inflammation

inflammation,

reaction of the body to injury or to infectious, allergic, or chemical irritation. The symptoms are redness, swelling, heat, and pain resulting from dilation of the blood vessels in the affected part with loss of plasma and leucocytes (white blood cells) into the tissues. White blood cells communicate with each other via cytokines, which are polypeptides released by cells of the immune system that regulate other cells. They are a broad class of soluble compounds that signal one cell type to another, particularly in response to foreign substances. Granulomas are most common in infectious diseases such as tuberculosistuberculosis
(TB), contagious, wasting disease caused by any of several mycobacteria. The most common form of the disease is tuberculosis of the lungs (pulmonary consumption, or phthisis), but the intestines, bones and joints, the skin, and the genitourinary, lymphatic, and
..... Click the link for more information. , leishmaniasisleishmaniasis
, any of a group of tropical diseases caused by parasitic protozoans of the genus Leishmania. The parasites live in dogs, foxes, rodents, and humans; they are transmitted by the bites of sand flies.
..... Click the link for more information. , and schistosomiasisschistosomiasis
, bilharziasis
, or snail fever,
parasitic disease caused by blood flukes, trematode worms of the genus Schistosoma. Three species are human parasites: S. mansoni, S. japonicum, and S. haematobium.
..... Click the link for more information. , in which the body's defenses, unable to destroy the offending organisms, try to enclose them in a mass of inflammatory cells. Certain types of inflammation result in pus formation, as in an abscess. The leukocytes destroy harmful microorganisms and dead cells, preventing the spread of the irritation and permitting the injured tissue to repair itself.

Inflammation

a complex defense reaction of the body for dealing with harmful agents developed in the course of evolution and manifested by various vascular and tissue changes. Inflammation is one of the processes underlying many diseases with different clinical symptoms. The biological role of inflammation is to limit the spread of pathogenic agents in the body; sometimes the inflammatory process helps to destroy them. Intensive study of the mechanisms of inflammation began after R. Virchow advanced his theory of cellular pathology. According to this theory, inflammation is a local tissue reaction morphologically manifesting itself in protein dystrophy of cells. The German scientist J. Konheim regarded disturbances in the flow of blood and lymph in the inflammatory focus as the primary factor in inflammation. The Russian biologist E. Metchnikoff developed a fundamentally new approach to the analysis of inflammation with his general biological theory (1892) based on the results of a comparative pathological study of the process. Metchnikoff demonstrated the decisive significance of evolutionary characteristics and perfection of the organism in the development of inflammation. He also described phagocytosis as an inseparable part of the inflammatory process and scientifically substantiated the relationship between a focus of inflammation and the body as a whole.

The causes of inflammation may be either exogenous (external), such as bacteria and their toxins, mechanical injury, effects of radiation or electrical energy, and chemical substances, or endogenous (arising within the organism itself), including products of tissue necrosis and decomposition, thrombi, infarcts, hematomas, and deposits of salts. Depending on the course, inflammation may be acute, subacute, or chronic. An acute inflammation of the skin, such as an abscess or burn, is manifested by redness, swelling, elevated temperature in the area of inflammation, soreness, and functional impairment of the affected organs and tissues. Not all of the above symptoms are present in chronic inflammation or in inflammation of the internal organs.

Inflammation consists of a vascular reaction, alteration, and proliferation. The vascular reaction is manifested first by a transient vascular spasm in the inflammatory focus followed by dilation of the arterioles and capillaries, which undergo an intensified filling with blood (arterial hyperemia). The external signs are elevated temperature in the focus, redness, and pulsation. These vascular changes are due to an accumulation in the inflammatory focus of substances that affect the tone of the vascular wall, such as acetylcholine, histamine, and adenine nucleotides. The next phase of the vascular changes involves dilation of the venous network and slowing of the blood flow. Because of an increased permeability of the vascular walls, plasma (the liquid part of the blood) and leukocytes (exudation) emerge into the surrounding tissues. The causative agent of the inflammation greatly affects the nature of the exudative process and composition of the exudate (inflammatory effusion). The exudate can be serous (from serum), fibrinous (with an increased amount of protein), leukocytic (with many leukocytes), purulent, or hemorrhagic (with many erythrocytes). The exudate causes the swelling of tissues in the focus of inflammation. It can accumulate in cavities, for example, in pleuritis. Pain is caused by compression of the edema and by irritation of the nerve endings in the inflammatory focus by the metabolic products. During the vascular changes the leukocytes approach the vascular wall (phenomenon of margination of leukocytes), after which they emerge from the vascular stream (diapedesis) and migrate to the focus of inflammation. Here they carry out phagocytosis. The migration of leukocytes to the focus is caused by chemotaxis (drawing of leukocytes from the blood by chemical agents accumulating in the inflammatory focus), by the appearance in the inflammatory focus of substances capable of decreasing the surface tension of leukocytes and of substances that convert leukocyte protoplasm from a sol to a gel, and by electrokinetic factors.

Circulatory disturbances in a focus of inflammation are accompanied by the development of thrombi and protein coagula (protein flakes) in the blood vessels and lymphatics, by the filling of their lumens with various cellular elements that enter the exudate in profusion, and by increased vascular tone and compression of the small vessels by edema. These processes eventually block the efferent blood vessels and lymphatics, thus making it difficult for bacteria and the toxic products formed by tissue breakdown to become absorbed and enter the bloodstream; that is, the focus of inflammation is separated from healthy tissue. The presence of a greater or lesser admixture of multiplying mesenchymal cells stimulates the subsequent regenerative processes in the injured tissues.

Alteration (lesion) of tissues in inflammation is reflected in structural and functional changes in the injured tissue. The tissue changes range from dystrophy (protein, fatty, and hyaline) to necrosis (death) of tissues, and they are the result of nutritional and metabolic disorders. All the metabolic processes (the “fire of metabolism”) are sharply intensified and qualitatively changed in a focus of inflammation. Glucose is excessively consumed in inflamed tissue at a time when the oxygen is relatively inadequate. Moreover, the respiratory coefficient decreases and anaerobic glycolysis intensifies. The accumulation of lactic acid and other incompletely oxidized metabolic products produces acidosis, fatty acids increase, and the content of ketone bodies increases in blood flowing from the focus. In the inflamed tissue protein decomposition also intensifies. The metabolic disturbances give rise to increased osmotic and oncotic pressure in the focus.

Proliferation (multiplication of cellular elements) takes place on the periphery of a focus of inflammation against a background of exudation and alteration processes, and it is most pronounced in the final stages of the process. Proliferation is followed by gradual regeneration (repair of tissues), which completes the inflammatory process. Inflammation may be exudative, alterative, or proliferative, depending on the particular component that is dominant. Inflammation always results in the death of tissues. The outcome of the inflammation depends on the condition of the body, the form of inflammation, and the size of the focus. Inflammation may be normergic (characteristic of a healthy body) or hyperergic, when the body is sensitized. The latter form is characterized by intensive alteration, for example, Pirquet’s reaction. Hypoergic inflammation occurs in the presence of immunity to the factor that caused the inflammation and when the body is exhausted. Development of the inflammatory process is also largely a function of age, nutrition, and metabolism. The nervous and endocrine systems play a major role in the development of inflammation. Excitation of the sympathetic nervous system decreases the inflammatory phenomena, while excitation of the parasympathetic nervous system intensifies them. Hormones also influence the course of inflammation in different ways. Thus, the adenocorticotropic hormone (ACTH) of the hypophysis and the glucocorticoids of the suprarenal gland inhibit the development of inflammation while the mineralocorticoids of the suprarenal gland activate it. Dysfunction of the pancreas (diabetes mellitus) causes a predisposition to stubborn pyoderma. Inflammation is severe with increased thyroid function (hyperthyroidism). Small thrombi and dead tissues are resorbed in the final stage of inflammation (enzymic splitting, phagocytosis). The large defects formed in the tissues as a result of fibrinous-necrotic inflammation are replaced by scar tissue, which impairs the function of organs (for example, cirrhosis of the liver after hepatitis) and deforms them (for example, deformity of the heart valves after endocarditis). Inflammation of the tubular organs (esophagus, uterine tubes, intestines) may result in their becoming constricted and their lumens closing completely (obliteration). When the exudate is resorbed from the body cavities (abdominal, pleural, and others), the fibrin remaining on the surface of the serous membranes forms adhesions.

Inflammation may provoke a greater or lesser reaction throughout the body, depending on where it originates and on the size of the focus. The body mobilizes its defensive forces and creates antibodies. Moreover, symptoms of intoxication (poisoning) may appear when the products of the vital activity of the causative agents and the products of tissue decomposition are resorbed. They include chiefly fever, an increased number of leukocytes in the peripheral blood (leukocytosis), and an accelerated erythrocyte sedimentation rate (ESR). When the bacteria are carried to parts of the body remote from the focus of inflammation, metastatic inflammatory foci may arise.

REFERENCES

Al’pern, D. E. Vospalenie (Voprosy patologii). Moscow, 1959.
Metchnikoff, E. Lektsii o sravnitel’noi patologii vospaleniia. Moscow, 1947.
Menkin, V. Dynamics of Inflammation. New York, 1940.

V. A. FROLOV

inflammation

[‚in·flə′mā·shən] (medicine) Local tissue response to injury characterized by redness, swelling, pain, and heat.

inflammation

the reaction of living tissue to injury or infection, characterized by heat, redness, swelling, and pain

Inflammation

inflammation

[in″flah-ma´shun] a localized protective response elicited by injury or destruction of tissues, which serves to destroy, dilute, or wall off both the injurious agent and the injured tissue. adj., adj inflam´matory.
The response" >inflammatory response can be provoked by physical, chemical, and biologic agents, including mechanical trauma, exposure to excessive amounts of sunlight, x-rays and radioactive materials, corrosive chemicals, extremes of heat and cold, or by infectious agents such as bacteria, viruses, and other pathogenic microorganisms. Although these infectious agents can produce inflammation, infection and inflammation are not synonymous.
The classic signs of inflammation are heat, redness, swelling, pain, and loss of function. These are manifestations of the physiologic changes that occur during the inflammatory process. The three major components of this process are (1) changes in the caliber of blood vessels and the rate of blood flow through them (hemodynamic changes); (2) increased capillary permeability; and (3) leukocytic exudation.
Hemodynamic changes begin soon after injury and progress at varying rates, according to the extent of injury. They start with dilation of the arterioles and the opening of new capillaries and venular beds in the area. This causes an accelerated flow of blood, accounting for the signs of heat and redness. Next follows increased permeability of the microcirculation, which permits leakage of protein-rich fluid out of small blood vessels and into the extravascular fluid compartment, accounting for the inflammatory edema.
Leukocytic exudation occurs in the following sequence. First, the leukocytes move to the endothelial lining of the small blood vessels (margination) and line the endothelium in a tightly packed formation (pavementing). Eventually, these leukocytes move through the endothelial spaces and escape into the extravascular space (emigration). Once they are outside the blood vessels they are free to move and, by chemotaxis, are drawn to the site of injury. Accumulations of neutrophils and macrophages at the area of inflammation act to neutralize foreign particles by phagocytosis.
Chemical mediators of the inflammatory process include a variety of substances originating in the plasma and the cells of uninjured tissue, and possibly from the damaged tissue. The major kinds of mediators are (1) vasoactive amines, such as histamine and serotonin; (2) plasma endopeptidases that comprise three interrelated systems, the kinin system that produces bradykinin, the complement system that produces proteins that interact with antigen--antibody complexes and mediate immunologic injury and inflammation, and the clotting system that increases vascular permeability and chemotactic activity for the leukocytes; (3) prostaglandins, which can reproduce several aspects of the inflammatory process; (4) neutrophil products; (5) lymphocyte factors; and (6) other mediators, such as substance of anaphylaxis" >slow-reacting substance of anaphylaxis and pyrogen" >endogenous pyrogen.
Hormonal Response. Some hormones, such as cortisol, have an antiinflammatory action that limits inflammation to a local reaction while others are proinflammatory. Thus, the endocrine system has a regulatory effect on the process of inflammation so that it can be balanced and beneficial in the body's attempts to recover from injury.

Cellular changes in inflammation. 1, Margination of neutrophils brings these inflammatory cells in close contact with the endothelium. 2, Adhesion of platelets results in the release of mediators of inflammation and coagulation. Fibrin strands are the first signs of clot formation. 3, Pavementing of leukocytes is mediated by adhesion molecules activated by the mediators of inflammation released from platelets and leukocytes. RBC, red blood cells. From Damjanov, 2000. acute inflammation inflammation, usually of sudden onset, marked by the classical signs of heat, redness, swelling, pain, and loss of function, and in which vascular and exudative processes predominate.catarrhal inflammation a form affecting mainly a mucous surface, marked by a copious discharge of mucus and epithelial debris.chronic inflammation prolonged and persistent inflammation marked chiefly by new connective tissue formation; it may be a continuation of an acute form or a prolonged low-grade form.exudative inflammation one in which the prominent feature is an exudate.fibrinous inflammation one marked by an exudate of coagulated fibrin.granulomatous inflammation a form, usually chronic, attended by formation of granulomas.interstitial inflammation inflammation affecting chiefly the stroma of an organ.parenchymatous inflammation inflammation affecting chiefly the essential tissue elements of an organ.productive inflammation (proliferative inflammation) one leading to the production of new connective tissue fibers.pseudomembranous inflammation an acute response" >inflammatory response to a powerful necrotizing toxin (such astoxin" >diphtheria toxin), characterized by formation on a mucosal surface of a false membrane composed of precipitated fibrin, necrotic epithelium, and inflammatory leukocytes.purulent inflammation suppurative inflammation.serous inflammation one producing a serous exudate.subacute inflammation a condition intermediate between chronic and acute inflammation, exhibiting some of the characteristics of each.suppurative inflammation one marked by pus formation.toxic inflammation one due to a poison, e.g., a bacterial product.traumatic inflammation one that follows a wound or injury.ulcerative inflammation that in which necrosis on or near the surface leads to loss of tissue and creation of a local defect (ulcer).

in·flam·ma·tion

(in'flă-mā'shŭn), Avoid the misspelling inflamation.A fundamental pathologic process consisting of a dynamic complex of histologically apparent cytologic changes, cellular infiltration, and mediator release that occurs in the affected blood vessels and adjacent tissues in response to an injury or abnormal stimulation caused by a physical, chemical, or biologic agent, including the local reactions and resulting morphologic changes; the destruction or removal of the injurious material; and the responses that lead to repair and healing. The so-called cardinal signs of inflammation are rubor, redness; calor, heat (or warmth); tumor, swelling; and dolor, pain; a fifth sign, functio laesa, inhibited or lost function, is sometimes added. All these signs may be observed in certain instances, but none is necessarily always present. [L. inflammo, pp. -atus, fr. in, in, + flamma, flame]

inflammation

(ĭn′flə-mā′shən)n.1. The act of inflaming or the state of being inflamed.2. A localized protective reaction of tissue to irritation, injury, or infection, characterized by pain, redness, swelling, and sometimes loss of function.

inflammation

A response to injury which is characterized by pain, swelling, heat, redness, and/or loss of function. See Round cellinflammation.

in·flam·ma·tion

(in'flă-mā'shŭn) A fundamental, stereotyped complex of cytologic and chemical reactions that occur in affected blood vessels and adjacent tissues in response to an injury or abnormal stimulation caused by a physical, chemical, or biologic agent. Redness (rubor), heat (calor), swelling (tumor), and pain (dolor) are signs generally associated with inflammation.[L. inflammo, pp. -atus, fr. in, in, + flamma, flame]

inflammation

The response of living tissue to injury, featuring widening of blood vessels, with redness, heat, swelling and pain-the cardinal signs ‘rubor’, ‘calor’, ‘tumor’ and ‘dolor’ of the first century physician Celsus. Inflammation also involves loss of function and is the commonest of all the disease processes. It is expressed by the ending ‘-itis’. Inflammation involves release of PROSTAGLANDINS which strongly stimulate pain nerve endings. It is, in general, protective and assists the immune system to restore normality, but persistent (chronic) inflammation may lead to the formation of undesirable scar tissue.

inflammation

a local response to injury or damage, by which HISTAMINES are released that trigger a number of effects including dilation of blood vessels, and the invasion of blood proteins, blood fluid and LEUCOCYTES into the tissues to combat invading bacteria.

Inflammation

The body's immune reaction to presumed foreign substances like germs. Inflammation is characterized by increased blood supply and activation of defense mechanisms. It produces redness, swelling, heat, and pain.Mentioned in: Acetaminophen, Analgesics, Analgesics, Opioid, Ankylosing Spondylitis, Antacids, Antiarrhythmic Drugs, Antiasthmatic Drugs, Antibiotics, Antibiotics, Topical, Antigastroesophageal Reflux Drugs, Antimigraine Drugs, Antiprotozoal Drugs, Antiretroviral Drugs, Antirheumatic Drugs, Antispasmodic Drugs, Antiulcer Drugs, Aspirin, Bronchodilators, Buerger's Disease, Bursitis, Cancer Therapy, Supportive, Canker Sores, Cellulitis, Cephalosporins, Corneal Ulcers, Corticosteroids, Costochondritis, Crohn's Disease, Dermatomyositis, Diuretics, Encephalitis, Erythromycins, Exophthalmos, Fluoroquinolones, Gammaglobulin, Graft-vs.-Host Disease, Hyperlipoproteinemia, Immunologic Therapies, Immunosuppressant Drugs, Keratitis, Leukocytosis, Myopathies, Nonsteroidal Anti-Inflammatory Drugs, Periodontal Disease, Physical Allergy, Pleurisy, Pulmonary Fibrosis, Q Fever, Relapsing Polychondritis, Rheumatic Fever, Sulfonamides, Trichinosis, Ulcerative Colitis, Vaginal Pain, Vasculitis

inflammation

A complex reaction that occurs in response to injury, infection, irritation, toxicity or hypersensitivity. The reaction is characterized by redness, heat, pain and swelling to different degrees. Treatment depends on the cause. See antiinflammatory drug; infection.

in·flam·ma·tion

(in'flă-mā'shŭn) Avoid the misspelling inflamation.Fundamental pathologic process consisting of a dynamic complex of histologically apparent cytologic changes, cellular infiltration, and mediator release that occurs in the affected blood vessels and adjacent tissues in response to an injury or abnormal stimulation caused by a physical, chemical, or biologic agent.[L. inflammo, pp. -atus, fr. in, in, + flamma, flame]

Patient discussion about Inflammation

Q. What causes inflammation of the knee joint? A. It depends on many things - the age of the person, other diseases he or she may have, whether he experienced any trauma to the joint, drugs or other substances he or she uses. Generally speaking, it may be caused by an infection (usually after trauma, very painful and abrupt inflammation, necessitates rapid treatment), rheumatologic diseases (such as rheumatoid arthritis or others, reaction to drugs or as a feature of other diseases.
You may read more here: http://en.wikipedia.org/wiki/Arthritis

Q. what is fragments of endocervical glandular mucosa with inflammation and squamous metaplasia fragments of endocervical glandular mucosaA. It means that part of the mucose on the cervix area has changes from a certain kind of mucose cells to another, and that there is a bit of an inflammation around it. This should be brought to the knowledge of a gynecologist and be monitored by him/her.

Q. Does anyone know how to relieve chronic back pain due to inflammation and arthritis? I have tried OTC arthritis pain meds they don't offer much relief for me. I have had surgery for herniated disc. My doctor says that there is a lot of inflammation and arthritis in my back. You can't get Vioxx anymore. Is there an alternative?A. there also is a drug called diclofenac(cataflam) ask your DR.

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noun swelling

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noun a response of body tissues to injury or irritation

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