What is Pathology - How does apoptosis begin?
Apoptosis can be triggered in a variety of ways. The following are the two most important routes: Extrinsic route: This pathway is triggered by the activation of death receptors on the cell membrane's surface. Proteins like tumour necrosis factor or Fas ligand act as ligands for these receptors. Intrinsic mitochondrial pathway: This mechanism is started by increased mitochondrial permeability, which releases proapoptotic chemicals like cytochrome, which act on the initiator caspases, similar to the extrinsic pathway. Apoptosis can be triggered by a variety of factors, including radiation, medications, hormones, and immunological responses (e.g., cytotoxic T lymphocytes). Apoptosis can also be caused by the removal of hormones and growth factors that are necessary for the cell's survival. Castration, for example, is accompanied by a drop in testosterone levels in the blood, which causes prostatic cells to die.
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What is Pathology - What exactly is apoptosis?
Apoptosis is a type of cell death characterised by the activation of "death genes" and "suicide pathway enzymes" in a specific order. It's also referred to as "planned cell death." What is Pathology - What happens when you have necrosis?
Restitution in full: The deceased cells are replaced by nearly parenchymal cells in a process known as regeneration. Organs made up of facultative mitotic cells, such as the kidneys and liver, regenerate. Repair: Fibrous tissue replaces the deceased cells, leaving microscopic or macroscopic scars. In the heart, for example, phagocytes remove dead myocardial cells and replace them with a fibrous scar. Calcification: The necrotic tissue is sometimes contaminated with calcium salts (dystrophic calcification). Resorption of necrotic tissue: Macrophages in the brain remove necrotic tissue, transforming the infarct into a fluid-filled pseudocyst. What is Pathology- What is Fibrinoid Necrosis?
Fibrinoid necrosis is a type of necrosis caused by fibrin. Fibrinoid necrosis is a condition that affects only tiny blood vessels. It usually involves autoimmune illnesses (e.g., systemic lupus erythematosus) or malignant hypertension affecting tiny arteries, arterioles, and glomeruli. In normal hematoxylin-eosin (H&E)–stained slides, the walls of necrotic arteries or glomeruli are coated with fibrin and look uniformly red. Other plasma proteins are present in these deposits, according to a detailed investigation; nonetheless, fibrin dominates other proteins in histologic slides, giving the lesion its name. Fibrinoid necrosis is only visible in histologic preparations and has no macroscopic symptoms. What is Pathology - What is the definition of fat necrosis?
Fat cells in and around the pancreas, the omentum, and the abdominal cavity wall are commonly involved. It is characterised by lipolysis, which happens when lipase and other lytic enzymes released from injured pancreas cells infiltrate fat cells. Acute pancreatitis is the most common cause of this. The fat tissue appears squishy and fluid at first, but it eventually turns into chalky white patches made up of calcium soaps. Fat cells lose their shapes and become blurry histologically. Calcium deposition gives necrotic fat cells a bluish tint. What is Pathology - What is caseous necrosis, and how does it affect the tissue ?
Tuberculous and fungal granulomas are the most common sites for caseous necrosis. On first glance, it appears to be soft and greasy, similar to cottage cheese. The necrotic tissue has lost its usual structure and appears amorphous and coarsely granular on histological examination. What is Pathology - Give a few examples of necrosis that is liquefactive.
Brain infarct: The necrotic area softens (encephalomalacia), and macrophages phagocytize the necrotic tissue debris. Diffusion of fluid from the surrounding interstitial spaces of the brain fills the residual void ("the body abhors a vacuum"). A fluid-filled pseudocyst like this can last indefinitely. Abscess: This is caused by a purulent infection that is localised. It usually manifests as a pus-filled cavity, which is made up of liquefied tissue from the diseased organ infiltrated by dead and dying neutrophils. Wet gangrene of the extremities: This is a type of coagulative necrosis with a bacterial infection that is commonly found in diabetic individuals. Bacterial lytic enzymes break down the tissue, causing it to liquefy. What is Pathology - What is liquefactive necrosis, and how does it happen?
Liquefactive necrosis is defined by the necrotic tissue softening to the point that it becomes a pastelike mush or watery waste. The action of hydrolytic enzymes released from dead cells, as in a brain infarct, or from the lysosomes of invading inflammatory cells, as in an abscess, causes tissue liquefaction. What is Pathology - What does coagulative necrosis look like?
The rapid termination of basic cell activity induced by a blockade of most enzymes is known as coagulative necrosis. There is no tissue dissolving since the action of hydrolytic cytoplasmic enzymes is also stopped (i.e., there is little autolysis). As a result, the general shape of the dead tissue is conserved. The necrotic tissue is paler than normal and has a boiled meat appearance. What is Pathology - What type of necrosis is the most common?
Coagulative necrosis is the most prevalent type of necrosis. It's common in myocardial infarction, as well as infarcts of the kidney, spleen, and a variety of other organs. Coagulative necrosis can occur even in infarcted tumours. |
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