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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
The comprehensive overview of the essential discipline of pathophysiology in small animal disease
Textbook of Small Animal Pathophysiology provides a complete and accessible overview of disease mechanisms and pathophysiological consequences in the field of small animal medicine. The text focuses on the relationship between pathophysiology and disease of any etiology to aid better diagnostics and targeted therapy.
The text includes general pathophysiology of key organ systems such as cardiac, respiratory, gastrointestinal, neural, and more. Core information such as diagnostic methods and therapeutic options is presented in tabular form and clear full-color illustrations are featured throughout to aid in seamless reader comprehension.
Written by a highly qualified professional with significant firsthand experience in the field, Textbook of Small Animal Pathophysiology includes information on:
- Common pathological mechanisms, such as inflammation, sepsis and cytokine storm, fibrosis, degeneration, obesity, ischemia, hypoxia, cell death, apoptosis, necrosis, neoplasia, infection, ageing and pain
- General clinical manifestations, like abdominal enlargement, ataxia, constipation, cough, diarrhea, dyschezia, dysphagia, dyspnea, effusion, fatigue, fever, inappetence, jaundice, oedema, polyphagia, pruritus, regurgitation, seizure, shock, syncope, urinary disorders, vomitus, and weight loss
- Pathophysiology of organ systems cardiac system, hypertension, respiratory system, gastrointestinal system, hepatobiliary system, exocrine pancreas, urinary system, electrolyte system and acid-base balance, endocrine system, reproduction system, nerve system, joints, haematology and infectious diseases
Written to be a complete resource on the subject, Textbook of Small Animal Pathophysiology enables its readers to develop a clear understanding of how each disease works in order to improve decision making and patient outcomes. It is essential reading for veterinary students and a highly useful reference for small animal clinicians.
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Seitenzahl: 970
Veröffentlichungsjahr: 2024
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Table of Contents
Cover
Table of Contents
Title Page
Copyright Page
Preface
Further Reading
Abbreviations
Part I: General Pathological Mechanisms
1 Inflammation
Definition
Trigger
Defence Cascade of the Body
Player of the Inflammation
Course of the Acute Inflammation
References
2 Sepsis and Cytokine Storm
Further Reading
3 Fibrosis
Definition
Cells of Fibrosis Initiation
Course of the Fibrosis
References
4 Degeneration
Definition
Aetiology
Cellular Disturbances in Degeneration
Degenerative Tissue Changes
Further Reading
5 Obesity
Definition
Fat Metabolism
Fat Transport
Mechanism of Obesity
Consequences of Obesity
Further Reading
6 Ischaemia, Hypoxia
Importance of Oxygen
The Physiological Way of Oxygen
Definition of
Hypoxia
,
Ischaemia
Acute Hypoxia
Chronic Hypoxia
References
Further Reading
7 Cell Death
Definition
Necroptosis
Autophagy
Pyroptosis
Further Reading
8 Neoplasia
Definition
Causes
Neoplastic Transformation
Metastasis
Pathophysiology
Local Processes
Systemic Processes
Paraneoplastic Syndrome
Tumour Cachexia
References
9 Infections
Virus
Bacteria
Parasites
Further Reading
10 Ageing
Molecular Aspects of Ageing
Cell Ageing and Telomere Length
Cell Ageing and Transcription and Translation
Cell Ageing and Mitochondrial Function
Cell Ageing and the Cytoskeleton
Ageing and Extracellular Matrix
Ageing in the Dog
Ageing in the Cat
Clinical‐Pathological Changes in Old Age
References
Further Reading
11 Pain
Definition
Classification of Pain
Influence of Pain on the Organism
Reference
Further Reading
12 Hypothalamus Function
Functions
The Control Circuits in Detail
References
Further Reading
Part II: General Clinical Manifestations (Alphabetical)
13 Abdominal Enlargement
Definition
Aetiology
Organ Enlargement
Reduced Muscle Tone
Reference
Further Reading
14 Ataxia
Definition
Physiology of Movement Coordination
Aetiology
Pathogenesis
Further Reading
15 Constipation
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
Reference
Further Reading
16 Cough
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
Reference
Further Reading
17 Diarrhoea
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
References
Further Reading
18 Dyschezia
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
Further Reading
19 Dysphagia
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
Reference
Further Reading
20 Dyspnoea
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
Reference
Further Reading
21 Effusions
Definition
Physiological Basics
Aetiology
Transudate
Exudate
Abdominal Bleeding
Uroabdomen
Bile Peritonitis
References
Further Reading
22 Fatigue
Definition
Aetiology
Pathogenesis
References
Further Reading
23 Fever
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
References
Further Reading
24 Inappetence
Definition
Aetiology
Pathogenesis
Pathophysiologic Consequences
References
25 Jaundice
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
References
Further Reading
26 Oedema
Definition
Aetiology
Pathogenesis
Pathophysiologic Consequences
Further Reading
27 Polyphagia
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
Further Reading
28 Pruritus
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
References
29 Regurgitation
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
Further Reading
30 Seizure
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
Further Reading
31 Shock
Definition
Aetiology
Pathogenesis
Pathophysiologic Consequences
Further Reading
32 Syncope
Definition
Physiological Basics
Aetiology
Pathogenesis
Pathophysiologic Consequences
References
Further Reading
33 Urinary Disorders
Definition
Physiological Basics
Aetiology
Pathogenesis
Further Reading
34 Vomiting
Definition
Aetiology
Pathogenesis
Pathophysiologic Consequences
References
35 Weight Loss
Definition
Aetiology
Pathogenesis
Pathophysiologic Consequences
References
Part III: Pathophysiology of Organ Systems
36 Cardiac System, Hypertension
36.1 Physiological Functions and General Pathophysiology of Organ Insufficiency
Anatomy of the Heart
Electrophysiological Automatism
Electromechanical Coupling
Physiological Heart Action
Factors Influencing Heart Action
Basic Disorders of Cardiac Function
General Consequences of Impaired Cardiac Function
Compensation Mechanisms
Reference
Further Reading
36.2 Congenital Cardiac Diseases
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
36.3 Atrioventricular Valvular Diseases
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
36.4 Cardiomyopathy, Hypertrophic
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
36.5 Cardiomyopathy, Dilated
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
36.6 Heart Arrhythmia
Definition
Aetiology
Diagnostics
Pathophysiologic Consequences
Therapy
References
36.7 Pericardial Disease
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
36.8 Hypertension
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
37 Respiratory System
37.1 Physiological Functions and General Pathophysiology of Organ Insufficiency
Functions
Pathological Mechanisms
References
37.2 Brachiocephalic Syndrome
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
37.3 Acute Respiratory Distress Syndrome (ARDS)
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
37.4 Asthma (Feline Lower Respiratory Tract Disease)
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
37.5 Chronic Obstructive Bronchitis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
37.6 Pneumonia
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
37.7 Idiopathic Lung Fibrosis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
38 Gastrointestinal System
38.1 Physiological Functions and General Pathophysiology of Organ Insufficiency
Digestion
Gut‐associated Lymphoid Tissue (GALT)
References
Further Reading
38.2 Megaoesophagus
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
38.3 Gastritis/Ulceration
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
38.4 Gastric Dilatation–Volvulus Syndrome
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
38.5 Enteritis/Inflammatory Bowel Disease
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
38.6 Intestinal Lymphangiectasias
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
38.7 Intestinal Obstruction
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
39 Hepatobiliary System
39.1 Physiological Functions and General Pathophysiology of Organ Insufficiency
Functions
References
39.2 Acute Hepatic Failure
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
39.3 Chronic Hepatitis; Liver Fibrosis and Cirrhosis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
39.4 Portosystemic Shunts/Hepatoencephalopathy
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
39.5 Feline Hepatic Lipidosis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
39.6 Cholangiohepatitis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
40 Exocrine Pancreas
40.1 Physiological Functions and General Pathophysiology of Organ Insufficiency
Functions
Formation of the Digestive Secretion
Control of Pancreatic Secretion
Digestion of the Nutrients
Reference
Further Reading
40.2 Acute Pancreatitis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
40.3 Chronic Pancreatitis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
40.4 Exocrine Pancreas Insufficiency
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
41 Urinary System
41.1 Physiological Functions of the Kidneys and General Pathophysiology of Organ Insufficiency
Functions
Acid‐Base Regulation
Bone Metabolism
Blood Pressure
Erythropoiesis
Gluconeogenesis
Further Reading
41.2 Glomerulonephritis/Nephrotic Syndrome
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
41.3 Tubular Disease/Fanconi Syndrome
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Reference
Further Reading
41.4 Acute Renal Failure
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
41.5 Chronic Kidney Disease
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
41.6 Urinary Tract Infection
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
41.7 Urolithiasis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
42 Electrolyte System and Acid-Base Balance
42.1 Acid‐Base Balance
Physiology
The Buffering of Protons
The Elimination of CO
2
via the Lungs (Respiratory Regulation)
Elimination of Protons via the Kidney and Reabsorption of Bicarbonate (Renal Regulation)
Disorders in the Acid‐Base Balance
Pathophysiologic Consequences
Therapy
Further Reading
42.2 Hypo‐/Hypernatraemia
Physiology
Hypernatraemia
Causes of Hypernatraemia
Pathophysiologic Consequences
Hyponatraemia
Therapy
Further Reading
42.3 Hypo‐/Hyperkalaemia
Physiology
Hyperkalaemia
Hypokalaemia
Therapy
Further Reading
43 Endocrine System
43.1 General Physiology
Further Reading
43.2 Pituitary Gland
43.2.1 Acromegaly
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
43.2.2 Pituitary Dwarfism
Definition
Aetiology
Pathogenesis and Pathophysiology
Diagnostics
Therapy
References
Further Reading
43.2.3 Diabetes Insipidus
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
43_3 Thyroid Gland
43.3.1 Physiology of the Thyroid Gland
Functions
General Consequences of the Malfunction
References
Further Reading
43.3.2 Hyperthyroidism
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
43.3.3 Hypothyroidism
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
43.4 Parathyroid Gland
Physiology
Hyperparathyroidism
Hypoparathyroidism
References
Further Reading
43.5 Endocrine Pancreas
43.5.1 Physiology of Endocrine Pancreas
Functions
Further Reading
43.5.2 Diabetes Mellitus
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
43.5.3 Diabetic Ketoacidosis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
43.5.4 Insulinoma
Definition
Aetiology and Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
43.6 Adrenal Gland
43.6.1 Physiology of the Adrenal Gland
Functions
Reference
Further Reading
43.6.2 Hyperadrenocorticism
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
43.6.3 Hypoadrenocorticism
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Reference
Further Reading
43.6.4 Hyperaldosteronism
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
43.6.5 Pheochromocytoma
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
44 Reproduction System
44.1 Pyometra
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
44.2 Prostate Diseases
Aetiology and Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Reference
Further Reading
45 Nerve System
45.1 Brain Tumours
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
45.2 Idiopathic Epilepsy
Definition/Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
45.3 Intervertebral Disc Disease
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
45.4 Peripheral Neuropathy
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
46 Joints
46.1 Arthritis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
46.2 Osteoarthritis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
47 Haematology
47.1 Physiological Functions of Red Blood Cells
Functions
Haemoglobin Formation
Iron Metabolism
References
47.2 Erythrocytosis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
47.3 Anaemia
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
47.4 Coagulation Disorders
Definition
Physiological Basics
Aetiology
Pathogenesis
Deficiency of Clotting Factors
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
47.5 Hypercoagulability
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
48 Infectious Diseases
48.1 Feline
48.1.1 Feline Leukaemia Virus Infection
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
48.1.2 Feline Infectious Peritonitis
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
48.1.3 Feline Immunodeficiency Virus Infection
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
48.2 Canine
48.2.1 Distemper
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
48.2.2 Canine Parvovirus
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
48.3 Bacterial Diseases
48.3.1 Anaplasmosis
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
48.3.2 Borreliosis
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
48.3.3 Ehrlichiosis
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Reference
Further Reading
48.3.4 Leptospirosis
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
48.4 Protozoal Infections
48.4.1 Babesiosis
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Reference
Further Reading
48.4.2 Giardiasis
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
48.4.3 Leishmaniasis
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
49 Common Immune‐mediated Diseases
49.1 Autoimmunity
Definition
Aetiology and Pathogenesis
Further Reading
49.2 Lupus Erythematosus
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
References
Further Reading
49.3 Myasthenia Gravis
Definition
Aetiology
Pathogenesis
Diagnostics
Pathophysiologic Consequences
Therapy
Further Reading
50 Common Clinical Biochemical Parameters (Alphabetical)
50.1 Alanine Aminotransferase (ALT)
Physiology
Variations
50.2 Albumin
Physiology
Variations
50.3 Alkaline Phosphatase (ALP)
Physiology
Variations
50.4 Ammonia
Physiology
Variations
50.5 Aspartate Aminotransferase (AST)
Physiology
Variations
50.6 Bile Acids
Physiology
Variations
50.7 Bilirubin
Physiology
Variations
5.8 Calcium
Physiology
Variations
50.9 Cholesterol
Physiology
Variations
50.10 Creatinine
Physiology
Variations
50.11 Creatine Kinase
Physiology
Variations
50.12 Glucose
Physiology
Variations
50.13 Glutamate Dehydrogenase (GLDH)
Physiology
Variations
50.14 Lipase
Physiology
Variations
50.15 Phosphorus
Physiology
Variations
50.16 Potassium
Physiology
Variations
50.17 Sodium
Physiology
Variations
50.18 Total Protein
Physiology
Variations
50.19 Urea
Physiology
Variations
Index
End User License Agreement
List of Tables
Chapter 1
Table 1.1 Common causes of inflammation in dogs and cats.
Table 1.2 Components of the epidermal extracellular matrix with function.
Table 1.3 Cytokines, resource, effect.
Table 1.4 Some eicosanoids with effect.
Table 1.5 Some acute phase proteins.
Chapter 2
Table 2.1 Clinical consequences of sepsis.
Chapter 3
Table 3.1 Functional cells of fibrosis.
Chapter 5
Table 5.1 Mediators from the adipose tissue.
Chapter 6
Table 6.1 Clinical causes of hypoxaemia.
Chapter 7
Table 7.1 Structural proteins influenced by caspases during apoptosis.
Table 7.2 Trigger of cell necrosis and the mechanism.
Chapter 12
Table 12.1 Physiological mechanisms influenced by the hypothalamus.
Chapter 13
Table 13.1 Abdominal organ enlargements.
Chapter 14
Table 14.1 Causes of vestibular diseases.
Chapter 15
Table 15.1 Interpretation of altered PCV and total protein.
Chapter 17
Table 17.1 Gut pathogenic microorganism causing acute diarrhoea.
Chapter 21
Table 21.1 Differential diagnosis for effusions.
Chapter 27
Table 27.1 Hormones with influence on food intake.
Chapter 28
Table 28.1 Mediators of pruritus triggering.
Chapter 30
Table 30.1 Neurotransmitters by chemical structure.
Chapter 32
Table 32.1 Consequences of hypoxia on different ion channels.
Chapter 33
Table 33.1 Causes for polyuria and polydipsia in dogs and cats.
Chapter 36_1
Table 36.1.1 Effects of the sympathetic and parasympathetic nervous system ...
Table 36.1.2 Examples of intracardiac and extracardiac arrhythmias.
Chapter 36_2
Table 36.2.1 Common congenital heart diseases in dogs and cats.
Chapter 36_3
Table 36.3.1 Causalities of mitral valve regurgitation.
Chapter 36_4
Table 36.4.1 Causes of cardiac hypertrophy.
Chapter 36_6
Table 36.6.1 Causes of bradyarrhythmia.
Table 36.6.2 Causes of tachyarrhythmia.
Chapter 36_8
Table 36.8.1 Mechanisms of hypertension in Cushing's disease.
Chapter 37_1
Table 37.1.1 Defence systems in the airways.
Table 37.1.2 Causes for the development of pulmonary oedema.
Chapter 37_3
Table 37.3.1 Aetiologies of ARDS.
Table 37.3.2 Phases of ARDS.
Table 37.3.3 Alveolar cells.
Chapter 37_5
Table 37.5.1 Causes of bronchitis.
Chapter 38_1
Table 38.1.1 Functions of the saliva.
Table 38.1.2 Stomach function.
Table 38.1.3 Important hormones of the digestive system with essential func...
Table 38.1.4 Overview of intestinal enzymes.
Table 38.1.5 List of quantitatively important bacterial strains in the micr...
Table 38.1.6 Consequences of malassimilation.
Chapter 38_5
Table 38.5.1 Cytokines, with their respective changes in IBD.
Chapter 38_6
Table 38.6.1 Functions of albumin.
Chapter 38_7
Table 38.7.1 Intestine‐associated tumours in dogs and cats.
Chapter 39_1
Table 39.1.1 Functions of the liver.
Table 39.1.2 Composition of bile.
Chapter 39_4
Table 39.4.1 Metabolites with significance in hepatoencephalic syndrome.
Chapter 40_1
Table 40.1.1 Pancreatic digestive enzymes.
Chapter 40_2
Table 40.2.1 Causes of pancreatitis in dogs and cats.
Table 40.2.2 Differentiation of different tests for the diagnosis of pancrea...
Chapter 40_4
Table 40.4.1 Influence of SIBO and IBD on serum concentrations of folic aci...
Chapter 41_1
Table 41.1.1 Kidney functions.
Table 41.1.2 Secretion and reabsorption in the tubular system.
Chapter 41_2
Table 41.2.1 Cells and mediators in the pathogenesis of glomerulonephritis....
Table 41.2.2 Summary of possible glomerular protein losses.
Chapter 41_4
Table 41.4.1 Uraemic toxins.
Chapter 41_5
Table 41.5.1 Metabolic acidosis consequences.
Chapter 42_2
Table 42.2.1 Hormones with sodium control.
Chapter 42_3
Table 42.3.1 Metabolic control of the potassium balance.
Table 42.3.2 Causes of hyperkalaemia.
Chapter 43_1
Table 43.1.1 Hormones of hypothalamus.
Table 43.1.2 Examples of cAMP‐induced cell metabolic processes.
Chapter 43_2_1
Table 43.2.1.1 Effects of growth hormone and IGF‐1.
Chapter 43_2_2
Table 43.2.2.1 Metabolic influence of GH and IGF‐1.
Chapter 43_3_1
Table 43.3.1.1 Effects of thyroid hormones.
Table 43.3.1.2 Alterations of the metabolism in hypo‐ and hyperthyroidism....
Chapter 43_3_2
Table 43.3.2.1 Influences on the metabolism of erythrocytes in hyperthyroid...
Chapter 43_3_3
Table 43.3.3.1 Common causes of hypothyroidism.
Chapter 43_5_3
Table 43.5.3.1 Major cations and anions in serum.
Chapter 43_6_1
Table 43.6.1.1 Functions of glucocorticoids.
Chapter 43_6_4
Table 43.6.4.1 Categories of hypertension in dogs and cats.
Chapter 43_6_5
Table 43.6.5.1 Target organs and selected effects of catecholamines.
Chapter 44_1
Table 44.1.1 Bacteria detected in pyometra.
Chapter 45_1
Table 45.1.1 Brain tumours in dogs and cats in descending frequency.
Chapter 45_2
Table 45.2.1 Breeds with predisposition to epilepsy.
Chapter 47_1
Table 47.1.1 Growth factors and cytokines in haematopoiesis.
Chapter 47_4
Table 47.4.1 Causes and mechanism of DIC.
Chapter 48_1_1
Table 48.1.1.1 Influence of cytokines on erythropoiesis.
Chapter 48_2_1
Table 48.2.1.1 Molecules of the canine distemper virus.
Chapter 48_2_2
Table 48.2.2.1 Mechanisms of virus replication.
Chapter 48_4_1
Table 48.4.1.1 Differentiation of some veterinary relevant babesias.
Chapter 49_2
Table 49.2.1 Triggers of systemic lupus erythematosus.
List of Illustrations
Chapter 1
Figure 1.1 Structure of the outer skin and development of keratinocytes.
Figure 1.2 Building up the defence system of the mucous membrane.
Figure 1.3 Defence mechanism by neutrophilic granulocytes.
Figure 1.4 Antigen presentation by macrophages.
Figure 1.5 Function of the eosinophilic granulocytes.
Figure 1.6 Function of the lymphocytes.
Figure 1.7 Induction of the acute phase response.
Figure 1.8 Overview of the inflammatory reaction.
Chapter 2
Figure 2.1 Pathophysiology of sepsis.
Figure 2.2 Effects of TNF‐α, IL‐1, IL‐6.
Chapter 3
Figure 3.1 Inflammatory cells with their influence on the myofibroblasts.
Figure 3.2 Mechanism of tissue fibrosis.
Figure 3.3 Relation between fibrosis and tumour (Rybinski et al. 2014).
Chapter 4
Figure 4.1 Hydropic swelling due to water retention.
Figure 4.2 Consequences of decreased cell pH.
Figure 4.3 Disturbances of lipid metabolism in hepatocellular fatty degenera...
Chapter 5
Figure 5.1 Mechanism of fat accumulation.
Figure 5.2 Hormones and cytokines produced by adipose tissue.
Figure 5.3 Influence of fat on different physiological mechanisms.
Figure 5.4 Connection between obesity and type II diabetes mellitus.
Figure 5.5 Obesity and hypertension.
Chapter 6
Figure 6.1 Consequences of cellular hypoxaemia.
Figure 6.2 Catabolic consequences of AMPK activation.
Chapter 7
Figure 7.1 Apoptosis, process.
Figure 7.2 Comparison of apoptosis and necrosis.
Chapter 8
Figure 8.1 Oncogenesis initiation, promotion, progression.
Figure 8.2 Mechanism of metastasis.
Figure 8.3 PTHrP effect.
Chapter 9
Figure 9.1 Course of an infection.
Figure 9.2 Schematic virus structure.
Figure 9.3 Mechanism of cellular viral infection.
Figure 9.4 Anatomy of a bacterium.
Chapter 10
Figure 10.1 Overview of cell ageing mechanisms.
Chapter 11
Figure 11.1 Irritation of the nociceptors.
Figure 11.2 Pain reflex arc.
Chapter 12
Figure 12.1 Physiological processes regulated by the hypothalamus.
Figure 12.2 Regulation of body temperature.
Figure 12.3 Control of stress.
Chapter 14
Figure 14.1 Simple reflex arc.
Figure 14.2 Synthesis and consequence of increased excitatory amino acids.
Chapter 15
Figure 15.1 Pathological consequences at the obstruction site.
Figure 15.2 Consequences of constipation.
Chapter 16
Figure 16.1 Mucociliary clearance.
Figure 16.2 Pathways of the cough.
Chapter 17
Figure 17.1 Mechanism of secretory diarrhoea.
Figure 17.2 Illustration of destruction in exudative diarrhoea.
Figure 17.3 Overview of molecular mechanisms of diarrhoea.
Chapter 18
Figure 18.1 Mechanism of defaecation.
Chapter 19
Figure 19.1 Pathogenesis of dysphagia.
Figure 19.2 Consequences of ptyalism.
Chapter 20
Figure 20.1 Breathing mechanism dog.
Figure 20.2 Mechanism of bronchoconstriction in feline lower respiratory dis...
Figure 20.3 Pathophysiologic consequences of dyspnoea.
Chapter 21
Figure 21.1 Physiology of thoracic and abdominal fluid formation.
Figure 21.2 Mechanism of transudate formation.
Figure 21.3 Mechanism of exudate formation.
Figure 21.4 Hypoxia consequences on kidney, liver, intestine and lungs.
Figure 21.5 Pathophysiologic consequences of increased reabsorption of uremi...
Chapter 22
Figure 22.1 Cytokine effects on the central nervous system.
Chapter 23
Figure 23.1 Mechanism of the fever.
Figure 23.2 Influence of fever on various organs.
Chapter 24
Figure 24.1 Pathophysiologic consequences of inappetence.
Chapter 25
Figure 25.1 Pathophysiology of jaundice.
Chapter 26
Figure 26.1 Cell‐to‐cell contact via cadherins.
Chapter 27
Figure 27.1 Hormonal effects on the appetite centre.
Chapter 29
Figure 29.1 Consequences of regurgitation.
Chapter 30
Figure 30.1 Pathogenesis of a seizure event.
Chapter 31
Figure 31.1 Pathomechanism of shock based on cardiogenic shock.
Figure 31.2 Septic shock process.
Chapter 32
Figure 32.1 Mechanism of blood pressure regulation.
Figure 32.2 Pathomechanism of hypoglycaemia.
Figure 32.3 Pathomechanism of hypokalaemic syncope.
Chapter 33
Figure 33.1 Mechanisms of polyuria.
Figure 33.2 Causes and localisation of dysfunctional micturition.
Chapter 34
Figure 34.1 Representation of emetic receptors and triggers.
Figure 34.2 Function of the chromaffin cells.
Figure 34.3 Consequences of chronic vomiting.
Chapter 35
Figure 35.1 Mechanism of cardiac cachexia.
Figure 35.2 Influence of tumour diseases on food intake and weight loss.
Figure 35.3 Influence of cachexia on different organ systems.
Chapter 36_1
Figure 36.1.1 Anatomical overview of the heart structure.
Figure 36.1.2 Ion fluxes and action potential structure in the P cells of th...
Figure 36.1.3 Ion fluxes in the generation of the action potential in the my...
Figure 36.1.4 Sequence of muscle contraction.
Figure 36.1.5 Illustration of the heart action.
Figure 36.1.6 Mechanism of impaired left‐sided cardiac function.
Figure 36.1.7 Mechanism of impaired right‐sided heart function.
Chapter 36_2
Figure 36.2.1 Illustration of the different heart malformations.
Figure 36.2.2 Pathophysiologic consequences of right heart failure.
Figure 36.2.3 Pathophysiologic consequences of the left‐right shunt.
Chapter 36_3
Figure 36.3.1 Morphological changes in mitral valve degeneration.
Figure 36.3.2 Pathophysiologic consequences of mitral valve regurgitation.
Figure 36.3.3 Pathophysiologic consequences of tricuspid regurgitation.
Chapter 36_4
Figure 36.4.1 Dystrophin associated glycoprotein complex.
Figure 36.4.2 Pathophysiologic consequences of hypertrophic cardiomyopathy....
Chapter 36_5
Figure 36.5.1 Pathogenesis of dilated cardiomyopathy.
Figure 36.5.2 Relationship between cardiac dysfunction and renal failure....
Figure 36.5.3 Pathophysiologic consequences of dilated cardiomyopathy.
Chapter 36_6
Figure 36.6.1 Summary of right and left‐heart failure.
Figure 36.6.2 Mode of action of the antiarrhythmic drugs.
Chapter 36_7
Figure 36.7.1 Histology of the pericardium.
Figure 36.7.2 Typical localisations of cardiac neoplasms.
Figure 36.7.3 Mechanism of blood clotting.
Figure 36.7.4 Mechanism of the ‘Pulsus paradoxus’.
Figure 36.7.5 Pathophysiologic consequences of pericardial disease.
Chapter 36_8
Figure 36.8.1 Physiology of blood pressure.
Figure 36.8.2 Pathophysiologic consequences of hypertension.
Chapter 37_1
Figure 37.1.1 Movement of the chest during breathing.
Figure 37.1.2 Illustration of mucociliary transport.
Figure 37.1.3 Alveolar gas exchange.
Figure 37.1.4 Cellular gas exchange.
Figure 37.1.5 Mechanisms of pulmonary oedema formation.
Figure 37.1.6 Mechanisms of emphysema formation.
Figure 37.1.7 Mechanisms of lung atelectasis.
Chapter 37_2
Figure 37.2.1 Localisation of stenoses in the respiratory system of brachioc...
Chapter 37_3
Figure 37.3.1 Mechanisms in ARDS.
Chapter 37_4
Figure 37.4.1 Pathomechanisms in asthma.
Chapter 37_5
Figure 37.5.1 Pathophysiologic consequences of chronic bronchitis.
Chapter 37_6
Figure 37.6.1 Mechanism of pneumonia.
Figure 37.6.2 Pathophysiologic consequences of pneumonia.
Chapter 37_7
Figure 37.7.1 Differentiation of fibroblasts into myofibroblasts.
Chapter 38_1
Figure 38.1.1 Intestinal sections with function.
Figure 38.1.2 Defence system in the intestinal wall.
Chapter 38_2
Figure 38.2.1 Pathophysiologic consequences in megaoesophagus.
Chapter 38_3
Figure 38.3.1 Pathogenesis and pathophysiologic consequences of gastritis.
Chapter 38_4
Figure 38.4.1 Mechanism of gastric torsion.
Figure 38.4.2 Pathophysiologic consequences of gastric torsion.
Chapter 38_5
Figure 38.5.1 Mechanism of secretory diarrhoea.
Figure 38.5.2 Molecular mechanisms of diarrhoea.
Figure 38.5.3 Pathophysiologic consequences of IBD.
Chapter 38_6
Figure 38.6.1 Structure of the intestinal lymphatic system.
Figure 38.6.2 Morphological changes in lymphangiectasia.
Figure 38.6.3 Protein electrophoresis in protein‐losing enteropathy.
Figure 38.6.4 Pathophysiologic consequences of lymphangiectasia.
Chapter 38_7
Figure 38.7.1 Pathophysiologic consequences of intestinal obstruction.
Chapter 39_1
Figure 39.1.1 Illustration of the liver lobule with the sinusoid.
Chapter 39_2
Figure 39.2.1 Pathogenesis and pathophysiologic consequences of acute liver ...
Figure 39.2.2 Mechanism of hepatoencephalopathy.
Chapter 39_3
Figure 39.3.1 Mechanism of hepatogenic fibrogenesis.
Figure 39.3.2 Pathophysiology of liver cirrhosis.
Chapter 39_4
Figure 39.4.1 Types of portosystemic shunts.
Chapter 39_6
Figure 39.6.1 Pathogenesis and pathophysiologic consequences of cholangitis....
Chapter 40_1
Figure 40.1.1 Structure of the exocrine pancreas.
Figure 40.1.2 Mechanism of bicarbonate secretion.
Figure 40.1.3 Control of pancreatic juice secretion.
Chapter 40_2
Figure 40.2.1 Pathogenesis and pathophysiologic consequences of acute pancre...
Figure 40.2.2 Mechanism of paralytic ileus.
Chapter 40_3
Figure 40.3.1 Pathogenesis of chronic pancreatitis.
Figure 40.3.2 Pathophysiologic consequences of chronic pancreatitis.
Chapter 40_4
Figure 40.4.1 Mechanism of and pathophysiologic consequences of exocrine pan...
Chapter 41_1
Figure 41.1.1 Nephron – the shortest functional unit of the kidneys.
Figure 41.1.2 Kidney and bone metabolism.
Figure 41.1.3 RAA‐system.
Figure 41.1.4 Erythropoietin pathway.
Chapter 41_2
Figure 41.2.1 Different forms of glomerulonephritis.
Figure 41.2.2 Pathogenesis of glomerulonephritis with nephrotic syndrome.
Figure 41.2.3 Pathophysiologic consequences of glomerulonephritis with nephr...
Chapter 41_3
Figure 41.3.1 Resorption disorders in Fanconi syndrome.
Figure 41.3.2 Pathophysiologic consequences of Fanconi syndrome.
Chapter 41_4
Figure 41.4.1 Mechanism of glomerular damage.
Figure 41.4.2 Mechanism of tubule damage.
Figure 41.4.3 Pathogenesis of acute renal failure.
Figure 41.4.4 Pathophysiologic consequences of acute renal failure.
Chapter 41_5
Figure 41.5.1 Pathogenesis of chronic renal failure, morphology.
Figure 41.5.2 Pathogenesis of chronic renal failure, function.
Figure 41.5.3 Pathophysiologic consequences of chronic renal failure.
Chapter 41_6
Figure 41.6.1 Pathomechanism and clinical consequences of bacterial cystitis...
Chapter 41_7
Figure 41.7.1 Mechanism of stone formation using the example of calcium oxal...
Figure 41.7.2 Pathophysiologic consequences of urethral obstruction.
Chapter 42_1
Figure 42.1.1 Function of bicarbonate buffering.
Figure 42.1.2 Pathogenesis of metabolic acidosis.
Figure 42.1.3 Pathogenesis of metabolic alkalosis.
Chapter 42_2
Figure 42.2.1 Pathomechanisms of hypernatraemia.
Chapter 42_3
Figure 42.3.1 Pathophysiologic consequences of hyperkalaemia.
Figure 42.3.2 Pathophysiologic consequences of hypokalaemia.
Chapter 43_1
Figure 43.1.1 Hierarchy of hormones.
Chapter 43_2_1
Figure 43.2.1.1 Pathophysiologic consequences of acromegaly.
Chapter 43_2_3
Figure 43.2.3.1 Pathogenesis and pathophysiologic consequences of diabetes i...
Chapter 43_3_1
Figure 43.3.1.1 Synthesis and transport of thyroid hormones.
Chapter 43_3_2
Figure 43.3.2.1 Pathophysiologic consequences of hyperthyroidism.
Chapter 43_3_3
Figure 43.3.3.1 Development of autoimmune thyroiditis.
Figure 43.3.3.2 Pathophysiologic consequences of hypothyroidism.
Chapter 43_4
Figure 43.4.1 Calcium metabolism.
Figure 43.4.2 Aetiology of hyperparathyroidism.
Figure 43.4.3 Pathophysiologic consequences of hypercalcaemia.
Figure 43.4.4 Pathophysiologic consequences of hypocalcaemia.
Chapter 43_5_1
Figure 43.5.1.1 Endocrine areas in the pancreas.
Figure 43.5.1.2 Overview of insulin functions.
Chapter 43_5_2
Figure 43.5.2.1 Effect of cortisol and progesterone on glucose metabolism.
Figure 43.5.2.2 Pathogenesis of type II diabetes mellitus.
Figure 43.5.2.3 Pathophysiologic consequences of diabetes mellitus.
Chapter 43_5_3
Figure 43.5.3.1 Pathogenesis and pathophysiologic consequences of ketoacidos...
Chapter 43_5_4
Figure 43.5.4.1 Relationship between blood glucose concentration and symptom...
Chapter 43_6_1
Figure 43.6.1.1 Synthesis of steroid hormones from cholesterol.
Chapter 43_6_2
Figure 43.6.2.1 Pathophysiologic consequences of hyperadrenocorticism.
Chapter 43_6_3
Figure 43.6.3.1 Pathophysiologic consequences of hypoadrenocorticism.
Chapter 43_6_4
Figure 43.6.4.1 Pathogenesis and pathophysiologic consequences of hyperaldos...
Chapter 43_6_5
Figure 43.6.5.1 Pathophysiologic consequences of pheochromocytoma.
Chapter 44_1
Figure 44.1.1 Pathogenesis of pyometra.
Chapter 44_2
Figure 44.2.1 Overview of prostate diseases.
Chapter 45_1
Figure 45.1.1 Pathogenesis of intracranial tumours.
Chapter 45_2
Figure 45.2.1 Pathogenesis of idiopathic epilepsy.
Chapter 45_3
Figure 45.3.1 Hansen type I and Hansen type II.
Figure 45.3.2 Consequences of the herniated disc.
Chapter 46_1
Figure 46.1.1 Mechanism of arthritis.
Chapter 46_2
Figure 46.2.1 Pathogenesis of the development of osteoarthritis.
Chapter 47_1
Figure 47.1.1 Development of the erythrocytes.
Figure 47.1.2 Iron metabolism.
Figure 47.1.3 Extramedullary haematopoiesis.
Chapter 47_2
Figure 47.2.1 Mechanisms of secondary polycythaemia.
Chapter 47_3
Figure 47.3.1 Non‐regenerative anaemia in CKD.
Figure 47.3.2 Mechanism of bleeding anaemia.
Figure 47.3.3 Pathophysiologic consequences of haemolytic anaemia.
Chapter 47_4
Figure 47.4.1 The coagulation cascade.
Chapter 47_5
Figure 47.5.1 Consequences of pulmonary emboli.
Chapter 48_1_1
Figure 48.1.1.1 Infection mode of FeLV.
Figure 48.1.1.2 Pathophysiology of FeLV infection.
Chapter 48_1_2
Figure 48.1.2.1 Course of coronavirus infection.
Figure 48.1.2.2 Pathophysiology of FIP.
Chapter 48_1_3
Figure 48.1.3.1 Course of an FIV infection.
Figure 48.1.3.2 Mechanisms of neuropathic dysfunction due to FIV.
Figure 48.1.3.3 Pathophysiology of FIV infection.
Chapter 48_2_1
Figure 48.2.1.1 Pathophysiology of distemper infection.
Chapter 48_2_2
Figure 48.2.2.1 Pathogenesis of parvovirus infection in dogs.
Figure 48.2.2.2 Influence of viral infection on lymphocyte count.
Figure 48.2.2.3 Pathophysiologic consequences of canine parvovirus infection...
Chapter 48_3_1
Figure 48.3.1.1 Pathogen uptake in the tick.
Figure 48.3.1.2 Infection of granulocytes by
A. phagocytophilum
.
Chapter 48_3_2
Figure 48.3.2.1 Mechanism of transmission of
Borrelia
by
Ixodes
.
Figure 48.3.2.2 Pathophysiology of Lyme borreliosis.
Chapter 48_3_3
Figure 48.3.3.1 Mechanism of infection of monocytes.
Chapter 48_3_4
Figure 48.3.4.1 Pathophysiology of leptospirosis.
Chapter 48_4_1
Figure 48.4.1.1 Babesiosis cycle.
Figure 48.4.1.2 Invasion of the erythrocytes and release of the parasites.
Figure 48.4.1.3 Pathophysiology of babesiosis.
Chapter 48_4_2
Figure 48.4.2.1 Cycle of giardiasis.
Figure 48.4.2.2 Mechanism of interaction between giardiasis and enterocytes....
Chapter 48_4_3
Figure 48.4.3.1 Leishmaniasis cycle.
Figure 48.4.3.2 Pathophysiology of leishmaniasis.
Chapter 49_1
Figure 49.1.1 The antigen presentation pathway.
Figure 49.1.2 Induction of autoimmunity.
Chapter 49_2
Figure 49.2.1 Pathogenesis of systemic LE.
Chapter 49_3
Figure 49.3.1 Pathomechanism of MG at the motor end plate.
Guide
Cover Page
Table of Contents
Title Page
Copyright Page
Preface
Abbreviations
Begin Reading
Index
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Textbook of Small Animal Pathophysiology
Stephan Neumann
Institute of Veterinary MedicineUniversity of GoettingenGoettingenGermany
This edition first published 2025© 2025 John Wiley & Sons Ltd
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Library of Congress Cataloging‐in‐Publication Data applied forHardback ISBN: 9781119824619
Cover Design: WileyCover Images: cat © SciePro/Shutterstock, dog © SEBASTIAN KAULITZKI/SCIENCE PHOTO LIBRARY/Getty Images, organ renderings – Courtesy of Stephen Neumann
Preface
This book was written to summarise the mechanisms of canine and feline disease in one book. Although the author believes that understanding the mechanisms of disease is essential to understanding the course, diagnosis, treatment and prognosis of disease, there are only few books that have focused on the mechanisms. This was the motivation for writing this book. Not all mechanisms presented in this book have been directly investigated in dogs and cats. Some of the findings originate from studies of other species and have been adapted to the conditions in dogs and cats. This is comparable to the human medical literature on this topic. The book is structured in such a way that first the general disease mechanisms are presented. In the second part of the book, the development of the clinical symptoms is explained. Finally, in the third part of the book, the mechanisms of important diseases in dogs and cats are presented. The chapters are structured in such a way that first the disease is defined and then aetiological factors are presented. The main causes are described. In the section on pathogenesis, the mechanisms by which the aetiology leads to the disease are described. Finally, the diagnostic possibilities are briefly summarised. The section on pathophysiology explains how the symptoms typical of the respective disease develop. Each chapter ends with a summary of therapeutic options. Knowledge of the mechanisms of diseases is constantly changing as a result of increasing knowledge. Accordingly, the explanations in the book reflect current knowledge.
This book is dedicated to all those who have accompanied me on my professional journey and have been my contact and support in hours of joy and pause.
I have written this book with great enthusiasm and would be delighted if you would read it with the same pleasure.
Stephan Neumann
Göttingen, April 2023
Further Reading
Besides the literature given at the end of each chapter, the following publications provided basic information for the realisation of this book:
Black, V.L., Murphy, K.F., Payne, J.R., and Hall, E.J. (2022).
Notes on Canine Internal Medicine, 4th ed
, 7e. New York: Wiley.
Blanco, A. (2022).
Medical Biochemistry
, 2e. St. Louis: Elsevier.
Blum, H.E. and Müller‐Wieland, D. (2020).
Klinische Pathophysiologie
, 11. Auflage. Stuttgart: Thieme Verlag.
Bojarb, M.J. (2010).
Mechanisms of Disease in Small Animal Surgery
, 3e. Jackson: Teton New Media.
Cui, D. (2011).
Atlas of Histology: With Functional and Clinical Correlations
, 1e. Philadelphia: Wolters Kluwer.
Ettinger, S.J., Feldman, E.C., and Cote, E. (2017).
Textbook of Veterinary Internal Medicine
, 8e. St. Louis: Elsevier.
Feldman, E.C., Nelson, R.W., Reusch, C.E., and Scott‐Moncrieff, J.C.R. (2015).
Canine and Feline Endocrinology
, 4e. Philadelphia: Elsevier.
Gough, A. and Murphy, K. (2015).
Diagnosis in Small Animal Medicine
, 2e. New York: Wiley.
Greene, C.E. (2006).
Infectious Diseases of the Dog and Cat
, 3e. St. Louis: Elsevier.
Hartmann, H. and Meyer, H. (1994).
Klinische Pathologie der Haustiere
, 1. Auflage. Stuttgart: Gustav Fischer Verlag.
Harvey, R.A. and Ferrier, D.R. (2011).
Lippincott’s Illustrated Reviews: Biochemistry
, 5e. Philadelphia: Wolters Kluwer.
Huether, S.E.
Understanding Pathophysiology
, 7e. St. Louis: Elsevier.
Kaneko, J.J., Harvey, J.W., and Bruss, M.L. (2008).
Clinical Biochemistry of Domestic Animals
, 6e. Burlington: Academic Press.
Kierszenbaum, A.L. and Tres, L.L. (2020).
Histology and Cell Biology. An Introduction to Pathology
, 5e. Philadelphia: Elsevier.
Klein, B.G. (2020).
Cunningham’s Textbook of Veterinary Physiology
, 6e. Philadelphia: Elsevier.
Kumar, V., Abbas, A.K., and Fausto, N. (2005).
Pathologic Basis of Disease
, 7e. Philadelphia: Elsevier.
Nelson, R.W. and Couto, G. (2014).
Small Animal Internal Medicine
, 5e. St. Louis: Elsevier.
Rastogi, S.C. (2007).
Animal Physiology
, 4e. New Delhi: New Age International (P) Limited, Publishers.
Schmidt, R.F., Lang, F., and Heckmann, M. (2010).
Physiologie des Menschen
, 31. Auflage. Berlin: Springer Verlag.
Silbernagl, S. and Lang, F. (2019).
Taschenatlas Pathophysiologie
, 6. Auflage. Stuttgart: Thieme Verlag.
Sjaastad, O.V., Sand, O., and Hove, K. (2016).
Physiology of Domestic Animals
, 3e. Oslo: Scandinavian Veterinary Press.
Stockham, S.L. and Scott, M.A. (2002).
Fundamentals of Veterinary Clinical pathology
, 1e. Ames: Iowa State Press.
Sturgess, K. (2013).
Notes on Feline Internal Medicine
, 2e. New York: Wiley.
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Abbreviations
ACh
Acetylcholin
ACTH
Adrenocorticotropic hormone
ADH
Antidiuretic hormone
ALP
Alkaline phosphatase
ANP
Atrial natriuretic peptide
APC
Antigen presenting cells
ARDS
Acute Respiratory Distress Syndrome
ATP
Adenosine triphosphate
cAMP
cyclic Adenosine monophosphate
BALT
Bronchus‐Associated Lymphoid Tissue
BCS
Body condition score
BMP
Bone morphogenic protein
CCK
Cholecystokinin
CFU
Colony forming units
CKD
Chronic kidney disease
CNS
Central nervous system
COB
Chronic obstructive bronchitis
CRH
Corticotropin‐releasing hormone
CRP
C‐reactive protein
DAGPC
Dystrophin‐associated glycoprotein complex
DAMPS
Danger‐associated molecular patterns
DIC
Disseminated intravascular coagulation
ECM
Extracellular matrix
EGF
Epidermal growth factor
FeLv
Feline leukaemia virus
FGF
Fibroblast growth factor
FIP
Feline infectious peritonitis
FIV
Feline immunodeficiency virus
FSH
Follicle stimulating hormone
GH
Growth hormone
GnRH
Gonadotropin‐releasing hormone
HPA
Hypothalamic–pituitary–adrenal axis
IBD
Inflammatory bowel disease
IGF
Insulin‐like growth factor
LE
Lupus erythematosus
LH
Luteinisation hormone
LPS
Lipopolysaccharides
MAPK
Mitogen‐activated protein Kinase
MG
Myasthenia gravis
MHC
Major histocompatibility complex
MMP
Matrix metalloproteinase
MPS
Mononuclear phagocytic system
Na
Sodium
NGF
Nerve growth factor
NK‐cells
Natural killer cells
NO
Nitric oxide
PAF
Platelet‐activating factor
PAMPS
Pathogen‐associated molecular pattern molecules
PRP
Pattern‐recognition receptors
PTH
Parathormone
RAAS
Renin‐Angiotensin‐Aldosterone System
ROS
Reactive oxygen species
SIBO
Small intestine bacterial overgrowth
SIRS
Systemic inflammatory response syndrome
SLE
Systemic lupus erythematosus
SMAD
Small mothers against decapentaplegic
TAP
Trypsinogen activation peptide
TGF
Transforming growth factor
TLR
Toll‐like receptor
TRPM8
Transient receptor potential cation channel subfamily M (melastatin) member 8
TRPV 1
Transient receptor potential cation channel subfamily V member 1
TSH
Thyroid‐stimulating hormone
UTI
Urinary tract infection
VEGF
Vascular endothelial growth factor
VLDL
Very‐low‐density lipoproteins
vWF
von Willebrand factor
Part IGeneral Pathological Mechanisms
1Inflammation
Definition
Inflammation is by definition a defensive reaction of the body with the aim of eliminating the trigger of the inflammation and repairing the damage caused, either by restoring the tissue of origin (restitutio) or by a replacement tissue, the scar (reparatio).
Trigger
Inflammation is triggered by any stimuli, called ‘noxae’, that overcome the organism's defence‐compensation mechanisms. By definition, a noxious agent is a substance or event that causes damage to a biological organism. The noxious agent can be divided according to its origin into internal and external, and according to its structure into physical, chemical or biological triggers (Table 1.1).
Defence Cascade of the Body
Numerous defence mechanisms exist to protect an organism. These are particularly effective at the ‘contact surfaces’ between the organism and the environment. There, the penetration of the noxious agent is prevented by mechanical as well as biological defence mechanisms.
The skin prevents the penetration of the noxious agent under physiological conditions due to its structural design. For this purpose, the skin consists of different layers with different functions (Figure 1.1).
The outer layer of the skin, the epidermis, is made up of the layers – stratum corneum, lucidum, granulosum, spinosum and basale from the outside inwards. The main cell type in the epidermis is the keratinocyte. This differentiates in the stratum basale from epidermal stem cells. In the stratum spinosum, the cells begin to remodel with an increase in volume and a change in shape and width. In the further course, keratohyalin grains are formed in the stratum granulosum, and further remodelling processes take place. The cells become flattened, the nucleus is lost, shrinkage occurs due to fluid loss, and finally cornification takes place. Eventually, no more keratinocytes can be detected in the stratum corneum. Keratinocytes become corneocytes. The cornification process builds up a mechanical protection for the skin. In addition, penetration of a noxious substance is ensured by a close connection between the keratinocytes through tight‐junctions. The tight‐junctions consist of connections of transmembrane proteins, such as claudin and occludin. Intracellularly, these proteins are connected to the cytoskeleton. The tight‐junctions connect the cells into a bandage that forms a barrier to the paracellular penetration of a noxious agent.
In addition, defence cells such as Langerhans cells are localised in the epidermis.
These are tissue macrophages that are capable of phagocytosis but also differentiate into antigen‐presenting cells after contact with an antigenically active noxious agent, which can initiate an immune response.
Finally, the extracellular matrix in the epidermis forms a molecular association that can prevent the penetration of a noxious agent. The molecules of the extracellular matrix include, for example, keratins and collagens as structural proteins and ceramides, which are lipids composed of a sphingosine molecule and fatty acids that provide protection against hydrophilic noxae (Mitamura et al. 2021) (Table 1.2).
Table 1.1 Common causes of inflammation in dogs and cats.
Physical
Chemical
Biological
Infectious agents
Heat
Environmental toxins
Viruses
Cold
Endogenous toxins
Tumours
Bacteria
Degenerations
Fungi
Parasites
Figure 1.1 Structure of the outer skin and development of keratinocytes.
Table 1.2 Components of the epidermal extracellular matrix with function.
Molecule
Function
Keratin
Intermediate filament, structural element of keratinocytes
Collagen
Tight protein of the ECM, adhesion molecule
Elastin
Elastic protein of the ECM
Fillagrin
Structural protein
Ceramide
Hydrophobic protection
The mucous membranes of the body form the inner boundary layer between the organism and the environment. The microscopic structure of the mucous membranes already reflects defence competences. This includes the contact of the mucosal cells through tight‐junctions. These form a tight connection between the cell membrane of neighbouring cells through proteins such as occludin. This prevents the paracellular penetration of extracorporeal noxae.
Another superficial defence mechanism is the synthesis of mucins. Mucins are glycoproteins that are synthesised by goblet cells and form a protective layer several micrometres thick on the mucosa. In the process, defence functions of the mucins develop due to their gel‐like structure, which enables mechanical protection of the underlying mucosal cells. Chemically, for example, bicarbonate residues of the mucins can bind and inactivate acids, and biologically, mucins can prevent bacteria from invading by binding them.
Cells localised in the mucosa (Paneth cells) secrete lysozyme or defensins to inactivate germs. The latter are differentiated into α‐, β‐ and θ‐defensins based on their molecular structure (Lehrer and Ganz 2002).
The effects of defensins are antimicrobial and immunomodulatory. The former effect is based on their positive molecular charge, which enables a charge‐dependent interaction with the negatively charged bacterial cell wall, especially the lipopolysaccharides (Scott and Hancock 2000). The binding of the defensins results in pore formation. The consequence is a depolarisation of the bacterial cell membrane and thus a breakdown of the membrane potential and lysis of the cell (Scott and Hancock 2000; Sahl et al. 2005).
In addition, defensins show immunomodulatory functions. Defensins have a chemotactic effect on dendritic cells and memory T cells, and thus represent a link between innate and adaptive immune responses. In addition, some defensins act chemotactically on monocytes and macrophages, and in some cases induce mast cell activation and degranulation. As a result, histamine and prostaglandins are released, which promote the migration of neutrophilic granulocytes. Degranulation of the recruited neutrophilic granulocytes in turn releases defensins again, resulting in a positive feedback loop (Yang et al. 2002).
The secretion of lysozyme is another defence mechanism against bacterial invasion of the mucous membranes. Lysozyme is an enzyme that cleaves murein. Murein is a peptidoglycan and a component of the bacterial cell wall. Due to the hydrolytic cleavage of murein, the bacterial cell wall loses its selective permeability and rupture of the bacterial cell wall occurs due to increased water influx.
Another defence mechanism in the mucosa is the mucosa‐associated lymphoid system located in the lamina propria, which is called ‘gut associated lymphoid tissue’ (GALT) in the gastrointestinal tract and bronchial associated lymphoid tissue (BALT) in the respiratory tract. This system includes numerous cells of the non‐specific and specific defence response, such as macrophages and lymphocytes (Figure 1.2).
Figure 1.2 Building up the defence system of the mucous membrane.
Player of the Inflammation
The inflammatory process is maintained by some so‐called ‘inflammatory cells’. These combine some properties that predispose them to fulfil the definitional task of inflammation. This states that inflammation is a reaction of the body that serves to eliminate a noxious agent and its consequences.
The following cells are involved in the inflammatory process:
Neutrophilic granulocytes originate from the leukocyte pool of the bone marrow and are distributed throughout the blood. The residence time in the blood is a few hours (6–12 hours). Subsequently, the neutrophilic granulocytes leave the blood capillaries under the influence of chemoattractive substances. These are released as part of the local inflammatory process. The process of neutrophilic granulocyte emigration from the blood vessels takes place via adhesion and transmigration. Integrin‐mediated, the neutrophilic granulocytes adhere to the surfaces of the endothelial cells. In the process, the cells change their shape from roundish to an amoeboid cell shape. The cells can now migrate trans‐ and paracellularly through the vascular endothelial layer.
