acute inflammation
TRANSCRIPT
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Inflammation
Dr. Mehzabin Ahmed
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Inflammation ?
• It is a complex reaction in the vascularised tissues in response to cell injury, leading to accumulation of – fluid, – proteins and – leucocytes in extravascular tissues.
• It is described by adding the suffix –itis to the name of the organ or tissue involved.
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Types of inflammation
• Acute inflammation is typically of short duration, few minutes to few days, in which neutrophils predominate, usually occurs with protein exudate.
• Chronic inflammation occurs over a duration of days to years, characterized by mainly lymphocytic and macrophage infiltrate with proliferation of blood vessels, tissue necrosis and fibrosis.
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Acute inflammation
• It is the most common early tissue response to tissue damage and destruction.
• An inflammatory exudate fills up the site of damage.
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Differences between Exudate & Transudate
The inflammatory fluid is called an exudate when it is
• Rich in proteins • Cells and tissue
debris• Has a specific
gravity greater than 1.020.
It is called a transudate when there is
• Less protein • Less number of
cells• Has a specific
gravity less that 1.012.
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Clinical effects of acute inflammation
The cardinal signs of inflammation are• tumor (swelling) due to accumulation of exudate
• rubor (redness) due to vessel dilatation & blood
• calor (heat) flow to the inflamed area
• dolor (pain) due to pressure on the nerve endings from the swelling & due to chemical mediators
• loss of function due to swelling & pain
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Components of acute Inflammation
• 1) Vascular component- in the local vascular flow and alteration of the vascular permeability in acute inflammation.
• 2) Cellular component- Neutrophils are the main effector cells of acute inflammation. They attach themselves to
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Vascular component
* local vascular flow* Altered vascular
permeability
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Cellular component
It involve neutrophils as the main effector cells of acute inflammation. The cellular events are:
1) Extravasation 2) Transmigration of leukocytes3) Chemotaxis 4) Phagocytosis
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Cellular componentExtravasation of the PMN occurs by the following
process:1) Margination: Movement of the PMN cells close to
the vessel wall in the blood stream 2) Rolling: the PMN cells roll along the vessel wall3) Adhesion: attach themselves to activated
endothelial cells of the blood vessels4) Aggregation: collection of adjacent PMN cells
and these undergo shape changes
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Transmigration: movement of the PMN cells out of the vessel lumen to the tissue space around the vessels.
Chemotaxis: Movement of the PMN cells along a concentration gradient of chemotactic factors to reach the site of inflammation.
Phagocytosis: process by which the PMN cells engulf and digest the injurious agent by releasing enzymes and superoxides
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Some mediators come from plasma in precursor
forms that are activated.
Cell bound mediators are found in granules and
released immediately. Others are newly
synthesized, usually from mast cells, platelets,
neutrophils, or monocytes.
Their action is usually short- lived and decay, often
within seconds.
Mediators of Inflammation
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Chemical mediators of inflammation by function:
1. Increase vascular permeability: histamine, C3a, C5a, PAF, bradykinin, LTC, LTD, LTE (leukotrienes C,D,E)
2. Chemotaxis: C5a, LTB4, chemokines, IL-8
3. Vasodilation: NO, PGI 2 (prostaglandin I 2)
4. Systemic signs: TNF (tumor necrosis factor), IL-1, IL-6
5. Pain: bradykinin, prostaglandins
6. Tissue Destruction: leukocyte lysosomal enzymes, NO (nitric oxide), reactive O2 (reactive oxygen species)
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Outcomes of Acute Inflammation
1.Resolution: The return to normal architecture and removal of dead cellular debris
2.Fibrosis: is scar formation with loss of original architecture from more significant injury.
3.Organization: denotes connective tissue replacement of functional tissue and occurs with marked protein exudates, lots of fibrin exudation from plasma, areas where exudate cannot be adequately absorbed.
4.Abscesses: localized collection of pus may form in some bacterial infections.
5.Chronic inflammation: Acute inflammation can continue and progress to chronic form
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TISSUE DAMAGE
Acute inflammation
Damage neutralized & Damage neutralized & Damaging agent persists
Cells can regrow Cells cannot regrow with tissue damage
Regeneration Organization through Organization with Phagocytosis & Healing contd. inflammation
by repair of damaged tissueRestoration of CHRONIC normal structure Scar formation INFLAMMATION& function or FIBROSIS
& loss of Damaging agent specialized function overcome
RESOLUTION Persistence
Yes No