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Pathology Pt. 1, Fibrinoid necrosis is a specific pattern of irreversible,…

- - - - Cellular injury is detected by:
        
        Macrophages, Dentrtic cells, Mast Cells = release mediators
        
        Oponised antigens (ie Antibodies or Complement)
    - - a) Dilation
        
        Warmth/redness
        
        mediated by histamines/prostaglandins
        
        Acts on arterioles/capilaries
      - b) Permeability
        
        Retracted endothelial cells allow for fluid/protein to flow out (Exudate)
        
        Swelling/odema
        
        Transudate (just fluid) vs exudate (fluid/proteins)
      - c) Emigration
        
        Endothelial activation via IL-1 & TNF-α
        
        Selectins (High + Low affinity) appear
        
        Margination/rolling (low affinity selectins)
        
        Adherence (high affinity selectins)
        
        Transmigration (movement through vessek into tissue)
        
        Chemotaxis (movement to site of injury along chemical gradient)
    - - Phagocytosis
        
        Recognition - via phagocytic receptors
        
        Engulfment
        
        pesopedia engulf debris o become a phagosome
        
        phagosome fuses w/ lysosomes to become phagolysome
        
        Breakdown
        
        Release of reactive O2 and N2, lysoszymes, microbiocidal ect DESTROY!!
    - - Cessation of actue response
        
        Offending agents removed, mediators degraded, WBCs stopped recuited, nueral impulses ceased
    - - Sequale of acute inflammation
        
        Resolution
        
        Clearance of injurious stimulus, mediators and inflam cells
        
        Replacement of injured cells
        
        Normal function restored
        
        Healing
        
        Pus (liquefactive) / abcess formation
        
        Fibrosis (scar) = LOSS OF FUNCTION
        
        Progression
        
        Chronic Inflammation
        
        Angiogenesis, mononulcear cell infiltrate, fibrosis
  - - - Mediated by the cytokine release (IL-1, 6 & TNF-α)
      - Rasied platelets on FBC
      - Raised C-Reactive Protein (Inflammatory marker)
      - Associated fever, elevated HR, RR (IL-6)
  - - - Histamine, Prostaglandin
    - - Histamine, C3a, C5a, Leukotienes
    - - TNF, IL-1, Chemokines, C3a/5a
    - - IL-1, 6, TNF
    - - Bradykinin, prostaglanins
  - - - C3b is deposited on microbe
        
        C3/5a is detected by leuckocytes for recruitment causing inflammation
        
        Recognised c3b by phagocyte cuases phagocytosis of microbe
        
        Casues fomation of the membrane attack complec (MAC) destroying microbe
- - - - Cell Enlargement, nuclei kerolysis, membrane disrupted, inflammtory
      - Types: Coagulative, liqefactive, caseous
    - - Programmed cell death (loss of survival GTH)
      - Cell reduced, nuclei fragmented, membrane intact, no inflammation
      - Aopototic bodies phagocytosed
    - - Acutet w/ Intact framework
        
        Regeneration
        
        Liver cells or skin wounds
      - Acute w/ Damaged framework
        
        Healing with reapair/scar formation
        
        Myocardial infacrts (coagulatic necrosis) or deep incisonal wounds
      - Persistent Damage
        
        Fibrosis
        
        Cirrhosis, pancreatitis, pulmonary fibrosis
- - - - Macrophages
        
        Classical activated macrophage
        
        Monocytes are activated to become macrophages and destroy the noxious stimuli but also release mediators to promote inflammation (IL-1, 6 and TNF-a, chmokines)
        
        Alternatively activated macrophage
        
        promote tissue repair/fibrosis and have antiinflammatory effects (growth factors, IL-10)
      - Lymphocytes
        
        Antigens activate T and B lymphocytes which amplify and propagate chronic inflammation
        
        Recuited by cytokines (IL-1, TNF-a) released from macrophages
        
        TH1 cells produce IFN-Gamma which causes classical activation of macrophages
        
        TH2 cells secrete IL-4, IL-5 and IL-13 which recruit eosinophils and cause alternative activation of macrophages
      - Other Cells
        
        Plasma cells = produce ab
        
        Eosinophils = granular cells (histamines) - allergy reactions
        
        Mast cells = granular cells (histamine), mediated by IgE, hypersensitivity
    - - Role is in the THIRD stage of wound healing = proliferative
        
        Immune (protect wound from further injury),
        
        Proliferative (full wound with new cells/tissue)
        
        Plug (replace necrotic tissue until scar tissue is formed)
      - Granulation tissue is a complex connective tissue w/ fibroblasts, endothelial cells, and immune cells
        
        Fibroblasts synthesis collagen and ECM (initally collagem type 3, but this is eventually repalced with collagen type 1)
        
        Endothelial cells are responsible for angiogensis which aids in the formation of granulation tissue and the whole healing process
        
        myofibrobalsts (mediated by fibroblasts) aid in the wound contraction
      - Errors in the formation of granulation tissue (ie foregin bodies) can result in chronic wound formation/poor wound healing
        
        Both healing and inflammation will then exist at the site
    - - Chronic Ulcer - thickened(hyperplastic healing) epithelium, chronic inflammatory cells, granulation tissue
    - - Epithelioid cells (activated macrophages) = wall off an offending agent with associated mononuclear inflammatory cells
      - Can fuse togther to become a multinuleate giant cell (MNG)
        
        Capable of more phagocytosis
      - Causes of granulomas
        
        Foreign body graulomas - suture materials
        
        Infectious - ie TB
        
        Autoimmune = sarcoidosis
      - NB: a periapical granuloma is a collection of granulation tissue in an area where we have chronic inflammation (NOT A TRUE GRANULOMA) ie no immune cells
  - - - Persistent infections
        
        Ex. H pylori, (gram-ve infection) causing gut inflammation and ulcerations
      - Hypersensitivity diseases
        
        Endogenous = Own tissues VS Exogenous = environemtal allergens
        
        Type 1 = anaphylaxis, Type 2, Ab mediated, Type 3 = Immune complex (SLE), Type IV = Cell-mediated (Dermatitis, DM)
      - Ongoing exposure to potentially toxic agents
        
        Exogenous = Asbestos, silica
        
        Endogenous = athersclortic laques
  - - - No. Chronic inflammation can arise from autoimmune disease, foregin bodies. endogenous toxins or infections
    - - No necessisairly, as acute can regenerate or heal only progress to chronic if persistent