proliferative inflammation


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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 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).

pro·lif·er·a·tive in·flam·ma·tion

an inflammatory reaction in which the distinguishing feature is an actual increase in the number of tissue cells, especially the reticuloendothelial macrophages, in contrast to cells exuded from blood vessels; in addition, exudates of various types are likely to be observed in granulomas and other forms of proliferative inflammation, but the latter may occur without an exudate being formed (as in certain infections caused by virus).

pro·lif·er·a·tive in·flam·ma·tion

(prō-lif'ĕr-ă-tiv in'flă-mā'shŭn)
An inflammatory reaction in which the distinguishing feature is an increase in the number of tissue cells, especially the reticuloendothelial macrophages, rather than of cells exuded from blood vessels.
Synonym(s): hyperplastic inflammation.

inflammation

(in?fla-ma'shon) [L. inflammare, to kindle]
An immunological defense against injury, infection, or allergy, marked by increases in regional blood flow, immigration of white blood cells, and release of chemical toxins. Inflammation is one way the body uses to protect itself from invasion by foreign organisms and to repair wounds to tissue. Clinical hallmarks of inflammation are redness, heat, swelling, pain, and loss of function of a body part. Systemically, inflammation may produce fevers, joint and muscle pains, organ dysfunction, and malaise. Synonym: inflammatory response See: table; autoimmune disease; infection

The Inflammatory Process

Local inflammatory responses begin when traumatized or infected tissues activate the humoral and cellular immune systems. Complement proteins and cytokines are manufactured. These signaling proteins start a cascade of chemical events that result in increases in local blood flow and the attraction of white blood cells to the damaged tissue. White blood cells in turn consume foreign or injured cells and release arachidonic acid metabolites, kinins, histamines, and more complement, thereby amplifying and perpetuating the immune response. The white blood cells also release toxic oxygen radicals, nitric oxide, and tissue-destroying enzymes in an attempt to kill any invading microorganisms. In healthy people, the process continues until all damaged tissues or invading pathogens are removed (usually about 5 days); an inpouring of fibroblasts, which repair the injury and form a healed scar, follows.

Systemic inflammatory responses occur when foreign proteins are recognized, e.g., in the bloodstream, and immune complexes are formed or cytotoxic T cells are activated. If sepsis triggers the immune response, these agents may help clear microorganisms from the blood.

Autoimmune illnesses occur when the chemical and cellular tools of inflammation are directed against the body's own tissues.

Diagnosis

Nonspecific test results that suggest inflammation include an elevated white blood cell count, erythrocyte sedimentation rate, or C-reactive protein level.

Treatment

Mild inflammation (such as the inflammatory change from minor injuries) often resolves with the topical application of ice packs or cold water. Nonsteroidal anti-inflammatory drugs (such as ibuprofen) and steroids (such as prednisone) are useful in managing more severe inflammation, as are many disease-modifying antirheumatic drugs, such as methotrexate or azathioprine.

acute inflammation

The early response to tissue injury, marked by the influx of white blood cells and inflammatory mediators into damaged tissues. Most of the response takes place in 12 to 24 hr.

adhesive inflammation

Inflammation of the serous membrane, enhancing the likelihood of attachments.

chronic inflammation

Inflammation that persists weeks to months after tissue damage. Its pathological hallmarks include simultaneous tissue repair and destruction.

exudative inflammation

Inflammation in which the fluid leaving the capillaries is rich in plasma proteins.

fibrinous inflammation

Inflammation in which the exudate is rich in fibrin.

hyperplastic inflammation

Inflammation characterized by excess production of young fibrous tissue. Synonym: proliferative inflammation

inflammation of jejunum

Jejunitis.

inflammation of liver

Hepatitis.

interstitial inflammation

Inflammation involving principally the noncellular or supporting elements of an organ.

lung inflammation

Pneumonia.

productive inflammation

An infrequently used term for any inflammatory process in which there is marked cellular proliferation, e.g., in proliferative retinopathy.

proliferative inflammation

Hyperplastic inflammation.

pseudomembranous inflammation

Inflammation in which a shelf of fibrin and white blood cell debris forms on an epithelial lining, usually from a toxin that necroses tissue. This type of inflammation is most often seen in colitis caused by Clostridium difficile. Before there were vaccinations against diphtheria, this inflammation was frequently found in the oral cavities of those infected with that pathogen.

purulent inflammation

Inflammation in which pus is formed. Synonym: suppurative inflammation

serous inflammation

Inflammation of a part with serous exudate, or inflammation of a serous membrane.

simple inflammation

Inflammation without pus or other inflammatory exudates.

subacute inflammation

Mild inflammation with minimal signs and symptoms. It may become chronic and gradually damage tissues.

suppurative inflammation

Purulent inflammation.

ulcerative inflammation

The formation of an ulcer over an inflamed area.
FactorsSourceEffect
Arachidonic acid metabolites (prostaglandins and leukotrienes)Phospholipids of cell membranes, especially mast cellsPrimary mediators of late-stage (> 6 hr) inflammation; increase dilation and permeability of blood vessels; stimulate neutrophil adhesion to endothelial tissue; bronchoconstriction; anaphylaxis
BradykininKinin system of plasma proteinsPrimary mediator of prolonged (> 1 hr) inflammation; vasodilation and increased permeability of blood vessels; pain; release of leukotrienes and prostaglandins
Complement proteinsMacrophages; liver endotheliumIncrease vasodilation and vascular permeability; coat antigens to enhance phagocytosis; attract neutrophils; destroy pathogens
Histamine and serotoninMast cells; basophilsPrimary mediators of early (=30 min) inflammation; rapid dilation and increase in permeability of venules; bronchoconstriction; stimulation of prostaglandin production
Interleukin 1 (IL-1)Macrophages; B cells, dendritic cells, neutrophils, other nucleated cellsIncreased production and activity of other chemical mediators, phagocytes and lymphocytes; promotes release of acute-phase proteins; causes fever
Interleukin 8 (IL-8)T lymphocytes; monocytesAttracts neutrophils and more T cells
Platelet-activating factor (PAF)PlateletsReleases chemical mediators; activates neutrophils; dilates and increases permeability of vessels
Transforming growth factor ß (TFGß)Activated macrophages and T lymphocytesAttracts neutrophils and monocytes; stimulates growth of connective tissue; inhibits other mediators
Tumor necrosis factors (TFNa)Activated macrophages and some lymphocytesIncrease synthesis of other cytokines; induce formation of new blood vessels; increase adhesion of neutrophils to endothelium; cause fever and cachexia
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