The basic pathologic changes of inflammation in the site of injury are alteration, exudation, and proliferation.

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Section 2 Basic Pathologic Changes

• The basic pathologic changes of inflammation in
  the site of injury are alteration, exudation, and
  proliferation.
• 1. Alteration
• (1) Definition The tissues or cells in the
  inflammatory site become degeneration and/or
  necrosis.

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• (2) Causes and mechanism
• Be damaged by inflammatory factors directly.
• Local blood circulation disturbance
• Be affected by inflammatory mediators.
• (3) Morphology
• Parenchyma cells edema, fatty change, necrosis
  etc.
• Interstitium edema, mucoid degeneration,
  fibrinoid degeneration, necrosis, etc.

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• 2. Vascular changes
• (hyperemia and exudation)
• (1) Changes in vascular flow and caliber
• ? Changes in caliber
• Transient arteriolar constriction
• Persistent vasodilatation

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• ? Changes in flow
• a. Initially rapid as a result of vasodilatation
  (active hyperemia)
• b. Slowing and disturbance of axial flow as a
  result of increased blood viscosity secondary to
  loss of plasma into the tissue (congestion and
  edema)

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• ? Changes in the endothelium
• Increased vascular permeability leading to the
  escape of a protein-rich fluid (exudates) into
  the interstitium.
• a. Endothelial cell contraction, or increased
  transcytosis across the endothelial cytoplasm.
• b. Direct endothelial injury, resulting in
  endothelial cell necrosis and detachment
• c. Leakage from regenerating capillaries

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• (2) Fluid exudate
• Normally the walls of small blood vessels are
  freely permeable to water and crystalloids but
  relatively impermeable to plasma proteins. The
  formation of protein-rich fluid exudates is
  facilitated by separation of the intercellular
  junction of the endothelium.

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• The fluid exude carries into the inflamed area
  the following important constituents
• ? Serum bactericidal factors
• a. Antibodies which act by opsonising bacteria
  prior to phagocytosis and by neutralizing
  exotoxins
• b. Components of the complement system

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• ? Interferon a non-specific antiviral agent
• ? Fibrinogen which is converted to fibrin. Fibrin
  is important in providing
• a. Cement substance uniting severed tissues
• b. Scaffold for repair processes
• c. Barrier to the spread of organisms
• d. Surface against which phagocytosis of
  adherent organisms is enhanced
• ? Therapeutic agents-antibiotics,
  anti-inflammatory drugs, etc.

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• (3) Leukocyte exudates and phagocytosis
• ? Leukocytic margination,rolling
• ? Adhesionby the binding of adhesion
• molectures (selections,
  immunoglobulins,
• intergrins, mucin-like glycoproteins)

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• ? Emigrating
• It refers to the process by which motile white
  cells migrate out of blood vessels.
• Although all leukocytes are more or less
  motile, the most active are the neutrophils and
  monocytes the most sluggish are the lymphocytes.
• While cell emigration is an active,
  energy-dependent process.
• Red blood cell out of blood vessels, called
  diapedesis, is believed to be passive loss of red
  blood cells through the points of rupture
  (blooding).

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The molecular mechanism of Leukocyte emigration
(?? Robbins Basic Pathology,2003)
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White cell transmigration

• It is include following handings
• ?WBC margination
• ?
• ?WBC adhesion with endothelial surface adhesion
  molecule
• ?
• ?WBC transmigration
• 2-12 minute

EM White cell transmigration
(????? ??????????,??)
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Leukocyte exudates
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• ? Chemotaxis
• Following extravasations, leukocytes emigrate
  in tissues toward the site of injury by a process
  called chemotaxis.
• Exogenous chemo attractants bacterial products,
  etc.
• Endogenous chemo attractants components of the
  (LTB4), cytokines, etc.

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• ? Phagocytosis
• Recognition and attachment of the particle to
  the surface of the phagocyte? engulfment? killing
  and degradation

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The mode of Phagocytosis (?? Robbins
Basic Pathology,2003,??)
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• Types of leukocyte (inflammatory cells)
• Leukocytes are out of blood vessels that are
  known as inflammatory cells.
• a. Neutrophils
• Small phagocytic cell
• The two types of granules in the cytoplasm
• Azurophil granules and specific granules.
• The first cells to appear in perivascular
  spaces are the neutrophils.
• Commonly seen in early stage of inflammation,
  and acute inflammation, and purulent inflammation.

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• b. Macrophages
• Tissue macrophages are derived from blood
  monocytes that emigrate from blood vessels under
  influence of chemotactic factors.
• Commonly seen in later stage of inflammation,
  chronic inflammation, non-purulent inflammation,
  and viral, or protozoal, or fungal infections.
  And macrophages are also related to specific
  immune response.

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• dusty cell
  Langhans giant cell
• foamy cell
• Macrophages could epithelioid cell
• Formation heart failure cell
• 
  Multinucleate giant-cells foreign-body giant
  cell

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• c. Eosinophilia
• Commonly seen in hypersensitivity reaction and
  human parasitological infections.
• d. Lymphocytes and plasma cells
• Commonly seen in virus infection and chronic
  inflammation.
• e. Basophilic and mast cell

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MacrM
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• 3. Proliferation
• Proliferate constitution
• Endothelium, macrophages, and fibroblasts
  commonly seen in later stage of inflammation