Arkhiv patologii
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The analysis of 7 cases of subacute spongiform encephalopathy, the Creutzfeldt-Jacob disease (CJD), is given. Three main morphological features are typical for this disease: spongiform change of the grey matter, progressive neuronal loss and proliferation of the astroglia cells. ⋯ As a rule, the disease affects at first the cortex of the cerebral hemispheres, then subcortical nuclear groups, cerebellum and more rarely nuclear groups of the brain stem. The demyelinization of the white matter of the cerebral hemispheres is not obligatory for the CJD and appears in cases with a severe lesion of the grey matter.
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The main principles of quantitative morphology allowing an objective study of chronopathology are presented. Three main types of chronopathology associated with changes in the rate of development, dyschronization, and dyscyclicity of pathomorphological processes are considered. Mathematical models of the main types of chronopathology are presented.
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Examinations of 43 section observations of shock established that the role of the syndrome of disseminated intravascular blood coagulation (DIBC) in the development of shock was variable: in some cases it caused the shock condition (embolism with amniotic waters, premature desquamation of the placenta), in others it is its consequence (hemorrhagic, cardiogenic shock). Morphogenesis of the DIBC syndrome is different depending on its role in the development of the shock condition. ⋯ The characteristic morphological features of DIBC as the consequence of the shock include incomplete thrombus formation processes with the presence of pre-thrombi and/or strands and filaments of fibrin, involvement of the adrenals, the presence of the phenomenon of fibrin lining of vascular walls. The time of development of intravascular coagulation does not coincide with shock occurrence and may be different in various parts of the microcirculatory bed.
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The results of experimental reproduction in dogs of some components of closed thoracic injury: traumatic injuries of the lungs and disturbed carcass of the thorax which led to the development of acute respiratory insufficiency are presented. Morphological manifestations of the latter consisted in hemorrhages of various sizes and atelectasis, as well as marked hemodynamic disorders developing, according to electron microscopy, at the level of aerohematic barrier. The concurrent arterial hypoxemia facilitated the development of hypoxic lesions in the myocardium. These studies demonstrated that myocardial lesions may aggravate the severity of respiratory insufficiency.