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factors for Inflammation.ppt

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factors for Inflammation.ppt

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									Inflammation:

 From L. inflammare-to set on fire
  A complex progression of vascular
   changes in response to tissue injury.
  It is a defensive response which
   destroys, dilutes or neutralizes harmful
   agents (microbes, toxins) and repairs the
   damaged tissues.
Components of Acute and Chronic
Inflammation
Components of Inflammation
    Circulating cells – neutroplils, eosinophils,
     basophils, monocytes, lymphocytes,
     thrombocytes
    Circulating Proteins – clotting factors,
     kininogens, and complement factors
    Vascular wall cells – Endothelial cells,
     smooth muscle cells
    Connective tissue cells – mast cells,
     macrophages, lymphocytes, fibroblasts
    Exracellular matrix – collagen and elastin,
     proteoglycans, adhesive glycoproteins
Types:

   Inflammation is of two types: acute and
   chronic.
  Acute inflammation is of short duration
   – a few hours or days and characterized
   by exudation of fluid and plasma proteins
   (edema) and emigration of leukocytes,
   mainly neutrophils.
   Chronic inflammation is of longer
    duration (weeks and months) and
    associated with mononuclear cells
    (lymphocytes and macrophages) and
    proliferation of fibrous connective tissue
    and blood vessels.
Acute Inflammation:
 Causes:
 1. Infectious agents including bacteria,
    viruses, fungi, protozoa, helminths etc.
 2. Chemical agents like toxins, acids,
    alkalies etc.
 3. Physical agents such as burns,
    electricity, radiation, excessive cold,
    trauma etc.
4.   Immunological reactions:
     Tissue damaging antigen-antibody
     reactions like hypersensitivity and
     autoimmune diseases.
5.   Necrotic tissue:
     Ischemia, toxins and infectious agents
     may directly cause necrosis and
     necrotic tissues release mediators
     which cause inflammation.
Cardinal signs of inflammation:

    Celsus, a roman philosopher, described
     4 principal signs of inflammation in 38
     AD i.e. redness, swelling, heat and pain.

    The 5th cardinal sign, loss of function,
     was added in 1858 by Virchow.
1.   Redness (L. rubor)
     It is due to increase of blood in the inflamed
     area as a result of hyperemia.
2.   Swelling (L.tumor)
     Due to hyperemia and exudation of protein –
     rich fluid and leukocytes.
3.   Heat (L.calor)
     Due to increased arterial blood flow and
     increased metabolism in the area of acute
     inflammation.
4.   Pain (L. dolor)
     Caused by pressure on sensory nerve
     endings by the exudate and irritation by the
     chemical mediators like 5HT (serotonin)
     kinins (bradykinin) and prostaglandins.

5.   Loss of function (L. functio laesa)
     Due to combination of pain, swelling and
     tissue destruction.
Vascular changes in inflammation:

  Vascular changes, first described by the
  German pathologist – Cohnheim in 1877
  play an important role in acute
  inflammation.

  The cardinal signs of inflammation are
  attributed to the vascular changes
  including:
1) Changes in the blood vessels:
a) Momentary constriction:
   Immediately after the injury (irritation) arterioles
   undergo vasoconstriction lasting for only a few
   seconds, possibly caused by neurogenic stimuli
   or chemical mediators.
b) Vasodilation:
   Normally many capillaries remain collapsed but
   in an area of inflammation all the arterioles and
   capillaries are dilated by the action of chemical
   mediators of inflammation. The area appears to
   be more vascular, with heat and redness.
Vascular Changes
2) Changes in the rate of flow:
i)  Increased vascular permeability:
    Vasodilation is immediately followed by
    increased blood flow and then a slowdown and
    exudation of protein – rich fluid into the
    interstitial spaces, forming inflammatory edema
    (exudate).
Plasma proteins – albumin, fibrinogen, globulins etc
    leave the blood vessels due to increased
    vascular permeability resulting in
    hemoconcentration, increased blood viscosity
    and stasis.
Mechanism of increased vascular permeability


a) Formation of endothelial gaps in
   venules:
    chemical mediators of inflammation increase
    vascular permeability by opening endothelial cell
    junctions – due to contraction of endothelial cells
    0.5-1.0um gaps appear between them.
     Most commonly it is produced by histamine,
      bradykinin and leukotrienes.
      Called immediate transient response (15 to 30
      minutes), is reversible and affects only
      venules.
b) Endothelial cell retraction:

 Cytokines interleukin – 1, tumour necrosis
  factor and interferon – gamma cause
  changes in cellular cytoskeleton, cellular
  retraction and formation of endothelial
  gaps.
 This change occurs after 4-6 hours and
  lasts for 24 hrs or longer.
c) Direct endothelial injury:

    It follows necrosis and detachment of
     endothelial cells after severe injuries due
     to burns or injuries. It persists until vessel
     is thrombosed or repaired.
d)   Delayed prolonged leakage:
     It is caused by mild to moderate thermal
     injuries, some bacterial toxins, u.v.
     radiation etc. It continues for several hours
     and days.
e) Leukocyte - Dependant Endothelial Injury:

   Leukocytes release toxic oxygen – free
   radicals and proteolytic enzymes which
   cause endothelial injury.
ii) Slowing down of circulation:
 Early vasodilation results in increased blood
   flow, followed by slowing of circulation
   which is essential for emigration of
   leukocytes.
Retardation of blood flow is caused by:

     a) Increased capillary bed.
     b) Swelling of endothelial cells.
     c) Hemoconcentration.
     d) Margination of leukocytes.
iii) Stasis:
     A condition of stasis is produced following
     slowing down of circulation. This is ideal for
     escape of large molecules and cellular
     elements from blood vessels and formation of
     exudate.
Sequence of events in leukocyte
emigration in inflammation
3) Changes in the bloodstream:
  Slowing down of blood circulation changes
  the blood stream from axial to laminar flow
  i.e. from centripetal to centrifugal. This
  leads to margination, rolling and adhesion
  or pavementing of leukocytes to the
  endothelium.
4) Exudation of plasma:
  The fluid part of blood escapes blood
  vessels due to increased vascular
  permeability and produces exudate.
5) Emigration of leukocytes:

5 The Process by which leukocytes come
  out of the blood vessels is called
  emigration.

6) Diapedesis of erythrocytes:
   Erythrocytes are pushed out of the vessels
   passively by increased hydrostatic
   pressure. These bring oxygen and
   nutrients to cells and tissues.

								
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