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Book Details
Abstract
Understanding the normal functions of the body is essential for successful veterinary practice and for understanding the mechanisms of disease. The 5th edition of Textbook of Veterinary Physiology approaches this vast subject in a practical, user-friendly way that helps you understand how key concepts relate to clinical practice. From cell physiology to body system function to homeostasis and immune function, this comprehensive text gives you the solid foundation you need to provide effective veterinary care.
- Clinical Correlations boxes present case studies that illustrate how to apply physiology principles and concepts to the diagnosis and treatment of veterinary patients.
- Key Points at the beginning of each chapter introduce new concepts and help you prepare for exams.
- Practice questions at the end of each chapter test your understanding of what you’ve just read and provide valuable review for exams.
- Full-color format highlights helpful information and enhances learning with a wealth of illustrations that visually depict specific functions and conditions.
- Expanded resources on the companion Evolve website include state-of-the-art 3D animations, practice questions, a glossary, and additional Clinical Correlations not found in the text.
Table of Contents
| Section Title | Page | Action | Price |
|---|---|---|---|
| Front cover | cover | ||
| Endsheets 2-3 | FM1 | ||
| Evolve page | FM3 | ||
| Cunningham's Textbook of Veterinary Physiology | i | ||
| Copyright page | iv | ||
| Dedication | v | ||
| Contributors | vi | ||
| Preface | ix | ||
| Table of Contents | xi | ||
| Section I The Cell | 1 | ||
| Chapter 1 The Molecular and Cellular Bases of Physiological Regulation | 1 | ||
| Key Points | 1 | ||
| All Physiological Change Is Mediated by Proteins | 1 | ||
| Protein Function Depends on Protein Shape and Shape Changes | 2 | ||
| A Series of Enzymatic Reactions Converts Tyrosine into the Signaling Molecules Dopamine, Norepinephrine, and Epinephrine | 3 | ||
| Muscle Contraction and its Initiation and Cessation Depend on the Binding Specificity and Allosteric Properties of Proteins | 4 | ||
| Biological Membranes Are a Mosaic of Proteins Embedded in a Phospholipid Bilayer | 5 | ||
| Transport | 7 | ||
| Only Small, Uncharged Molecules and Oily Molecules Can Penetrate Biomembranes Without the Aid of Proteins | 7 | ||
| Molecules Move Spontaneously from Regions of High Free Energy to Regions of Lower Free Energy | 7 | ||
| Important Transport Equations Summarize the Contributions of the Various Driving Forces | 8 | ||
| Starling’s Hypothesis Relates Fluid Flow Across the Capillaries to Hydrostatic Pressure and Osmotic Pressure | 9 | ||
| Membrane Proteins that Serve the Triple Functions of Selective Transport, Catalysis, and Coupling Can Pump Ions and Molecules to Regions of Higher Free Energy | 9 | ||
| Many Membrane Proteins Selectively Facilitate the Transport of Ions/Molecules from High to Low Electrochemical Potential | 11 | ||
| Passive Transport of K+ Across the Plasma Membrane Creates an Electrical Potential | 12 | ||
| Spatial Organization of Active and Passive Transport Proteins Enables Material to Pass Completely Through the Cell | 13 | ||
| Membrane Fusion Allows for a Combination of Compartmentalization and Transport of Material | 14 | ||
| Information Transmission and Transduction | 15 | ||
| Cell Signaling Usually Occurs by a Lengthy Chain of Sequential Molecular Interactions | 15 | ||
| Signaling Pathways Begin with the Binding of an Extracellular Molecule to a Receptor | 16 | ||
| Specific Physiological Information Is Inherent in the Receptor/Ligand Complex, Not in the Hormone/Neurotransmitter Molecule | 16 | ||
| G-Protein–Coupled Receptors Are the Largest Family (a Superfamily) of Receptors and Help Regulate Almost All Physiological Processes | 16 | ||
| Most G-Protein–Linked Information Is Sent to the Cytoplasm by Second Messengers | 19 | ||
| Ca2+ Transport Across Plasma and Intracellular Membranes Is an Important Second Messenger | 19 | ||
| Cyclic Amp Is Produced by Activation of a Membrane-Bound Enzyme in Response to Hormone/Neurotransmitter Binding to Receptors | 20 | ||
| The Receptor-Mediated Hydrolysis of a Rare Phospholipid of the Plasma Membrane Produces Two Different Second Messengers with Different Actions | 23 | ||
| Steroid Hormones and Other Lipid Signals Interact with Nuclear Receptors, Which Are Transcription Factors Within the Cell | 24 | ||
| Clinical Correlations | 25 | ||
| Peripheral Edema | 25 | ||
| History. | 25 | ||
| Clinical Examination. | 26 | ||
| Comment. | 26 | ||
| Treatment. | 26 | ||
| Practice Questions | 26 | ||
| Bibliography | 26 | ||
| Chapter 2 Cancer: | 27 | ||
| Key Points | 27 | ||
| Cancer Arises from Genetic Dysfunction in the Regulation of the Cell Cycle, Cell Life Span, and Cell Suicide | 28 | ||
| Control of the Cell Cycle (Proliferation) | 29 | ||
| Cell Division Is the Result of a Clocklike Cell Cycle | 29 | ||
| Cyclin-Dependent Kinases Are the “Engines” Driving the Cell Cycle | 29 | ||
| The CDK “Engines” Are Controlled by Both Throttle (Oncogene) and Brake (Tumor Suppressor) Controls | 30 | ||
| Growth Factor Pathway: Stimulator of Cell Proliferation | 31 | ||
| The Cell Cycle Is Stimulated by Growth Factors that Bind to and Activate Receptor Tyrosine Kinases | 31 | ||
| The Ras Oncogene Contributes to Many Cancers and Serves as a Model for Understanding Small G Proteins | 32 | ||
| The MAP Kinase Pathway Leads to the Expression of Cyclins and Other Stimulators of the Cell Cycle | 33 | ||
| The MAP Kinase Pathway also Mediates the Stimulation of the Cell Cycle by Cell Adhesion | 33 | ||
| Tumor Suppressors: Inhibitors of Cell Cycle | 34 | ||
| Checkpoints in the Cell Cycle Are Manned by Tumor Suppressors | 34 | ||
| The Retinoblastoma and P53 Proteins Are the Main Gatekeepers for the Cell Cycle | 35 | ||
| Mechanisms Regulating Cell Suicide and Cell Life Span | 37 | ||
| Apoptosis Is the Process of Cell Suicide | 37 | ||
| Resistance to Apoptosis Via the Intrinsic Pathway Is a Hallmark of Cancer | 38 | ||
| Cellular Life Span Is Determined by Dna Sequences at the Ends of Chromosomes | 39 | ||
| Tumor Origin and the Spread of Cancer | 40 | ||
| Cancer Cells May Be Related to Stem Cells | 40 | ||
| Death by Cancer Is Usually the Result of Its Spread, Not the Original Tumor | 41 | ||
| Growth of Solid Tumors Depends on Development of New Blood Vessels | 43 | ||
| Prospective Cancer Therapy | 44 | ||
| Cancer Therapy Has a Hopeful but Challenging Future | 44 | ||
| Clinical Correlations | 45 | ||
| Dog That Collapsed While Running | 45 | ||
| History. | 45 | ||
| Clinical Examination. | 45 | ||
| Comment. | 46 | ||
| Treatment. | 46 | ||
| Practice Questions | 46 | ||
| Vocabulary | 46 | ||
| Bibliography | 47 | ||
| Section II Neurophysiology | 48 | ||
| Chapter 3 Introduction to the Nervous System | 48 | ||
| Key Points | 48 | ||
| The Neuron Is the Major Functional Unit of the Nervous System | 48 | ||
| The Mammalian Nervous System Has Two Major Subdivisions: the Central Nervous System and the Peripheral Nervous System | 48 | ||
| The Central Nervous System Can Be Divided Into Six Anatomical Regions | 49 | ||
| The Central Nervous System Is Protected By the Meninges and Cerebrospinal Fluid | 51 | ||
| The Nervous System Collects and Integrates Sensory Information, Formulates a Response Plan, and Produces a Motor Output | 51 | ||
| Clinical Correlations | 52 | ||
| Neurological Disease in a Horse | 52 | ||
| History. | 52 | ||
| Clinical Examination. | 52 | ||
| Comment. | 52 | ||
| Treatment. | 52 | ||
| Practice Questions | 52 | ||
| Bibliography | 52 | ||
| Chapter 4 The Neuron | 53 | ||
| Key Points | 53 | ||
| Neurons Have Four Distinct Anatomical Regions | 53 | ||
| Neuronal Membranes Contain a Resting Electrical Membrane Potential | 54 | ||
| The Resting Membrane Potential Is the Result of Three Major Determinants | 54 | ||
| The Resting Membrane Potential Can Be Changed By Synaptic Signals from a Presynaptic Cell | 56 | ||
| Action Potentials Begin at the Axon’s Initial Segment and Spread Down the Entire Length of the Axon | 57 | ||
| Clinical Correlations | 58 | ||
| Hypoglycemia | 58 | ||
| History. | 58 | ||
| Clinical Examination. | 58 | ||
| Comment. | 58 | ||
| Section III Cardiovascular Physiology | 158 | ||
| Chapter 18 Overview of Cardiovascular Function | 158 | ||
| Key Points | 158 | ||
| Because Normal Cardiovascular Function Is Essential for Life and Health, a Practical Understanding of Cardiovascular Function and Dysfunction Is Vital to the Veterinary Clinician | 158 | ||
| Cardiovascular Dysfunctions Sometimes Reflect Primary Cardiovascular Disturbances or Diseases, But More Often They Are Secondary Consequences of Noncardiovascular Disturbances or Diseases | 159 | ||
| Substances Transported by the Cardiovascular System Include Nutrients, Waste Products, Hormones, Electrolytes, and Water | 159 | ||
| Two Modes of Transport Are Used in the Cardiovascular System: Bulk Flow and Diffusion | 160 | ||
| Because Diffusion Is Very Slow, Every Metabolically Active Cell in the Body Must Be Close to a Capillary Carrying Blood by Bulk Flow | 160 | ||
| The Pulmonary and Systemic Circulations Are Arranged In Series, But the Various Organs Within the Systemic Circulation Are Arranged in Parallel | 162 | ||
| Cardiac Output Is the Volume of Blood Pumped Each Minute by One Ventricle | 163 | ||
| The Perfusion Pressure for the Systemic Circulation Is Much Greater Than the Perfusion Pressure for the Pulmonary Circulation | 163 | ||
| Each Type of Blood Vessel Has Physical Properties Suited to Its Particular Function | 164 | ||
| Blood Is a Suspension of Cells in Extracellular Fluid (Plasma) | 165 | ||
| The Cellular Component of Blood Includes Red Blood Cells, White Blood Cells, and Platelets | 166 | ||
| Most of the Oxygen in Blood Is Carried in Chemical Combination with the Protein Hemoglobin Within Red Blood Cells | 167 | ||
| Clinical Correlations | 168 | ||
| Lethargic Kid Goat | 168 | ||
| History. | 168 | ||
| Clinical Examination. | 168 | ||
| Section IV Physiology of the Gastrointestinal Tract | 263 | ||
| Chapter 27 Regulation of the Gastrointestinal Functions | 263 | ||
| Key Points | 263 | ||
| The Gastrointestinal Tract, or Gut, Supplies the Body with Nutrients, Electrolytes, and Water by Performing Five Functions: Motility, Secretion, Digestion, Absorption, and Storage | 263 | ||
| Intrinsic and Extrinsic Control Systems Regulate Various Functions of the Gut | 263 | ||
| The Intrinsic Neuronal Control System of the Gastrointestinal Tract Is the Enteric Nervous System | 265 | ||
| The Intrinsic Hormonal Control System of the Gut Consists of Five Hormones Including Secretin, Gastrin, Cholecystokinin, Gastric Inhibitory Polypeptide, and Motilin | 268 | ||
| Secretin | 269 | ||
| Gastrin | 269 | ||
| Cholecystokinin | 270 | ||
| Gastric Inhibitory Polypeptide | 270 | ||
| Motilin | 270 | ||
| The Immune System of the Gut Is Extensive and Interacts with the Gastrointestinal Regulatory Systems to Control the Various Functions of the Gut | 270 | ||
| The Extrinsic Neuronal Control System of the Gut Is Comprised of Two Nerves: the Vagus and the Splanchnic | 270 | ||
| The Vagus Nerve | 270 | ||
| The Splanchnic Nerve | 271 | ||
| The Extrinsic Hormonal Control System of the Gut Is Limited to One Hormone: Aldosterone | 271 | ||
| Aldosterone | 271 | ||
| Acknowledgment | 271 | ||
| Practice Questions | 272 | ||
| Bibliography | 273 | ||
| Chapter 28 Motility Patterns of the Gastrointestinal Tract | 274 | ||
| Key Points | 274 | ||
| Slow Waves of Electrical Depolarization Are a Unique Feature of Gut Smooth Muscle | 274 | ||
| When Slow Waves Reach Sensitized Smooth Muscle Cells, Action Potentials and Contraction Result | 275 | ||
| Coordinated Motility Enables the Lips, Tongue, Mouth, and Pharynx to Grasp Food and Propel It Down the Gastrointestinal Tract | 276 | ||
| Motility of the Esophagus Propels Food from the Pharynx to the Stomach | 277 | ||
| The Function of the Stomach Is to Process Food into a Fluid Consistency and Release It into the Intestine at a Controlled Rate | 278 | ||
| The Proximal Stomach Stores Food Awaiting Further Gastric Processing in the Distal Stomach | 278 | ||
| The Distal Stomach Grinds and Sifts Food Entering the Small Intestine | 278 | ||
| Control of Gastric Motility Differs in the Proximal and Distal Stomach | 279 | ||
| The Rate of Gastric Emptying Must Match the Small Intestine’s Rate of Digestion and Absorption | 279 | ||
| Between Meals, the Stomach Is Cleared of Indigestible Material | 280 | ||
| Vomiting Is a Complex Reflex Coordinated from the Brainstem | 280 | ||
| Motility of the Small Intestine Has Digestive and Interdigestive Phases | 281 | ||
| The Ileocecal Sphincter Prevents Movement of Colon Contents Back into the Ileum | 281 | ||
| Motility of the Colon Causes Mixing, Retropulsion, and Propulsion of Ingesta | 281 | ||
| The Colon Is an Important Site of Storage and Absorption in All Animals | 282 | ||
| Despite Large Anatomical Differences in the Colons of Herbivores Compared to Omnivores and Carnivores, There Are Similarities in Motility | 283 | ||
| The Anal Sphincter Has Two Layers with Separate Innervation | 283 | ||
| The Rectosphincteric Reflex Is Important in Defecation | 283 | ||
| Major Differences Between Avian and Mammalian Digestive Systems Include, in Birds, Both the Lack of Teeth and the Separation of Gastric Functions into Distinct Anatomical Regions | 284 | ||
| Clinical Correlations | 285 | ||
| Equine Rabies | 285 | ||
| History. | 285 | ||
| Clinical Examination. | 285 | ||
| Comment. | 285 | ||
| Treatment. | 285 | ||
| Practice Questions | 285 | ||
| Bibliography | 286 | ||
| Chapter 29 Secretions of the Gastrointestinal Tract | 288 | ||
| Key Points | 288 | ||
| The Salivary Glands | 288 | ||
| Saliva Moistens, Lubricates, and Partially Digests Food | 288 | ||
| Salivary Secretions Originate in the Gland Acini and Are Modified in the Collecting Ducts | 288 | ||
| Salivary Glands Are Regulated by the Parasympathetic Nervous System | 289 | ||
| Ruminant Saliva Is a Bicarbonate-Phosphate Buffer Secreted in Large Quantities | 289 | ||
| Gastric Secretion | 289 | ||
| Depending on the Species, There May Be Two General Types of Gastric Mucosa: Glandular and Nonglandular | 289 | ||
| The Gastric Mucosa Contains Many Different Cell Types | 290 | ||
| The Gastric Glands Secrete Hydrochloric Acid | 290 | ||
| Pepsin Is Secreted by Gastric Chief Cells in an Inactive Form and Is Subsequently Activated in the Stomach Lumen | 291 | ||
| The Parietal Cells Are Stimulated to Secrete by the Action of Acetylcholine, Gastrin, and Histamine | 291 | ||
| The Pancreas | 291 | ||
| Pancreatic Exocrine Secretions Are Indispensable for the Digestion of the Complex Nutrients: Proteins, Starches, and Triglycerides | 291 | ||
| Acinar Cells Secrete Enzymes, Whereas Centroacinar Cells and Duct Cells Secrete an Electrolyte Solution Rich in Sodium Bicarbonate | 291 | ||
| Pancreatic Cells Have Cell Surface Receptors Stimulated by Acetylcholine, Cholecystokinin, and Secretin | 292 | ||
| Bile Secretion | 292 | ||
| The Liver Is an Acinar Gland with Small Acinar Lumina Known as Canaliculi | 292 | ||
| Bile Contains Phospholipids and Cholesterol Maintained in Aqueous Solution by the Detergent Action of Bile Acids | 293 | ||
| The Gallbladder Stores and Concentrates Bile During the Periods Between Feeding | 294 | ||
| Bile Secretion Is Initiated by the Presence of Food in the Duodenum and Stimulated by the Return of Bile Acids to the Liver | 294 | ||
| Clinical Correlations | 294 | ||
| Horse in Pain with Weight Loss | 294 | ||
| History. | 294 | ||
| Clinical Examination. | 294 | ||
| Comment. | 294 | ||
| Section V Endocrinology | 359 | ||
| Chapter 33 The Endocrine System | 359 | ||
| Key Points | 359 | ||
| General Concepts | 359 | ||
| Hormones Are Chemicals Produced by Specific Tissues That Are Transported by the Vascular System to Affect Other Tissues at Low Concentrations | 359 | ||
| The Endocrine and Nervous Systems Are Integrated in Their Control of Physiological Processes | 360 | ||
| Synthesis of Hormones | 360 | ||
| Protein Hormones Are Initially Synthesized as Preprohormones and Then Cleaved in the Rough Endoplasmic Reticulum to Form Prohormones and in the Golgi Apparatus to Form the Active Hormones, Which Are Stored in Granules Before Being Released by Exocytosis | 360 | ||
| Steroids Are Synthesized from Cholesterol, Which Is Synthesized by the Liver; Steroids Are Not Stored but Are Released as They Are Synthesized | 361 | ||
| Transport of Hormones in the Blood | 361 | ||
| Protein Hormones Are Hydrophilic and Carried in the Plasma in Dissolved Form | 361 | ||
| Steroids and Thyroid Hormones Are Lipophilic and Carried in Plasma in Association with Both Specific and Nonspecific Binding Proteins; the Amount of Unbound, Active Hormone Is Relatively Small | 363 | ||
| Hormone-Cell Interaction | 363 | ||
| Protein Hormones Have Specific Receptors on Target Tissue Plasma Membranes, Whereas Steroids Have Specific Receptors Within the Cytoplasm or Nucleus | 363 | ||
| Postreceptor Cell Responses | 363 | ||
| Steroids Interact Directly with the Cell Nucleus Through the Formation of a Complex with Its Cytosolic Receptor, Whereas Protein Hormones Need a Messenger Because They Cannot Enter the Cell | 363 | ||
| Metabolism of Hormones | 365 | ||
| Steroid Hormones Are Metabolized by Conjugation with Sulfates and Glucuronides, Which Makes Steroids Water Soluble | 365 | ||
| Feedback Control Mechanisms | 365 | ||
| The Most Important Feedback Control for Hormones Is the Negative-Feedback System, in Which Increased Hormone Concentrations Result in Less Production of the Hormone, Usually Through an Interaction with the Hypothalamus or Pituitary Gland | 365 | ||
| Endocrine Secretory Patterns Can Be Influenced by Factors Such as Sleep or Light and Can Produce Circadian Rhythms | 366 | ||
| The Hypothalamus | 366 | ||
| The Hypothalamus Coordinates the Activity of the Pituitary Gland Through the Secretion of Peptides and Amines | 366 | ||
| The Pituitary Gland | 366 | ||
| The Neurohypophysis Has Cell Bodies That Originate in the Hypothalamus, with Cell Endings That Secrete Oxytocin and Vasopressin | 366 | ||
| Oxytocin and Vasopressin Are Synthesized in Cell Bodies Within the Hypothalamus and Are Carried by Axon Flow to the Posterior Lobe, Where They Are Released | 367 | ||
| The Main Effects of Oxytocin Are on the Contraction of Smooth Muscle (Mammary Gland and Uterus); the Effects of Vasopressin Are Primarily on the Conservation of Water (Antidiuresis) and Secondarily on Blood Pressure | 367 | ||
| Plasma Osmolality Controls the Secretion of Vasopressin | 367 | ||
| The Anterior Pituitary Produces Growth Hormone, Prolactin, Thyroid-Stimulating Hormone, Follicle-Stimulating Hormone, Luteinizing Hormone, and Corticotropin | 369 | ||
| Adenohypophyseal Activity Is Controlled by Hypothalamic Releasing Hormones, Which Are Released into the Portal System, Which in Turn Connects the Median Eminence of the Hypothalamus and the Anterior Pituitary Gland | 370 | ||
| Clinical Correlations | 372 | ||
| Equine Cushing’s Disease | 372 | ||
| History. | 372 | ||
| Clinical Examination. | 372 | ||
| Comment. | 372 | ||
| Section VI Reproduction and Lactation | 408 | ||
| Chapter 35 Control of Gonadal and Gamete Development | 408 | ||
| Key Points | 408 | ||
| Development of the Reproductive System | 408 | ||
| Organization of the Gonads Is Under Genetic Control (Genetic Sexual Differentiation) | 408 | ||
| Sexual Orientation of the Genitalia and Brain Depends on the Presence or Absence of Testosterone | 408 | ||
| Hypothalamopituitary Control of Reproduction | 410 | ||
| The Hypothalamus and Anterior Pituitary (Adenohypophysis) Secrete Protein and Peptide Hormones, Which Control Gonadal Activity | 410 | ||
| The Adenohypophysis (Pars Distalis) Produces Follicle-Stimulating Hormone, Luteinizing Hormone, and Prolactin, All of Which Control Reproductive Processes | 410 | ||
| Modification of Gonadotropin Release | 411 | ||
| The Pulsatile Release of Gonadotropin Releasing Hormone (GnRH) Induces the Critical Pulsatile Production of the Gonadotropins, Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH) | 411 | ||
| Gonadotropin Release Is then Modulated by the Process of Negative Feedback from Estrogen and Progesterone | 411 | ||
| Ovarian Follicle Development | 413 | ||
| Gamete Development Occurs Initially Without Gonadotropin Support and Subsequently with Pulsatile Gonadotropin Secretion | 413 | ||
| In the Preantral Follicle, Gonadotropin Receptors for Luteinizing Hormone Develop on the Theca, Which Results in Androgen Synthesis; Follicle-Stimulating Hormone Directs the Granulosa to Transform the Androgens to Estrogens | 413 | ||
| Late in the Ovarian Follicular Phase, Luteinizing Hormone Receptors Develop on the Granulosa, Which Permits the Preovulatory Surge of Luteinizing Hormone to Cause Ovulation | 414 | ||
| Clinical Correlations | 414 | ||
| Androgen Insensitivity | 414 | ||
| History. | 414 | ||
| Clinical Examination. | 414 | ||
| Comment. | 414 | ||
| Treatment. | 414 | ||
| Practice Questions | 414 | ||
| Bibliography | 415 | ||
| Chapter 36 Control of Ovulation and the Corpus Luteum | 416 | ||
| Key Points | 416 | ||
| Ovulation | 416 | ||
| Ovulatory Follicles Are Selected at the Onset of Luteolysis (in Large Domestic Animals) | 416 | ||
| Ovulation Is Caused by an Estrogen-Induced Preovulatory Surge of Gonadotropins | 416 | ||
| Corpus Luteum | 418 | ||
| The Corpus Luteum Secretes Progesterone, Which Is Essential for Pregnancy | 418 | ||
| Luteinizing Hormone Is Important for the Maintenance of the Corpus Luteum | 418 | ||
| Regression of the Corpus Luteum in Nonpregnant Large Domestic Animals Is Controlled by Uterine Secretion of Prostaglandin F2α | 418 | ||
| Changes in Luteal Life Span in Large Domestic Animals Occur Because of Changes in Prostaglandin F2α Synthesis by the Uterus | 419 | ||
| Ovarian Cycles | 420 | ||
| In Spontaneously Ovulating Animals, Ovarian Cycles Have Two Phases: Follicular and Luteal; Animals That Require Copulation for Ovulation Can Have Only a Follicular Phase | 420 | ||
| The Luteal Phase Is Modified by Copulation in Some Species | 420 | ||
| Clinical Correlations | 420 | ||
| Inability to Impregnate a Mare | 420 | ||
| History. | 420 | ||
| Clinical Examination. | 420 | ||
| Comment. | 420 | ||
| Treatment. | 420 | ||
| Persistent luteal phase in the mare | 421 | ||
| History. | 421 | ||
| Clinical Examination. | 421 | ||
| Comment. | 421 | ||
| Treatment. | 421 | ||
| Practice Questions | 421 | ||
| Bibliography | 422 | ||
| Chapter 37 Reproductive Cycles | 423 | ||
| Key Points | 423 | ||
| Reproductive Cycles | 423 | ||
| The Two Types of Reproductive Cycles Are Estrual and Menstrual | 423 | ||
| Puberty and Reproductive Senescence | 424 | ||
| Puberty Is the Time When Animals Initially Release Mature Germ Cells | 424 | ||
| Reproductive Senescence in Primates Occurs Because of Ovarian Inadequacy, Not Inadequacy of Gonadotropin Secretion | 426 | ||
| Sexual Behavior | 426 | ||
| Sexual Receptivity Is Keyed by the Interaction of the Hormones Estrogen and Progesterone via Gonadotropin-Releasing Hormone in the Female and Testosterone in the Male | 426 | ||
| External Factors Controlling Reproductive Cycles | 427 | ||
| Photoperiod, Lactation, Nutrition, and Animal Interaction Are Important Factors That Affect Reproduction | 427 | ||
| Photoperiod | 427 | ||
| Lactation | 428 | ||
| Pheromones | 428 | ||
| Inadequate Nutrition Results in Ovarian Inactivity, Especially in Cattle | 429 | ||
| Clinical Correlations | 429 | ||
| Sexual Attractiveness in the Spayed Bitch | 429 | ||
| Section VII Renal Physiology | 460 | ||
| Chapter 41 Glomerular Filtration | 460 | ||
| Key Points | 460 | ||
| Introduction to the Physiology of the Kidney | 460 | ||
| The Glomerulus Filters the Blood | 460 | ||
| The Structure of the Glomerulus Allows Efficient, Selective Filtration | 460 | ||
| Glomerular Filtration Rate Is Determined by the Mean Net Filtration Pressure, Permeability of the Filtration Barrier, and Area Available for Filtration | 462 | ||
| The Filtration Barrier Is Selectively Permeable | 463 | ||
| Glomerular Filtration Rate Is Regulated by Systemic and Intrinsic Factors | 464 | ||
| Glomerular Filtration Rate Is Measured by Determining the Plasma Clearance Rate of a Substance | 466 | ||
| Clinical Correlations | 466 | ||
| Chronic Renal Failure | 466 | ||
| History. | 466 | ||
| Section VIII Respiratory Function | 495 | ||
| Chapter 45 Overview of Respiratory Function: | 495 | ||
| Key Points | 495 | ||
| Respiratory Function | 495 | ||
| The Respiratory System’s Primary Function Is the Transport of Oxygen and Carbon Dioxide Between the Environment and the Tissues | 495 | ||
| Ventilation | 495 | ||
| Ventilation Is the Movement of Gas Into and Out of the Lung | 495 | ||
| Ventilation Requires Muscular Energy | 497 | ||
| The Respiratory Muscles Generate Work to Stretch the Lung and Overcome the Frictional Resistance to Airflow Provided by the Airways (Airway Resistance) | 498 | ||
| Lung Elasticity Results from Tissue and Surface Tension Forces | 498 | ||
| The Lung Is Mechanically Connected to the Thoracic Cage by the Pleural Liquid | 499 | ||
| Airflow Is Opposed by Frictional Resistance in the Airways | 500 | ||
| Smooth Muscle Contraction Affects the Diameters of the Trachea, Bronchi, and Bronchioles | 501 | ||
| Dynamic Compression Can Narrow the Airways and Limit Airflow | 502 | ||
| The Distribution of Air Depends on the Local Mechanical Properties of the Lung | 503 | ||
| In Some Species, Air Travels Between Adjacent Regions of Lung Through Collateral Pathways | 503 | ||
| Clinical Correlations | 504 | ||
| Lung Fibrosis in the Dog | 504 | ||
| Section IX Homeostasis | 543 | ||
| Chapter 51 Fetal and Neonatal Oxygen Transport | 543 | ||
| Key Points | 543 | ||
| The Fetus Depends on the Placenta for the Exchange of Gas, Nutrients, and Metabolic Byproducts | 543 | ||
| The Efficiency of Gas Exchange at the Placenta Depends on the Species-Variable Arrangement of Fetal and Maternal Blood Vessels | 543 | ||
| The Fetal Circulation Mixes Oxygenated and Deoxygenated Blood at Several Points, So the Fetus Exists in a State of Hypoxemia | 545 | ||
| Fetal Oxygen Transport Is Assisted by Fetal Hemoglobin, Which Has a High Affinity for Oxygen | 546 | ||
| The Lung Develops in Three Stages, and Pulmonary Surfactant Must Be Present at Birth | 546 | ||
| At or Shortly After Birth, Umbilical Vessels Rupture, Pulmonary Vascular Resistance Decreases, and the Foramen Ovale and Ductus Arteriosus Close | 547 | ||
| Clinical Correlations | 547 | ||
| Patent Ductus Arteriosus in a Pomeranian | 547 | ||
| History. | 547 | ||
| Clinical Examination. | 547 | ||
| Comment. | 547 | ||
| Treatment. | 548 | ||
| Practice Questions | 548 | ||
| Bibliography | 548 | ||
| Chapter 52 Acid-Base Homeostasis | 549 | ||
| Key Points | 549 | ||
| Acid-Base Regulation | 549 | ||
| Relative Constancy of the Body’s pH Is Essential Because Metabolism Requires Enzymes That Operate at an Optimal pH | 549 | ||
| Hydrogen Ion Concentration Is Measured as pH | 549 | ||
| An Acid Can Donate a Hydrogen Ion, and a Base Can Accept a Hydrogen Ion | 550 | ||
| Buffers Are Combinations of Salts and Weak Acids That Prevent Major Changes in pH | 550 | ||
| Hemoglobin and Bicarbonate Are the Most Important Blood Buffers | 550 | ||
| The First Defense Against a Change in Blood pH Is Provided by the Blood Buffers, but the Lungs and Kidneys Must Ultimately Correct the Hydrogen Ion Load | 551 | ||
| Changes in Ventilation Can Rapidly Change Carbon Dioxide Tension and Therefore Alter pH | 551 | ||
| Metabolic Production of Fixed Acids Requires That the Kidneys Eliminate Hydrogen Ions and Conserve Bicarbonate | 552 | ||
| Intracellular pH Is Regulated by Buffers and Ion Pumps | 552 | ||
| Acid-Base Disturbances | 552 | ||
| Acid-Base Abnormalities Accompany Many Diseases, and Restoration of Normal Blood pH Should Be a Consideration in the Treatment of Any Disease | 552 | ||
| Respiratory Acidosis Is Caused by the Accumulation of Carbon Dioxide, Which Decreases Blood pH | 552 | ||
| Respiratory Alkalosis Is Caused by the Loss of Carbon Dioxide, Which Increases Blood pH | 553 | ||
| Metabolic Acidosis Is Caused by the Accumulation of Fixed Acids or the Loss of Buffer Base, Which Decreases Blood pH | 553 | ||
| Metabolic Alkalosis Is Caused by the Excessive Elimination of Hydrogen Ions or by the Intake of Base, such as Bicarbonate, Which Increases Blood pH | 554 | ||
| Respiratory Compensations for Acid-Base Abnormalities Occur Rapidly; Renal Compensations Occur Over Several Hours | 554 | ||
| Hydrogen and Potassium Ions Are Interrelated in Acid-Base Homeostasis | 554 | ||
| The Diagnosis of Acid-Base Disturbances Depends on Interpretation of Measurements of Arterial Blood pH and Carbon Dioxide Tension, from Which Bicarbonate Concentration and Total Buffer Base Are Calculated | 554 | ||
| Over the Years, Many Terms Have Been Used to Explain Acid-Base Balance | 555 | ||
| Clinical Correlations | 555 | ||
| Upper Airway Obstruction in a Boston Terrier | 555 | ||
| Section X The Immune System | 569 | ||
| Chapter 54 Antigens and Innate Immunity | 569 | ||
| Key Points | 569 | ||
| Antigens | 569 | ||
| Antigens (or Immunogens) Stimulate Immune Cells to Induce an Immune Response | 569 | ||
| The Degree of Immune Response Depends on Several Characteristics of the Antigen | 570 | ||
| Body’s Defense Against Invading Antigens | 571 | ||
| Both Nonimmune and Immune Mechanisms Defend Against Invading Antigens | 571 | ||
| A First Line of Defense Includes Physical and Chemical Barriers such as the Skin and Internal Body Fluids | 571 | ||
| A Second Line of Defense Consists of Phagocytic Cells of the Myeloid and Macrophage-Monocyte Lineages | 572 | ||
| Macrophage-Derived Cytokines Can Induce a Variety of Physiological Processes to Help Combat Infectious Antigens | 574 | ||
| Clinical Correlations | 575 | ||
| Swollen Lymph Nodes in a Colt | 575 | ||
| History. | 575 | ||
| Clinical Examination. | 575 | ||
| Comment. | 575 | ||
| Appendix A Answers to Practice Questions | 587 | ||
| Index | 588 | ||
| A | 588 | ||
| B | 590 | ||
| C | 590 | ||
| D | 593 | ||
| E | 594 | ||
| F | 595 | ||
| G | 595 | ||
| H | 596 | ||
| I | 597 | ||
| J | 598 | ||
| K | 598 | ||
| L | 598 | ||
| M | 599 | ||
| N | 600 | ||
| O | 601 | ||
| P | 601 | ||
| Q | 603 | ||
| R | 603 | ||
| S | 604 | ||
| T | 606 | ||
| U | 607 | ||
| V | 607 | ||
| W | 608 | ||
| Y | 608 | ||
| Z | 608 | ||
| PageBurst page | BM1 | ||
| Endsheets 6-7 | BM2 |