Library of Congress Cataloging-in-Publication
Trowbridge, Henry O.
Inflammation : a review of the process / Henry O. Trowbridge,
Robert C. Emiling. – – 5th ed.
p. cm.
Includes bibliographical references and index.
ISBN 0-86715-310-5 | eISBN 978-0-86715-895-3
1. Inflammation. I. Emling, Robert C. II. Title.
[DNLM: 1. Inflammation. QZ 150 T863i 1997]
RB131.T76 1997
616’.0473 – – dc21
DNLM/DLC
| for Library of Congress | 96-39904 |
| CIP |
Fifth Edition
© 1997 by Quintessence Publishing Co, Inc
Quintessence Publishing Co, Inc
551 North Kimberly Drive
Carol Stream, IL 60188
All right reserved. This book or any part thereof may not be reproduced, stored in a retieval system, or transmitted in any form or by any means, electronics, mechanical, photocopying, or otherwise, without prior written permission of the publisher.
Fourth edition copyrighted 1993
Editor: Betsy Solaro
Production: Eric S. Przyblyski
Cover design: Jennifer A. Sabella
Printed in the United States of America
Preface
Introduction
Abbreviations
Part I
Acute Inflammatory Process
1 Vascular Response to Injury
Quick review
The vascular events
Exudation, transudation, and edema
The lymphatic system
Postscript
2 Chemical Mediators of the Vascular Response
Histamine
Serotonin
Plasma proteases
The kinin system
The fibrinolytic system
Advice from some old friends
The complement system
Eicosanoids
Platelet activation factor
Nitric oxide
Neuropeptides
Other mediators
3 The Blood Leukoctyes
The cells involved
The individual leukocytes
The mononuclear-phagocytic system
4 Systemic Manifestations of Inflammation
Part II
Immunity
5 The Immune System
The opponents
The defenders
Antigen-presenting cells
The system
Immunoglobulins
General battle plan
Duration of antibody repsonses
6 Hypersensitivity Reactions
Type I—Immediate-type hypersensitivity
Type II—Immune cytotoic reactions
Type III—Immune complex hypersensitivity
Type IV—Delayed-type hypersensitivity
Immunologic tolerance
Immunodeficiency
7 Chronic Inflammatory Processes
General considerations
Causes of chronic inflammation
Factors contributing to chronicity
Maintenance of chronicity
Other cells involved
Tissue damage
Chemical mediators
Essential elements
Granulomatous inflammation
Control of inflammation
Part III
Repair of Host Tissues
8 Healing
Resolution vs repair
Regeneration
Fibrous repair
Cell-matrix interaction
Cell-cell interaction
The role cells play in wound healing
What is organization?
Epithelialization
Strength of healing wounds
Remodeling wounds
Local and systemic factors influencing healing
Part IV
Application of Basic Principles
9 Clinical Connections
Inflammation of the tooth pulp (pulpitis)
Inflammatory lesions of the periapical tissues
Acute pyogenic osteomyelitis of the jaws
Chronic osteomyelitis of the jaws
Cellulitis
Periodontal disease
Acquired immunodeficiency syndrome
Answers to Self-Test and Charts
Index
Over the past few years, we have witnessed an explosion of information concerning the processes of inflammation and immunity and how they protect, and in some instances, harm the host. In revising the fourth edition of this book, we have drawn extensively from the most upto-date journals and textb.ooks. We do not attempt a comprehensive treatment of these processes, complete with references and background material. Full detail would merely mean another book of esoteric language and of necessity would be hundreds of pages long. The amount of detail has therefore been purposefully kept at an “essential” level with the needs of the practicing professional always in mind.
The book is designed on the premise that the reader possesses a background understanding of the basic sciences.
Each chapter builds on that background and introduces “new” concepts in a careful and studied manner. Two chapters have been added in the fifth edition, one concerning the systemic manifestations of inflammation, and the other applying what has been covered in the preceding chapters to specific clinical conditions.
With our combined backgrounds in pathology and education, we have creijted a “self-study” book that will bring readers up to date b_n the fundamentals of inflammation and immunology at)a;, further, will help them understand related materials they \/Viii come across in journals and at meetings. It will also be useful for graduate students in specialty pro grams when pieparing for specialty board examinations.
This book is also designed with a teaching methodology. Based on research and experience in higher education, and especially in continuing education, this methodology involves modes of quick comprehension and strategically placed review mechanisms. This structure enables you to read, study, and comprehend, while moving through the material. In other words, this is a “workbook” of sorts. Take time to understand each chapter before moving on to the next. In this way, as the material builds, you will be able to follow the development and fully understand the referrals back to earli er passages.
The book is divided into four sections. The first covers the various components of inflammation, both local and systemic; the second provides a review of immunology and immunopathology; and the third explains healing, the final stage of inflammation. The fourth section is new in this edition. It consists of familiar clinical conditions. We hope that by applying what you have learned in the first three sections, you will gain new insights into these disease processes and that as a result, your therapeutic decisions will have a strong scientific basis. As you proceed through the book, you will be amazed at how effective our host defensive system is. At times these defenses may harm the host, but for most of us, they provide a long and healthy life.
The wide acceptance of this book since its first appearance in 1978 has been most gratifying. A special thanks goes to Professor Masaki Shimono, Department of Pathology, Tokyo Dental College, for the use of some illustrations. We acknowledge with heartfelt gratitude our benefactor, Dr J.B. Bender, foremost among those to whom we are indebted. Without his impelling influence this book never would have been launched.
Inflammation is a defense reaction of higher animals to the presence of any injurious stimulus. An irritant can be physical in nature, such as heat, or it can be chemical, or bacterial. One can look upon inflammation as an immunologic mechanism of definite significance in bodily economy.
To inflame means to “set afire,” which conjures up the color red, a sense of heat, and often pain. The word comes to us by way of Middle English (enflamme), from the Middle French (enflamm), and from Latin (enflammare). The word inflammation is particularly appropriate as a descriptive term for the physiological response of the body to injury.
The inflammatory reaction tends to be stereotyped. Regardless of the nature of the stimulus, a sequence of events occurs whereby the deleterious agent tends to be localized and ultimately destroyed. To avoid confusion, a distinction should be made between acute and chronic inflammation. Acute refers to a response that is abrupt in onset and of short duration. Thus, acute inflammation may become chronic (in the temporal sense) if the injurious agent is persistent.
Chronic inflammation is characterized by a proliferation of fibroblasts and .small blood vessels, as well as an influx of chronic inflamq:iatory cells (lymphocytes, plasma cells, macrophages). At times, chronic inflammation is primary and is not preceded by an acute inflammatory response. This is the case in certain immunologic conditions. Chronic inflam mation also differs from acute inflammation in that it is orchestrated almost entirely by cells of the immune system.
We must hasten to add that there is a great deal of overlap between acute inflammation, chronic inflammation, and healing, but for the sake of simplicity we often consider them separately. Although frequently regarded as a separate process, healing commences soon after injury, while acute inflammation is still in full swing. Chronic inflammation is very similar to repair; in fact, it is often referred to as “frustrated repair” because healing is held in abeyance until the injurious agent has been completely eliminated. Do keep this overlap in mind as you proceed through the book.
Ab antibody
ACTH adrenocorticotropic hormone
ADCC antibody-dependent cell-mediated cytotoxicity
ADP adenosine diphosphate
Ag antigen
AIDS acquired immunodeficiency syndrome
AMP adenosine monophosphate
APC antigen-presenting cell
APR acute phase reaction
BMP bone morphogenetic protein
CD cluster designation
CD4 surface marker on T-effector/helper lymphocyte surface
CD8 marker on T-cytotoxic/suppressor lymphocyte
CGRP ca/citonin gene-related peptide
CMI cell-mediated immunity
CMV cytomegalovirus
CRP C-reactive protein
CSF colony-stimulating factors
CTL cytotoxic T lymphocyte
DTH delayed-type hypersensitivity
EBV Epstejn-Barr virus
ECM extritcellu/ar matrix
EGF epitdermal growth factor
ELAM endothelial leukocyte adhesion molecule
ESR erythrocyte sedimentation rate
Fc portion of immunoglobulin molecule
FDC follicular dendritic cell
FGF fibroblast growth factor
GALT gut-associated lymphoid tissue
GF growth factor
GM-CSF granulocyte-macrophage colony-stimulating factor
GMP guanosine monophosphate
H histamine
5-HPETE 5-hydroperoxyeicosatetraenoic acid
5-HT 5-hydroxytryptamine (serotonin)
H2O2 hydrogen peroxide
HLA human lymphocyte antigen
HMP hexosemonophosphate
HOCI hypochlorous acid
ICAM intracellular adhesion molecule
Ig immunoglobulin
IGF insulin-like growth factor
IL interleukin
INF interferon
JP juvenile periodontitis
LAK lymphokine-activated killer (NK cell)
LPS lipopolysaccharide (endotoxin)
LT leukotriene
MAC membrane attack complex
MHC major histocompatibility complex
MIF macrophage inhibition factor
NADPH nicotinamide adenine dinucleotide phosphate (reduced form)
NGF nerve growth factor
NK natural killer (cell)
NO nitic oxide
PAF platelet activating factor
PBL peripheral blood lymphacyte
PDGF platelet-derived growth factor
PDL periodontal ligament
PG prostoglandin
PMN polymorphonuclear neutrophil
RD reparative dentin
SC secretory component (of IgA)
SP substance P
SRS-A slow-reacting substance of anaphylaxis
TCR T-cell receptor
TGF transforming growth factor
Th1 T-helper cell subset
Th2 T-helper cell subset
TNF tumor necrosis factor
VEGF vascular endothelial growth factor
The vascular response to injury is a reactionary process that sets up the “delivery system” of inflammation. What is needed at the site of an injury is a way to deliver supplies and materials for defense. By initially opening up the vascular delivery system, more supplies and materials are shipped into an area than would normally pass that way. Without something else, however, the supplies would rapidly pass right on by. Therefore, the system builds in a slowing-down process once the supplies are on location. Finally, the system must get the supplies unloaded from the delivery system and across the country to the injury site.
Injury to an organ or tissue results in progressive changes in the damaged area. The main signs of such a response are redness, heat, and swelling. These signs are the result of vascular alterations in the area of injury. The redness and heat result from an increase in blood flow, which in turn is the result of vasodilatation, first involving arterioles, and then capillaries and venules. Swelling is the result of alterations in vascular permeability leading to exudation of fluid, plasma proteins, and white blood cells.
Certain blood vessels are involved in the response to injury. These vessels constitute the microvasculature. Since numerous references will be made to these vessels in the first section of this book, a quick review is in order (Fig 1-1).
Arteriole: Smaller than an artery, it consists of an inner layer of endothelial cells, a middle layer in which there is at least one layer of smooth muscle, and an outer layer of adventitia.
Fig 1–1 Microvasculature. (A) Adventitia; (SM) smooth muscle; (E) endothelium; (PS) precapillary sphincter; (1) arteriole; (2) metarteriole; (3) capillary; (4) venule.
Metarterioles: Branches of arterioles that are similar to capillaries except for the presence of muscle fibers that encircle the lining of endothelial cells. The muscle fibers do not form a continuous layer but tend to occur in groups.
Precapillary: May arise from either an arteriole or a metarteriole and is distinguished by the presence of a few muscle fibers that form a sphincter around the underlying endothe lial cells.
Capillary: The structural unit of the circulatory system. Except for the capillaries, the blood is normally contained within relatively heavy-walled, impervious tubes. Even in the capillary network the plasma and cells of the blood are separated from the tissues they serve by a thin sheet of endothelial cells that form the capillary wall. Fluid and metabolites are transported through the walls of the capillaries and reach the tissues by diffusion. Capillaries are surrounded by a basement membrane.
Fig 1–2 Fluid exchange across walls of small blood vessels.
Venules: Blood is drained from the capillaries by these vessels. They possess a basement membrane and an adventitia but lack smooth muscle fibers.
The movement of fluid in and out of arterioles, capillaries, and venules is regulated by the balance between intravascular hydrostatic pressure, which tends to force fluid out of the vessels, and the opposing effects of osmotic pressure exerted by the plasma proteins, which tend to retain fluid within the vessels (Fig 1-2). This is often referred to as Starling’s law.
During the acute inflammatory response, swelling results from (1) an increase in the hydrostatic pressure in the micro-circulation (this forces more fluid out of the vessels), and (2) the passage of fluid from small vessels (principally venules), which become more permeable to plasma proteins. When these proteins leave the vessels and enter the extravascular space, they increase the osmotic pressure in the tissue. This draws more fluid out of the blood vessels and into the tissues. The fluid that accumulates in the tissues is termed edema fluid.
The immediate responses to injury produced by physical, chemical, or microbial agents are quite similar, suggesting that injurious agents mediate their effects through common pathways. Thus, the acute inflammatory response is determined more by the severity of the injury than the actual cause.
The vascular response to injury is variable and may be reversible. The amount of variability and reversibility depends more upon the severity of injury than the kind of injury.
Following a very brief period of vasoconstriction, the arterioles dilate (vasodilation, Fig 1-3) and the microvasculature at the site of injury becomes filled with blood (congestion). Thus, the process of increased “delivery” is set in motion. This process is known as active hyperemia.
Fig 1–3 Vasodilation.
Fig 1–4 Increase in blood flow associated with inflammation. (A) Arteriole; (V) venule.
Vasodilation results from a relaxation of the smooth muscle layer of arterioles and the sphincter of precapillaries. This opens previously inactive capillaries and may result in as much as a tenfold increase in blood flow in the injured area (Fig 1-4). Postcapillary venules dilate as more blood flows in through the capillaries.
From the thousands of letters we have received about vascular permeability it is clear that you want to know why a vessel becomes leaky. Your long wait is over. . . .
Vessels become leaky for a couple of reasons (more detailed discussion later). For now, you should know that first the vessel dilates. The cells of the endothelium, which make up the inner layer, then contract. (This happens only in small postcapillary venules.) When the endothelial cells contract and draw away from each other, gaps form between the cells through which fluid and plasma proteins can move (Fig 1-5).
Another mechanism by which vessels may become more leaky is through an injury that causes destruction of endothelial cells but does not damage the basement membrane that surrounds the vessel. (If the basement membrane remains intact there is no hemorrhage.) Now this is more of the useful information we promised to deliver. Next time you see a bruise on your squash partner’s leg, you can comment with assurance, “Oh . . . I see your basement membrane was not intact!” As he tries to figure you out, you can probably nail down a couple more squash points. This destruction of endothelial cells can occur in capillaries and arterioles, as well as in venules.
Fig 1–5 Intercellular gaps.
1. In mild injury it is principally the postcapillary venules that become more permeable.
2. In moderate injury the capillaries as well as the small venules become more permeable.
3. In very severe injury the capillaries, venules, and arterioles may all become leaky.
Now you can see why the pattern of vascular permeability is known to be related more to the intensity of the injury than to the nature of the injury.
At first there is an escape of fluid (but not red or white blood cells) from the microvasculature due to (1) an increase in hydrostatic pressure inside the blood vessels, (2) increased vascular permeability, and (3) increased osmotic pressure in the extravascular tissue fluid (remember Starling’s law!).
Because fluid is lost from the vessels while blood cells are retained, there is an increase in the viscosity of the blood (hemoconcentration), and this tends to slow the flow of blood right at the site, where it is needed to deliver supplies.
Leukocytes (white blood cells) commence to stick to the endothelium of the venules (leukocyte margination or pavementing) producing an increase in resistance to blood flow, which in turn increases the hydrostatic pressure in the venules and capillaries.
As the blood flow continues to decrease there may be an eventual complete stagnation (vascular stasis). This is particularly likely to occur in the postcapillary venules where, because of increased vascular permeability, the loss of fluid is greatest. In mild injury, it may take 15–20 minutes for stasis to develop. In severe injury, stasis may occur within a few minutes.
In vascular stasis, because of an increase in the resistance to the flow of blood, there is an increase in hydrostatic pressure within the capillaries and venules. This pressure increase contributes to vascular permeability as well.
Plasma proteins that leave leaky vessels include albumin, fibrinogen, immunoglobulins, and other high molecular weight proteins. Thus, an inflammatory exudate consisting of fluid and plasma proteins accumulates in the tissue as a result of increased vascular permeability.
The vascular changes resulting from a mild mechanical injury of skin are often referred to as the “Triple Response of Lewis” (he was the first to characterize them). These changes consist of a flush, flare, and wheal and are most clearly seen in the reaction of the skin to a sharp blow or smack (as with a ruler) (Fig 1-6):
1. An immediate reddening, or flush, occurs at the site of injury producing vasodilation due to smooth muscle relaxation in the walls of arterioles (Fig 1-7). This response is primarily generated by the release of histamine.
Fig 1–6 Sharp smack to the skin with a ruler.
Fig 1–7 Immediate reddening or flush.
Fig 1–8 Red flare spreading outward from the wound.
Fig 1–9 Swelling (wheal) associated with accumulation of edema fluid.
2. Soon a red flare spreads outward from the injured area. The flare is partly of nervous origin (“neurogenic inflammation”) resulting from vasodilation associated with the release of neuropeptides (Fig 1-8).
3. Eventually, increased vascular permeability produces a swelling, or wheal, as edema fluid accumulates in the tissue (Fig 1-9).
(Notice the military flavor to this whole book? Not yet? Well, you will. . . .) At each self-test it would be a good idea to make sure you really understand before moving on.
Self-test 1-1
1. What causes heat and redness in an acute inflammatory response?
2. What is Starling’s law and how does it relate to vascular reactions?
3. In acute inflammation, what causes tissues to swell?
4. What is the most important factor in determining the extent of the immediate acute response?
5. What is meant by active hyperemia?
6. What does relaxation of the precapillary sphincters accomplish?
7. What causes hemoconcentration?
8. How does vascular stasis develop?
9. Which type(s) of vessel become(s) more permeable in mild injury?
10. What produces gaps between endothelial cells?
11. When vascular permeability is increased, which plasma proteins may be found in the exudate?
Answers on .
These terms are associated with similar processes, so we need to clarify what they are and how they are related to the defensive posture.
Increased vascular permeability allows fluid and plasma proteins to leave the blood vessels. This process is termed exudation, and the substances that leave the vessels and enter the tissues are collectively called the exudate. Couldn’t be easier, right?
The amount of protein in an exudate is variable. There are several categories of exudates, depending on the amount of proteins and/or cells that leave the vessels. For example:
1. Serous exudate is associated with mild inflammation. The fluid is usually clear with a relatively low protein content and very few cells. (The fluid in a blister is a good example.)
2. Fibrinous exudate is rich in protein, particularly fibrinogen. When it enters the tissue, the exudate clots due to the formation of fibrin. An example is the collection of fibrinous exudate on the surface of the lung (pleurisy) due to bacterial pneumonia.
3. Suppurative (or purulent) exudate is rich in neutrophils (PMNs) and is recognized clinically as pus.
Actually, exudates play a useful role in addition to just being good-looking! The fluid dilutes bacterial toxins. The deposition of fibrin may act as a mechanical obstruction to the spread of bacteria or aid in phagocytosis by providing a surface against which bacteria can be trapped. In addition, exudates contain antibody and complement molecules that are extremely important, as will be clarified later.
As you’ve seen, exudation is an inflammatory process and is associated with increased vascular permeability. Transudation is also the movement of fluid and some proteins from blood vessels; however, it is different from exudation in that it occurs in noninflammatory conditions (Table 1-1). Examples would be fluid collecting in the lungs (pulmonary edema) in cases of congestive heart failure and ascites in cirrhosis. Transudation can occur in any or all of the following:
1. Increase in hydrostatic pressure in small blood vessels
2. Decrease in osmotic pressure in small blood vessels
3. Increase in osmotic pressure in the extravascular compartment
Table 1-1 Comparison of transudate and exudate |
||
|
Transudate |
Exudate |
Amount of protein |
Low (specific gravity <1.015) |
High (specific gravity >1.015) |
Type of protein |
Albumin |
All plasma proteins |
Fibrin |
No |
Yes |
Cells |
None |
Inflammatory |
One word often associated with the vascular changes seen in the body and with exudation and transudation is edema. Edema refers to an abnormally large amount of leakage of fluid from the bloodstream into the surrounding tissues. Edema can be associated with either exudation or transudation.
Why should edema be considered part of the defensive system? Clearly, inflammatory edema is associated with increased vascular permeability and the exudation of plasma proteins, and there are some very positive aspects of inflammatory edema for defense.
The positive aspects of inflammatory edema are as follows:
1. Dilutes toxins in the tissue
2. Inactivates toxins by action of proteolytic enzymes contained in the fluid
3. Provides nutrients for inflammatory cells
4. Contains antibodies that help protect the host
5. Contains complement proteins
6. Often contains fibrinogen, which, when converted to fibrin, facilitates movement of inflammatory cells into the wound and enhances phagocytosis
Inflammatory edema is associated with increased vascular permeability and the exudation of plasma proteins.
In addition to the terms exudate and transudate you should be familiar with the term effusion. Effusion is the passage of an exudate from blood vessels into the tissues or a cavity of the body (eg, pleural effusion, pericardial effusion).
So far we have made the point that the vascular response to injury is quite variable and that part of the variability is dependent upon the degree of injury sustained (mild, moderate, or severe).
There is another point to be made about variability, that is, the duration of the vascular response. Remember, the body can be engaged in a quick skirmish or find itself in a protracted conflict over life and death! So, the defense system must be able to somehow determine how much support is needed and for how long. In a nutshell, when the insult is major, the response should be also. As a result, not only is the kind of response variable, but so is the duration, and it’s all predicated upon the severity of injury.
The duration is controlled by chemical mediators (from the National Vascular Mediation Board). We will mention them by name only and detail them later in Chapter 2.
Fig 1–10 Immediate and delayed vascular response.
This occurs soon after mild injury and lasts about 10–15 minutes. It mainly involves small and medium-sized post-capillary venules. The immediate transient response is shown in Figure 1-10. The response appears to be mediated primarily by histamine and can often be suppressed by antihistamines.
This occurs with more severe injury and involves capillaries as well as venules. The sustained phase follows from several minutes to an hour after the immediate transient phase and may last for hours or even days (Fig 1-10). Chemical mediators probably include bradykinin early on and later prostaglandins, leukotrienes, anaphylatoxins, oxygen-derived free radicals, and still others. It can be suppressed by salicylates and glucocorticoids.
In this case, injury does not evoke an immediate response (sunburn is an example). Prostaglandins and leukotrienes probably mediate this response.
This occurs in the severest of injuries and involves a marked vascular response (venules, capillaries, and arterioles).
Vascular permeability increases immediately and continues to remain high. This is probably due to an overlapping of the immediate (histamine-mediated) and delayed responses medi ated by bradykinin, prostaglandins, leukotrienes, etc. (The reason we have emphasized the overlapping aspect here is because, as with all superb defensive systems, there is what we generals like to call “redundancy.” We will be coming back to redundancy later; it is a very important concept. It’s good insurance, and it can be essential for bringing about a compound effect.)
So, here we are. The system is delivering supplies to the battleground; the transport system is pouring in the “right stuff”! But you cry, “Where’s the discipline?” The arena is in danger of being overwhelmed and swamped. What is to happen to the excess fluid and proteins that accumulate as a result of increased vascular permeability? Did you really think that the system had no mechanism for this contingency? Where’s your faith?
Much of the fluid is removed by the lymphatic system. Venules may also participate in this. Lymphatics are endothelial-lined channels with loose intercellular junctions, sparse basement membranes, and no muscular lining (except in the larger lymphatic ducts).
The lymphatics play an important role in draining the exudate (fluid, leukocytes, cell debris, plasma proteins, and fibrin) from the site of inflammation (Fig 1-11). In this way foreign antigens can be transported to lymph nodes, where they initiate an immune response. Drainage of chemical irritants or bacteria may irritate the lymphatic vessels and produce lymphangitis, which means inflammation of the lymphatic vessels. (Lymphadenitis means that the draining lymph nodes are inflamed.)
Fig 1–11 Dilated lymphatic vessel (arrow) in inflamed skin.
You should now be able to fill in Chart 1. Do this by placing an X in each box that applies (answers on ).
Chart 1
Some clinicians might use the more traditional Latin names for the cardinal signs of inflammation we have been describing. These are:
Calor—Heat, the result of increased blood flow
Rubor—Redness, also the result of increased blood flow
Tumor—Swelling, the result of exudation and inflammatory edema
Dolor—Pain, the result of tissue pressure due to hyperemia and edema and the release of algogenic (pain producing) inflammatory agents such as bradykinin (more on this later)
Functio laesa—Loss of function, the result of swelling and/or pain
The events of the vascular response to injury are not necessarily in a precise sequence. In fact, several events may be occurring simultaneously or even overlap each other.
Self-test 1-2
1. Name the three principal phenomena associated with the acute inflammatory response.
2. In acute inflammation, what produces increased permeability of blood vessels?
3. What determines the duration of the vascular response?
4. What is the process of exudation?
5. What is edema?
6. How does a serous exudate differ from a fibrinous exudate?
7. What is meant by the term “biphasic” response?
8. What is the difference between exudation and transudation?
9. In inflammation, what do lymphatics do besides remove fluid from the tissues?
10. Besides the lymphatics, how else can fluid be removed?
Answers on .
In this chapter we have reviewed the following:
1. The components of the vascular system.
2. The vascular response to injury.
3. Starling’s law and how it applies to exudation and transudation.
4. Vasodilation.
5. Increased vascular permeability.
6. Vascular stasis.
7. The triple response of Lewis.
8. Exudation and exudates.
9. Duration of increased vascular permeability.
10. The lymphatic system.
11. The cardinal signs of inflammation.
Chandrasoma P, Taylor CR. Concise Pathology, 2nd ed. Norwalk, Conn: Appleton & Lange; 1995:35–46.
Cotran RS, Kumar V, Robbins SL. Pathologic Basis of Disease, 5th ed. Philadelphia: WB Saunders; 1995:51–57.
Ritchie AC. Boyd’s Textbook of Pathology, 9th ed. Philadelphia: Lea & Febiger; 1990:60–81.
Walker BAM, Fantone JC. The inflammatory response. In: Sigal LH, Ron Y, eds. Immunology and Inflammation. New York: McGraw-Hill; 1994:359–383.
Officers control troops with predetermined strategies and regulations. Sometimes, external forces dictate and control military actions and reactions, but usually the internal chain of command sets the pace. Inflammation is controlled by the presence of a group of substances called chemical mediators, each with a specific role at some definite stage of the inflammatory reaction. These mediators may be exogenous (arise from bacteria or chemical irritants) or endogenous in origin. In this section we will be dealing with the latter.
It is important to note that the exact sequence of the appearance of various mediators and their dependence on, or independence of, each other is still largely speculative. Furthermore, other mediators have probably not yet been identified.
Before we get into a description of the endogenous chemical mediators, it might be helpful to understand that:
1. The body needs some mechanism for “immediate” action on the battle front, which will also initiate other events. The first mediator in this section, histamine, serves this function. In order to be immediately effective (as in “ready to go”) this mediator is already present in the tissues before the damage occurs. Histamine just sits tight and usually exerts its effect only after injury releases it. (Note: Some allergic reactions also cause its release.)
2. Other mediators must be produced at the site, or by migrating leukocytes attracted to the injury.
Fig 2–1 Histamine release.