Necrosis: causes, forms, diagnosis, outcome in necrosis
In apoptosis, cell death is a normal physiological condition caused by the action of an immune factor, which ensures a constant replacement of diseased, damaged and infected cells and structural components to prevent the spread of infection.
There is a constant, carefully balanced physiological renewal, thereby confirming the vital activity of the body.
Necrosis does not give a single chance to the dead cells for regeneration, since such a process is not genetically embedded in the life program, every second a millionth army of cells divides and dies, ceases to function, excluding structural and biochemical adaptation.
According to the formation of dystrophic changes in the period preceding the formation of pathology, numerous changes occur in the morphological structure:
- 1) The morphology of nuclear structures is expressed by karyopicosis - the nuclei change in size, shrivel, change density, petrification and encapsulation of necrotic sites. Kernels can be prone to karyorexis - rupture of the nucleus or lysis - dissolution. With a rapid course of the disease, dissolution can pass without breaks in the nucleus.
- 2) The change in the cytoplasm is expressed by a "gap" in the plasmolemma, which leads to the destruction of membranes and the dissolution of cells that have undergone necrosis, already six hours later.
- 3) Changes in the intercellular substance - manifested by inflammatory processes in the interstitial substance and fibrous structures, transforming them into a dense basophilic mass. With the subsequent occurrence of edema, dissolution and mucosal structures.
What are the causes of the defeat?
There are many factors for the manifestation of the disease.
- 1) Physiological causes - with gunshot wounds, radiation exposure. As a result of injuries from electric shock, burns and frostbite.
- 2) As a result of toxic effects - the effect of acids and alkalis, drug and alcohol poisoning, as a result of prolonged exposure to heavy metals.
- 3) The biological effect factor is a consequence of bactericidal and viral infection.
- 4) Allergic causes - allergic and autoimmune reactions
- 5) Pathologies of vascular nature - the development of infarctions of various etiologies.
- 6) Consequence of trophoneurologic manifestations - as a result of non-healing wounds and bedsores
Morphogenesis and forms of necrosis
There are multiple forms of the disease. Differences between them determine:
- morphologenesis and its changes;
- is a structurally functional feature of tissues and organs;
- rate of development of pathological process;
- type, cause of occurrence, and development conditions.
Got its name because of the external manifestation-it is expressed by the drying out of deadened areas with subsequent mummification. The consequence of a bactericidal and viral infection that caused oxygen deficiency and blood circulation disorders, as a result of multiple damaging effects.
Internal organs are affected, their color changes:
- spleen is sharply enlarged, has a bright red color, is covered with nodules of various sizes of variegated color - evidence of lymphogranulomatosis;
- foci of myocardial damage are highlighted in light yellow;
- kidney damage occurs with a hemorrhage and a sharp increase in the adrenal gland.
- 1) The most frequent is vascular necrosis. Consequence of ischemia.
- 2) Specific, curd, caseous type, mixed necrosis - with this type of disease, parenchyma and stroma die( cell elements and tissues).In addition to the dry parts of the lesion, pasty globules resembling glue are formed. It appears due to tuberculosis lesions, leprosy, granulomatous disease of Wegener. The affected areas are pink.
- 3) With the Center, Waxy type as a result of severe infectious lesions, necrosis affects the abdominal wall, skeletal muscles and hips. Due to cholera, abdominal or typhus. The foci have a glossy yellowish gray tint similar to wax.
- 4) Necrosis of the fibrinoid species, expressed by stromal-vascular dystrophy and affection of connective tissue - fibrinoid dysplasia. It manifests itself in rheumatoid factor and allergic diseases with a high production of autoimmune killer cells.
- 5) Fatty necrosis - enzyme( steanonecrosis), non-enzyme and traumatic type.- subcutaneous layers of the mammary glands, peritoneum and omentum are affected, as a consequence of hemorrhages and bruises, rupture of the capsule and destruction in the tissues of the pancreas.
- 6) Gangrenous types - dry and moist necrosis, gas "Antonov fire" type, and pressure sores. Contact with the external environment causes the penetration of bacterial infections, which causes additional transformations, in accordance with clinical and morphological features.
- dry appearance of gangrene is manifested without the intervention of microorganisms, is the consequence of ischemia. The result of vascular lesions of extremities lining atherosclerosis, capillary thrombosis;
- moist type of gangrene is characterized by an additional bacterial infection of already necrotic areas. Occurs in the affected areas of the intestine, lungs, extremities, on the cheeks and in the perineum, accompanied by an unpleasant ambre, as a result of the decay products. When the surface layers are damaged, sensitivity is lost. The pathology of the deep layers is expressed by the manifestation of high fever, acute pain and severe general condition;
- manifestation of gas gangrene - the result of the action of anaerobic infections, differs from the wet type by the defeat of extensive areas with gassing, as a result of bacterial fermentation. With stagnant inflammatory crepitations, there is an obvious characteristic cracking of gas bubbles;
- one of the varieties of gangrene are bedsores - are expressed by defeat and necrosis, as a result of constant pressure on the cutaneous fatty tissue and bone protrusions, which disrupts the cellular nutrition that ensures the preservation of the tissue structure and organs. A characteristic manifestation in bedridden patients.
A vivid example is the foci of softening the end of the chordal central nervous system located in the cranium, with ischemia, when after a very short time, the area of the brain melts, forming a serous fluid and pus. In this case, a cavity is formed - the cyst. Formation of dead areas is possible with osteomyelitis - purulent capsules are formed. There is a real threat of mutation - spontaneous rejection of both affected organs and tissues.
What is the outcome for necrosis?
The outcome, with such a serious illness is often unfavorable and often leads to the death of the patient. Everything depends on the form, localization and course of the disease. Fatal risk factors are necrosis:
- in the myocardium;
- in the brain;
- is a lesion of the cortical renal substance;
- progressive pathology in the adrenal and liver
- purulent fusion, in which there is a high probability of developing the sepsic state of the patient.
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