Pathophysiology-病理生理學(xué)

內(nèi)容概要

　　In recent years many foreign students from various countries have come to Chinafor higher medical education or advanced studies.To adapt to ever-increasinginternational communication，bilingual education is inevitable for universities.It is necessary to teach pathophysiology in English for foreign students whohave difficulty communicating in Chinese.We have designed this textbook toaid these students with their studies and to help them master necessary Chinesepathophysiological terminology.This textbook is designed to provide a concise summary of pathophysiology.It contains a learning guide， case files，main teaching content， exerases，and also provides some professional terminology in Chinese. We hope these students will find that this book provides useful reading material to assist them in understanding pathophysiology and enhanang their Chinese proficiency.This book is also suitable for Chinese students to improve their English level for academic purposes.This work is supported by the Capital Medical University of China. We wish to express our heartfelt thanks to Professor Xinliang Ma，at thomas Jefferson University USA，and Professor Like Zhang，at Capital Medical University of China，for their valuable review.We are especially grateful to Yunhui Du，PhD，for her assistance of proofing the whole book. We are also heartily thankful to co-editors that contributed their time and effort to this book and all the other contributors of this book for their excellent work to make this book available.

書(shū)籍目錄

Chapter 1 Introduction  1.1 The Function and Elements of Pathophysiology 1.2 The Major Research Methods Involved in Pathophysiology Chapter 2 Concept of Disease 2.1 Concepts of Health and Disease 2.2 Etiology 2.3 Pathogenesis  2.4 Clinical Manifestations 2.5 Diagnosis 2.6 Clinical Course 2.7 Outcome of Disease  Chapter 3 Water and Electrolyte Metabolism 3.1 Water and Sodium Metabolism Disorders 3.2 Disorders of Potassium Metabolism Chapter4 Acid-base Disturbance 4.1 The Regulation of Acid-base Homeostasis 4.2 Simple Acid-base Disorders  4.3 Complex Acid-base Disorders 4.4 Clinical Measurements and Analysis of Acid-base Disorders Chapter 5 Stress 5.1 Stressor  5.2 Stress Response 5.3 Altered Metabolism and Function  5.4 Stress Diseases and Stress Related Diseases 5.5 Pathophysiological Basis of Prevention and Treatment for Stress Disorders Chapter 6 Fever 6.1 Etiology  6.2 Stages and Manifestation  6.3 Altered Metabolism and Function  6.4 Pathophysiological Basis of Prevention and Treatment Chapter 7 Hypoxia， 7.2 Classification, Etiology and Mechanisms of Hypoxia  7.3 Alterations of Metabolism and Function in the Body  7.4 Pathophysiological Basis of Prevention and Treatment of Hypoxia Chapter 8 Disorders of Balance between Coagulation and Anticoagulation 8.1 Normal Balance between Coagulation and Anticoagulation 8.2 Disseminated Intravascular Coagulation (DIC) Chapter 9 Ischemia-reperfusion Injury 9.1 Etiology 9.2 Duration of lschemia 9.4 Alterations of Metabolism and Function in Myocardial Ischemia-reperfusion Injury 9.7 Pathophysiological Basis of Prevention and Treatment Chapter 10 Shock 10.1 The Etiology and Classification of Shock  10.2 The Development Process and Underlying Mechanisms of Shock 10.3 Cell Injury and Metabolic Changes in Shock  10.4 0rgan Dysfunction during Shock 10.5 Treatment of Shock andlts Rationale  Chapter 11 Heart Failure 11.1 Etiology of Cardiac Insuffiaency  11.3 CompensatoryResponsesinCardiaclnsufficiency  11.5 Alterations of Metabolism and Function in Cardiac Insufficiency  11.6 Pathophysiological Basis of Prevention and Treatment for Cardiac Insufficiency Chapter 12 Respiratory Failure 12.1 The Etiology and Pathogenesis 12.2 The Alteration of Function and Metabolism 12.3 The Pathophysiological Basis of Treatment Chapter 13 Hepatic Insufficiency 13.1 Hepatic Insufficiency  13.2 Hepatic Encephalopathy 13.3 Hepatorenal Syndrome  Chapter 14 Renal Failure 14.1 Etiology and Pathogenesis of Acute Renal Failure 14.2 Alterations of Metabolism/Function during ARF 14.3 Acute Renal Failure Management

章節(jié)摘錄

版權(quán)頁(yè)：   插圖：   (3) Increased β-adrenergic receptor activity. For instance, epinephrine, salbutamol, etc. can activate Na+-K+ pump through cAMP mechanisms to pro-mote the ability of cells to take in potassium. (4) Some toxicant, such as barium poisoning,can cause blocking in potassium channel, which pro-hibits the transference of potassium. (5) Hypokalemic periodic paralysis. It is a rare autosomal dominant genetic disease, which results in skeletal muscle paralysis and hypokalemia. 3.2.2.1.1.2 Insufficient intake of potassium Hypokalemia usually does not occur in people with normal diet. But for those patients with the di-gestive tract obstruction, coma, and anorexia nervo-sa, dieting to lose weight and those who deliberately prolongs fast after surgery, if potassium is not given in intravenous transfusion, hypokalemia can occur. 3.2.2.1.1.3 Excessive loss of potassium It is the most common causes for potassium de-ficiency and hypokalemia. (1) The excessive loss through kidney 1) Diuretics. Most diuretics, except for spirono-lactone and triamterene, can increase excretion of potassium with urine. The mechanisms are as fol-lows. Diuretics induces an increase in distal flow.Secondary excessive secretion of aldosterone occurs after diuretics taking. Chlorine can be lost after tak-ing diuretic, and thus potassium secretion increases continually in distal nephron. 2) Renal tubular acidosis. Type I is also called the distal convoluted tubule acidosis, in which pro-ton pump (H+ pump) in collecting tubule is in dis-orders and the excretion and reabsorption of K+ is blocked, which leads to acid retention and potassium loss. Type I , also known as proximal tubular acido-sis, is induced by reabsorption disturbance of K+ in proximal tubule.

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