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10CHARACTERISTIC MORPHOLOGICAL CHANGES OF SECONDARY
PLACENTARY DEFICIENCY
Bakhtiyar Abdurasulovich Sanoev Gulmira Hasanovna Mukhidova
Bukhara State Medical Institute
ABSTRACT
The aim of this study was to supplement the data on morphological changes characteristic of secondary placental insufficiency in the placenta. To achieve the goal, the placental tissue of 22 postpartum women with a history of causes of secondary placental insufficiency was studied morphologically. The results showed that changes in the placenta are characteristic of secondary placental insufficiency, proliferation of primary and secondary mammary vascular wall cells, vasoconstriction leading to ischemia, low stratification of connective tissue cells. observed. The abundance of Kashchenko-Gofbauer macrophages in the stroma of semi-stratified terminal suckers, the lack of capillaries, syncytiocapillary barriers, different levels of trophoblasts indicate the underdevelopment of suckers.
Keywords: pregnancy, placenta, deficiency, partial stratification, circulatory, atrophy.
The urgency of the problem. Placental insufficiency is a syndrome based on morphofunctional changes in the placenta, during which the fetus slows down and hypoxia develops. R02 - Diseases of the fetus and baby due to complications of the placenta, umbilical cord and amniotic membranes.R05 - Stopping fetal growth and malnutrition.
Placental insufficiency is a common complication of pregnancy, observed in 5077% of fetal infertility, 32% in preeclampsia, 25-45% in extragenital diseases, and up to 60% in combination with viral and bacterial infections . Placental insufficiency occurs in 10.3% of women with premature rupture and up to 49% in premature births. Placental insufficiency causes fetal developmental delay in 60% of cases. Placental insufficiency by time and developmental mechanism: primary - develops from implantation and placental abnormalities before 16 weeks of gestation, secondary - develops after 16 weeks of gestation due to exposure of the fetus and placenta to exogenous factors .
Placental insufficiency can be compensatory and decompensating, depending on the change in functional status. Compensatory PE is normal in uterine and fetal blood circulation, but is observed in disorders of metabolic processes in the placenta. Decompensator PE - develops in uterine and fetal-circulatory disorders . Morphofunctional changes of the placenta in the case of placental insufficiency are poorly studied, especially in secondary placental insufficiency. It is known that the
causes of secondary placental insufficiency are exogenous pathological factors: radiation, physical and chemical effects, drugs and under the influence of these factors, uterine-circulatory disorders develop in several stages: endovascular migration of trophoblasts, lack of invasion of the placenta, satellite differentiation. Our goal is to supplement the data on morphological changes specific to secondary placental insufficiency in the placenta.
Materials and methods. In order to achieve the goal, the placental tissue of 22 postpartum women with a history of causes of secondary placental insufficiency was studied morphologically. In this general hematoxylin and eosin stain of general morphology, as well as semi-thin sections were stained with toluidine blue. For general morphology, 3 pieces from each satellite, ie 1.5x1.5 cm from the center, middle and periphery, were cut and solidified in 10% neutralized formalin. After washing for 2-4 h in running water, it was dehydrated in concentrated alcohols and chloroform, then paraffin was poured and the blocks were prepared.
Incisions of 5-8 ^m were made from paraffin blocks and stained with hematoxylin and eosin. To obtain semi-thin incisions, the satellite fragments were solidified in osmium 4 oxide, dehydrated, epon wax was poured, and blocks were prepared. Semi-thin incisions 1 ^m thick were obtained from Epon bricks on Leyka ultramicrotomy and stained with toluidine blue. Histological preparations were studied under 10, 20, 40 lenses of a light microscope and the required areas were photographed.
Inspection results and discussion. In order to make the results of morphological examination clear and reliable, we aimed to identify endovascular migration of trophoblasts, invasion of the non-placental part of the placenta, changes in placental differentiation, which may develop as a result of uterine circulatory disorders characteristic of secondary placental insufficiency.
Changes specific to circulatory disorders in the placenta were detected in primary and secondary suckers. It is found that the proliferation of both endothelial and pericardial cells in the vascular wall in the stroma of the mammary glands is narrowed, the endothelial surface is twisted (Pic. 1). The connective tissue stroma around the vessels is dense due to proliferation of cells and fibers. In the trophoblastic layer on the surface of the suckers, foci of vacuolation and necrosis are detected. In the mother's blood in the space between the suckers, erythrocytes are observed to shrink, deform and fragment.
Narrowing and ischemia of the coronary arteries of the placenta are associated with a decrease in the number of terminal suckers, hypoplasia, small size, atrophy of all structural units of the component. In the stroma of one type of terminal suckers, the number of blood vessels is small, the interstitial connective tissue is swollen, the connective tissue cells are sparsely located, and young and immature cells are visible from the staining of the nucleus. The number of capillaries in the sucking stroma is
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small and they are also of different diameters, only one of which formed a syncytiocapillary barrier (Pic. 2).
The structural units of the capillary wall are not fully developed, i.e. the endothelial layer is thin, the nucleus is not visible in most capillaries, with the erythrocytes in the cavity adhering to each other. The trophoblasts on the surface of this type of terminal suckers are dense in some areas and sparse in others. The nuclei of trophoblasts in dense areas are deformed, the karyolemma is uneven, bulges appear, chromatin is dense, these changes indicate atrophy and aging of cells. Circulatory disorders in the placenta, as noted above, lead to premature development, hypoplasia of the mammals, and the preservation of large numbers of immature mammals. This microscopic image shows an unsealed sucker (Figure 3). The main sign of insufficiency is the
underdevelopment of the stroma, in which the capillaries are scarce, the connective tissue is thin and swollen. Boron 2 capillaries are also very small, not fully developed, did not form a syncytiocapillary barrier. The suction stroma is lightly stained, with almost no connective tissue fibers. Among the cells of connective tissue, most are young, poorly developed, most of them have sparse chromatin in the nucleus, and they are Kashchenko - Gofbauer cells. Thus, it can be concluded that the large number of Kashchenko-Gofbauer macrophages preserved in the satellite stroma indicates that lactation perfection is lagging behind.
The smaller the number of these cells, the less developed the capillaries in the sucker (2, 5).
Disorders of blood circulation in the uterine system lead to ischemia, microcirculatory disorders, accumulation of immune compounds in the basal layer of trophoblasts, lagging behind angiogenesis. As a result, impaired placental stratification is an important factor in the development of placental insufficiency. At the same time, satellite suckers age rapidly, are incompletely developed, and different types of suckers appear in the satellite (5).
The formation of the syncytiocapillary border is disrupted, which slows down the metabolism due to the formation of fibroblasts and collagen fibers. This microscopic image shows an incomplete set of suckers (Picture 4). In all of them the stroma is young, the capillaries are small, the syncytiocapillary barrier is not formed, the surface trophoblasts are also underdeveloped, thin, the nuclei are atrophied and some are fragmented.
The abundance of Kashchenko-Gofbauer macrophages around the basement membrane of trophoblasts, the lack of capillaries, indicates that these suckers are not well differentiated.
Conclusions
1. As a characteristic change in the placenta secondary placental insufficiency, proliferation of cells of the vascular wall of the primary and secondary mammary glands, vascular narrowing leading to ischemia, low stratification of connective tissue cells were identified.
2. There is a high incompleteness of the structure of the terminal suckers, the predominance of dystrophy, atrophy, destruction in the structural units.
3. The abundance of Kashchenko-Gofbauer macrophages in the stroma of semi-stratified terminal suckers, the lack of capillaries, syncytiocapillary barriers, different levels of trophoblasts indicate the underdevelopment of suckers.
Picture 1. Satellite secondary suction, vascular wall cells proliferated, cavity narrowed, stroma dense, vacuolated in trophoblasts and necrotic foci. Semi-thin cut, dye: toluidine blue. X: 10x40.
Picture 2. Terminal suction, capillaries, syncytiocapillary barrier low, stroma swollen, trophoblasts atrophied. Half-thin cut, stained with toluidine blue. X: 10x40.
Picture 3. Unfinished terminal suction. The stroma is young, Kashchenko - Gofbauer macrophages are preserved, capillaries are small, trophoblasts are unevenly located. Half-thin cut, stained with toluidine blue. X: 10x40.
Picture 4. A set of semi-stratified terminal suckers. Half-thin cut, stained with toluidine blue. X: 10x40.
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