acute inflammation

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Related to acute inflammation: chronic inflammation


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 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 slow-reacting substance of anaphylaxis and 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 inflammatory response to a powerful necrotizing toxin (such asdiphtheria 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).
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

a·cute in·flam·ma·tion

any inflammation that has a fairly rapid onset, quickly becomes severe, and is usually manifested for only a few days, but that may persist for even a few weeks; characterized histologically by edema, hyperemia, and inflitrates of polymorphonuclear leukocytes.
Synonym(s): active inflammation
Farlex Partner Medical Dictionary © Farlex 2012

a·cute in·flam·ma·tion

(ă-kyūt' in'flă-mā'shŭn)
Any inflammation that has a fairly rapid onset, quickly becomes severe, and is usually manifested for only a few days; characterized histopathologically by edema, hyperemia, and infiltrates of polymorphonuclear leukocytes.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

a·cute in·flam·ma·tion

(ă-kyūt' in'flă-mā'shŭn)
Any rapid-onset inflammation that quickly worsens but resolves in a few days to weeks; characterized histologically by edema, hyperemia, and inflitrates of polymorphonuclear leukocytes.
Medical Dictionary for the Dental Professions © Farlex 2012
References in periodicals archive ?
Although increased numbers of eosinophils and mast cells are detected in acute appendicitis (19,20), the absence of acute inflammation in 3 of 4 patients with tip obliteration supports the possible profibrogenic effect of eosinophils in fibrous obliteration of the appendix.
Wound healing involves inflammation, tissue formation, and tissue remodeling phases and begins with acute inflammation during which increased vascular permeability and vasodilatation occurs (14,16).
Conclusion: The results of the experiment showed that the crude extract of Berberis lycium (Bl.Cr) has been found more effective against acute inflammation (carrageenan-induced paw edema and xylene-mediated ear edema) than the chronic inflammation (formalin-evoked arthritic inflammation).
Acute inflammation is a form of innate immune defense and is the primary response to injury and infection.
The basal mean paw volume was comparable in all the three groups in carrageenin-induced paw edema model of acute inflammation in rats.
Mean age of patients in acute inflammation group was 46.36 +- 13.47 years, 44.10 +- 12.28 years in chronic inflammation group and 43.08 +- 13.14 yearsin no inflammation group.
Kupffer Cells Are Not Involved in the Pathogenesis of Chemically Induced Extrahepatic Acute Inflammation. Next, we examined the influence of KC deletion on dextran sodium sulfate- (DSS-) induced colitis as a model of extrahepatic acute inflammation, which shows features of ulcerative colitis with inflammation and exhibits features of Crohn's disease such as Th1 dependency [23, 24].
Histopathological evaluation overall (Figure 4) revealed less acute inflammation and fewer architectural changes when compared to her prior biopsies but was suggestive of an evolving autoimmune enterocolopathy with villous blunting of the duodenum and absence of goblet and Paneth cells in the colon.
Swelling, acute inflammation infiltration, necrotic tissue, and mass inflammatory cell were observed in all the groups on day 3.
Although regulation of lymphangiogenesis has been demonstrated in experimental models of chronic inflammatory diseases such as chronic skin inflammation (16), chronic inflammatory arthritis (23), and corneal inflammation (24), the functional role of the lymphatic vasculature in acute inflammation remains unclear.
ProThera has developed a novel process to purify Inter- alpha Inhibitor Proteins from human plasma, and has conducted research into the usage of IAIP to fight acute inflammation across multiple indication areas.

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