Acute Inflammation 1

Acute Inflammation 1

1. Describe key inflammatory mediators and their effects

   • Histamine: vasoactive-dilation/permeability/sm. contraction (serotonin similar); mast cells/basophils in immediate phase
   • Kinin: active polypeptides, vascular effects + pain via axon reflex (bradykinin); activated from complement/plasmin (blood clotting)
     • Plasmin-> breaking doen fibrin (demolition phase)
   • Prostaglandins and Leukotrienes: fatty acids from phospholipids by activated cells (delayed phase); vasodilation/permeability PG, sm. contraction, LT pain PG, chemotaxis LT
   • Platelet activating factor: by activated mast cells from membrane phospholipids-> degranulation
     • Platelet released mediators: lysosomal granules (proteolytic/ cationic) + dense bodies (serotonin) also PROSTAGLANDINS
   • Complement System: C3a and C5a (anaphylotoxins)-> release of histamine from mast cells
   • Neutrophil released mediators: azurophillic lysosomal granules (degradative enzymes)-> tissue liquifaction/ inflammation amplification, specific granules (antibacterial/mast cell degranulation
   • Peptides: from digestion of exudate, increase vascular permeability
   • Microbial products: kinases, hyaluronindase, vaso-active toxins, haemolysins, leucocidins, proteases etc
   • Cytokines: IL-1, TNF-a, IFN-y produced by local cells; vascular dilation/permeability, production of proteolytic enzymes
   • Chemokines: chemoattractants for leukocytes

2. cardinal signs of inflammation

   • Heat + redness
     • Vasodilation + ^blood flow = accumulation of blood
   • Redness
     • ^Metabolic rate
   • Swelling
     • Accumulation of exudate + migration of inflammatory cells
   • Pain
     • ^Pressure from swelling + release of chemicals from damaged tissue which stimulate nerve endings
   • Loss of function
     • ^Pain (m + joint movement), cell/tissue destruction + vascular disturbances on normal physiology (secretion of glandular tissue e.g. udder)

3. Explain changes in vascular responses

   • Hyperaemia (increased blood flow into tissues)
   • Margination of leukocytes (stick to b.vessel wall)
   • Slowing of blood flow
     • Sludging of erythrocytes (rouleaux formation)
     • Stasis (thrombosis)
   • Changes in vessel walls + swelling of endothelial cells
   • Exudation of Fluid
     • ^Hydrostatic pressure, ^passive filtration
     • Escape of plasma proteins through transient gaps between endothelial cells

4. Principally a protective response but can become a major driver of disease/pathology if deregulated

   • Pathology dominant if reaction is very STRONG, PROLONGED or INAPPROPRIATE (autoimmunity/allergy)
   • Inflammation is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.
     • To dilute, destroy or neutralise harmful agents such as microbes and toxins., to remove dead and damaged tissue, to initiate repair
   • Components
     • Cells + molecules that can leave circulation
     • Macrophages, fibroblasts + ECM proteins
     • Endothelial + s.muscle cells of vessel wall

5. Name stimuli for inflammatory reactions

   • Physical
     • cuts, burns, fractures, foreign bodies
   • Chemical
     • acids, alkalis, industrial chemicals
   • Microbial
     • bacterial / fungal toxins & products, viral induced cell death, parasites
   • Immunological
     • Normal immune response to infectious agents, hypersensitivity reactions (I to IV)

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