Inf 3

• Fates (outcomes) of acute inflammation

  • Complete resolution
  • Healing & organization
  • Suppuration
  • Progression to chronic inflammation

  
• Complete resolution


  1. Removal of the exudate, fibrin & debris

  2. Reversal of the microvascular changes

  3. Regeneration of lost cells
• Healing & organization


  Connective tissue replacement
• Suppuration


  It may be diffuse in tissue, localized in tissue (abscess), on the surface of a wound, or in serous cavity
• Acute inflammation progresses


  Into chronic inflammation
• Ulcer


  Loss of continuity in an epithelial surface or excavation of the surface of an organ or tissue produced by the sloughing of inflammatory necrotic tissue
• Acute inflammation


  • Short duration: hours - days - weeks
  • Exudative fluid (protein rich fluid + inflammatory cells + debris)
  • Main inflammatory cells - N & Macrophage

  
• Chronic inflammation


  • Long duration: months - years
  • Fibrosis
  • Main inflammatory cells - L, M, plasma cells + fibroblasts & endothelial cells

  
• Chronic inflammation


  • A prolonged process in which inflammation and attempt of healing proceed at the same time
  • It is less uniform & productive
  • The main cells are mononuclear cells

  
• Tissue macrophage


  • The dominant cellular player in chronic inflammation
  • It is joined by lymphocytes and plasma cells, however mast cells and eosinophils are as well involved in chronic allergic diseases
• Tissue macrophage


  Blood monocyte migrates into tissue within 48 hours after injury and differentiates
• Types of tissue macrophages

  • Kupffer cell (liver)
  • Microglia (CNS)
  • Histiocytes (spleen)
  • Alveolar macs (lung)
• Ways chronic inflammation may arise

  • Progression from acute inflammation
  • Repeated episodes of acute inflammation
  • Primary chronic inflammation

  
• Causes of chronic inflammation

  • Persistent infection by certain micro-organisms
  • Prolonged exposure to potentially toxic agents (exogenous or endogenous)
  • Autoimmunity
• Outcomes of chronic inflammation

  • Ulcers
  • Fistulas
  • Granulomatous diseases
  • Fibrotic diseases (Scaring)
  • Combinations of the above

  
• Morphologic features of chronic inflammation


  • Infiltration with lymphocytes
  • Infiltration with plasma cells
  • Infiltration with eosinophils
  • Infiltration with mast cells
  • Infiltration with macrophage, activated to epitheliod cells, or fused together forming giant cell

  
• Primary chronic inflammation


  No initial phase of acute inflammation

  
• Causes of primary chronic inflammation

  • Certain infections
  • Prolonged exposure to potential toxic agents
  • Foreign body reactions
  • Some autoimmune diseases
  • Specific diseases of unknown etiology
  • Primary granulomatous diseases

  
• Granulomatous inflammation


  Special type of chronic inflammation in which the predominant cell type is an epitheloid macrophage
• Epitheloid macrophages


  Activated macrophage that has acquired an enlarged, elongated squamous cell-like appearance with secretory rather than phagocytic activity
• Macrophage giant cell


  A large cell having numerous nuclei, of two main types: Foreign body GC and Langhan's GC
• Granuloma


  An aggregate of epitheloid macrophages, surrounding rim of mononuclear infl cells, surrounding rim of fibroblast & fibrosis, with giant cells and central necrosis
• Causes of granulomatous inflammation


  • Specific infections
  • Foreign bodies
  • Chemicals
  • Unknown
• Macroscopic appearance of chronic inflammation

  • Chronic ulcer
  • Chronic abscess cavity
  • Induration & fibrosis
  • Thickening of the wall of the hallow viscous
  • Caseous necrosis
• Systemic effects of acute inflammation (acute phase response)

  • Fever
  • Increased pulse, blood pressure, Chills and anorexia
  • Leukocytosis
  • Neutrophilia and left shift of neutrophils
  • Lymphocytosis
  • Eosinophilia
  • Acute phase protein production in liver
• Erythrocyte Sedimentation Rate (ESR)


  Rate at which erythrocytes settle out of unclotted blood in one hour, increased due to presence of acute phase reactants
• Weight loss in chronic inflammation is due to actions of IL-1 and TNF alpha which increase catabolism in skeletal muscles, adipose tissue and the liver
• Other manifestations of acute inflammation

  • Increase pulse and decreased blood pressure
  • Sweating, rigors, chills
  • Anorexia, somnolence, and malaise
• In sepsis, there are systemic effects of acute inflammation