Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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VII. Toxins Affecting Erythrocytes and the Hematopoietic System 829 Angiotensin converting enzyme (ACE) is concentrated on the luminal surface of pulmonary endothelial cells. Most circulating ACE originates from the lung; however, many tissues including tubular epithelial and endocrine cells contain this enzyme ( Erdos, 1987 ). Serum ACE activity is altered in chronic and acute pulmonary disease ( Hollinger, 1983 ). Unfortunately, assay for this enzyme is not readily available in most veterinary clinical biochemistry laboratories, and ACE remains primarily a research tool. Acute pulmonary edema is the typical lesion resulting from toxins affecting the epithelial-endothelial interface of the alveolus. Because CO 2 is approximately 20 times more diffusible than O 2 , early pulmonary edema typically results in decreased P a O 2 , whereas P a CO 2 remains normal or may decrease with hyperventilation producing respiratory alkalosis. Severe pulmonary edema may result in elevated P a CO 2 (hypercapnia and respiratory acidosis) ( Carlson, 1997 ). Chronic insult to the alveolar epithelial-endothelial interface may progress to pulmonary fibrosis (e.g., paraquat intoxication) and be associated with low PaO 2 and elevated PaCO 2 . Pulmonary fibrosis impinging on the pulmonary vasculature may induce pulmonary hypertension and cor pulmonale associated with enzymological alterations suggestive of hepatoxicity resulting from passive hepatic congestion. Cattle are susceptible to several toxins that induce acute pulmonary edema including ingestion of perilla ketone in Perilla frutescens , 4-ipomeanol in sweet potatoes ( Ipomoea batatas ) infected with Fusarium solani ( Doster et al. , 1978 ), and the generation of 3-methyindole by ruminal Lactobacillus skatoli from tryptophan in lush pasture grasses ( Breeze and Carlson, 1982 ). Some of the pyrrolizidine alkaloids, notably monocrotaline from Crotolaria spectabilis , may induce chronic pulmonary arteriopathy resulting in pulmonary hypertension that progresses to right heart failure and elevation of enzymes suggestive of cardiotoxicity or hepatotoxicity. Similar pulmonary arteriopathy occurs in pigs with chronic fumonisin intoxication ( Casteel et al. , 1994 ). Organochlorines and organobromines include chlorinated naphthalenes, polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), and dibenzofurans. These industrial toxins are cumulative and result in hypovitaminosis A that is associated with squamous metaplasia of columnar epithelium of the respiratory tract and hyperkeratosis as discussed under integumentary toxins. The numerous chemotherapeutic agents that have been associated with pulmonary toxicity or hypersensitivity have been reviewed elsewhere ( Myers, 1993 ). VI . TOXINS AFFECTING THE GASTROINTESTINAL TRACT Disease affecting the gastrointestinal tract is often clinically apparent on the basis of vomiting or diarrhea. In veterinary medicine, these are more often the result of infectious disease rather than intoxication. However, the possibility of gastrointestinal toxins ( Table 27-5 ) should be considered, especially in acute outbreaks affecting several animals sharing the same environment. Vomiting and diarrhea may produce dehydration that results in mild to moderate elevations of BUN, plasma protein, packed cell volume (PCV), and urine specific gravity. Metabolic alkalosis (increased pH, normal or increased PCO 2 , increased HCO 3 and HCO 3 /H 2 CO 3 ) and hypochloridemia may result from chloride loss associated with vomiting ( Tennant and Hornbuckle, 1997 ) . Metabolic acidosis (decreased pH, normal or decreased PCO 2 , decreased HCO 3 and HCO 3 /H 2 CO 3 ) may result from secretory loss of bicarbonate in diarrhea. In the absence of evidence of malnutrition or hepatic or renal disease, chronic gastrointestinal malabsorption or protein loss should be considered as a potential cause of hypoproteinemia (Kaneko, 1997a) . Ingestion of strong acids or alkalis may induce immediate and severe damage to the gastrointestinal mucosa. The seleniferous plants, which may be associated with acute gastroenteritis in herbivores, are discussed under the integumentary system. Trichothecenes, especially T-2, produced by Fusarium spp. and the macrocyclic trichothecene produced by Stachybotrys alternans are highly irritant and produce acute ulceration and hemorrhage of the gastrointestinal tract. These mycotoxins also produce acute ulcerative and necrotizing lesions of the skin and chronic pancytopenia with hemorrhage. The estrogenic mycotoxin, zearalenone, may induce rectal prolapse in pigs in addition to affecting reproductive performance. VII . TOXINS AFFECTING ERYTHROCYTES AND THE HEMATOPOIETIC SYSTEM Toxins inducing hemolysis ( Table 27-6 ) may produce elevations of serum LDH, anemia, icterus, hemoglobinemia, hemoglobinuria with secondary nephrotoxicity, and unconjugated bilirubinemia. Chronic, drug-induced, immune-mediated hemolysis has been associated with para-aminosalicylic acid, chlorpromazine, dipyrine, insecticides, penicillin, phenacetin, quinine, quinidine, and sulfonamides ( Valli, 1993 ). Mellitin is a hemolyzing component of Hymenopterous toxins and comprises approximately 50% of bee venom ( Cheville, 1988 ). One report also attributes a case of immune-mediated hemolytic anemia in a young dog to exposure to bee venom ( Noble and Armstrong, 1999 ). Chronic nephrotoxicosis leading to uremia may decrease erythrocyte life span because products normally eliminated by the kidney are retained. This mechanism
830 Chapter | 27 Clinical Biochemistry in Toxicology TABLE 27-5 Toxins Affecting the Gastrointestinal Tract Toxins Disease Onset Geography Species Affected Acids/alkalis Acute Worldwide All Aleurites fordi (tung oil tree) Acute AUS, US B Arsenic Acute Worldwide All Asclepias spp. (milkweed) Acute N AM B, E, Cp, O Cantharidin (blister beetle) Acute US All Copper Acute Worldwide All Fluoroacetate Acute AUS, MEX, S AFR All Fluorensia cernua (blackbush/tarbush) Acute MEX, US Cp, O Hymenoxys odorata (bitterweed) Acute US O Isotropis spp. Acute AUS B, O Kerosene/petroleum Acute Worldwide All Nerium oleander (oleander) Acute Worldwide B, Cp, E, O Pyrrolizidine alkaloids Acute Worldwide B, Cp, E, O, P Ricinus communis (castor bean) Acute Worldwide B, E Robinia pseudoaca-cia (Black locust) Acute N AM B, E Solanaceae Acute Worldwide All Selenium Acute Worldwide B, Cp, E, O, P Tannins ( Quercus spp., oaks) Acute Worldwide B, Cp, O Tricothecenes Acute Worldwide All Urginea maritima (sea onion) Acute Worldwide Cn, F, P Zearalenone ( Fusarium roseum ) Chronic Worldwide P Zinc Acute Worldwide B, Cn, O Abbreviations: B, bovine; Cn, canine; Cp, caprine; E, equine; F, feline; O, ovine; P, porcine. TABLE 27-6 Toxins Inducing Hemolysis Toxins Disease Onset Geography Species Affected Allium spp. (onion) Acute Worldwide B, Cn, E, O Acer rubrum (red maple) Acute US E Brassicae Acute Worldwide B, O Copper Acute Worldwide Cn, O Drug-induced immune mediated anemia Chronic Worldwide All Mellitin Acute Worldwide All Methylene blue Acute Worldwide F Molybdenum Chronic Worldwide B, Cp, O Naphthalene Acute Worldwide Cn Nephrotoxins Chronic All Phenothiazine Acute Worldwide E, O Snake venoms Acute Worldwide All Zinc Acute to chronic Worldwide B, Cn, O, P Abbreviations: B, bovine; Cn, canine; Cp, caprine; E, equine; F, feline; O, ovine; P, porcine.
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Preface It has been more than a dec
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viii Contributors Björn P. Meij (5
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2 Chapter | 1 Concepts of Normality
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10 Chapter | 1 Concepts of Normalit
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Chapter 2 Comparative Medical Genet
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I. Introduction 29 Green Red Green
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I. Introduction 31 A1 genetic map d
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I. Introduction 33 of genomes of va
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36 Chapter | 2 Comparative Medical
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46 Chapter | 3 Carbohydrate Metabol
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IX. Disorders of Carbohydrate Metab
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X. Disorders of Ruminants Associate
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X. Disorders of Ruminants Associate
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References 79 Kaneko , J. J. , Luic
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Chapter 4 Lipids and Ketones Michae
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II. Long Chain Fatty Acids 83 FIGUR
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II. Long Chain Fatty Acids 85 Plasm
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IV. Phospholipids 87 The regulation
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V. Cholesterol 89 V. CHOLESTEROL A.
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VI. Lipoproteins 91 TABLE 4-1 Compo
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VI. Lipoproteins 93 TABLE 4-2 Apoli
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96 Chapter | 4 Lipids and Ketones B
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98 Chapter | 4 Lipids and Ketones
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Chapter 5 Proteins, Proteomics, and
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III. Metabolism of Proteins 119 C .
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IV. Plasma Proteins 121 NH 4 HCO
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V. Methodology 123 molecule. The gl
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V. Methodology 125 has occurred wil
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V. Methodology 127 Although attempt
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V. Methodology 129 kD 94 67 43 2 2
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V. Methodology 131 D . Specific Pro
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VI. Normal Plasma and Serum Protein
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VII. Interpretation of Serum Protei
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References 149 Andersson , M. , Ste
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References 151 response of haptoglo
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References 153 dogs with metastasiz
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References 155 Watson , T. D. G. (
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158 Chapter | 6 Clinical Veterinary
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V. Methods for Evaluation of the Im
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VI. Laboratory Diagnosis of Disease
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Chapter 7 The Erythrocyte: Physiolo
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II. Hematopoiesis 175 progenitor ce
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III. Developing Erythroid Cells 177
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IV. Mature RBC 185 immune-mediated
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IV. Mature RBC 187 TABLE 7-3 Erythr
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IV. Mature RBC 189 TABLE 7.5 Erythr
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IV. Mature RBC 191 Echinocyte forma
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IV. Mature RBC 193 Pig RBC isoantig
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IV. Mature RBC 195 occurs in chicke
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IV. Mature RBC 197 inorganic phosph
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IV. Mature RBC 199 (a) FIGURE 7-6 T
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IV. Mature RBC 201 RBC 2,3DPG incre
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IV. Mature RBC 203 mechanisms would
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IV. Mature RBC 205 released during
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IV. Mature RBC 207 reduced by ascor
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V. Determinants of RBC Survival 209
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V. Determinants of RBC Survival 211
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VI. Inherited Disorders of RBCs 213
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described in people. They include a
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References 221 Boas , F. E. , Forma
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References 223 Della Rovere , F. ,
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References 225 Gedde , M. M. , Davi
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References 227 phosphofructokinase-
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References 229 Knight , A. P. , Las
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References 231 Martinovich , D. , a
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References 235 Shadduck , R. K. ( 1
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References 237 Tennant , B. , Dill
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References 239 Williams , D. M. , L
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Chapter 8 Porphyrins and the Porphy
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II. Porphyrins 243 two vinyl groups
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II. Porphyrins 245 TABLE 8-2 Nomenc
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IV. Porphyrias 247 6. Uroporphyrins
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IV. Porphyrias 249 i . Urine It is
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IV. Porphyrias 251 to localize the
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IV. Porphyrias 253 FIGURE 8-6 Metab
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IV. Porphyrias 255 estrogens. The d
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References 257 and hexachlorobenzen
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Chapter 9 Iron Metabolism and Its D
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II. Iron Distribution 261 plasma of
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IV. Plasma Iron Transport 263 pathw
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VI. Iron Metabolism in Cells 265 of
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VI. Iron Metabolism in Cells 267 in
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VII. Tests for Evaluating Iron Meta
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VII. Tests for Evaluating Iron Meta
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VIII. Disorders of Iron Metabolism
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References 279 ( Norrdin et al ., 2
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References 281 Fresco , R. ( 1981 )
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References 283 Moore , C. V. , Duba
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References 285 Weiden , P. L. , Hac
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288 Chapter | 10 Hemostasis TABLE 1
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292 Chapter | 10 Hemostasis The pro
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294 Chapter | 10 Hemostasis exhibit
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298 Chapter | 10 Hemostasis that is
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302 Chapter | 10 Hemostasis However
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304 Chapter | 10 Hemostasis 2. Comp
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306 Chapter | 10 Hemostasis is a re
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308 Chapter | 10 Hemostasis 2. Asse
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310 Chapter | 10 Hemostasis necessi
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312 Chapter | 10 Hemostasis disease
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314 Chapter | 10 Hemostasis concent
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316 Chapter | 10 Hemostasis the rol
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318 Chapter | 10 Hemostasis proport
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320 Chapter | 10 Hemostasis a consi
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322 Chapter | 10 Hemostasis Bakhtia
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324 Chapter | 10 Hemostasis Dowd ,
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326 Chapter | 10 Hemostasis Kier ,
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328 Chapter | 10 Hemostasis Nielsen
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330 Chapter | 10 Hemostasis Tablin
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332 Chapter | 11 Neutrophil Functio
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352 Chapter | 12 Diagnostic Enzymol
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380 Chapter | 13 Hepatic Function L
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382 Chapter | 13 Hepatic Function e
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384 Chapter | 13 Hepatic Function p
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386 Chapter | 13 Hepatic Function m
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388 Chapter | 13 Hepatic Function s
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390 Chapter | 13 Hepatic Function f
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392 Chapter | 13 Hepatic Function T
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394 Chapter | 13 Hepatic Function 2
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396 Chapter | 13 Hepatic Function u
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398 Chapter | 13 Hepatic Function 2
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400 Chapter | 13 Hepatic Function c
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402 Chapter | 13 Hepatic Function F
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404 Chapter | 13 Hepatic Function A
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406 Chapter | 13 Hepatic Function E
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408 Chapter | 13 Hepatic Function K
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410 Chapter | 13 Hepatic Function R
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412 Chapter | 13 Hepatic Function W
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414 Chapter | 14 Gastrointestinal F
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Chapter 15 Skeletal Muscle Function
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II. Specialization of the Sarcolemm
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II. Specialization of the Sarcolemm
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III. Heterogeneity of Skeletal Musc
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III. Heterogeneity of Skeletal Musc
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V. Exercise and Adaptations to Trai
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VI. Diagnostic Laboratory Methods f
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VI. Diagnostic Laboratory Methods f
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IX. Selected Neuromuscular Disorder
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IX. Selected Neuromuscular Disorder
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References 479 and, recently, there
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References 481 Engel , A. G. ( 2004
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References 483 Paciello , O. , Maio
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Chapter 16 Kidney Function and Dama
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II. Kidney Morphology and Function
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II. Kidney Morphology and Function
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III. Tests of Kidney Function 491 (
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III. Tests of Kidney Function 493 T
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III. Tests of Kidney Function 495 B
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6 5 4 3 2 1 0 Dog Cat Equine Cattle
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III. Tests of Kidney Function 499 d
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IV. Tests of Kidney Damage 501 1000
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IV. Tests of Kidney Damage 503 and
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IV. Tests of Kidney Damage 505 Enzy
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V. Biochemical Changes in Kidney Di
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V. Biochemical Changes in Kidney Di
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References 511 were reported to occ
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References 513 Bovee , K. C. ( 1969
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References 515 Deguchi , E. , and A
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References 521 Kühl , S. , Mischke
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References 523 creatinine measureme
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Chapter 17 Fluid, Electrolyte, and
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532 Chapter | 17 Fluid, Electrolyte
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VIII. Clinicopathological Indicator
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References 555 plasma water, electr
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References 557 Krzywanek , H. ( 197
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References 559 Strombeck , D. R. (1
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562 Chapter | 18 Pituitary Function
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606 Chapter | 19 Adrenocortical Fun
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624 Chapter | 20 Thyroid Function a
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626 Chapter | 20 Thyroid Function t
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628 Chapter | 20 Thyroid Function A
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630 Chapter | 20 Thyroid Function S
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632 Chapter | 20 Thyroid Function a
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634 Chapter | 20 Thyroid Function O
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636 Chapter | 21 Clinical Reproduct
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664 Chapter | 22 Trace Minerals the
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666 Chapter | 22 Trace Minerals the
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668 Chapter | 22 Trace Minerals P i
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670 Chapter | 22 Trace Minerals be
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Copper Cuproreductase Cytochromes C
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674 Chapter | 22 Trace Minerals 2 .
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676 Chapter | 22 Trace Minerals Cor
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678 Chapter | 22 Trace Minerals inf
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680 Chapter | 22 Trace Minerals tis
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682 Chapter | 22 Trace Minerals VI
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684 Chapter | 22 Trace Minerals red
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686 Chapter | 22 Trace Minerals of
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692 Chapter | 22 Trace Minerals Liu
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Chapter 23 Vitamins Robert B. Rucke
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III. Fat-Soluble Vitamins 697 TABLE
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III. Fat-Soluble Vitamins 699 Carot
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III. Fat-Soluble Vitamins 701 Major
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III. Fat-Soluble Vitamins 703 doses
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III. Fat-Soluble Vitamins 705 Diet
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III. Fat-Soluble Vitamins 707 conta
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III. Fat-Soluble Vitamins 709 immun
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IV. Water-Soluble Vitamins 711 are
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IV. Water-Soluble Vitamins 713 abil
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IV. Water-Soluble Vitamins 715 5’
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IV. Water-Soluble Vitamins 717 H 2
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IV. Water-Soluble Vitamins 719 Enzy
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722 Chapter | 23 Vitamins When biot
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724 Chapter | 23 Vitamins Cyanocoba
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726 Chapter | 23 Vitamins V . VITAM
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728 Chapter | 23 Vitamins nature, r
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730 Chapter | 23 Vitamins Stites ,
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732 Chapter | 24 Lysosomal Storage
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Chapter 25 Tumor Markers Michael D.
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II. Serum Tumor Markers 753 also be
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III. Flow Cytometry 755 cancer of t
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V. Immunohistochemistry/Immunocytoc
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V. Immunohistochemistry/Immunocytoc
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References 761 analysis will facili
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References 763 Fernandez , N. J. ,
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References 765 Meinecke , B. , and
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References 767 Walter , J. ( 2000 )
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770 Chapter | 26 Cerebrospinal Flui
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Appendix VI Nomogram for Computing
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t0100 Appendix VIII Blood Analyte R
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884 Appendix | VIII Blood Analyte R
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890 Appendix | IX Blood Analyte Ref
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Appendix X Blood Analyte Reference
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Appendix XI Blood Analyte Reference
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Appendix XII Urine Analyte Referenc
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902 Appendix | XIII Cerebrospinal F
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904 Appendix | XIV Cerebrospinal Fl
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