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Cell Death - Coggle Diagram

- - - - The cytoplasm forms bubbles, and endonucleases cause nuclear fragmentation, resulting in apoptotic bodies that are phagocytized by macrophages.
- - - - Granuloma formation occurs when the immune system is unable to eliminate foreign stimuli, leading to containment rather than eradication.
        
        This response involves fibroblasts, leukocytes, and Langhans giant cells, resulting in a structure with a distinct border encasing a necrotic core.
        
        The core, surrounded by inflammation and fibroblasts, appears yellow-white and contains debris.
        
        This process signifies an inability to fully eliminate the noxious agent, resulting in containment rather than eradication.
    - - Gangrene, commonly used clinically, lacks a specific cell death pattern. It occurs in extremities, particularly the lower limbs, due to severe ischemia.
        
        Dry gangrene, with coagulative necrosis, is associated with conditions like severe frostbite.
        
        Wet gangrene, involving liquefactive necrosis, may occur with bacterial infection.
        
        Clinical features include black skin, a mummified appearance, and potential odor indicating infection.
        
        The choice between dry and wet gangrene is based on histological traits, with ischemia suggesting dry gangrene and bacterial infection suggesting wet gangrene.
        
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    - - Tissue liquefaction, often associated with infections, involves the breakdown of dead cells into a viscous liquid mass.
    - - Fat necrosis doesn't signify a specific necrosis pattern but describes fat destruction, often due to pancreatic lipases released in conditions like acute pancreatitis.
        
        Enzymes liquefy fat cell membranes, releasing fats that combine with calcium, creating chalky-white areas.
        
        Causes include infections, trauma, and toxins. In breast tissues, trauma can also trigger fat necrosis.
        
        Histologically, it presents as a soft chalky-white area with basophilic calcium deposits, anucleated adipocytes, pink cytoplasm, and inflammation.
    - - Coagulative necrosis typically results from infarction, affecting various organs except the brain.
        
        Cells become dry, hard, and white, maintaining architectural integrity for some days.
        
        Coagulation involves protein degradation and denaturation, forming an opaque film. A pale, firm segment contrasts with surrounding healthy tissues.
        
        Eosinophilia and anucleated cells with preserved outlines are characteristic features of a microscopic examination in certain conditions.
    - - Fibrinoid necrosis is associated with vascular damage and plasma protein exudation, often due to type 3 hypersensitivity. Immune complexes (Ag-Ab) deposit in vessel walls, triggering inflammation, complement activation, and phagocytic cell recruitment.
        
        This can lead to the release of oxidants and enzymes, causing damage. Fibrin, leaked from vessels, creates a bright pink, amorphous appearance in H&E stains.
        
        The term 'fibrinoid' reflects this fibrin-like quality.
        
        Grossly not discernible, microscopically, it appears as intensely pink fibrinoid necrosis surrounding blood vessels with inflammation.