Veterinary Pathology: Necrosis and Gangrene

A type of cell death characterized by the coagulation of necrotic tissue, resulting in a firm, dry, and preserved tissue architecture. It is often caused by ischemia, infections, and mild irritants.

Fat necrosis is a specific form of necrosis that occurs in adipose tissue, usually due to the leakage of pancreatic enzymes. It results in the breakdown of fat cells and the formation of chalky white deposits.

Apoptosis is a programmed cell death that is characterized by a series of biochemical events that lead to the orderly dismantling of the cell. It's a normal physiological process and is essential for maintaining homeostasis.

A form of cell death characterized by enzymatic digestion of cells by intracellular hydrolases, leading to the formation of a soft, creamy, liquid mass. It is often seen in brain and spinal cord infections.

This is a specific type of necrosis primarily found in tuberculosis infections. It is characterized by a cheesy, yellow-white appearance of the necrotic tissue. The tissue is firm and dry with a granular appearance.

The condensation of chromatin material within the nucleus, giving it a dark, reduced, and deeply stained appearance. It is a typical feature observed in cell death.

The dissolution of the nucleus into small fragments. Karyolysis is a distinctive feature of necrotic cells and often precedes complete cell death.

Necrobiosis is the natural physiological cell death that occurs after a cell completes its functional life. It is a normal process in the development and aging of tissues.

A process involving the breakdown of cells and tissues by their own enzymes. It starts after cell death and occurs in the absence of inflammation.

Refers to the changes that occur to the nucleus during necrosis. These changes include pyknosis (condensation of chromatin), karyolysis (dissolution of the nucleus), and karyorrhexis (fragmentation of the nucleus).

This type of clot is formed after death and is not firmly attached to the endothelium. They are typically composed of blood components that have separated out during coagulation.

The primary cause of decreased ATP in the body after death is hypoxia, which occurs due to the cessation of oxygen supply. This leads to the depletion of ATP reserves and ultimately to cell death.

The color of the organ (often grayish-white) after coagulative necrosis is due to the denaturation of proteins and the coagulation of the cytoplasm. This process makes the tissue opaque and firm.

The gross appearance of necrotic tissue is typically pale, soft, friable, and sharply demarcated from viable tissue. This is due to the changes in cell structure and the breakdown of cellular components.

The presence of a cavity within necrotic tissue characterizes liquefactive necrosis. This cavity is formed due to the enzymatic digestion of the cells and the release of fluid into the surrounding area.

The microscopic feature of coagulative necrosis is the absence of the nucleus or the presence of a pyknotic nucleus. This is because the DNA within the nucleus is degraded during the process of necrosis.

The etiology of coagulative necrosis refers to the factors that cause it. These include infections, ischemia, and mild irritants. The presence of these factors disrupts cellular function and leads to cell death.

The enzyme responsible for the formation of fibrin in coagulative necrosis is thrombin. This enzyme plays a crucial role in the clotting process and contributes to the coagulation of necrotic tissue.

The tissue consistency in caseous necrosis is described as firm and dry, similar to cheese. This is because the tissue is characterized by a cheesy, yellow-white appearance due to the breakdown of cells and the accumulation of inflammatory cells.

The characteristic of the dead tissue in caseative/caseous necrosis is a grainy, cheesy appearance. This is due to the breakdown of cells and the accumulation of inflammatory cells, which give the tissue a distinctive yellow-white color.

The etiology of caseative/caseous necrosis involves chronic infections, particularly those caused by Mycobacterium tuberculosis. These infections trigger an immune response that leads to the formation of granulomas, which can undergo caseous necrosis.

The primary cause of fat necrosis is the leakage of pancreatic juice into the surrounding adipose tissue. The pancreatic enzymes, such as lipase, hydrolyze the fat cells, resulting in the formation of chalky white deposits.

The primary distinguishing feature of autolysis from putrefaction is the uniform destruction of cells without inflammation in autolysis. Putrefaction, on the other hand, involves the action of bacteria, leading to a foul smell and the production of gases.

The source of thrombokinase (or thromboplastin) in post-mortem clotting is dying leucocytes and endothelial cells. These cells release thrombokinase, which initiates the coagulation cascade leading to the formation of clots.

The difference between red and yellow post-mortem clots is the distribution of blood components within the clot. Red clots have a larger amount of blood cells and are more homogeneous. Yellow clots are more fibrinous and have a paler appearance.

The primary function of lysosomal enzymes in the process of autolysis is to digest cells and tissues. These enzymes break down cellular components into simpler molecules, contributing to the breakdown of the cell.