Inf 1

• "Inflame"


  To set fire
• Inflammation


  A dynamic response of living vascularised tissue to injury
• Inflammation is a protective response that serves to bring defense & healing mechanisms to the site of injury
• Inflammation


  A reaction of a living tissue & its micro-circulation to a pathogenic insult
• Inflammation


  A defense mechanism for survival
• Inflammation


  • Reaction of tissues to injury, characterized clinically by: heat, swelling, redness, pain, and loss of function
• Inflammation


  • Pathologically by: vasoconstriction followed by vasodilatation, stasis, hyperemia, accumulation of leukocytes, exudation of fluid, and deposition of fibrin

  
• How Inflammation Occurs


  Tissue injury or death --> Release mediators

  
• Etiologies of Inflammation


  • Microbial infections: bacterial, viral, fungal, etc.
  • Physical agents: burns, trauma--like cuts, radiation
  • Chemicals: drugs, toxins, or caustic substances like battery acid
  • Immunologic reactions: rheumatoid arthritis
• Cardinal Signs of Inflammation

  • Redness: Hyperaemia
  • Warm-heat: Hyperaemia
  • Pain: Nerve, Chemical mediators
  • Swelling: Exudation
  • Loss of Function: Pain
• Acute inflammation


  Less than 48 hours
• Chronic inflammation


  Greater than 48 hours (weeks, months, years)
• Cell types in inflammation

  • Acute inflammation: Neutrophils
  • Chronic inflammation: Mononuclear cells (Macrophages, Lymphocytes, Plasma cells)
• Pathogenesis of Inflammation


  1. Increased blood flow (redness and warmth)

  2. Increased vascular permeability (swelling, pain & loss of function)

  3. Leukocytic Infiltration

  
• Mechanism of Inflammation


  1. Vaso dilatation

  2. Exudation - Edema

  3. Emigration of cells

  4. Chemotaxis

  
• Exudate


  A filtrate of blood plasma mixed with inflammatory cells and cellular debris
• Pus


  A purulent exudate: an inflammatory exudate rich in leukocytes (mostly neutrophils) and parenchymal cell debris
• Leukocyte exudation


  1. Margination, rolling, and adhesion to endothelium

  2. Diapedesis (trans-migration across the endothelium)

  3. Migration toward a chemotactic stimuli from the source of tissue injury

  4. Phagocytosis

  
• Phagocytosis


  1. Recognition and attachment

  2. Engulfment

  3. Killing or degradation

  
• Chemical Mediators of Inflammation

  • Histamine by mast cells - vasodilatation
  • Prostaglandins – Cause pain & fever
  • Bradykinin - Causes pain
• Morphologic types of acute inflammation

  • Exudative or catarrhal Inflammation: excess fluid
  • Fibrinous – pneumonia – fibrin
  • Membranous inflammation
  • Suppuration/Purulent – Bacterial - neutrophils
  • Serous – excess clear fluid – Heart, lung
  • Allergic inflammation
  • Haemorrhagic – b.v. damage - anthrax
  • Necrotising inflammation (tissue loss)

  
• Outcomes of Acute Inflammation

  • Abscess formation
  • Progression to chronic inflammation
  • Resolution--tissue goes back to normal
  • Repair--healing by scarring or fibrosis
• Abscess


  A localized collection of pus (suppurative inflammation) appearing in an acute or chronic infection, and associated with tissue destruction, and swelling
• Abscess sites


  • skin, subcutaneous tissue, internal organs like brain, lung, liver, kidney
• Pathogenesis of Abscess


  The necrotic tissue is surrounded by a pyogenic membrane, which is formed by fibrin and helps in localizing the infection
• Carbuncle


  • An extensive form of abscess in which pus is present in multiple loci open at the surface by sinuses, occurring in the back of the neck and the scalp

  
• Furuncle or boil


  • Skin abscesses caused by staphylococcal infection, which involve a hair follicle and surrounding tissue
• Cellulitis


  • An acute diffuse suppurative inflammation caused by streptococci, which secrete hyaluronidase & streptokinase enzymes that dissolve the ground substances and facilitate the spread of infection