scholarly journals ПАТОМОРФОЛОГІЧНІ ЗМІНИ ЛЕГЕНЕВОЇ ТКАНИНИ ЗА ІНФЕКЦІЙНОГО ПЕРИТОНІТУ КОТІВ

2016 ◽  
Vol 18 (3(70)) ◽  
pp. 161-167
Author(s):  
G. Kotsiumbas ◽  
V. Pritsak ◽  
M. Khalaniia

The article presents the results of pathoanatomical, pathohistological and histochemical researches of the lung tissue for exudative form of the spontaneous infectious peritonitis of cats. The results of researches allow us to analyze pathoanatomical, microstructural changes in lung tissue of cats in various forms of peritonitis infectious and to define the mechanism of the pathological process that cause lethal consequence.The pathoanatomical research of dead bodies of 4 cats has been carried out: a 3 year–old cat and 1 year and 2 month–old cat and 1 year and 5 month–old with symptoms of exudative pleurisy; a 2 year–old cat with clear signs of exudative peritonitis and pleurisy. Peritoneal fluid and lung tissue fragments for cytological and pathohistological examination were selected. At pathoanatomical autopsy accumulation in the thoracal, abdominal cavities and pericardial space fluid with the flakes of fibrin were revealed, thickening of the serous membranes, layering them fibrin. At the pathohistological research in lung tissue noted the consequences of hemodynamic disturbances in the form of multiple perivascular hemorrhage, interstitial pneumonia, atelectasis and emphysematous cells and signs of fibrinous pleurisy in the state organization have been noted. The hardest changes were developed in the structures of the vascular system and are characterized by the damage of vascular endothelium, the development of productive meso– and periarteritis, syndrome of disseminated intravascular coagulation, stasis and hemolysis of erythrocytes in small vessels of interalveolar septum leading to the oppression of hemocirculation. In lungs, the mononuclear–macrophage infiltration prevailed, especially in periarteritis zone, indicating the presence of productively–necrotic vasculitis.The development of the syndrome disseminated intravascular coagulation led to the formation of multiple micro–blood clots, aggregated cells in vascular channel, the presence of which has led to the development of thrombi and then hemorrhages. The blockade microcirculation, in their turn, led to tissue hypoxia, acidosis and, as a result, distrophic changes in the past. The discovered processes in the vascular system of the lung tissue caused the insufficient flow of blood, irreversible changes of homeostasis and a sharp decline in adaptive capacity. 

2019 ◽  
Vol 2019 ◽  
pp. 1-2
Author(s):  
Jeremy Chuang ◽  
An Uche ◽  
Rohan Gupta ◽  
Kim Margolin ◽  
Phyllis Kim

Acute disseminated intravascular coagulation (DIC) is a pathological process involving dysfunction of the coagulation cascade. In this case report, we discuss a 33-year-old woman with BRAF V600E-mutated metastatic melanoma who presented in fulminant DIC with concurrent hemorrhagic and thrombotic manifestations and discuss the patient’s brief response to combination therapy. In our discussion, we highlight the current understanding of DIC and also identify opportunities for future research to elucidate the genetic aberrations in melanoma that may result in treatment resistance to combination therapy.


2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Jae C. Chang

Abstract Disseminated intravascular coagulation (DIC) can be correctly redefined as disseminated intravascular microthrombosis based on “two-path unifying theory” of in vivo hemostasis. “DIC” is a form of vascular microthrombotic disease characterized by “microthrombi” composed of platelets and unusually large von Willebrand factor multimers (ULVWF). Microthrombotic disease includes not only “DIC”, but also microthrombosis occurring in thrombotic thrombocytopenic purpura (TTP), TTP-like syndrome, and focal, multifocal and localized microthrombosis. Being a hemostatic disease, microthrombotic disease occurs as a result of lone activation of ULVWF path via partial in vivo hemostasis. In endothelial injury associated with critical illnesses such as sepsis, the vascular damage is limited to the endothelial cell and activates ULVWF path. In contrast, in intravascular traumatic injury, the local damage may extend from the endothelial cell to subendothelial tissue and sometimes beyond, and activates both ULVWF and tissue factor (TF) paths. When endotheliopathy triggers exocytosis of ULVWF and recruits platelets, ULVWF path is activated and promotes microthrombogenesis to produce microthrombi composed of microthrombi strings, but when localized vascular damage causes endothelial and subendothelial tissue damage, both ULVWF and TF paths are activated and promote macrothrombogenesis to produce macrothrombus made of complete “blood clots”. Currently, “DIC” concept is ascribed to activated TF path leading to fibrin clots. Instead, it should be correctly redefined as microthrombosis caused by activation of ULVWF path, leading to endotheliopathy-associated microthrombosis. The correct term for acute “DIC” is disseminated microthrombosis-associated hepatic coagulopathy, and that for chronic “DIC” is disseminated microthrombosis without hepatic coagulopathy. TTP-like syndrome is hematologic phenotype of endotheliopathy-associated microthrombosis. This correct concept of “DIC” is identified from novel theory of “in vivo hemostasis”, which now can solve every mystery associated with “DIC” and other associated thrombotic disorders. Thus, sepsis-associated coagulopathy is not “DIC”, but is endotheliopathy-associated vascular microthrombotic disease.


2020 ◽  
Author(s):  
Sandeep Chakraborty

Disseminated intravascular coagulation (DIC) is a serious disorder characterized by small blood clots de- veloping throughout the bloodstream, blocking small blood vessels, depleting platelets and clotting factors leading to excessive bleeding. Lately, it is been reported that Covid19 is more of a vascular problem, than one of the lungs. Here, I enumerate studies of Lemierre’s syndrome with DIC, and also papers highlighting the Covid19 cases - this is based on my hypothesis that Covid19 is very similar to Lemierre’s Syndrome, wherein an anaerobic bacteria is enabled by a virus (SARS-Cov2/EBV) to form an abscess, from which a blood clot (carrying the bacteria) disseminates through the blood stream [1].


Author(s):  
M. G. Williams ◽  
C. Corn ◽  
R. F. Dodson ◽  
G. A. Hurst

During this century, interest in the particulate content of the organs and body fluids of those individuals affected by pneumoconiosis, cancer, or other diseases of unknown etiology developed and concern was further prompted with the increasing realization that various foreign particles were associated with or caused disease. Concurrently particularly in the past two decades, a number of methods were devised for isolating particulates from tissue. These methods were recently reviewed by Vallyathan et al. who concluded sodium hypochlorite digestion was both simple and superior to other digestion procedures.


Author(s):  
Jerrold L. Abraham

Inorganic particulate material of diverse types is present in the ambient and occupational environment, and exposure to such materials is a well recognized cause of some lung disease. To investigate the interaction of inhaled inorganic particulates with the lung it is necessary to obtain quantitative information on the particulate burden of lung tissue in a wide variety of situations. The vast majority of diagnostic and experimental tissue samples (biopsies and autopsies) are fixed with formaldehyde solutions, dehydrated with organic solvents and embedded in paraffin wax. Over the past 16 years, I have attempted to obtain maximal analytical use of such tissue with minimal preparative steps. Unique diagnostic and research data result from both qualitative and quantitative analyses of sections. Most of the data has been related to inhaled inorganic particulates in lungs, but the basic methods are applicable to any tissues. The preparations are primarily designed for SEM use, but they are stable for storage and transport to other laboratories and several other instruments (e.g., for SIMS techniques).


2003 ◽  
Vol 23 (03) ◽  
pp. 125-130 ◽  
Author(s):  
S. Zeerleder ◽  
R. Zürcher Zenklusen ◽  
C. E. Hack ◽  
W. A. Wuillemin

SummaryWe report on a man (age: 49 years), who died from severe meningococcal sepsis with disseminated intravascular coagulation (DIC), multiple organ dysfunction syndrome and extended skin necrosis. We discuss in detail the pathophysiology of the activation of coagulation and fibrinolysis during sepsis. The article discusses new therapeutic concepts in the treatment of disseminated intravascular coagulation in meningococcal sepsis, too.


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