Inflammation I

Causes of infection

  • Infection
  • Trauma
  • Foreign bodies
  • Immune reaction
  • Necrosis

Vascular changes in response to injury

  • Changes in blood flow and blood vessel caliber - vasodilation
  • Changes mediated by histamine and nitric oxide
  • Results in calor and rubor

Cellular changes in response to injury

  1. Stasis
    1. Blood flow slows as a result of vasodilation
  1. Margination
    1. Slowed blood flow enables WBCs to accumulate near the blood vessel wall
      1. Neutrophils are the main cell of acute inflammation
  1. Rolling
    1. Selectins stimulate WBCs to roll along cell wall
  1. Adhesions
    1. Endothelial expression of cell adhesion molecules (ICAM and VCAM)
    2. Adhesion molecules also expressed on WBCs - integrins, selectins
    3. Low affinity initially - affinity increased by proteoglycans + prostaglandins (VCAMs and ICAMs) and histamine + thrombin (selectins)
  1. Transendothelial migration
    1. WBCs able to move through vascular endothelium (leaky)
      1. Caused by endothelial contraction, mediated by histamine, bradykinin, substance n and leukotrienes
      2. Direct damage
    2. Pass through junctions - diapedesis, transcytosis

Chemotaxis

  • Occurs after WBC has left blood vessel
  • Cells follow chemical gradient and move along it

Phagocytosis

  1. Recognition and attachment
    1. Opsonins
  1. Engulfment
  1. Killing and degradation
    1. Reactive oxygen species - NADPH oxidase
    2. Reactive nitrogen species - nitric oxide synthase

Clinical features of inflammation

Rubor (redness) and calor (heat) caused by:

  • Increased perfusion
  • Slow flow
  • Increased permeability of vessels

Tumor (swelling) caused by vascular changes

  • Proteins exit the leaky blood vessels causing change in osmotic pressure

Dolor (pain)

  • Mediated by prostaglandins and bradykinin

Functio laesa

  • Loss of function