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

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850 Chapter | 28 Avian Clinical Biochemistry VI . HEPATOBILIARY DISEASE A . Clinical Enzymology Clinical enzymology is described more fully in a separate chapter in this book, so only a brief synopsis is given here. Enzymes occur normally in the cytoplasm (e.g., aspartate aminotransferase [AST], alanine aminotransferase [ALT], lactic dehydrogenase [LDH]), mitochondria (glutamate dehydrogenase [GLDH] and AST), nucleus, or membranes (alkaline phosphatase [AP], gamma glutamyl transferase [GGT, γ GT]) of body cells, where they catalyze specific reactions. The distribution of various enzymes is markedly different among organs and animal species, which explains the variation in organ and tissue specificities among animal species. Generally, increased plasma enzyme concentrations indicate recent organ damage rather then decreased organ function. Increased enzyme production has been reported in cholestatic liver disease in mammals (AP and GGT). Sometimes a decreased activity is of diagnostic value (e.g., decreased cholinesterase activity in organophosphate toxicity). Baseline activity of an enzyme in plasma is generally a reflection of the amount and turnover of the tissue that contains this enzyme. For example, the creatine kinase (CK) activity in plasma increases in direct proportion to the increase of skeletal muscle mass as a result of training. Increases in CK may also be observed simply as a result of the muscle cellular damage associated with capture and restraint. Conversely, in chronic liver diseases with severe fibrosis and a reduction in the number of functional hepatocytes, plasma activities of liver enzymes may be within normal limits. The increase of a particular enzyme also depends on factors such as its rate of release, rate of production, and rate of clearance from plasma. Cytoplasmatic enzymes will be released early in cell degeneration, whereas mitochondrial enzymes will be released after advanced cell damage (necrosis). Enzymes with high tissue concentrations but with short elimination half-lives are of limited value in clinical enzymology because of their rapid disappearance from plasma. Generally, EDTA samples are not appropriate for enzyme assays, because this anticoagulant may chelate metal ions, which are required for maximal enzyme activity. Plasma and cells should be separated immediately after sampling to prevent leakage of intracellular enzymes into the plasma. Even if the cellular elements are separated from the plasma, freezing/thawing and refrigeration of plasma samples for several days may severely decrease enzyme activity and therefore should be avoided unless the effects of the storage procedure used is known. B . Enzyme Activities in Avian Tissues Enzyme profiles of the various organs have been studied in chickens, mallards, turkeys, racing pigeons, budgerigars and African grey parrots ( Lumeij 1994d ; Figs. 28-13 through 28-15 ). C . Clearance of Enzymes from Plasma The half-life of an enzyme is defined as the time required for its concentration to be reduced by half. When an enzyme is injected into plasma, its clearance from the plasma generally follows a biphasic exponential decline. Initially, there is a rapid decline, which is the primary mixing or distribution phase, followed by a slower secondary decline phase, which is the actual clearance of the enzyme from the plasma. During this secondary phase, a constant fraction of enzyme present is cleared per unit of time; hence, the decline is linear on a semilogarithmic scale. The (t½ β)half-life of the enzyme can be calculated from the regression function of the secondary linear phase of the semilogarithmic concentration-time curve and is independent of plasma enzyme activity. Clearance half-lives of various enzymes considered to be of use for the differential diagnosis of liver and muscle disease in pigeons have been established by studying the disappearance rates of enzymes from plasma after IV injections of supernatants of homologous liver and muscle homogenates ( Lumeij et al ., 1988a ). For AST, ALT, and LD, the half-lives of the respective enzymes from liver and muscle were compared, whereas for GLDH and CK, only liver and muscle were used, respectively ( Table 28-1 ). D . Experimentally Induced Liver and Muscle Disease Plasma enzyme profiles after experimentally or spontaneously occurring liver disease have been studied in a number of avian species. The results of studies in racing pigeons ( Lumeij et al ., 1988a, 1988b ) with two different types of liver disease were compared to plasma chemistry changes after muscle injury. Liver disease was induced by ethylene glycol or D-galactosamine, and muscle injury was induced by an intramuscular injection of doxycycline in three groups of six pigeons each. Plasma chemical changes were correlated with histological findings from organ samples taken just after the last blood collection ( Fig. 28-16 , Table 28-2 ). Plasma AST activity and bile acid (BA) concentration were the most sensitive indicators of liver disease in the racing pigeon, followed by ALT, GGT, and LD. Although all pigeons with histological proven ethylene glycol- or galactosamine-induced liver damage had increased AST activity and BA concentrations in their plasmas, these constituents were not raised at every sampling time. Increased plasma GLDH activities were associated with large necrotic areas in the liver. Moderate necrosis of liver cells resulted in slightly elevated GLDH activities. Degeneration
Racing pigeon ALAT (IU/g tissue) Racing pigeon -GT (IU/g tissue) H 0.7 0.2 H 0 L 11.2 1.2 L 0 Mp 5.8 1.2 Mp 0 Mq 1.1 0.3 Mq 0 D 0.8 0.2 D 0 K 10.4 0.7 K 2.3 0.3 B 2.0 0.2 B 0.2 0.02 Racing pigeon ASAT (IU/g tissue) Racing pigeon AP (IU/g tissue) H 89.3 13.7 H 0 L 69.9 2.6 L 0.4 0.1 Mp 64.9 9.7 Mp 0 Mq 23.5 2.3 Mq 0.25 0.04 D 14.4 1.6 D 11.0 2.4 K 111.0 5.0 K 54.2 8.6 B 40.2 1.9 B 1.4 0.4 Racing pigeon GLDH (IU/g tissue) Racing pigeon CK (IU/g tissue) H 1.7 0.8 H 552 51 L 25.2 6.9 L 8 1 Mp 0.2 0.1 Mp 1916 162 Mq 0.6 0.1 Mq 2900 430 D 2.1 0.4 D 244 26 K 31.0 5.0 K 99 13 B 35.0 2.6 B 433 35 Racing pigeon LD (IU/g tissue) 0 20 40 60 80 100 (%) H L Mp Mq D K B 181.3 10.6 125.5 4.9 114.8 17.7 84.7 13.4 35.8 5.1 215.0 41.5 149.5 12.0 H Heart L Liver Mp M.pectoralis Mq M. quadriceps femoris D Duodenum K Kidney B Brain 0 20 40 60 80 100 (%) FIGURE 28-13 Relative distribution of various tissue enzymes in supernatants of pigeon tissue homogenates. Mean SEM, U/g wet tissue, n 6. Reprinted with permission from Lumeij et al . (1988a).
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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 233 Pearson , W. , Boerm
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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 519 Harvey , D. G. ( 197
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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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688 Chapter | 22 Trace Minerals Per
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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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TABLE 26-7 Continued Constituent Ro
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Page 830 and 831: References 837 Solaiman , S. G. , M
Page 832 and 833: 840 Chapter | 28 Avian Clinical Bio
Page 844 and 845: Budgerigar ALAT (IU/g tissue) Budge
Page 866 and 867: 874 Appendix | I SI Units TABLE E S
Page 868 and 869: Appendix II Conversion Factors of S
Page 870 and 871: Appendix IV Stability of Serum Enzy
Page 872 and 873: Appendix VI Nomogram for Computing
Page 874 and 875: t0100 Appendix VIII Blood Analyte R
Page 876 and 877: 884 Appendix | VIII Blood Analyte R
Page 882 and 883: 890 Appendix | IX Blood Analyte Ref
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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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