Acute And Chronic Inflammatory Processes

Inflammation is a living tissue reaction against all forms of injury. In this reaction contributed to the blood vessels, nerves, fluids and cells in the lesion.Inflammatory processes destroy, dissolve or restrict the causative agent of injury and paved the way for the restoration of damaged tissue in that place. To achieve these objectives, an inflammatory reaction often cause clinical symptoms such as pain. Inflammatory reaction can be divided into two, namely acute inflammation and chronic inflammation.


A. acute inflammation
Acute inflammation is the answer immediately or directly and early response to injury agents. This response is relatively short, lasting only a few hours or days.Immediate introduction to the entry of lesion agent will have two important effects, namely: berhimpunnya antibodies around agents injury, emigration of leukocytes from the blood vessels into the affected tissue lesion agent. Thus the acute inflammation has the following components:

1. Changes in blood vessel cross-section with a result of increased blood flow
Immediately after injury, local arteriolar dilation is preceded by a brief vasoconstriction. Prakapiler sphincter opening resulted in increased capillary blood flow, as well as capillary matting previously inactive opens. As a result, post-capillary venular woven dilated and filled with blood flowing. Thus micro vaskulator on lesion location dilated and filled with blood unstoppable.

2. Structural changes in micro blood vessels that allow the plasma proteins and leukocytes to leave the blood circulation
Increased vascular permeability accompanied by the release of plasma protein and white blood cells into the tissue, called exudation and a prominent feature of acute inflammation. Normal movement of fluid takes place out in the micro vaskulator regulated by the balance between intra vascular hydrostatic pressure and colloid osmotic pressure opposing effects by plasma proteins. At the end of the capillary arterioles, high hydrostatic pressure urging the fluid out into the interstitial tissue spaces by means of ultra filtration, thereby increasing the concentration of plasma proteins and colloid osmotic pressure increases. The normal exchange will leave little fluid in the interstitial tissue that runs from the room through a network of lymphatic channels. In general, the capillary wall can be passed water, salt and a solution to the density of 10,000 Dalton. Movement of plasma proteins with density above 10,000 Dalton will be inhibited because of the size of the protein molecule increases. Extravascular inflammatory liquid with high specific gravity above 1.020 called exudate, containing protein 2 to 4 mg% and the white blood cells that do emigration. These fluids accumulate as a result of increased vascular permeability, increased intravascular hydrostatic pressure as a result of increased local blood flow and leukocyte emigration event.

3. Aggregation of leukocytes at the site of injury
Hoarding of white blood cells, especially neutrophils and monocytes to the site of injury is the most important aspect of the inflammatory reaction. White blood cells capable of devouring material which is salty including bacteria and necrotic cell debris, and lysosomal enzymes that help the body's defenses contained therein. The series of white blood cell aggregation behavior in inflammatory sites include:

a. Marginasi and layered arrangement
In the early inflammatory focus microcirculation dam would cause red blood cells to clot and form aggregates larger than leukocytes. According to the laws of physics, the mass of red blood cells will be found in the middle in the axial flow, and white blood cells move to the edge (marginasi) so as to make contact with the endothelial surface. At first these white blood cells move slowly along the endothelial surface in the flow of stuttering but then will stick and coat the endothelial layer.

b. Emigration
Emigration is the process of moving the white blood cells that move out of the blood vessels. The main place of emigration of white blood cells is a meeting between endothelial cells. Neutrophils are the first cells to appear in perivaskuler space, usually followed by monocytes. Neutrophils do not exceed the age of more than 24-48 hours outside of the blood vessels and monocytes will replace it.

c. Chemotaxis
After leaving the blood vessels, leukocytes move toward the main lesion location.Migration of white blood cells are directed is caused by chemical influences that can diffuse and therefore called chemotaxis. The most reactive to stimuli chemotaxis of neutrophils and monocytes it is. Chemotactic factors can be derived from plasma proteins endogenous or exogenous bacteria such products.

d. Phagocytosis
Phagocytosis begins with the attachment of particles on the surface of phagocytes, pelahapan and annihilation and destruction of microorganisms or particles are eaten.

Events associated with acute inflammatory process largely made possible by the production and release of a wide variety of chemical mediators. Although this type of injury can influence various and different tissue accompanying inflammation, mediators are released the same, so the response to inflammation appears stereotypes. So infections caused by bacteria, injury due to heat, cold or radiation energy, electrical or chemical injury, and trauma mechanics will give the same immediate inflammatory reaction.


B. chronic inflammatory
Chronic inflammation caused by stimuli that settled, often within a few weeks or months, causing mononuclear infiltration and proliferation of fibroblasts. White blood cells that accumulate, mostly consisting of macrophages and lymphocytes and occasional plasma cells were also found. So exudate leukocytes in chronic inflammation called monomorfonuklear to distinguish from polymorphonuclear exudate in acute inflammation.
Chronic inflammation can occur through one or two roads. Can occur following acute inflammation, or the response from the beginning is chronic. Acute inflammation becomes chronic changes take place when the acute inflammatory response may not occur, due to the settling agent causes injury or there is interference with the normal healing process. For example, pulmonary bacterial infection may begin as a focus of acute inflammation (pneumonia) but failure to perform the resolution can cause extensive tissue damage and the formation of a cavity with a fixed malignant inflammatory process and can lead to chronic lung abscess.
Sometimes chronic inflammation since the beginning of the primary process, often causing injury have low toxicity compared to the causes that give rise to acute inflammation. Known three major groups:
1. Persistent infection by intracellular microorganisms such as tubercle bacillus, Treponema pallidum and certain fungi. These organisms have low toxicity and an immune response called delayed hypersensitivity. Inflammatory response often have a distinctive pattern called granulomatik reaction.
2. Contact long with a material that is not easily broken. This material includes particles of silica, which can cause chronic inflammatory response in the lung is called silicosis, when inhaled in a long time. Silica can work in the form of chemical and mechanical. Instead foreign objects such as broken glass large, stitches may result in chronic inflammation due to irritation of physics and mechanics. Response in the above case is called a foreign body reaction and is often accompanied by the formation of Datia cells as a function of macrophages.
3. In certain circumstances, an immune reaction against the individual's own tissues and menyebaban auto-immune diseases. In this disease the auto antigens induce an immune reaction that berlangsun itself continuously and resulted in several chronic inflammatory diseases such as rheumatoid arthritis.

Some types of inflammation is difficult to distinguish as chronic or acute, in the absence of explicit restrictions that distinguish clinically and morphology. It is said when the inflammation lasts longer than 4-6 weeks is called chronic inflammation, but because many effective response dependence of the host and the nature of the injury then the time limit is meaningless.
Chronic inflammation is characterized by the presence of mononuclear cells, namely macrophages lymphocytes and plasma cells. Traditionally macrophages are considered as a cleaner, but is now known to also have some other functions that are important in inflammation and immunity. Tissue macrophages only one component only of the mononuclear phagocyte system (MPS), formerly known as the reticulo-endothelial system (RES). The latter was found to be scattered everywhere in the connective tissue or in groups in organ such as the liver (Kupffer cells), spleen and lymph node (sinus histiocytes), and lung (alveolar macrophages).All derived from the same precursor in the bone system that produces blood monocytes from blood monocytes migrate into various tissues and transformed into macrophages.
In addition to macrophage phagocytosis has several other aspects that are important for its role as inflammatory cells. Mononuclear phagocytes capable to be made active, a process which results in cell shape more active and more importantly, a greater ability of phagocytosis that kills microbes to eat. Once activated macrophages secrete biologically active products are largely role associated with inflammation and recovery.
More than 50 bioactive products derived from macrophages has been known. The products are classified into the following main categories:
a. Enzymes: Protease neutral or acidic. Some neutral proteases such as elastase and collagenase was once referred to as inflammatory mediators in the affected tissue. Others such as plasminogen activators, stimulate the formation of plasmin and greatly strengthen the formation of ingredients pro-inflammatory.
b. Plasma proteins: included in this class is the complement protein (C1 - C5, properdin) and coagulation proteins such as tissue factor and factor V, VII, IX and X
c. Active metabolites of oxygen.
d. Lipid mediators including amino acids and aseter PAF
e. The factors that regulate cell proliferation and other fusion, ie interferon, fibroblast growth factor, endothelial cells and primitive myeloid cells and interleukin-1 molecule with an immense impact, as well as the occurrence of fever (fibrogen endogenous), activation of T and B lymphocytes, stimulation of the formation of collagenase by fibroblasts and liver secretion of acute phase reactants.

Back in the presence of macrophages in chronic inflammation sites is clear that they are derived from blood monocytes who emigrated from the blood vessels under the influence of chemotactic factors. Liberation factors derived from lymphocytes are important mechanisms making further macrophages remain buried in chronic inflammation sites.

BIBLIOGRAPHY

Kumar-Robbins Basic Pathology Part 1, WB Saunders Company, Philadelphia, 1987

Price, Sylvia Anderson and Wilson, Lorraine McCarty, Pathophysiology-Clinical Concepts of Desesase Processes, Fourth edition, Mosby Year Book Inc., Michigan, 1992 

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