Please enable JavaScript.

Coggle requires JavaScript to display documents.

Cell Injury and Death (Mechanisms of Cell Injury (Influx of intracellular…

- - - - Antioxidants
      - Iron and copper binding proteins
      - Scavenging enzyme systems
  - - - If cells switch to glycolysis glycogen is depleased and lactic acid and inorganic phosphates accumulate which decreases intracellular pH, resulting in decreased activity of some cellular enzymes
      - As ATP depletion continues, ribosomes detach from RER leading to decreased protein synthesis
      - Failure of Ca pump causes excess Ca to enter cell, damages systems by increased enzyme activity
      - Protein misfolding occurs leading to further cell injury
      - Plasma membrane Na, K, ATP pumps fail & Na enters the cell and water follows leading to cell swelling and dilation of RER
- - - - Light microscopy: hypereosinophilic (takes up more pink dye, eosin) due to loss of RNA in the cytoplasm (RNA and DNA stain with the blue dye, hemotoxylin) and denatured cytoplasmic proteins
      - Calcification of cells may occur
      - EM: membrane disruption, dilated mitochondria with large amorphous densities, and cytoplasmic myelin figures
    - - Light microscopy: due to breakdown of DNA
        
        Pyknosis: nuclear skrinkage and increased basophilic
        
        Karyorrhexis: nucleus fragments (usually following pyknosis)
        
        Karyolysis: fading or disappearance of the nucleus
  - - - occurs most commonly with bacterial, fungal, or lytic viral infections and the cells are digested by their own enzymes, bacterial toxins, or enzymes of leukocytes
      - cells are replaced by neutrophils and macrophages
      - focal collections of white blood cells (pus) and cellular debris are called abscesses
    - - not a separate type of necrosis but refers to enzymatic destruction of fat (usually by pancreatic enzymes in acute necrotizing pancreatitis) with subsequent mineralization (saponification)
    - - occurs most often with ischemia or toxins and for a few days the cells maintain their basic outline
      - eventually enzymatic action and entering leukocytes leads to proteolysis and loss of the cell outline
      - Ischemic necrosis of an extremity with subsequent coagulation necrosis is called dry gangrene
      - when the action of bacteria causes liquefaction of the gangrenous tissues it is called wet gangrene
    - - not a separate type of necrosis but is used for cheese-like gross appearance of coagulation necrosis with subsequent (often granulomatous) inflammation and sometimes calcification that occurs with some bacteria
- - - - Caspases cleave cytoskeletal and nuclear membrane proteins
      - Caspases activate a DNAase that induces internucleosomal cleavage of DNA
    - - Dying cells attract phagocytes by molecular markers on their surface
      - Macrophages remove dead cells without causing inflammation
    - - via either the extrinsic (death receptor mediated) or intrinsic (mitochondrial) pathway
      - Caspases become catalytically active
- - - - Membrane alterations
      - Mitochondrial swelling
      - Dilation of the endoplasmic reticulum
      - Clumping of nuclear chromatin
- - - - More than once cause may be at work for any given disease
    - - The response to injury depends on the type, duration, and severity of the injury
    - - Cells differ in their capacity to withstand injury and in their ability to regenerate following injury
    - - Following initial injury, if the injury persists, secondary effects rapidly occur
    - - Ultrastructural changes are the first to be visible, gross changes take the longest
- - - - may be difficult to distinguish from necrosis histologically
        
        involves entire tissue
        
        no associated inflammatory response
        
        red blood cells in adjacent blood vessels are also autolyzed