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Inflammation

The inflammatory process is a mechanism of tissue reaction so there is a disposal, clearance and destruction of the cause of aggression. This process is characterized by the output of liquid and cells ( exudation ) and induces the process of cell repair.
 

Inflammation can be acute or chronic , however, the initial mechanisms are the same for both types . Therefore , what differentiates this division is the time of exposure to the offending agent , the agent and the type of immune response.
 

There are five signals in the inflammatory process that are called cardinal signs : heat, redness , tumor, pain and loss of function . The heat and redness are due to vasodilatation of the affected site leads to a larger amount of blood ( hyperemia ) , and therefore , there is an increase in temperature by increasing the blood concentration and for redness of blood. The tumor is caused by the increase of vascular permeability which allows leakage of liquid and therefore the edema which is synonymous with tumor. The pain appears both by compression of nerves by the tumor or by chemical mediators released as prostraglandinas E2 and kinin . The loss of function can be total or partial and occurs as a result of the other four cardinal signs . Throughout the inflammatory process, there is a release of chemical mediators that will be addressed later on.
 

For the inflammatory process occurs , there are five steps ( 5 R's ) : Recognition of the offending agent , recruitment of cells that assist in the process , removal of the offender , regulation and resolution of inflammation .
 

Acute inflammation


From a irritative phenomenon as trauma , infection or foreign body , there is a rapid response with polymorphonuclear leukocytes ( neutrophils) called acute inflammation.


At this moment , there are vascular , exudative and proliferative phenomena . It is important to know that these phenomena are not characteristic of acute inflammation and also occur in chronic . The vascular phenomena are transient vasoconstriction mediated by thromboxane to prevent possible bleeding and also to direct the blood to the site you need most ; vasodilation mediated by vasoactive amines ( such as histamine ) , nitric oxide ( NO) , prostraglandinas , kinins and fragments complement (C3a and C5a) to keep the blood concentrated, and thus have a greater number of leukocytes to the inflammatory process and increase the permeability to assist in the output cells of the immune system. From there , there are exudative phenomena . As a result of hyperemia, blood velocity decreases ( stasis ) and promotes leukocyte margination to the endothelial wall. When the leukocyte endothelium meets the wall , there is a rolling process in which leukocytes bind to expressions molecules ( selectins and integrins ) and begin to roll down the endothelial wall until they find a space between endothelial cells and pass procedure called transmigration ( diapedesis ) in which the leukocytes migrate into the vessel wall with the aid of mediators such as complement fragments that are responsible for chemotaxis , that is, the direction given to leukocytes to the harmful agent . At the time of transmigration , a fibrin network serves as a support for migration. Once out of the blood vessel , leukocyte meets the harmful agent . For this cell of the immune system to recognize the harmful agent , antibodies surround the agent. So, the leukocyte approaches , recognizes the agent and embraces by endocytosis , then forming an endocytic vesicle . It is within this vesicle that leukocyte make the death of the agent and their digestion by lysosomal enzymes .
 

Thus, the acute inflammation can progress to chronicity ,regeneration or healing.


Chronic inflammation


If in acute inflammation characteristic cell is the neutrophil ( polymorphonuclear leukocyte ) in chronic inflammation are mononuclear leukocytes ( lymphocytes and macrophages ) . All vascular , exudative and proliferative phenomena also occur in chronic inflammation , however, the difference is that this inflammation occurs due to persistent infections and autoimmune diseases for example .


Chronic inflammation can be divided into specific ( granuloma ) and nonspecific (granulation tissue ) . The granuloma is a specific pattern of chronic inflammation in an attempt to contain a lesion that is difficult to eradicate . Epithelioid cells , ie activated macrophages that have changed their morphology , form granulomas with giant cells and lymphocytic halo. This process occurs when there is a specific agent such as, for example, a non-absorbable suture wire . There are some types of granuloma as tuberculous one . Granulation tissue (or granulomatous ) comprises chronic non-specific inflammation. In this tissue there are immune cells , fibroblasts and new blood vessels ( angiogenesis ) that are responsible for bringing more nutrients to the affected site .


The intense activity of leukocytes with the inflammatory process triggers tissue to repair .

Cardinal signs.

Formation of transudate and exudate

Vascular phenomena of inflammation

Exudative phenomena

Leukocyte activation

Acute inflammatory processes

Events in the resolution of inflammation

Formation of chemical mediators

Morphology of an ulcer

Chemical mediators

NO effects on inflammation

TNF and IL-1 effects on inflammation

Activation of macrophages

Relationship between mediators

Macrophage-lymphocyte interaction

Exudative phenomena of the inflammatory process

Bibliography:

 

KUMAR V, ABBAS AK, FAUSTO N. Robbins & Cotran: Bases Patológicas das Doenças. 8ª edição. Rio de Janeiro: Elsevier, 2008.

BRASILEIRO FILHO, G. Bogliolo: Patologia. 7ª edição. Rio de Janeiro: Guanabara Koogan, 2006.
RUBIN E, GORSTEIN F, RUBIN R, SCHWARTING R, STRAYER D. Rubin: Bases Clínico-Patológicas da Medicina. 4ª edição. Rio de Janeiro: Guanabara Koogan, 2006.
BRASILEIRO FILHO, G. Bogliolo: Patologia Geral. 4ª edição. Rio de Janeiro: Guanabara Koogan, 2009.
MONTENEGRO MR, FRANCO M. Patologia: Processos Gerais. 4ª edição. São Paulo: Atheneu, 1999.

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