Injury > Inflammation

PLASMA DERIVED MEIATORS
1. HAGERMAN FACTOR
  1. XIIa
    1. KININ
      1. Bradikinin
        ↑ Histamine, ↑ VascPermeability, ↑ Vasodilation, BronchoSpasm
      2. FIBRINOLYTIC
        Plasminogen
        Plasmin
        Fibrin
        Fibrinogen
        COMPLEMENT
        ↑ VascPermeability, ↑ Leuk activation, adhesion, chemostaxis, Phagocytosis
        Inactivates thrombin to limit clotting
    2. CLOTTING
      1. Prothrombin
        Thrombin
        Acute Inflammation
        Cleaves fibrinogen > clot formation, binds to platelets and EN
  2. BM, Collagen, Platelets
VASCULAR PHASE
1. ↑ VASODILATION
  1. Red/hot/swollen
  2. ↑ Blood to area > ↑ WBC
  3. ↑ in hydrostatic P > Transudate
2. ↑ PERMEABILITY
  1. ↓ Colloid Osmotic P > Exudate
  2. ↑ WBC to tissue > Activated (mediators) > ↑ function and phagocytosis
ACUTE PHASE REACTION
1. VASCULAR CHANGES
  1. 1. Vasodilation
    1. Mast cells > histamine > relax smooth muscle of vessels
    2. ↑ hydrostatic P > Transudate
    3. Slows bloodflow > marginalisation of leukocytes
  2. 2. Vascular permeability
    1. Release mediators from cells (Histamine, Serotonin, Bradykinin, Leukotriens, NO)
    2. Endothelial cell contraction > ↑ permeability
    3. Fluid + protein into ECM > ↓ Colloid osmoric P > Exudate
    4. ↑ sludging and marginalisation
  3. 3. Lyphatic vessels
    1. Clears inflammation: oedema, inflammation cells, detritis
2. CELLULAR CHANGES
  1. 1. Leukocyte recruitment
    1. (1) Adhesion (2) Transmigration (3) Chemotaxis
    2. Chemotaxis stimulated by bacterial products, complement med, leukotriens
    3. Chemotaxis of (1) Neutrophils (first responders) (2) Monocytes (replace neutrophils)
  2. 2. Leukocyte actication
    1. Phogocytosis (1) Recognise and attach (2) Engulf (3) Kill
    2. Opsonisation > engulfment
    3. Produce lysosomal enzymes: destroy phagocytosed microbes and dead tissue
    4. Produce mediators > amplify inflammation
  3. 3. Tissue injury
    1. Leukocyte induced injury d/t tissue clearing and progression to AI dx
CELL DERIVED MEDIATORS
1. VASO ACTIVE AMINES
  1. Histamine
    1. ↑ Vasodilation, ↑ VascPermeability, BronchoSpasm (Mast)
  2. Serotonin
    1. Vasoconstriction (Pl)
2. ARACHADONIC ACID METABOLISM
  1. Phospholipases
  2. Lipoxygenase
    1. Lipoxins
      1. ↑ Vasodilation, ↓ Neutrophils, ↑ Monocytes
    2. Leukotrienes
      1. Vasoconstriction, ↑ VascPermeability, BronchoSpasm (Mast)
  3. Cyclooxygenase
    1. Prostacyclin
      1. ↑ Vasodilation, ↓ Platelet aggregation (EC)
    2. Thromboxane
      1. Vasoconstriction, ↑ Platelet aggregation (Pl)
    3. Prostaglandin
      1. ↑ Vasodilation, Potentiate oedema (Pl, Leuk, EC)
3. PAF
  1. ↑ Platelet aggregation, cause degranulation
4. CYTOKINES
  1. TNF
    1. ↑ EN thrombogenicity, ↑ Neutrophil aggregation and actrivation
  2. IL-1
    1. Activate tx fibrblasts, ↑ ECM proliferation
  3. Fever, lethargy, cacexia, anorexia
5. CHEMOKINES
  1. Chemo-attractants for leukocytes
6. REACTIVE OXYGEN SPECIES
  1. Produced in lysosomes and released byNeutrophils and macrophages
  2. Low: ↑ immune response
  3. High: EN damage, protease activation, direct injury to cell
7. NITRIC OXIDE
  1. ↑ Vasodilation, ↓ Platelet aggregation, ↓ lLeukocyte adhesion, Microbicidal in macrophages

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Injury > Inflammation

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	Created by Lindie Metz over 8 years ago