Inflammation is a very common and important basic pathological process. Traumatic infection of body surface and the most common and frequently-occurring diseases of various organs (such as furuncle, carbuncle, pneumonia, hepatitis, nephritis, etc.). ) is an inflammatory disease. The defensive response of living tissues with vascular system to injury factors is called inflammation.

Etiology of inflammation

Any factor that can cause tissue damage may be the cause of inflammation, that is, inflammatory factors. Can be summarized into the following categories:

biotic factor

Bacteria, viruses, rickettsia, mycoplasma, fungi, spirochetes and parasites are the most common causes of inflammation. Inflammation caused by biological pathogens is also called infection. Exotoxin and endotoxin produced by bacteria can directly damage tissues; The virus replicates in infected cells, leading to cell necrosis; Some antigenic pathogens can damage tissues by inducing immune response after infection, such as parasitic infection and tuberculosis.

(2) Physical factors

High temperature, low temperature, radioactive substances, ultraviolet rays and mechanical damage.

(3) Chemical factors

Strong acid, strong alkali, turpentine, mustard gas and other exogenous chemicals. Endogenous toxic substances such as decomposition products of necrotic tissue and metabolites accumulated in the body under certain pathological conditions such as urea.

(4) Foreign bodies

Foreign bodies that enter the human body through various ways, such as various metals, sawdust, dust particles, surgical sutures, etc., will cause different degrees of inflammatory reactions due to their different antigenicity.

(5) necrotic tissue

Ischemia or hypoxia can lead to tissue necrosis, which is a potential inflammatory factor. The hyperemia and bleeding area and inflammatory cell infiltration at the edge of fresh infarction are all manifestations of inflammation.

(6) Allergy

When the immune response state of the body is abnormal, it can cause inappropriate or excessive immune response, cause tissue and cell damage, and lead to inflammation. Tissue damage caused by immune response is the most common in all kinds of hypersensitivity reactions: type I allergy such as allergic rhinitis and urticaria, type II allergy such as anti-basement membrane glomerulonephritis, type III allergy such as glomerulonephritis caused by immune complex deposition, type IV allergy such as tuberculosis and typhoid fever. In addition, there are many autoimmune diseases such as lymphocytic thyroiditis and ulcerative colitis.

Pathological changes of inflammation

The basic pathological changes of inflammation are usually summarized as deterioration, exudation and proliferation of local tissues.

acidification

The degeneration and necrosis of inflammatory local tissues are called lesions. Deterioration is an injury process caused by inflammatory factors, and it is a morphological observation of the changes of metabolism and physical and chemical properties of local cells and tissues. Both parenchyma cells and interstitial cells can undergo metamorphosis. The degeneration of parenchymal cells is often manifested as edema, steatosis, coagulative necrosis and liquefactive necrosis. Interstitial degeneration usually manifests as mucinous degeneration, connective tissue glassy degeneration and fibrotic necrosis.

Deterioration is the direct result of inflammatory factors, or local blood circulation disorder and immune mechanism in the process of inflammation, and the introduction of inflammatory reaction products. The severity of the deterioration depends on the nature and intensity of inflammatory factors and the reactivity of the body. The hydrolase released after the degeneration and necrosis of tissue cells makes the damaged tissue cells dissolve and liquefy, which further causes the deterioration of surrounding tissue cells and leads to organ dysfunction.

give?off

The process of liquid and cellular components in the blood vessels of inflammatory local tissues entering interstitial tissue, body cavity, mucosal surface and body surface through the blood vessel wall is called exudation. Exudates and cells are collectively referred to as exudates or exudates. During inflammation, exudation contains high protein, more cellular components and their disintegration products. These exudative components play an important defensive role in inflammatory reaction and play a positive role in eliminating pathogenic factors and harmful substances. Exudative lesion centered on vascular reaction is the most typical change of inflammation. In this process, the vascular reactions mainly show hemodynamic changes (inflammatory congestion), increased vascular permeability (inflammatory exudation), fluid exudation and cell exudation (inflammatory infiltration). Changes of bleeding dynamics

That is, changes in blood loss and vascular caliber generally occur in the following order:

Short-term contraction of arterioles? Vasodilation and blood flow acceleration (inflammation and congestion)? Slow blood flow (white blood cells released from blood vessels and leaked red blood cells form venous congestion)

(2) Increased vascular permeability

It is the main cause of exudation of local fluid and protein in inflammation. The exudation of this fluid is mainly related to the destruction of the integrity of vascular intima. The factors affecting the integrity of vascular endothelial cells are: contraction of endothelial cells, remodeling of endothelial cytoskeleton, injury of endothelial cells, enhancement of cell transition of endothelial cells, and increase of permeability of new blood vessel wall.

(3) liquid leakage

When inflammation occurs, the permeability of blood vessels increases until the protein-rich liquid in blood vessels reaches the outside of blood vessels through the blood vessel wall. This process is called liquid exudation. The exudate rich in protein is exudate, and the accumulation of exudate in the stroma is called inflammatory edema. If it accumulates with the body cavity, it is called inflammatory effusion.

Cell exudation

In the process of inflammation, there are not only fluid exudation, but also cell exudation, and leukocyte exudation is the most important feature of inflammatory reaction. The process of various white blood cells swimming out of blood vessels through blood vessel walls is called cell exudation. White blood cells oozing out during inflammation are called inflammatory cells. The phenomenon that inflammatory cells enter the stroma under the action of chemokines is called inflammatory cell infiltration, which is an important morphological feature of inflammatory reaction.

hyperplasia

Stimulated by inflammatory factors, tissue disintegration products or some physical and chemical reasons, the regeneration and proliferation of inflammatory local cells is called proliferation. Proliferating cells include parenchymal cells and interstitial cells. The proliferation of parenchymal cells, such as hepatocytes in chronic hepatitis and epithelial cells and glands in nasal mucosa in nasal polyps. The proliferation of interstitial cells includes macrophages, lymphocytes, vascular endothelial cells and fibroblasts. Proliferative reaction is generally more obvious in the late stage of inflammation or chronic inflammation, while proliferative lesions are more prominent in the late stage of chronic inflammation or inflammation. For example, acute glomerulonephritis and typhoid fever have obvious cell proliferation in the early stage.

Inflammatory hyperplasia is an important defensive reaction, which can limit the spread and spread of inflammation and make damaged tissues regenerate and repair. For example, in the early stage of inflammation, proliferating macrophages have the function of devouring pathogens and removing tissue disintegration products; In the late stage of inflammation, the proliferating fibroblasts and vascular endothelial cells * * * jointly form granulation tissue, which is helpful to the localization of inflammation and eventually form scar tissue for repair. However, excessive tissue proliferation is harmful to the body, such as excessive granulation, damage to the original parenchymal cells, and influence on organ function, such as viral hepatitis cirrhosis and myocardial sclerosis after myocarditis.

inflammatory reaction

As early as the first century A.D., the Roman writer Cornelius celsus suggested that inflammation mainly manifested in four symptoms: redness, swelling, heat and pain. It was not until the19th century that the famous German pathologist Virchow listed local dysfunction as the fifth symptom of inflammation.

Local manifestation

Inflammation on the body surface is the most obvious, often manifested as redness, swelling, heat, pain and dysfunction. The mechanism is as follows:

1. Red: It is caused by hyperemia of inflammatory focus. In the early stage of inflammation, due to arterial congestion, local oxygenated hemoglobin increased, so it was bright red. With the development of inflammation, blood flow is slow, blood stasis is stagnant, and reduced hemoglobin in local tissues increases, so it is dark red.

2. Swelling: mainly exudate, especially inflammatory edema. In chronic inflammation, the proliferation of tissues and cells can also cause local swelling.

3. Heat: Heat is caused by arterial congestion and accelerated metabolism. Leukocytes can produce interleukin-I (IL-1), tumor necrosis factor (TNF) and prostaglandin E(PGE), which can cause fever.

4. Pain: The factors causing local pain of inflammation are related to many factors. The accumulation of potassium ions and hydrogen ions in local inflammatory lesions, especially the stimulation of inflammatory mediators such as prostaglandin, 5- hydroxytryptamine and bradykinin, is the main cause of pain. The exudation in the inflammatory focus makes the tissue swell and tension increase, and the compression of nerve endings can cause pain, so the pain of loose tissue is relatively light during inflammation, while the inflammation of pulp and periosteum often causes severe pain; In addition, the inflamed organ swells, which increases the tension of the capsule rich in sensory nerve endings, and the nerve endings are pulled and cause pain.

5. Dysfunction: such as degeneration, necrosis and abnormal metabolic function of parenchymal cells in inflammatory lesions, mechanical obstruction and oppression caused by inflammatory exudate, etc. , may cause inflammatory organ dysfunction. Pain can also affect the activity function of limbs.

General reaction

Inflammatory lesions are mainly local, but local lesions and the whole are interactive. In serious inflammatory diseases, especially when pathogenic microorganisms spread in the body, obvious systemic reactions often occur.

(1) fever

Infection by pathogenic microorganisms often causes fever. Pathogenic microorganisms and their products can be used as fever activators, which act on EP-producing cells to produce EP, and the latter acts on the thermoregulatory center to move its regulatory point up, thus causing fever.

A certain degree of body temperature increase can enhance the body's metabolism, promote the formation of antibodies, enhance the phagocytic function of phagocytes and the barrier detoxification function of the liver, thus improving the body's defense function. However, if the fever exceeds a certain degree or lasts for a long time, it can affect the metabolic process of the body and cause dysfunction of multiple systems, especially the central nervous system. If the inflammatory lesion is serious, but the body temperature does not rise, it means that the body has poor reactivity and low resistance, which is a sign of poor prognosis.

(2) Leukocytosis

In acute inflammation, especially acute inflammation caused by bacterial infection, the white blood cell count in peripheral blood can be significantly increased. In severe infection, the proportion of naive neutrophils in peripheral blood often increases, which is clinically called? The nucleus moves to the left? . This reflects the patient's strong resistance to infection and the severity of infection. In the process of some inflammatory diseases, such as typhoid fever, viral diseases (influenza, viral hepatitis and infectious atypical pneumonia), rickettsia infection and some autoimmune diseases (such as SLE), white blood cells in the blood often do not increase, but sometimes decrease. When bronchial asthma and parasitic infection occur, the eosinophil count in blood increases.

(3) Cell proliferation of mononuclear phagocyte system

Cell proliferation of mononuclear phagocyte system is a manifestation of the body's defense response. In the process of inflammation, especially inflammation caused by pathogenic microorganisms, the cells of mononuclear phagocyte system often proliferate to varying degrees. Often manifested as local lymph nodes, hepatosplenomegaly. Macrophages in bone marrow, liver, spleen and lymph nodes proliferate, and their phagocytic and digestive abilities are enhanced. B and T lymphocytes in lymphoid tissue also proliferate, and their functions of releasing lymphatic factor and secreting antibodies are enhanced.

Damage to parenchymal organs