Acute inflammation : Microscopic changes

September 5, 2012 | By | Reply More

Acute inflammation : Microscopic changes

Mediated by endogenous chemicals released by cells (histamine, prostaglandins, leukotrienes, serotonin, and lymphokines) and plasma factors (complement, kinin, coagulation, and fibrinolytic cascades). Changes are as follows.
  • Changes in vessel calibre and flow.
    • Immediate and transient smooth muscle vasoconstriction.
    • Vasodilation (active hyperaemia) lasting 15min to hours.
    • Capillaries, then arterioles dilate to increase blood flow.
  • Increased vascular permeability and fluid exudate.
    • Capillary hydrostatic pressure is increased.

    • Endothelial cells contract, creating gaps.
    • Plasma proteins escape into extracellular space.
    • Increase in colloid osmotic pressure draws more fluid.
  • Formation of cellular exudates.
    • Accumulation of neutrophil polymorphs in extracellular space.
    • Begins with margination of neutrophils (flow next to vessel walls).
    • Neutrophils then adhere to vessel walls: mechanism unknown.
    • Migrate by amoeboid movement through gaps between cells.
    • Neutrophil polymorphs phagocytose debris and kill microbes intracellularly using oxygen-dependent (H2O2 and hydroxyl radicals) and -independent (lysosymes) means.

Category: Pathology, Surgery

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