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Liquefactive necrosis (or colliquative necrosis) is a type of necrosis which results in a transformation of the tissue into a liquid viscous mass. [1] Often it is associated with focal bacterial or fungal infections, and can also manifest as one of the symptoms of an internal chemical burn . [ 2 ]
Lung abscess is a type of liquefactive necrosis of the lung tissue and formation of cavities (more than 2 cm) [1] containing necrotic debris or fluid caused by microbial infection. This pus -filled cavity is often caused by aspiration, which may occur during anesthesia, sedation, or unconsciousness from injury.
Necrosis can also result from chemical trauma, with alkaline and acidic compounds causing liquefactive and coagulative necrosis, respectively, in affected tissues. The severity of such cases varies significantly based on multiple factors, including the compound concentration, type of tissue affected, and the extent of chemical exposure.
Caseous necrosis in T.B. is most common site of dystrophic calcification. Liquefactive necrosis in chronic abscesses may get calcified. Fat necrosis following acute pancreatitis or traumatic fat necrosis in breasts results in deposition of calcium soaps. Infarcts may undergo D.C. Thrombi, especially in veins, may produce phleboliths.
Necrotizing pneumonia (NP), also known as cavitary pneumonia or cavitatory necrosis, is a rare but severe complication of lung parenchymal infection. [ 1 ] [ 2 ] [ 3 ] In necrotizing pneumonia, there is a substantial liquefaction following death of the lung tissue, which may lead to gangrene formation in the lung.
Micrograph showing contraction band necrosis, a histopathologic finding of myocardial infarction (heart attack).. Histopathology (compound of three Greek words: ἱστός histos 'tissue', πάθος pathos 'suffering', and -λογία-logia 'study of') is the microscopic examination of tissue in order to study the manifestations of disease.
Granulomatosis with polyangiitis may have areas of liquefaction necrosis caused by vasculitis. A triad of vasculitis, necrosis and granulomatous inflammation may be observed. In secondary Sjögren’s syndrome, periglandular fibrosis with the absence of inflammation may also be observed in addition to that of myoepithelial sialadenitis from the ...
The bacteria gains access to the periapical region of the tooth through deeper infection of the pulp, traveling through the roots. The resulting pulpal necrosis causes proliferation of epithelial rests of Malassez which release toxins at the apex of the tooth. The body's inflammatory response will attack the source of the toxins, leading to ...