicates inﬂammation some- where in the urinary tract or contamination from the genital tract c. Clumped WBCs are typically due to infectious organisms d. Causes of pyuria include urinary tract inﬂammation or genital tract contamination 4. Epithelial cells a. Squamous epithelial cells (1) Large, polygonal cells with small, round nuclei (2) Common in voided or catheterized samples b. Transitional epithelial cells (1) A small number is normal Figure 1-1 Photomicrograph of an epithelial cell cast in urine. Small renal (2) Increased in infection, irritation, or epithelial cells can be identiﬁed in this case (white arrows). (Courtesy Nancy neoplasia Facklam; from Ettinger SJ, Feldman EC. Textbook of Veterinary Internal Medicine, 6th ed. St Louis, 2005, Saunders.) 4 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE h. Urate crystals are associated with liver disease and portosystemic shunt i. Calcium oxalate crystals are found in acidic urine j. Cystine crystals are found in acidic urine and are associated with cystinuria k. Bilirubin crystals may be found normally in concentrated dog urine l. Oxalate monohydrate (“hippurate-like”) crystals are found in acute renal failure owing to ethylene glycol ingestion 8. Miscellaneous a. Sperm is common in urine from intact males b. Amorphous debris may be seen in those with acute intrinsic renal failure c. Mucous threads or ﬁbrin strands may be seen in association with lower urinary tract or genital inﬂammation Figure 1-2 Photomicrograph of a ﬁnely granular case in urine. (From Ettinger SJ, Feldman EC. Textbook of Veterinary Internal Medicine, d. Parasite ova from Dioctophyma renale or 6th ed. St Louis, 2005, Saunders.) Capillaria plica are rarely seen e. Lipid droplets are associated with cellular degeneration f. Foreign material may be present, especially d. Waxy casts represent the ﬁnal stage of in voided samples degeneration of granular casts. They sug- g. Precipitates of urine stain may look like gest chronic intrarenal stasis and are found urinary crystals in advanced chronic renal disease e. Broad casts are wide casts that form in FLUIDS AND ACID-BASE METABOLISM collecting ducts or dilated distal nephron. They suggest severe intrarenal stasis and I. Dehydration tubular obstruction A. Status 6. Organisms 1. Total body water is about 60% of body a. Normal urine is sterile weight; about half is extracellular and half is b. Large numbers of bacteria present (in associa- intracellular tion with pyuria) in urine collected by cathe- 2. Very mild dehydration occurs with water loss terization or cystocentesis strongly suggest of 1% to 4% of body weight. Clinical signs are the presence of UTI not detectable c. The presence of bacteria without pyuria 3. Mild dehydration occurs with water loss of should arouse suspicion for bacterial con- 5% to 6% of body weight. Clinical signs include tamination. However, dogs with hyperadre- dry mucous membranes, slight loss of skin nocorticism, diabetes mellitus, or immuno- turgor, injected conjunctiva, and inelasticity suppression and cats with chronic renal of skin disease can have bacteriuria with pyuria 4. Moderate dehydration occurs with water loss d. The absence of bacteria does not rule out of 7% to 9% of body weight. Clinical signs UTI include loss of skin turgor with slow return, e. Yeast and fungal hyphae in sediment are prolonged capillary reﬁll time (2-3 seconds), usually contaminants enophthalmos 7. Crystals 5. Severe dehydration occurs with water loss a. Crystals are often an artifact of storage time of 10% to 12% of body weight. Clinical signs and refrigeration include extreme loss of skin turgor, peripheral b. Struvite crystals are found in alkaline urine vasoconstriction, cold extremities, and pro- and may be found in normal animals or in longed capillary reﬁll time (3 seconds) those with struvite urinary stones 6. Very severe dehydration occurs with water loss c. Calcium phosphate crystals are found in of 13% to 15% of body weight; clinical signs in- alkaline urine clude vascular collapse, renal failure, and death d. Calcium carbonate crystals are found in B. Isotonic dehydration occurs with equal losses alkaline urine of water and solute e. Amorphous phosphate crystals are found 1. Sodium and chloride concentrations are not in alkaline urine affected f. Ammonium biurate crystals are found in 2. Increased packed cell volume (PCV) with alkaline urine increased plasma proteins g. Uric acid crystals are found in acidic urine 3. Occurs in some cases of diarrhea and renal and are associated with the Dalmatian breed disease CHAPTER 1 Clinical Pathology: Clinical Chemistry 5 C. Hypertonic dehydration occurs when more water 2. Compensation is via a change in urinary acidi- than solute is lost ﬁcation to alter HCO3. This process is slower 1. Concentration of sodium and chloride increases than compensation in ventilation 2. PCV increases, with increased plasma proteins E. Simple acid-base disorders occur when there is a 3. Occurs most commonly in diabetes insipidus primary change, but no compensation has taken 4. Species that produce hypotonic sweat (cattle) place or little sweat (dogs, cats) develop hypertonic F. Compensated acid-base disorders occur when dehydration with heat stress primary changes are present, along with evidence D. Hypotonic dehydration occurs when more solute of a compensatory change in the complementary than water is lost system. The pH rarely returns to normal with 1. Concentrations of sodium and chloride compensation decrease G. Combined acid-base disorders occur when there 2. This results in a contraction of the extracellu- are changes in the same direction in both lar ﬂuid (ECF) volume with expansion of intra- systems cellular ﬂuid (ICF) volume to restore osmotic H. Metabolic acidosis equilibrium 1. Primary change is decreased HCO3 3. Most common type of dehydration, where the 2. PCO2 will decrease in compensation solute loss induces a secondary loss of water I. Metabolic alkalosis 4. Hypotonic dehydration from heat stress occurs 1. Primary change is increased HCO3 in species that produce hypertonic sweat 2. PCO2 will increase in compensation (horses) J. Respiratory acidosis II. Acid-base metabolism 1. Primary change is increased PCO2 A. Henderson-Hasselbach equation 2. HCO3 will increase in compensation 1. pH pKa log [A-]/[HA] 3. There is a larger compensation in chronic 2. The carbonic acid-bicarbonate system is usu- respiratory acidosis compared with an acute ally used: pH pKa log [HCO3-]/[H2CO3] event 3. pH 6.1 log[HCO3-]/0.03(PCO2) K. Respiratory alkalosis B. To characterize acid-base disorders, blood pH, 1. Primary change is decreased HCO3, and PCO2 are measured (Table 1-1) 2. PCO2 1. A decrease in pH is acidosis; an increase is 3. HCO3 will decrease in compensation alkalosis 4. There is a larger compensation in chronic 2. A decrease in HCO3 is a metabolic acidosis; an respiratory alkalosis compared with an acute increase is a metabolic alkalosis event 3. A decrease in PCO2 is a respiratory alkalosis; an L. Base excess and base deﬁcit increase is a respiratory acidosis 1. Calculated from blood gas parameters by the 4. If HCO3 measurement is unavailable, total CO2 blood gas analyzer. This calculation is based from a chemistry proﬁle can be used as an es- on human relationships and is probably valid timate. Total CO2 is about 1 to 2 mmol/L for dogs and cats. This calculation might not greater than the HCO3 concentration be valid for other species C. Metabolic disorders 2. Increased values reﬂect a base excess corre- 1. Characterized by changes in HCO3 sponding to metabolic alkalosis 2. Compensation is via rapid changes in ventila- 3. Decreased values reﬂect a base deﬁcit, corre- tion to alter PCO2 sponding to metabolic acidosis D. Respiratory disorders M. Anion gap 1. Characterized by changes in PCO2 1. Anion gap (Na K) – (Cl HCO3); the ob- jective is to estimate changes in the unmea- sured anions and cations without having to measure them a. Unmeasured anions include sulfate, Table 1-1 Characteristics of Primary Acid-Base lactate, phosphate, pyruvate, albumin, Disturbances and ketoacids b. Unmeasured cations include primarily pH [H] [HCO3] Pco2 calcium and magnesium 2. If the anion gap increases, then unmeasured Metabolic alkalosis ↑ ↓ ↑↑ ↑ anions have increased. If the anion gap Metabolic acidosis ↓ ↑ ↓↓ ↓ decreases, then unmeasured cations have Respiratory acidosis ↓ ↑ ↑ ↑↑ increased Respiratory alkalosis ↑ ↓ ↓ ↓↓ III. Osmolality GI loss (vomiting, A. Osmolality is the concentration or number of os- diarrhea) motically active particles in an aqueous solution B. Osmolal gap is the difference between the actual measured serum osmolality and the calculated es- Primary events are indicated by double arrows. timate of osmolality 6 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE 1. Calculated osmolality (mOsm/L) 1.86 [Na 3. Solute gain occurs with salt poisoning, hyper- (mmol/L)] [glucose (mg/dL)/18] [BUN tonic ﬂuid administration, hyperadrenocorti- (mg/dL)/2.8] 9 cism, hyperaldosteronism 2. The osmolal gap increases when there is an in- II. Chloride crease in any osmotically active particles that A. Roles are not included in the calculated equation 1. Principal anion in ECF 3. The osmolal gap will increase whenever the 2. Chloride usually accompanies sodium to main- anion gap is increased tain neutrality 4. Used commonly in cases of ethylene glycol 3. Normal fractional excretion is less than 1% but toxicity may be elevated in large animals fed a diet a. Ethylene glycol is a small osmotically active higher in chlorine particle B. The same conditions causing hypernatremia b. The osmolal gap correlates well with the and hyponatremia also cause hyperchloremia concentration of ethylene glycol in serum and hypochloremia III. Potassium A. Roles ELECTROLYTE METABOLISM 1. Principal cation of the ICF I. Sodium 2. Determines resting cell membrane potential A. Roles B. Hypokalemia (typically associated with 1. Principal cation in ECF alkalosis) 2. Important in movement of ﬂuids across epithe- 1. Decreased intake lial surfaces a. Anorexia B. Hyponatremia b. Dietary deﬁciency 1. Pseudohyponatremia c. Administration of potassium-free ﬂuids a. Occurs with hyperlipidemia or hyperpro- 2. Translocation between ECF and ICF teinemia a. Metabolic alkalosis, respiratory alkalosis b. Plasma sample is diluted by the excess lipid b. Glucose or insulin administration or protein and thus the measured sodium c. Catecholamines concentration is falsely lowered 3. Increased loss 2. Hyperosmolal, hypervolemic conditions include a. GI loss hyperglycemia and mannitol administration (1) Vomiting 3. Hypoosmolal hypervolemic conditions (2) Diarrhea a. Occurs when there is excess water reten- b. Third-space syndrome tion with dilution of the plasma (1) GI obstruction (especially displaced b. Causes include nephrotic syndrome, abomasum) chronic liver disease, chronic renal failure, (2) Peritonitis and congestive heart failure (3) Ascites 4. Hypoosmolal euvolemic conditions include hy- c. Urinary loss potonic ﬂuid infusion,antidiuretic hormone (1) Hyperadrenocorticism (ADH) administration, inappropriate secretion (2) Acute renal failure (nonoliguric) of ADH, and psychogenic polydipsia (3) Postobstructive diuresis 5. Hypoosmolal hypovolemic conditions include (4) Chronic renal failure (cats) the following: (5) Potassium-losing diuretics a. Dietary deﬁciency of sodium (6) Fanconi syndrome b. GI loss from vomiting or diarrhea (7) Renal tubular acidosis c. Third-space syndrome (GI obstruction, peri- (8) Primary hyperaldosteronism tonitis, uroabdomen, ascites) d. Cutaneous loss (burns) d. Urinary loss from hypoadrenocorticism, 4. Feline kaliopenic nephropathy-polymyopathy nonoliguric acute renal failure, diuretics, syndrome and Fanconi syndrome a. Characterized by hypokalemia, increased e. Cutaneous losses (burns) fractional excretion of potassium, azotemia, C. Hypernatremia and metabolic acidosis 1. Pure water deﬁcits occur in dietary deﬁciency, b. Chronic decrease of potassium leads to de- central or nephrogenic diabetes insipidus, pri- crease in aldosterone, which leads to distal mary hypodipsia, heat stress, and fever renal tubular acidosis 2. Hypotonic ﬂuid loss occurs with the following: C. Hyperkalemia (typically associated with a. GI loss owing to vomiting or diarrhea acidosis) b. Third-space syndrome (peritonitis, ascites) 1. Pseudohyperkalemia (in vitro translocation of c. Urinary loss from osmotic diuretics (manni- potassium to plasma) tol, diabetes mellitus), chronic renal failure, a. Thrombocytosis nonoliguric acute renal failure, postobstruc- b. Leukemia tive nephropathy c. Hemolysis (equine, bovids) d. Cutaneous loss (burns) d. Akita dogs CHAPTER 1 Clinical Pathology: Clinical Chemistry 7 2. Increased intake or oversupplementation of B. Hypomagnesemia ﬂuids with potassium 1. Most often occurs after excessive 3. Translocation between ICF and ECF magnesium loss a. Respiratory or metabolic acidosis a. GI tract (malabsorption syndromes, b. Hyperkalemic periodic paralysis diarrhea) c. Ischemia or reperfusion injury b. Renal loss (ﬂuid diuresis, diuretic therapy, 4. Decreased urinary excretion renal disease) a. Anuric or oliguric renal failure 2. Iatrogenic deﬁciency occurs during ﬂuid b. Urinary tract obstruction therapy as most ﬂuids contain little or no c. Ruptured urinary bladder magnesium d. Hypoadrenocorticism 3. Metabolic disorders (diabetes mellitus, pri- e. Potassium-sparing diuretics mary hyperparathyroidism, primary hypopara- f. Nonsteroidal antiinﬂammatory drugs thyroidism, hyperaldosteronism, third-space (NSAIDs) syndrome, hypophosphatemia) g. Angiotensin-converting enzyme (ACE) 4. Ruminants inhibitors a. Milk tetany, in which calves are fed a IV. Phosphorus magnesium-deﬁcient milk diet A. Roles b. Grass tetany, which occurs in adults fed on 1. Found mostly in ICF lush, green pasture that is high in potas- 2. Regulated through interactions with calcium sium, which blocks magnesium absorption and calcium metabolic hormones from the rumen a. Calcitriol increases phosphorus resorption C. Hypermagnesemia from bone, increases GI phosphorus absorp- 1. Renal disease (both acute and chronic) tion, and increases urinary fractional excre- 2. Increased renal tubular reabsorption of magne- tion of phosphorus sium during dehydration, salt depletion, and b. The concentrations of calcium and phos- hypoadrenocorticism phorus are reciprocally related and are 3. Overadministration of magnesium-containing kept relatively constant antacids B. Hypophosphatemia VI. Calcium 1. Increased cellular uptake of phosphorus A. Roles (glucose administration) 1. Major structural role in the skeleton 2. Acid-base balance 2. Important in regulation of ions across a. Respiratory alkalosis membranes b. Metabolic acidosis (enhanced urinary 3. Cofactor in many metabolic processes excretion of phosphates); often in diabetic 4. Major role in signal transmission, skeletal ketoacidosis muscle contraction, and cardiovascular 3. Abnormalities in renal tubular phosphate function reabsorption B. Measurement of calcium a. Hyperparathyroidism 1. Ionized calcium should be measured for an b. Fanconi syndrome accurate assessment of calcium status c. Aminoglycoside nephrotoxicosis 2. Adjustment formulas for total calcium should 4. GI absorption not be used because they do not reliably pre- a. Decreased phosphorus in diet dict ionized calcium concentration b. Vomiting 3. Acidosis increases ionized calcium concentra- c. Diarrhea tion, and alkalosis decreases ionized calcium d. Intestinal malabsorption syndromes concentration e. Excessive ingestion of phosphate binders C. Hypocalcemia C. Hyperphosphatemia 1. Primary hypoparathyroidism is characterized 1. Redistribution between ICF and ECF by hypocalcemia with a low or low-normal con- 2. Cellular damage centration of parathyroid hormone (an inap- 3. Acute acidosis (chronic metabolic acidosis propriate response). Hypomagnesemia may causes hypophosphatemia usually) also be seen. Primary hypoparathyroidism can 4. Decreased renal blood ﬂow and GFR (resulting be spontaneously occurring; result from para- in secondary hyperparathyroidism) thyroiditis or parathyroid adenoma infarction; 5. Ruptured urinary bladder or occur postoperatively after removal of a 6. Hypertonic sodium phosphate enemas parathyroid adenoma or any other neck sur- 7. Excessive dietary intake (with secondary hy- gery that can interrupt the blood supply to the perparathyroidism) parathyroid glands V. Magnesium 2. Common causes of hypocalcemia include A. Roles hypoalbuminemia, chronic renal failure (ionized 1. Magnesium is an important cofactor for many hypocalcemia), eclampsia, acute renal failure, enzymatic reactions acute pancreatitis, and urethral obstruction 2. Inﬂuences cell membrane properties in cats 8 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE 3. Occasional causes of hypocalcemia include EVALUATION OF THE LIVER soft tissue trauma, rhabdomyolysis, ethylene glycol poisoning, phosphate enemas, post I. Enzymes in the liver bicarbonate administration, and critical illness A. Leakage enzymes: alanine aminotransferase or sepsis (ALT), aspartate aminotransferase (AST), sorbitol 4. Uncommon causes of hypocalcemia include dehydrogenase (SDH), and glutamate dehydroge- EDTA contamination, dilution with calcium-free nase (GLDH) IV ﬂuids, intestinal malabsorption, hypovitamin- B. Induced enzymes: alkaline phosphatase (ALP), osis D, pancreatitis, citrated blood transfusions, GGT hypomagnesemia, and tumor lysis syndrome II. Tests for hepatocyte injury D. Hypercalcemia A. Alanine aminotransferase (ALT) 1. Neoplasia is the most common cause of ion- 1. Previously called serum pyruvic transaminase ized hypercalcemia in dogs. Neoplasia is char- (SGPT) acterized by an elevation of both total and ion- 2. Not liver speciﬁc; leakage enzyme ized calcium, with parathyroid hormone 3. In dogs and cats, ALT is present mostly in suppressed into the lower part of or below the hepatocytes, but increases can be seen reference range (a parathyroid- independent with muscle injury (especially extensive in- hypercalcemia) jury) a. In dogs, the most common neoplasm caus- 4. Horses and ruminants have little ALT in hepa- ing hypercalcemia is lymphoma. Other tocytes, so elevations of ALT usually indicate neoplasms include anal sac apocrine gland muscle damage adenocarcinoma, thymoma, carcinomas B. Aspartate aminotransferase (AST) (lung, pancreas, mammary gland, skin, na- 1. Previously called serum glutamic oxaloacetic sal cavity, thyroid, adrenal medulla), and transaminase (SGOT) hematologic malignancies (multiple my- 2. Present in hepatocytes and in skeletal and car- eloma, lymphoma, myeloproliferative dis- diac muscle cells ease, leukemia) 3. Not liver speciﬁc; leakage enzyme b. In cats, the most common neoplasias are 4. Increased AST can be due to hepatocyte death, lymphoma and squamous cell carcinomas. hepatocyte injury, muscle cell death and mus- Other neoplasms include multiple myeloma, cle cell injury leukemia, osteosarcoma, ﬁbrosarcoma, and 5. Not as speciﬁc in the dog and cat as ALT; more bronchogenic carcinoma speciﬁc than ALT in horses and ruminants 2. Idiopathic hypercalcemia is the most common C. Sorbitol dehydrogenase (SDH) cause of ionized hypercalcemia in cats. 1. Liver speciﬁc; leakage enzyme Idiopathic hypercalcemia is also a parathyroid 2. Increase suggests hepatocyte death or injury independent hypercalcemia 3. Very short half-life, and values return to nor- 3. Renal disease is a common cause of an eleva- mal within a few days tion of serum total calcium but not ionized 4. Not very stable in serum samples; stable for calcium. With renal disease, serum ionized about 48 hours if frozen calcium concentration is typically normal 5. In horses and ruminants, SDH is preferable to to low AST for detecting injury to hepatocytes 4. Vitamin D toxicity from oversupplementation D. Glutamate dehydrogenase (GLDH) with vitamin D, ingestion of plants containing 1. Liver speciﬁc; leakage enzyme calcitriol glycosides (Cestrum diurnum), 2. Increase suggests hepatocyte death or injury ingestion of cholecalciferol rodenticides, or 3. More stable than SDH but still not very stable ingestion of antipsoriasis cream (Dovonex). III. Tests for cholestasis Vitamin D toxicity is a parathyroid-independent A. ALP is an induced enzyme hypercalcemia, and an elevation in phosphorus 1. Bone origin (BALP) is typically observed a. Mild increase associated with increased os- 5. Primary hyperparathyroidism causes an teoblast activity elevation of both serum total and ionized cal- b. Will be higher in young growing animals cium with lack of suppression of parathyroid c. May be elevated in association with primary hormone production. Parathyroid hormone or secondary hyperparathyroidism (effects concentration may be still within normal of PTH on bone) limits, or it may be elevated 2. Liver origin (LALP) 6. Other causes of hypercalcemia include a. An increase is associated with cholestasis hypoadrenocorticism, osteolytic processes, b. LALP usually increases before an increase granulomatous disease, grape or raisin toxic- in bilirubin with cholestasis ity, dehydration, vitamin A toxicity, aluminum 3. Corticosteroid-induced (CiALP) toxicity, excessive calcium carbonate supple- a. Induced by corticosteroids and also anti- mentation, intestinal phosphate binders, convulsants thiazide diuretics, acromegaly, or severe b. Chronic disease (including chronic cho- hypothermia lestasis) can induce CiALP CHAPTER 1 Clinical Pathology: Clinical Chemistry 9 4. In cats, the half-life of ALP is very short (about or indirect. Most bilirubin in horses is un- 6 hours); thus the increase of ALP in choles- conjugated tatic disease is signiﬁcantly less than in other d. Once in hepatocytes, bilirubin is conju- species gated, and most is secreted into bile. A 5. Increases in horses with cholestasis are not small amount passes through the sinusoidal well documented side back into the blood. Conjugated biliru- 6. In ruminants, increases in ALP are usually due bin is also termed direct bilirubin to cholestasis or osteoblastic activity 2. Abnormal metabolism B. GGT a. Historically, both unconjugated and conju- 1. Considered to be an induced enzyme; however, gated bilirubin have been measured, but acute injury can cause elevations of GGT currently a total bilirubin measurement is 2. Elevated primarily in cholestasis. May also be usually determined induced by glucocorticoids and anticonvulsants b. Bilirubin is increased when there is in- 3. GGT is superior to ALP in horses and rumi- creased hemoglobin production (increased nants for the detection of cholestasis RBC destruction), decreased uptake and 4. GGT is present in very high levels in cattle and conjugation of bilirubin by hepatocytes, and sheep colostrums, resulting in very high levels a decrease in outﬂow of conjugated biliru- of serum GGT in calves and sheep that have bin (cholestasis, etc.) consumed colostrum c. Bilirubin is not consistently elevated in ru- IV. Tests of liver function minants with liver disease A. Bilirubin B. Bile acids 1. Normal metabolism 1. Fasting and postprandial samples are usually a. The heme portion of hemoglobin is split collected in dogs and cats into iron and protoporphyrin 2. The postprandial bile acid concentration is b. Protoporphyrin is converted to biliverdin, usually greatly exaggerated with portosystemic then to bilirubin shunt c. Bilirubin is released from macrophages, at- 3. Increases in fasting, postprandial, or both sam- tached to albumin or other globulins, trans- ples may occur with portosystemic shunts, ported to the liver, released from albumin cholestasis, cirrhosis, necrosis, hepatitis, he- or globulins, and enters hepatocytes. This patic lipidosis, steroid hepatopathy, and neo- circulating bilirubin is termed unconjugated’ plasia (Figure 1-3) Systemic circulation ↑ Bile acids C B A D Portal venous Biliary circulation system Bile acids Intestines Figure 1-3 The increase in the bile acid level in the circulation is generally caused by one of four disorders: congenital portosystemic shunting (A), hepatic microvascular dysplasia (B), intrahepatic colestatic disease (C), or extrahepatic bile duct obstruction (D). (From Meyer D, Harvey JW. Veterinary Laboratory Medicine: Interpretation and Diagnosis, 3rd ed. St Louis, 2004, Saunders.) 10 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE 4. One sample is collected in horses and rumi- F. Steroid hepatopathy nants. An increase in bile acids suggests he- 1. Most common in dogs patic disease 2. Leakage enzymes are mildly increased C. Ammonia concentration is usually increased in 3. Induced enzymes are markedly increased those with portosystemic shunts or if more than 4. Bilirubin may be mildly increased 60% of liver mass is lost G. Biliary disorders D. Albumin decreases when 60% to 80% of liver func- 1. Induced enzymes are markedly increased tion is lost 2. Leakage enzymes may be mildly increased E. Globulins may be increased, especially in horses as a result of hepatocyte injury from the F. Glucose cholestasis 1. The liver converts glucose to glycogen 3. Bilirubin and bile acids are also typically in- 2. Glucose may be increased if there is decreased creased glucose uptake by the liver H. Chronic liver disease 3. Glucose may be decreased if there is de- 1. Leakage enzymes may be increased, depending creased gluconeogenesis or glycogenolysis on the extent and rate of progression of the G. Urea is synthesized in the liver from ammonia disease 1. BUN decreases with liver failure 2. Induced enzymes are usually mildly to moder- 2. Blood ammonia concentration increases with ately increased liver failure 3. Bilirubin concentration is normal to mildly in- H. Cholesterol creased in those with more advanced disease 1. Can be decreased if there is decreased synthe- I. End-stage liver disease sis of cholesterol with liver failure 1. Occurs when 60% to 80% of liver mass has 2. Can be increased if cholestasis is present, been lost which prevents excretion of cholesterol in bile 2. Leakage enzymes may be normal to mildly in- I. Coagulation factors are commonly decreased in creased because of the overall loss of liver dogs with liver failure mass V. Changes in selected liver diseases 3. Induced enzymes are moderately to markedly A. Portosystemic shunt increased, as are bilirubin and bile acid con- 1. If portosystemic shunts occur because of se- centrations vere cirrhosis, then changes as seen in end- 4. Many have increased ammonia, decreased stage liver disease are expected BUN, decreased albumin, and abnormal coagu- 2. Early portosystemic shunts do not cause much lation tests active hepatocyte damage; thus leakage en- zymes are usually not elevated EVALUATION OF THE PANCREAS a. Induced enzymes are also not elevated be- cause there is little cholestasis I. Pancreatic injury b. Typically occurs in young, growing animals, A. Serum amylase so ALP may be elevated (BALP) 1. Dogs c. Bile acids are markedly elevated a. Highest concentrations in pancreas and d. Microcytic anemia with low iron concentra- small intestinal mucosa tion is typical b. Causes of increased serum amylase include B. Hepatic necrosis pancreatic injury, renal dysfunction, GI dis- 1. If focal, leakage enzymes may be normal or ease, hepatic disease, and neoplasia (lym- mildly elevated phoma, hemangiosarcoma) 2. Diffuse necrosis more often results in eleva- c. Magnitude of the increase may be helpful. tions in both leakage and induced enzymes. If amylase is elevated more than three-fold C. Hypoxia or mild toxic damage greater than the upper reference range 1. This process is diffuse, so leakage enzymes are limit, pancreatic injury is strongly usually mildly to moderately elevated suggested 2. Induced enzymes and bilirubin are not 2. Other species typically elevated a. Amylase is usually normal in cats with pan- 3. Bile acids may be mildly increased creatic injury and may be decreased D. Focal lesions b. Amylase is only slightly elevated in horses 1. Leakage enzymes may be normal to mildly with pancreatic injury and is elevated in increased most horses with proximal enteritis and 2. Induced enzymes are usually normal unless other causes of colic bile ﬂow is signiﬁcantly impaired B. Serum lipase E. Hepatic lipidosis 1. Dogs 1. Leakage enzymes are increased in most cats a. Causes of increased serum lipase include 2. ALP is also elevated in most, but GGT is ele- pancreatic injury, renal dysfunction, hepatic vated in only a small number disease, GI disease, corticosteroids (dexa- 3. Serum bilirubin is usually elevated, and bile ac- methasone can increase lipase ﬁve-fold), and ids are commonly increased neoplasia (lymphoma, hemangiosarcoma) CHAPTER 1 Clinical Pathology: Clinical Chemistry 11 b. An elevation greater than two-fold is sugges- 3. Dependent on the quantity of starch in the diet tive of pancreatic injury, except if the dog B. Fecal fat has received corticosteroids 1. Direct fecal fat detects undigested fat 2. Cats with pancreatic injury typically have nor- a. Stain feces with Sudan III or IV on slide and mal lipase activity examine C. Peritoneal ﬂuid b. The presence of undigested fecal fat indi- 1. If amylase or lipase activity is higher in perito- cates a deﬁciency in lipase neal ﬂuid than in serum, pancreatic injury is 2. Indirect fecal fat detects digested fat more likely a. Mix feces, acetic acid, and Sudan III or IV on 2. Consider measuring in cats or horses with sus- a slide; bring to a boil and examine pected pancreatic injury b. The presence of digested fat (in the absence D. Serum trypsin-like immunoreactivity (TLI) of undigested fat) suggests adequate lipase 1. TLI activity is proportional to trypsinogen and production but inadequate absorption of fat trypsin. Trypsinogen is secreted only by the C. Fecal proteolytic activity can be estimated but is pancreas and is converted to trypsin in the rarely performed anymore since the advent of se- small intestine rum TLI determination 2. TLI is increased in pancreatitis and is a more D. Fecal muscle ﬁbers sensitive indicator of early pancreatitis than 1. Stain brown with Lugol stain are amylase or lipase determination 2. Presence suggests inadequate fecal protease 3. TLI is also a sensitive and speciﬁc indicator for activity pancreatitis in the cat E. Fat absorption test (plasma turbidity test) II. Exocrine pancreatic insufﬁciency (see section below 1. After a 12-hour fast, orally administer corn oil, on intestinal absorption) then collect hourly plasma samples for a few hours 2. Turbidity of the samples should occur, indicat- EVALUATION OF DIGESTION ing the absorption of lipid AND INTESTINAL ABSORPTION 3. If turbidity does not occur, then repeat test I. Fecal parasites with corn oil that has been preincubated with A. Refrigerate fecal sample if cannot examine within pancreatic enzymes. If turbidity occurs, then 2 hours absorption occurred and the problem is with B. Direct smears are useful in detecting Strongyloi- digestion of fat des, Coccidia, Giardia, Balantidium, Entamoeba, 4. The sensitivity of this test is poor and Trichomonas spp. F. Serum TLI C. Wet mounts are useful to detect Giardia, Balantid- 1. Available for dogs and cats ium, and Entamoeba spp. 2. TLI is decreased in dogs and cats with EPI. It is D. Fecal ﬂotation normal in other small intestinal diseases 1. Best method for detecting parasitic ova and G. D-Xylose absorption test oocysts 1. Measure of intestinal absorption in dogs and 2. Different fecal ﬂotation solutions can be used, horses including a sugar solution, sodium chloride, 2. Xylose absorption is falsely decreased in those magnesium sulfate, zinc sulfate, or sodium ni- with delayed gastric emptying, bacterial over- trate solutions growth, and in some with exocrine pancreatic E. Baermann technique is most useful for detection insufﬁciency (EPI) of larvae in feces. H. Vitamin B12 and folate assays II. Fecal occult blood 1. Serum folate is decreased if there is malab- A. Performed in animals with chronic diarrhea or sorption in the proximal small intestine loose stools, microcytic anemia, a history of 2. Serum vitamin B12 is decreased if the malab- GI tumors, or in those treated with NSAIDs sorption is primarily in the distal small B. Positive test result suggests upper GI tract inﬂam- intestine mation, ulceration, or neoplasia 3. In cats with EPI, both serum vitamin B12 and fo- C. False positives may occur when consuming meats late levels are usually decreased. In dogs with or some vegetables. It is best to restrict the diet EPI, serum vitamin B12 is usually decreased, (rice and cottage cheese) for a few days before and folate is usually normal to increased the test 4. In small intestinal bacterial overgrowth, III. Fecal cytology vitamin B12 is decreased and folate is increased A. Look for types of bacteria present B. Evaluate for presence of inﬂammatory cells EVALUATION OF SERUM IV. Digestion and absorption tests AND PLASMA PROTEINS A. Fecal starch 1. Stain feces with Lugol solution I. Plasma versus serum 2. The presence of undigested starch suggests a A. Plasma contains albumin, and all globulins, which deﬁciency in starch-digesting enzymes or in- include antibodies, clotting factors, enzymes, and creased intestinal motility proteins 12 SECTION I GENERAL DISCIPLINES IN VETERINARY MEDICINE B. Serum contains no ﬁbrinogen and only contains exocrine pancreatic insufﬁciency, and glomeru- albumin and remaining globulins lar disease (loss of albumin) II. Total protein concentration 3. Hypoglobulinemia with normal or increased al- A. Can be measured with a refractometer. Excess bumin. Causes include failure of passive trans- lipid, hemoglobin, bilirubin, glucose, urea, fer, and immune deﬁciencies (inherited or ac- sodium, or chloride can falsely increase quired) total protein concentration as measured by B. Increased protein concentrations refractometry 1. Hyperalbuminemia occurs only in dehydration B. Spectrophotometric measurement is more accu- 2. Hyperalbuminemia with hyperglobulinemia oc- rate curs in dehydration III. Albumin concentration 3. Hyperglobulinemia A. Measured spectrophotometrically a. Increased -globulin concentration occurs B. At very low concentrations, albumin may be over- most commonly in acute inﬂammation estimated b. Increased -globulin concentration occurs IV. Globulin concentrations in acute inﬂammation, nephrotic syndrome, A. Fractions liver disease, and immune responses 1. The -fraction includes thyroxine-binding glob- c. Increased -globulin concentration (gam- ulin, transcortin, some lipoproteins (LPs), mopathies) ceruloplasmin, haptoglobin, antithrombin III, (1) Polyclonal gammopathies are present and 2-macroglobulin with chronic antigenic stimulation, 2. The fraction includes some LPs, transferrin, immune-mediated disease, liver ferritin, C-reactive protein, complement C3 and disease, lymphoma, and lymphocytic C4, plasminogen, and ﬁbrinogen (in plasma leukemia only) (2) Monoclonal gammopathies are present 3. The -fraction includes the immunoglobulins with multiple myeloma, extramedullary B. Measurement plasmacytoma, lymphoma, lymphocytic 1. The globulin concentration reported on a leukemia, chronic pyoderma, plasma- chemistry proﬁle is calculated by subtracting cytic enterocolitis, canine ehrlichiosis, serum albumin from total protein concentra- visceral leishmaniasis (dog), lympho- tion plasmacytic stomatitis (cats), and idio- 2. Accurate measurement is determined by se-

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