Fibrinoid necrosis
Fibrinoid necrosis is necrosis accompanied by the impregnation of the affected tissue with fibrin. It is characterized by the total destruction of connective tissue. Usually around the foci of necrosis, the reaction of macrophages is expressed, followed by the replacement of the necrotic focus with scar connective tissue. This type of necrosis occurs in rheumatic diseases, fibrinoid swelling, when the functions of the organ are disturbed and reduced, acute renal failure develops in malignant hypertension.
All these processes are accompanied by necrosis of arterioles and capillaries of the renal tissue.
As a result of fibrinoid necrosis, sclerosis or hyalinosis appears, the functions of the heart valves (heart defects) change. There is immobility of joints, narrowing of the lumen and loss of elasticity of the walls of blood vessels, hypoxia, atrophy and sclerosis of organs develop. Histochemical changes are determined by the influx of calcium ions into the cell; this is closely related to irreversible damage and the appearance of signs of necrosis.
One of the important signs of cell necrosis is a change in the structure of the nucleus. The chromatin of the dead cell is converted into large lumps. The core decreases in volume, shrinks, density and basophilicity increase (dark blue color). After the cell has undergone necrosis, its cytoplasm becomes homogeneous and brightly acidophilic, changes in its cytoplasm are determined.
First of all, specialized cell organelles disappear, mitochondrial swelling and destruction of organelle membranes take place, which causes vacuolization of the cytoplasm. Next, you can define cell lysis, the so-called autolysis. All this means that coagulation or thickening (coagulation) of proteins occurs in the cytoplasm instead of melting and liquefying masses of dry necrosis.
When the intercellular substance changes, both the interstitial substance and the fibrous structures change. This is characteristic of fibrinoid necrosis. Persistent arterial hypertension, acquiring a progressive character, although this rarely happens with timely treatment, is accompanied by changes in the fundus, such as hemorrhages, edema of the optic nerve head, and fluid filling of the fiber.
Severe headache, vomiting, decreased vision, paresis, seizures of epilepsy, possibly even coma, multiple small blood clots in the cerebral arteries, heart and renal failure, and oliguria are signs of not only cerebral edema, but also fibrinoid necrosis of the walls of small arteries and arterioles. If the treatment is carried out in the early stages of the disease, then it will be successful, and all changes will be reversible.
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Fibrinoid necrosis of the connective tissue of the vessel walls can be a consequence of fibrinoid swelling in allergic necrosis.
Fibrinoid changes in the arterial intima promote thrombosis and indirect necrosis of parts of organs. In atherosclerosis, prolonged spasms of arterioles and sudden increases in blood pressure are noteworthy. This creates conditions for the impregnation of fibrinogen, fibrin, and blood cells. The transformation of immune complexes with the fixation of a group of proteins circulating in the blood promotes an increase in soaking and the development of fibrinoid necrosis.
You can observe destructive processes expressed by dystrophy and death of muscle cells, followed by their lysis. Massive penetration of plasma proteins, their connection with the substance of the basement membranes leads to the accumulation of tropocollagen, proliferation of endothelial and smooth muscle cells and their death. All these changes occur as a result of acute fibrinoid necrosis.
With deep destruction of the vascular walls, perivascular exit of plasma from the bloodstream, hemorrhages, the formation of aneurysms and ruptures occur. Fibrinoid necrosis at the beginning of development captures the middle membrane of arterial vessels (media), and then spreads by foci to all the walls of the vessels. During this process, cellular infiltrates appear, with neutrophils predominating in them.
Further, pathological changes in the vessels end with the formation of stenoses and aneurysms. Most often, the kidneys, heart, and sometimes the peripheral nervous system, gastrointestinal tract, and skin are affected. The central nervous system, liver, spleen, adrenal glands, testes, and lungs can be vulnerable. Timely prescribed prednisone and cyclophosphamide reduce the severity of symptoms and reduce the death of the disease.
In the absence of kidney damage, the prognosis is better. The prognosis for the treatment of advanced stages in general, of course, is unfavorable, in the case of damage to several organs, the development of pathology occurs quickly, after the diagnosis is established, in most cases, people die within three months.
Article author: Mochalov Pavel Alexandrovich | d. m. n. therapist
Education: Moscow Medical Institute. IM Sechenov, specialty - "General Medicine" in 1991, in 1993 "Occupational Diseases", in 1996 "Therapy".
