英语医学文献2

Unit 1 PathologyText BInflammationDefinition and Nature of Inflammation1 When living tissues are injured, a series of changes, which may last for hours, days or weeks, occurs in and around the area of injury. This response to injury is known as inflammation, the term being derived from the Latin inflammare meaning to burn.2 The injury is abnormal but the body’s reaction, inflammation, is a normal, if complex, physiological reaction—the only one possible in the circumstances of that particular injury. This reactive nature of inflammation was first recognized by John Hunter (1794), who, after his studies of war wounds, conclude: “Inflammation is itself not to be considered as a disease, but as a salutary operation consequent either to some violence or some disease”.3 Many different types of injury may evoke inflammation. They may be classified as follows:1)Physical agents, such as excessive heating or cooling, ultra-violet or ionizingradiation or mechanical trauma.2)Chemical substances, including toxins from various bacteria.3)Hypersensitivity reactions. The reaction of antibody or of sensitized lymphocyteswith bacterial or other antigens may, by the mechanism of hypersensitivity release substances which cause an inflammatory response.4)Microbial infections are a very important cause of inflammation.Micro-organisms may injure tissue in several ways—by release of exo- or endo- toxins①, by hypersensitivity mechanisms or by intracellular multiplication followed by cell death as seen in many viral infections.5)Necrosis of tissue from almost any cause leads to release of substances whichinduce inflammation in adjacent living tissues.4 The reaction in the first few hours after injury is stereotyped and widely different kinds of injury cause a similar initial response—the acute inflammatory reaction. The inflammatory nature of a lesion is usually indicated by the suffix –itis. Thus inflammation of the appendix is appendicitis, of the liver hepatitis and so on. There are occasional historical exceptions. Inflammation of the lung is traditionally pneumonia, not pneumonitis②, and of the pleura pleurisy not pleuritis③. The term acute and chronic refer to the duration of the response. Acute inflammation lasts for ①refers to exotoxin (refers to a toxin that is secreted by microorganisms into the surrounding medium) or endotoxin (a toxin that is confined inside the microorganisms and is released only when the microorganisms are broken down or die)②means the inflammation of the lungs (NB: when we refer to inflammation of the lungs, we often use “pneumonia” instead of “pneumonitis”)③NB: “pleura” is used more often to refer to the thin serous membrane around the lungs and inner walls of the chest than “pleuritis”.days or a few weeks; chronic inflammation persists for weeks, months or even years.5 The inflammatory response is usually beneficial, indeed it is essential in combating most infections and in limiting the harmful effects of many toxic agents. However it is not always of benefit. There are many situations when destruction of tissue or other untoward effects are due not to the damaging agent but to one or other aspect of the body’s response to injury. For example in acute inflammation of the larynx there may be sufficient inflammatory swelling to obstruct the airway and cause death from asphyxia. In both the Arhus reaction④and the local response to the bites of certain ticks, necrosis of tissue is caused by substances liberated from polymorph nuclear leucocytes which accumulate at the site of injury as part of the inflammatory response: such necrosis does not occur in animals deprived of blood leucocytes by prior treatment with bone marrow poisons such as nitrogen mustard. Inflammation is best considered not as a single process but as a collection of distinct processes, each of which may have evolved for defense against injury, but each of which has also potentially deleterious effects.Acute Inflammation6 This is the immediate and early response to an injurious agent and affects the vascular and connective tissues adjacent to the injured cells. There are three major components in the process of acute inflammation: increased blood flow (vasodilation), increased vascular permeability (exudation) and egress of white blood cells into the injured tissue (emigration). These three components are coordinated and interrelated by numerous chemical mediators produced or released at the site of injury. Mediators include histamine, bradykinin, complement and many other pharmacologically active substances. The emphasis here is on the morphological aspects of the inflammatory process visible to the pathologist rather than on the pharmacological and biochemical events.7 Vasodilation. Vasodilation occurs directly after injury. The microvasculature at the site of jury becomes dilated and filled with blood (hyperaemia). Blood flow through the dilated microvasculature is initially rapid, but soon slows because a concomitant increase in vascular permeability and loss of plasma water raises the viscosity of the blood. In the slowly moving blood the pattern of flow changes. Red cells tend to clump in the centre of the vessel lumen and leucocytes assume a more peripheral position near the vessel wall. This margination of leucocytes is an important initial step in the emigration process. If flow becomes very slow, the blood may clot and form a thrombus.8 Exudation. This is the increased passage of fluid and solutes, notably proteins, through the vessel wall. The mechanisms leading to increased vascular permeability are complex and incompletely understood. They include endothelial cell concentration or damage, the effects of mediators, local haemodynamic forces and the ④In immunology, the Arthus reaction is a type of local type III hypersensitivity reaction（过敏反应）. Type III hypersensitivity reactions are immune complex-mediated, and involve the deposition of antigen/antibody complexes mainly in the vascular walls, serosa（膜，浆膜）(pleura（胸膜）, pericardium（心包膜）, synovium （滑膜）), and glomeruli（血管小球）.osmotic effects of proteins escaping into interstitial tissue. The leak of proteins is roughly in proportion to their molecular size. Albumin is in the greatest amount, but if vascular permeability is extensive, large amounts fibrinogen may leak out. Exudation is an important local defence mechanism. The increase in interstitial fluid dilutes toxins, and proteins such as globulins are effective in neutralising agents like bacteria. This increased fluid is sometimes called inflammatory oedema or simply oedema.9 Emigration. Emigration of white blood cells, principally neutrophils and monocytes is also an important defence mechanism. These are phagocytic cells which engulf and digest foreign particulate matter such as bacteria and the debris of dead cells. The emigration of leucocytes is an active process which occurs in two stages. The cells stick to the endothelial surface (pavementing) and then actively migrate through the gaps between the endothelial cells and into the tissue spaces. The mechanism by which leucocytes stick to the endothelial cells in unknown. Emigration is an active amoeboid process and once outside the vessel, neutrophils can move as fast as 20 µm per minute. Monocytes, which differentiate into macrophages, move more slowly. Movement of leucocytes in tissue spaces is polarized in the general direction of the site of injury. This process, known as chemotaxis⑤, is mediated by various chemical attractants such as components of the complement, kinin and clotting system. Because neutrophils are in greater number in the circulating blood and because they move faster than macrophages, the first phase of cellular infiltration into damaged tissue is dominated by neutrophils. With the passage of time macrophage number increase and after 2 or 3 days macrophages outnumber neutrophils in most inflammations.10 Variants. Whilst the major components of acute inflammation are present in all damaged tissue, the proportions vary according to the nature, duration and extent of injury and to the nature of the injured tissue itself. Qualifying terms may be used to specify the dominant features of the inflammation. For example, serous exudate refers to the fluid-filled blister after burn.11 Sequelae. Acute inflammation is the first step in a dynamic response to injury. The sequelae depend on the nature and extent of injury. Resolution means the complete restoration of normal conditions after the cause of the acute inflammation is removed. This occurs when there is minimal cell death and tissue damage, rapid elimination of the causal agent, and local condition favouring the removal fluid and debris by lymphatics and by phagocytosis.Source：彭杰青编译，《英汉对照医学读物—病理学》，上海科学技术出版社；P162-196Words: 1203⑤趋向性（taxis）是一生物（或细胞）天生的行为反应，指其对一指向性刺激（由特定方向给的刺激），会有趋进（正趋向性）或远离（负趋向性）刺激源的动作。