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

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References 447 characterized by reduced blood pH and HCO 3 concentration and by a fall in urine pH from a normal alkaline value to as low as pH 5. Fluid accumulates in the rumen because of the increased osmolality of the rumen fluid. This accumulation of fluid into the rumen causes hemoconcentration, which in turn may lead to hypovolemic shock and death. If affected animals survive the initial period of rapid fermentation, chemical rumenitis induced by the hyperosmolality of the rumen fluid and by the excess lactic acid may develop. Secondary mycotic rumenitis may then follow, which in severe cases can be fatal. In surviving cattle, metastatic hepatic abscesses may also occur. B . Acute Rumen Tympany (Bloat) The rumen of mature cattle can produce 1.2 to 2 liters of gas per minute ( Hungate et al., 1955, 1961 ). The gas is the product of rumen fermentation and is composed primarily of carbon dioxide (CO 2 ) and methane. CO 2 is also released when salivary HCO 3 comes in contact with the organic acids in the rumen. Under normal conditions, these large amounts of gas are continually removed by eructation. Any factor that interferes with eructation can produce acute tympany of the rumen (bloat) leading to rapid death. Interruption of the normal eructation reflex or mechanical obstruction of the esophagus typically results in free gas bloat. The most important form of bloat, however, is seen in cattle consuming large quantities of legumes or in feedlot cattle on high-concentrate diets. The primary factor in these more common forms of bloat is a change in the ruminal contents to a foamy or frothy character because of altered surface tension. Gas becomes trapped in small bubbles within the rumen and cannot be eliminated by eructation ( Clarke and Reid, 1974 ). The chemical changes that cause foam to form within the rumen are not fully understood. Some reports ( Nichols, 1966 ; Nichols and Deese, 1966 ) suggest that plant pectin and pectin methyl esterase, a plant enzyme, are critical factors. The enzyme acts on pectin to release pectic and galacturonic acids, which greatly increase the viscosity of the rumen fluid, resulting in formation of a highly stable foam. A soluble legume protein fraction with ribulose diphosphate carboxylase activity has been suggested as another important dietary factor in the pathogenesis of bloat ( Howarth, 1975 ). Slime-producing bacteria also have been incriminated in the pathogenesis of frothy bloat. These microorganisms produce an extracellular polysaccharide that results in stable foam formation. Effective medical treatment and control are directed toward decreasing or preventing foam formation. This has been accomplished with certain nonionic detergents with surfactant properties that break up or prevent formation of foam within the rumen ( Bartley, 1965 ). Another approach has been the prophylactic administration of sodium alkyl sulfonate, which inhibits pectin methyl esterase activity and prevents foam formation by eliminating the products of this enzyme reaction ( Nichols, 1963 ). Antifoaming agents such as poloxalene administered before ingestion of bloat-producing diets have been shown to be effective prophylactically ( Howarth, 1975 ). Silicone antifoaming agents also have been used for this purpose (Clark and Reid, 1974). Genetic selection of cattle that are less susceptible to rumen tympany has also been pursued ( Howarth, 1975 ). C . Urea Poisoning Unlike monogastric animals, ruminants, via their microbial flora, can effectively use nonprotein nitrogen (NPN) to meet some of their dietary protein requirements. Urea, biuret ( Oltjen et al., 1969 ), and ammonium salts ( Webb et al., 1972 ) can serve as dietary NPN sources. Urea, which is the most frequently used, is hydrolyzed by ruminal bacterial urease into CO 2 and NH 3 . The free NH 3 is incorporated into amino acids and protein by the rumen microorganisms. The bacterial protein is digested and absorbed in the abomasum and small intestine along with dietary protein. Signs of urea poisoning typically develop within minutes after consumption of food containing toxic amounts of urea. Clinical manifestations reflect the encephalotoxic effects of excess absorbed NH 3 ( Word et al., 1969 ). Tolerance to urea may be significantly increased by increasing the amount of urea in the diet gradually or by adding readily fermentable carbohydrate to the diet. Ruminants can actually adapt and thrive on a diet in which urea is the sole source of dietary nitrogen. However, if urea is fed at more than 3% in the diet in unadapted animals, toxic effects are likely to occur. Urea poisoning may occur accidentally when animals engorge on large amounts of urea-containing dietary supplement, when there has been an error in formulation of bulk feed, or when the urea-containing additive is incompletely mixed. Oral administration of acetic acid has been shown to reduce acute urea toxicity, apparently by decreasing absorption of free NH 3 from the rumen. Normally, NH 3 is in equilibrium: NH H → NH 3 4 with only 1% in the free form. Acidification shifts the equilibrium farther to the right, thereby reducing the amount of the NH 3 . Because only the free form crosses cell membranes, the net effect is a reduction of absorption of NH 3 by the cell. Acetic acid is used as a treatment for urea poisoning, but it is of more value as a prophylactic agent ( Word et al., 1969 ). REFERENCES Aclund , H. M. , Gunson , D. E. , and Gillette , D. M. ( 1983 ). Ulcerative duodenitis in foals . Vet. Pathol. 20 , 653 – 661 .
448 Chapter | 14 Gastrointestinal Function Alpers , D. H. ( 1969 ). Separation and isolation of rat and human intestinal beta-galactosidases . J. Biol. Chem. 244 , 1238 – 1246 . Alpers , D. H. , and Isselbacher , K. J. ( 1967 ). Protein synthesis by rat intestinal mucosa: the role of ribonuclease . J. Biol. Chem. 242 , 5617 – 5622 . Altamirano , M. ( 1963 ). Alkaline secretion produced by intra-arterial acetylcholine . J. Physiol. 168 , 787 – 803 . Alvarado , F. (1966a ). D-xylose active transport in the hamster small intestine . Biochim. Biophys. Acta 112 , 292 – 306 . Alvarado , F. (1966b ). Transport of sugars and amino acids in the intestine: evidence for a common carrier . Science 151 , 1010 – 1013 . Alvarado , F. , and Crane , R. K. ( 1962 ). Phlorizin as a competitive inhibitor of the active transport of sugars by hamster small intestine, in vitro . Biochim. Biophys. Acta 56 , 170 – 172 . Anderson , N. V. (1975). In
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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 231 Martinovich , D. , a
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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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390 Chapter | 13 Hepatic Function f
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394 Chapter | 13 Hepatic Function 2
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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 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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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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678 Chapter | 22 Trace Minerals inf
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684 Chapter | 22 Trace Minerals red
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686 Chapter | 22 Trace Minerals of
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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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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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III. Flow Cytometry 755 cancer of t
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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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Chapter 27 Clinical Biochemistry in
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II. Hepatotoxicity 823 Therefore, A
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III. Nephrotoxicity 825 suggested a
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IV. Toxins Affecting Skeletal and C
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IX. Toxins Affecting the Nervous Sy
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References 835 Plants classified as
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References 837 Solaiman , S. G. , M
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840 Chapter | 28 Avian Clinical Bio
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Budgerigar ALAT (IU/g tissue) Budge
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874 Appendix | I SI Units TABLE E S
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Appendix II Conversion Factors of S
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Appendix IV Stability of Serum Enzy
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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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