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cell injury, inflammation and healing - Coggle Diagram

- - - - because of prostaglandins from the injured cells
  - - - because of inflammation
      - fluid with plasma proteins and leukocytes cloudy
    - - hydrostatic pressure
      - just fluid clear
  - - - eosionphilia
        
        allergy or parasitic infection
      - lymphocytosis
        
        virus
      - neutrophilia
        
        bacteria
    - - increased ESR
      - increased c-reactive protein
- - - - cell membrane damage
      - cytoplasm leakage
      - nuclear changes
        
        karyorrhexis
        
        when the nucleus breaks down into small fragments
        
        karyolysis
        
        when the nucleus fade and chromatin lysed and DNA is lost
        
        pyknosis
        
        the nucleus shrinks and get denser and darker
    - - changes like hypoxia, partial damage of Na pump and swelling of the cell
  - - - considered as coagulative
      - in diabetic patients foot
      - if there is a bacterial infection it can be a wet gangrene
    - - combination of coagulative and liquefactive
      - the dead cells are not completely digested leaving granular particles
      - caused by tuberclosis typically in lungs
      - appearance of macrophages
      - white clumbed cheese
    - - the transformation of the tissue into liquid viscous
      - pus and abscess
      - cause of bacteria or fungal infections
    - - yellowish-whitened firm deposits
      - in organs with adipose tissue
      - necrotic cells will have a cloudy appearance
      - fat cells will release lipase which degrade the fat tissue into fatty acids that will bind to calcium and form white chalky deposits
    - - caused by infraction or ischemia
      - kidney, heart and adrenal glands
    - - damage of blood vessels
      - fibrin and other plasma proteins will deposit in the wall of arteris
  - - - reduced size of the cell
        
        fragmentation of nucleus
        
        intact plasma membrane
        
        intact
        
        no inflammation
        
        physiologic and pathologic role
    - - enlarged and swelling
        
        pyknosis and karyorrheixs and karolysis
        
        disrupted membrane
        
        digestion of the cellular contents
        
        there is inflammation
        
        pathologic role
- - - - replacement of necrotic tissue with new tissue
    - - proliferation of connective tissue and fibrosis and scarring
  - - - macrophages
      - granulation
      - collagen appear
      - epithelial cells continue to proliferate
    - - neovascularization
      - collagen bridge
      - epidermis recovers
    - - epithelial cells proliferate and meet in the midline
    - - collgen accumulate and fibroblast proliferate
      - leukocyte infiltration and edama are diminshed
    - - homeostasis and clot fomration
      - neutrophils come
      - increased mitotic activity of basal cells
  - - - clean and uninfected
      - surgically incised
    - - open and may be infected
      - cannot be surgically incised
    - - combine primary and secondary
      - left open for granulation for 5-7 days
      - when the risk of infection appear minimal the wound is sutured
  - - - poor blood supply
      - foreign bodies and infection
      - type, size and location of injury
      - less movement
    - - uncontrolled diabetes
      - history of glucocorticoids
      - nutrition
      - hematologic abnormalities
      - age
- - - - trauma
      - infection
    - - serosangiuneous
        
        serous exudate with blood
      - suppurative
        
        pus -yellowish creamy
      - serous exudate
        
        less cells
        
        yellow or straw like color
    - - progression to chronic inflammation
      - fibrosis
      - abscess formation
      - complete resoultion
  - - - persistant exposure
      - autoimmunity
      - persistant infection
    - - cirhosis
      - chronic organ insufficiency