Biomedical subjects
N K Permiakov
Publications and source records attributed to N K Permiakov.
[An introduction to iatrogenic pathology].
The authors presented the current conception of iatrogenesis in wide interpretation consistent with The International Classification of the Diseases and Causes of Death (the IX revision). The tendencies in iatrogenesis determination are analysed. Soviet and foreign literature data published on iatrogenic variants, frequency rate, problems for pathologists, classification, medical-pathological and social aspects are delineated.
[70 years of the Great October Socialist Revolution and the development of Soviet pathological anatomy].
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[Effect of tageflar, a synthetic analog of L-enkephalin, on the morphogenesis of experimental pancreatitis].
It has been substantiated that the use of a new synthetic drug tageflar analogous to L-enkephalin was accompanied by the depression in pancreatic enzyme activity in the blood of rats, acceleration of necrotic and lytic processes in irreversibly damaged exocrine pancreocytes in the course of experimental pancreatitis. The drug promoted microcirculation retention in the injury zone and acceleration of the arrangement and elimination of necrotic glandular tissue. The influence of tagaflar diminished the extent of perifocal necrobiotic zone and suppressed sclerotic processes and pancreatic lipomatosis.
[Ischemic diseases of the lower limbs].
On the material of 200 necropsies and 230 surgically amputated lower extremities in patients with an acute obstruction of the main arteries as well as the study of the limb muscles in the appropriate experimental models, the principal rules and the pathogenesis of the muscle damage in the ischemic disease of the lower extremities (IDLE) are described. Four clinico-anatomical variants of the acute IDLE are distinguished: (1) diffuse degenerative-necrotic muscle damage; (2) large-focal necrosis; (3) massive isolated necrosis of single muscles; (4) limb gangrene. Grave general and local somatic background in a patient, causes of death and role of the IDLE in thanatogenesis are characterized.
[Fibrofatty changes in the muscles in arterial occlusions of the extremities].
Widespread muscle alterations in the form of partial or full muscle fiber replacement by the fibrofatty tissue within the borders of the fascial sheath with the retention of the volume and topography of the muscles are observed in the obliterating atherosclerosis of the lower limbs arteries. These alterations are connected with a slowly progressing degenerative process due to chronic ischemia. The limb with a fibrofatty replacement (FFR) of the muscles is more resistant to the gangrene resulting from acute occlusion of the main arteries. The FFR should be correctly interpreted and considered when acute arterial occlusion of the lower limbs is diagnosed.
[False aneurysm of the heart after resection of a post-infarction aneurysm].
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[Pathological anatomy and pathogenesis of experimental pancreatitis].
The necrotic and inflammatory processes in the albino rats pancreas were studied by histological, immunomorphological and electron microscopic techniques after freezing of the pancreas. Early morphological sings of acinar cells destruction were revealed. The mechanism of secret "leakage" from zimogen granules into acinar cell cytoplasm was shown. The stages of pathologic process corresponding to different types of pancreatitis were established. The inflammatory reaction formed in the stage of parenchymal necrosis was characterised by an early activation of fibroblastic and macrophagal cells and by the delay of necrotic tissue elimination with their following calcification. The chronic pancreatitis developed on the immune basis in the intact parts of the pancreas.
[Postresuscitation encephalopathy].
On the basis of morphological examination of brain from 250 deceased patients who after clinical death showed, during 1-63 days, symptoms of grave anoxic encephalopathy as well as retrospective analysis of clinical biochemical data, and biochemical post-mortem study of the blood and liquor, the main pathological forms of postresuscitation encephalopathy are distinguished. These are as follows: diffuse-focal anoxic lesions of the brain and spinal cord, partial (complete and incomplete) necroses, isolated total brain necrosis, subtotal necrosis of the brain stem and cerebellum. Morphogenesis as well as extra- and intracranial factors enhancing the development of these forms of encephalopathy are described. Developmental stages of necrotic alterations are singled out, attention is drawn to the processes of organization and reparative regeneration of the brain structural elements in the postresuscitation period. The influence of certain grave metabolic and circulatory disorders on the postresuscitation encephalopathy morphology is shown.
[Macrofocal metabolic myocardial damage].
Eighteen observations of large-focal damage of the myocardium are analysed which macroscopically simulated myocardial infarction. Histologically the foci were represented by confluent areas of fatty and albuminous degeneration alternating with necrosis of individual cardiomyocytes. This condition is a complication of diseases having signs of intoxication, anemia, disorders of lipid metabolism and water-electrolyte balance combined with ischemic heart disease. The degree of heart function disturbance correlated with both the severity of concurrent diseases and the depth and size of cardiomyocyte damage.
[A method of dissection of the human lower limb in occlusion of the major arteries].
A simple and informative method of post-mortem dissecting the human lower limbs with the occlusion of main arteries. This method permits the examination of muscles and main vessels at their total length with the preservation of tissue topography and the possibility of taking the tissue pieces for the histological study from the standard areas.
[Central problems in the general pathology and pathologic anatomy of shock].
From the results of detailed clinico-anatomical studies of traumatic, exotoxic, burn, cardiogenic, bacterial, hemorrhagic, and other kinds of shock (1500 observations) and the data of the literature, the paper analyses some disputable aspects of shock: the role of neurogenic factors and vasomotor disorders in its pathogenesis, shock and collapse relationship, possibilities of shock diagnosis at autopsy, the concept of shock organ and shock cell. The importance in the pathoanatomic diagnosis of shock of hemodynamic disorders (sequestration of blood in the microcirculatory bed, shunting of the bloodstream in vital organs) and of hemocoagulation (liquid state of cadaver blood, DIBC) as well as of rapid mobilization of glycogen from tissue depots (liver) and circulatory-hypoxic injuries to the internal organs. The specific features of the individual kinds of shock are determined by different combinations of the above signs or predominant involvement of some internal organ. The lack of a single complete definition of the shock organ concept is indicated. The importance in the pathogenesis of shock of hemodynamic disorders, complications of the main disease, and pathology of therapy (the third factor) is emphasized.
[Repair processes in the pancreas after cold injury].
Electron microscopy of the pancreas has shown after focal ethyl chloride cooling that reparative processes spreading from the borders to the epicenter of the affected parts involved (1) intracellular regeneration of partially damaged acinar cells, (2) proliferation of the epithelium of unaffected ducts, (3) proliferation of fibroblasts and capillary endothelium to form a fibrous capsule around the focus of necrosis. After sequestration of the focus of necrosis the partially damaged acinar cells of the border area underwent amitosis without cytotomy followed by the recovery of lost organelles. No acinar cells were observed to occur. Canalicular proliferates became differentiated mainly in islet cells. However, the main mass of the canalicular acinar derivatives of the border area experienced atrophy and cicatrization to form a fibrous capsule around the focus of necrosis. The compensation of the lost part of the excretory parenchyma was preceded by hypertrophy of acinar cells of undamaged segments of the pancreas.
[Pathomorphology of recurrent pulmonary edema in myocardial infarction].
Morphological, including electron microscopical, dynamics of multiply recurrent pulmonary edema in myocardial infarction at intervals of 2 to 35 days is presented. The macroscopical picture of the lesion at that resembles croupous pneumonia. Microscopically, release of large disperse proteins and precipitation of fibrin in alveolar lumens, erythrocyte stasis in capillaries, and lipid vacuoles in their lumens are observed. Subsequently, the fibrin exudate in alveolis undergoes organization and carnification. In diffuse lesions this may cause acute respiratory insufficiency. Pathogenesis and morphogenesis of pulmonary changes as well as their importance in tanatogenesis are discussed. The patterns of changes in the lungs in recurrent edema allowed the authors to classify them as a new kind of pathology of intensive therapy caused by prolongation of the terminal condition.
[Morphology of thrombolysis as affected by a plasmakinase preparation].
The effect of a new thrombolytic preparation, plasmakinase, on experimental coagulates and thrombi was studied morphologically. Histological and electron microscopic studies revealed changes in the structure of fibrin fibers in the form of separation of fibers into individual protofibrils and subsequent degradation into globular particles. There were disorders in the fibrin association with blood cells, washing out of partially hemolyzed red blood cells into the bloodstream, decrease in the size of thrombi and restoration of the vessel lumen.
[Healing of compression anastomoses of the large intestine].
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[Bacterial shock].
Bacterial shock (BS) is a complication of infectious and suppurative surgical diseases caused mainly by gram-negative bacterial flora. The leading role in the pathogenesis of BS belongs to intoxication of the host by bacterial endotoxins resorbed from the primary focus, by products of protein disintegration, as well as hyperproduction of biologically active substances in the patient. The clinico-anatomical variants of BS are adequate to the quantity and quality of toxins resorbed from the primary focus. An accurate pathoanatomical diagnosis of BS is mandatory for its profound investigation. This diagnosis is possible on the basis of a careful clinico-anatomical analysis with due consideration of the morphological criteria of hemocoagulation and peripheral hemodynamics disorders (the liquid state of cadaver blood, disseminated intravascular coagulation, blood sequestration in some bassins, and intraorgan shunt of the bloodstream).
[Ultrastructural changes in the acinar cells of the pancreas after exposure to cold].
Electron microscopy of acinar cell (AC) of the pancreas cooled to -30 degrees C with subsequent thawing has disclosed the destruction of intracellular membranes, damage to the cell organelles followed by diffusion of the zymogen granule contents to the hyaloplasm and interstice. These changes corresponded to the phase of paranecrosis (cryogenic shock of the cell), whereas the AC lost its ability to autophagocytosis. Irreversible cryodestruction provoked complete cell necrosis during 3-6 hours. The less cold-affected cells were subsequently destroyed because of additional injurious action of enzymatic cytolysis and circulatory hypoxia.