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

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Chapter 14 Gastrointestinal Function William E. Hornbuckle Department of Clinical Sciences New York State College of Veterinary Medicine Cornell University Ithaca, New York Kenneth W. Simpson Department of Clinical Sciences New York State College of Veterinary Medicine Cornell University Ithaca, New York Bud C. Tennant Department of Clinical Sciences New York State College of Veterinary Medicine Cornell University Ithaca, New York I. INTRODUCTION II. SALIVARY SECRETIONS A. Mechanisms of Secretion B. Composition of Saliva C. Functions of Saliva III. GASTRIC SECRETIONS A. Composition of Gastric Secretions B. Control of Gastric Se cretion IV. BILIARY SECRETIONS A. Composition of Bile B. Properties of Bile C. Synthesis of Bile Acids D. Enterohepatic Circulation of Bile Acids V. EXOCRINE PANCREATIC SECRETIONS A. Composition of Pancreatic Juice B. Control of Pancreatic Secretions VI. OTHER GASTROINTESTINAL HORMONES A. Motilin B. Somatostatin C. Enteroglucagon VII. DIGESTION AND ABSORPTION A. Water and Electrolytes B. Carbohydrate Digestion and Absorption C. Proteins D. Lipids E. Cobalamin VIII. DISTURBANCES OF GASTROINTESTINAL FUNCTION A. Vomition B. Gastric Dilatation-Volvulus C. Ischemia-Reperfusion Injury D. Acute Diarrheas E. Malabsorption F. Tests of Malabsorption G. Bacterial Overgrowth H. Helicobacteria I. Intestinal Permeability J. Protein-Losing Enteropathy K. Ulcerative Colitis L. Equine Hyperammonemia M. Clostridial-Associated Diseases in Horses and Cows IX. DISTURBANCES OF RUMEN FUNCTION A. Acute Rumen Indigestion (Rumen Overload, Lactic Acidosis) B. Acute Rumen Tympany (Bloat) C. Urea Poisoning REFERENCES I . INTRODUCTION The digestive system is composed of the gastrointestinal (GI) tract or the alimentary canal, salivary glands, the liver, and the exocrine pancreas. The principal functions of the gastrointestinal tract are to digest and absorb ingested nutrients and to excrete waste products of digestion. Most nutrients are ingested in a form that is either too complex for absorption or insoluble and therefore indigestible or incapable of being digested. Within the GI tract, much of these substances are solubilized and further degraded enzymatically to simple molecules, sufficiently small in size and in a form that permits absorption across the mucosal epithelium. This chapter describes the normal biochemical processes of intestinal secretion, digestion, and absorption. Once these issues have been put in perspective, the chapter explores the pathogenesis of the important gastrointestinal diseases of domestic animals and the biochemical basis for their diagnosis and treatment. II . SALIVARY SECRETIONS A . Mechanisms of Secretion Saliva is produced by three major pairs of salivary glands and by small glands distributed throughout the buccal mucosa and submucosa. Two types of secretory cells are found in the acinar portions of the salivary glands: (1) the mucous cells, which contain droplets of mucus, and (2) the serous cells, which contain multiple secretory granules. Clinical Biochemistry of Domestic Animals, 6th Edition 413 Copyright © 2008, Elsevier Inc. All rights reserved.
414 Chapter | 14 Gastrointestinal Function In those species that produce salivary amylase (e.g., pig and human), the secretory granules are the zymogen precursors of this enzyme. A third cell type is found lining the striated ducts. The striations along the basal borders of these cells are caused by vertical infoldings of the cell membrane, a characteristic of epithelial cells involved in rapid movement of water and electrolytes. The primary secretion of the acinar cells is modified by active transport processes of the ductal epithelium. The distribution of the different types of secretory cells in the salivary glands varies among species. The parotid glands of most animals are serous glands, which produce a secretion of low-specific gravity and osmolality containing electrolytes and proteins including certain hydrolytic enzymes. The mandibular (submaxillary) and sublingual glands are mixed salivary glands that contain both mucous and serous types of cells and produce a more viscous secretion that contains large amounts of mucus ( Dukes, 1955 ). B . Composition of Saliva 1 . Mucus Mucus is an aqueous mixture of proteoglycans and glycoproteins. One of the most completely studied glycoproteins is mucin. Salivary mucins are O-glycosylated and consist of peptides with many oligosaccharides linked covalently to the hydroxyamino acid serine or threonine. The carbohydrate portion of submaxillary mucin from sheep is a disaccharide of N-acetylneuraminic acid (sialic acid) and N-acetylgalactosamine ( Carlson et al., 1973 ). The enzymes that link protein with hexosamine have been purified from the mandibular glands of sheep ( Carlson et al., 1973 ) and swine ( Schachter et al., 1971 ). The physiological functions of mucin are related to its high viscosity. N-acetylneuraminic acid is the component responsible for the formation of viscous aqueous solutions and, at physiological pH, causes expansion and stiffening of the mucin molecule. The resistance of mucin to enzymatic breakdown is also due to the presence of disaccharide residues. Removal of terminal N-acetylneuraminic acid residues by action of neuraminidase significantly increases the susceptibility of peptide bonds to trypsin. 2 . Electrolytes The principal inorganic constituents of saliva are sodium, potassium, chloride, and bicarbonate, which, with the exception of bicarbonate, originate directly from the plasma. Rates of salivary flow vary depending on stimulation, and there are wide variations in electrolyte concentration. Saliva is formed by a process that initially requires uptake of sodium and other electrolytes from the interstitium of the terminal structural unit of the salivary gland, the acinus or end piece. Water flows passively. This primary or precursor fluid has a sodium concentration similar to plasma, and the potassium concentration is similar to or slightly higher than plasma. As the primary fluid passes from the acinus along the duct system, the concentration of sodium, potassium, and other electrolytes changes. In most species, there is net sodium absorption and potassium secretion. Wide variations in electrolyte composition may occur depending on the flow rate ( Young and Schneyer, 1981 ), the salivary gland of origin, and the species ( Table 14-1 ). 3 . Amylase The saliva of rodents contains the α -amylase, ptyalin, but this enzyme activity is absent in the saliva of dogs, cats, horses, cattle, and sheep ( Dukes, 1955 ; Young and Schneyer, 1981 ). Salivary amylase splits the α 1,4-glucosidic bonds of various polysaccharides. Salivary amylase is similar in major respects to pancreatic α -amylase, which is described in Section V.B. Salivary amylase initiates digestion of starch and glycogen in the mouths of those species that secrete the enzyme. The optimal pH for amylase activity is approximately 7, so that this activity ceases when the enzyme mixes with acidic gastric contents. TABLE 14-1 Electrolyte Concentration of Mandibular Gland and Parotid Gland Saliva Observed during Maximum Rates of Secretion (mmol/l) Mandibular Gland Parotid Gland Na K HCO 3 Na K HCO 3 Sheep 20 7 23 160–175 9–10 113–140 Dog 70–100 12–15 10–30 80–110 6–14 50 Cat 40–51 9–10 26 — — — Rabbit 50–100 10–40 25 110–140 10 12–30
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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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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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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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III. Heterogeneity of Skeletal Musc
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References 479 and, recently, there
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References 481 Engel , A. G. ( 2004
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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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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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References 555 plasma water, electr
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562 Chapter | 18 Pituitary Function
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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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IV. Water-Soluble Vitamins 719 Enzy
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722 Chapter | 23 Vitamins When biot
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732 Chapter | 24 Lysosomal Storage
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Chapter 25 Tumor Markers Michael D.
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References 761 analysis will facili
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References 763 Fernandez , N. J. ,
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References 767 Walter , J. ( 2000 )
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770 Chapter | 26 Cerebrospinal Flui
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II. Hepatotoxicity 823 Therefore, A
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IV. Toxins Affecting Skeletal and C
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References 835 Plants classified as
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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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