Inflammation

By the related physical phenomenon to the ignition, it see Inflammation (Physical).

inflammation it is the form to pronounce many diseases. Forehead to the aggressions of means is a inespecífica answer, and is generated by the inflammatory agents. The inflammatory answer arises with the defensive aim to isolate and to destroy the harmful agent, as well as to repair to the weave or damaged organ. The inflammation is denominated in with the suffix - itis (faringitis, laryngitis, colitis...). The greater problem than arises from the inflammation is that the defense goes so much towards harmful agents as to nonharmful, causing damages in weaves u healthy.

Table of contents

Inflammatory agents

Historical evolution

In the first civilizations testimonies of their knowledge and its treatment exist.

In y exists writings of and Celso, of this last one the three signs are still conserved that characterize to the inflammation:

  • Tumor. Increase of size. It must to edema.
  • Flesh color. Reddening. It must to vasodilatación.
  • Heat. Increase of of the inflamed zone. It must to the vasodilatación and to the increase of the local consumption of .

Classically it is mentioned to pain as first sign of tétrada, but the pain is a given symptom its subjective character, whereas the rest is signs, by its objective character.

In the Average Age divine punishment was considered.

In century XVIII Hunter it was first in defining it like defense reaction.

In century XIX Cohnheim it investigated the inflammation in alive animals and with the optical microscope.

In century XX Metchnikoff it discovered .

Lewis discovered the chemical mediators of the inflammation, to which he called H, and defined the triple answer before the aggression that consisted of:

  • Eritema power station
  • Swelling
  • Peripheral Eritema

Depending on the temporary characteristics of the inflammation we defined two types of answer, inflammation acute and inflammation chronicle.

Acute inflammation

In the acute inflammation we distinguished three key points: hemodinámicos changes, alteration of the vascular permeability and modifications leucocitarias.

Hemodinámicos changes in the caliber and the flow

After a inconstante and transitory period of vasoconstricción to arteriolar, takes place vasodilatación and hiperemia activates (opening of new hair beds in the zone of the injury that produces an increase of flow) that causes to reddening and increase of the temperature. Later a passive period of hiperemia takes place in which it diminishes the flow by an increase of the microvascular permeability with extrusion of liquid and increase of sanguineous viscosity in the glasses of smaller caliber, than is what éstasis is denominated (total paralysis of the flow).

As it evolves the éstasis is taken place the peripheral direction (marginalization) of the leukocytes, that adhere to endotelio, they cross the vascular wall and they go to interstice.

Alteration of the vascular permeability

The morphologic bases of endotelio by action of the chemical mediators are altered. One takes place generally in vénulas.

In normal conditions endotelio does not allow the exit of and the interchange takes place by , but when it is altered the permeability is altered to the cellular unions and the negative loads of the basal membrane.

Majno and Palade they saw openings between the cells that were not defeats. This must to that the substances of the inflammation cause the abrupt contraction of filaments of and of the endoteliales cells that are dissuaded. Later the citoesqueleto is reorganized to maintain the contraction during more time.

The inflammatory substances must dissolve the basal membrane of these openings.

The central center is vénulas, but if he is very intense it reaches to capillaries and extrusion by breakage takes place.

In the cases in which the inflammation is pathological it produces necrosis of weaves and glasses.

Anatomical bases

  • Immediate answer: contraction of the endoteliales cells and widening of the intercellular union. Favored all this by substances like histamina, the bradiquinina and the leucotrienos.
  • Delayed answer: reorganization of citoesqueleto (endotelial retraction) and opening of the intercellular unions favored by substances like interleuquina-1 (IL-1), interferon - (IFN -) and factor of tumorlike necrosis (TNF).
  • Prolonged immediate answer: direct endotelial injury with necrosis and loosening of the endoteliales cells by excess of inflammatory agent in the glasses.

Chemical mediators

They can be present in it shapes and they must be activated to exert its function. Also it can be in the cells where they remain stored being secretadas or synthesized of I novate in answer to a stimulus. These cells are mainly plaquetas, polimorfonucleares, monocitos, macrophages and mastocitos.

These substances can have autocrinos, paracrinos effects or endocrinos.

Once released and activated they have very little average life due to its poisonous effect, the majority have detrimental indirect effect as they are the weave destruction, becoming therefore the inflammation a autoagresión.

Vasoactivas amines
  • Histamina: one is in cells barleys, basófilos and plaquetas stored in grains that secretan before inflammatory agents, molecules of the complement (Cá, Cä), lisosomales proteins, IL1, IL8. The histamina is the great mediator of the acute phase, its effects are:
    • Vasodilatación of arterioles and vénulas.
    • Alteration of the permeability in vénulas.
  • Serotonin: stored in cell enterocromoafines, plaquetas and cells of the nervous system. Its liberation takes place thanks to the factor activator of plaquetas (PAF). Their actions are very similar to those of the histamina.
Proteases plasmáticas
  • System of the complement: it can activate by the classic route or the alternative route freeing the factors of the complement that they have like main mission to vasodilatar the zone of the inflammation and the liberation of substances like the histamina or the leucotrienos, as well as to produce adhesion and quimiotaxis of leukocytes to which it activates, also favors .
  • Quininas: they along with activate the cascade of the coagulation. They promote increase of the vascular permeability, contraction of the smooth muscle and pain.
  • Coagulation system: when activating an increase of the permeability is promoted, quimiotaxis, adhesion and proliferation of fibroblasts.
Metabolitos of araquidónico acid
  • : PGE2, PGI2, PGD2 that produce vasodilatación, fever and pain.
  • Tromboxanos A2 (TXA2): they produce plaquetaria aggregation and vasoconstricción.
  • Leucotrienos LTC4, LTD2 and LTE4: they produce vasoconstricción, increase of the permeability and broncoespasmos.
  • Leucotrieno B4: that it promotes leucocitaria adhesion and quimiotaxis.
Lisosomales components of the leukocytes
  • Acid proteases: bacteria and cellular rest within fagolisosomas degrade.
  • Neutral proteases: like for example colagenasas, elastasas, proteinasas...
  • Catiónicas proteases: whose aim is to increase the permeability, to favor quimiotaxis and to activate to factors C3 and C5 of the complement.
Citocinas
  • IL1, TNF-&alfa; and, quimiocinas (IL8, MPC1), TGFB, PDCF. They have the assignment to promote the leucocitaria adhesion to endotelio, to foment the synthesis of prostaglandins, quimiotaxis and in addition they are factors of growth of fibroblasts and endotelio, which is important as far as the tissue necrosis.
Others
  • Nitric Oxide (NOT).
    • Short and local action.
    • Produced in , endoteliales macrophages and cells.
    • It is a relajante factor of smooth (vasodilatación).
    • In the macrophages the interleuquinas activate to the NO-sintasa.
    • When it is freed in uncontrolled amounts takes place peripheral vasodilatación and tissue necrosis.
  • Factor Activator of Plaquetas (PAF). One is in plaquetas, mastocitos, basófilos, PMN, monocitos, macrophages, endotelio. Their actions are:
    • Vasoconstricción and broncoconstricción.
    • Leucocitaria adhesion.
    • Quimiotaxis.
    • Degranulación.
    • Activation of the synthesis of eicosanoides.
  • Free Oxi'geno radicals (RLO). To low concentrations they activate quimiocinas, citocinas and molecules of endotelial leucocitaria adhesion: it increases the answer inflammatory.

Leucocitarias modifications

The leukocytes fagocitan to the pathogens, destroy the bacteria and to , and degrades the necrótico weave, but also they can prolong the tissue injury when releasing , mediating chemistries and RLO. The phases of the leucocitarias modifications are:

Marginalization and adhesion to the endoteliales cells

When the flow of vénulas is normal, the leukocytes move to the walls of the glass thanks to that the shear forces diminish, later adhere to endotelio transitorily (bearing) until they arrive at a point in which it adheres firmly. With time endotelio can be had with leukocytes (paving).

Emigration

The fixed leukocytes emit pseudópodos as a handle between the endoteliales cells, they introduce and they are left between these and the basal membrane. Finally, they release colagenasas in order to break it and they are able to cross it.

Molecules of adhesion
  • Selectinas.
  • Inmunoglobulinas.
  • Integrinas.

The inflammatory mediators activate to the selectinas, that are stored in grains of Weibel-Palade of the endoteliales cells and it redistributes itself quickly towards the cellular surface. The firm adhesion of the leukocytes to endotelio takes place thanks to the conformacional change of the integrinas.

The transmigración and the exit of leukocytes are in favor half-full of the PCAM-1.

Conglomeration

The inflamed weave contains acúmulo of neutrófilos.

Quimiotaxis

One is the locomotion oriented according to a chemical gradient towards the zone of injury.

The increase of intracellular calcium causes the contraction of actina filaments and miosina in a zone of the cytoplasm allowing the leucocitaria diapedesis. Also an increase of the adhesion and the affinity by the receiver of molecules exists.

In the inflammation they mainly appear PMN and in smaller amount monocitos.

Leukocytes PMN predominate more in the beginning, but in the final phases they predominate plus the monocitos, that have a longer average life and are more resistant to the inflammatory agent.

  • Quimiotácticas substances.
    • Bacterial products.
    • Components of the complement.
    • Metabolitos of araquidónico acid.
    • Lisosomales components.
    • Citoquinas.

Fagocitosis

  • Recognition and fixation of the inflammatory agent: the agents are recognized when they are covered with opsoninas that are united directly to leukocyte receivers.
  • Englobamiento: of the particle by means of pseudópodos until one forms fagosoma. Meanwhile I monomention and leukocyte desgranula.
  • Destruction or degradation of the fagocitado material: by means of oxidativos mecanisos, that take place in lisosoma or by means of proteolytic enzymes of fagolisosoma. If the lisosómicas enzymes are not able to destroy the agent, this one is multiplied and induced tissue injury and necrosis.

Evolution of the acute inflammatory answer

Destruction of the inflammatory agent

  • If tissue injury does not exist:
    • Resolution.
    • Organization of the exudate.
  • If tissue injury exists:
    • Regeneration: dead cells are replaced whereas it follows the conjuntivo frame intact.
    • Repair: the weave by cicatricial weave is replaced.

Persistence of the inflammatory agent

  • Abscesificación.
  • Chronic inflammation.

In case of resolution the bacteria also do not drain themselves and the infection by via extends lymphatic: linfangitis (inflammation of lymphatic glasses) and linfadenitis (inflammation of lymphatic ganglia).

Exudate

Extravascular liquid of inflammatory character that presents/displays discharge cellular protein concentration and many rest. Its presence indicates that a significant alteration in the normal permeability of the glasses of small caliber of the zone of the injury has taken place.

Trasudado

Liquid with low amount of proteins and few cellular rest. It is a ultrafiltrate of the plasma and the permeability must to the hydrostatic imbalance through endotelio vascular being normal.

Types of inflammation according to the exudate

It depends on the site, the inflammatory agent, the intensity and the duration of the inflammatory reaction.

  • Type 1: serosa inflammation: immediate, of minimum duration. The exudate contains few proteins and few cells. Little tissue injury exists. It happens on the serosas of the organism.
  • Type 2: fibrinosa inflammation: the exudate contains much fibrina that has formed once it has left from the fibrinógeno. Most favorable it is than it is degraded by the fibrinolítico system.
  • Type 3: inflammation purulenta: produced by producing germs of pus. (substance with high amount of polimorfonucleares (dead or alive PMN) and great amount of germs, that gives a more or less liquid consistency him). If she appears limited, surrounded by repair processes, abscess is denominated to him and had little risk of dissemination. If it does not have defined limits and it spreads by weaves destroying them, flemón is denominated to him (generally produced by more virulent and producing germs of hialuronidasa). If it happens in interio of cavities, or flemón or abscess, denominates empiema to him. Whereas pus exists, the treatment has not taken place. It can happen that it drains of natural form or that is opened of spontaneous form. In order to avoid that it is drained of artificial form.
  • Type 4: mucous or mucinosa inflammation: in organs with producing snot glands (respiratory and digestive) the exudate contains snot.
  • Type 5: hemorrágica inflammation: of intense red color, caused by serious infections or endogenous enzymes (like for example, pancreatitis necrohemorrágica).
  • Type 6: eosinofílica inflammation: exudate with many eosinófilos that when appears the antigen is protozoo.
  • Type 7: monocitaria inflammation: exudate constituted by lymphocytes, monocitos and plasmáticas cells, without being a chronic inflammation.
  • Type 8: ulcerosa inflammation: en órganos con luz la inflamación se puede desprender dejando un hueco llamado úlcera, el cual se produce sobre todo en el intestino.

Inflamación crónica

Se caracteriza por una duración prolongada, daño tisular reparado por tejido de cicatrización, angiogénesis, fibrinolisis e infiltrado de células como monocitos, linfocitos y células plasmáticas.

Se debe a la persistencia del agente inflamatorio o a agentes inflamatorios que desde el principio producen inflamación crónica (formas primarias).

La célula fundamental es el monocito, que contiene abudantes lisosomas que degradan mejor a los neutrófilos. Son más activos sintetizando y liberando sustancias al exterior.

Inflamación crónica granulomatosa

It is a specific type of chronic inflammatory reaction, that is characterized by the accumulation of modified macrophages (epitelioides cells) and that is initiated by diverse infectious and noninfectious agents. For the formation of granulomas the irritating product presence is necessary nondigeribles, of a half-full immune reaction by cells T in front of the irritating agent or of both.

I monomention evolves to macrophage, that is more active and has more powerful grains, ampler cytoplasm and with greater capacity of division. The macrophage activates by answer to a stimulus and it becomes one more a greater cell, with a ampler cytoplasm, more rough endoplasmic reticulum, more and an extended nucleus (epitelioide cell). The macrophage is sensible to inflammatory agents who are irritating and difficult to degrade, but that they are inert.

  • Granuloma: it is a local zone of the granulomatosa inflammation, that consists of the microscopic accumulation of macrophages transformed into epitelioides cells, surrounded by a necklace of mononuclear leukocytes, mainly lymphocytes and sometimes plasmáticas cells. Granulomas more evolved appears surrounded by fibroblasts. Frequently the epitelioides cells megre and form giant cells in the periphery of granulomas. They are constituted by a mass of cytoplasm that contains twenty or more dispersed nuclei by the same one (giant cells of type strange body), if they are arranged in the periphery denominate giant cells Langhans type and if they are central, with vacuolado cytoplasm, giant cells of Touton type are denominated. These cells can have cytoplasmic inclusions denominated conchoides bodies or of Schaumann.
    • Granuloma can go associate a:
      • Necrosis.
        • Caseosa: produced by mycobacteria.
        • Abscesificada: in , infections by bartonella...
      • Fibrosis: that it limits granuloma perfectly as it happens in the sarcoidosis.
      • Lymphocytes and plasmáticas cells: surrounding it.
      • Others granulomas: nonindividual, but fused (tuberculosis or brucelosis).

When much fibrosis exists is different granuloma perfectly and sarcoidosis is denominated: disease that mainly affects the lung, lymphatic ganglia, skin, conjuntiva, kidney...

Other times a space with gas can be formed, also can appear crystals of úrico acid, that are deposited forming that granuloma (drop). And in the tuberculosis granuloma is characterized by central caseosa necrosis without inclusions and fibrosis, which it difference of the sarcoidosis.

 

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