NURS 2090 Lecture Notes - Ibuprofen, Small Intestine, Synovectomy
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Inflammation and Tissue Repair
Goals of inflammation
1. Vascular Response- Increase blood flow to the site
2. Cellular Response- Increase healing cells at the site
3. Repair- Prepare for tissue repair (remove injured tissue)
Lines of Defense
First: Skin and mucous membranes. Areas not covered by skin are covered by chemically
coated mucous membranes that neutralize/ destroy invaders.
Second: Inflammatory response. Activated when first line is not adequate. It’s a non specific
response. Inflammatory response is identical regardless of cause.
Third: Immune response. Specific defense.
1. Vascular Response to Injury (increase in blood flow)
• Facilitated by chemical mediators
• Induces vasodilation (to accommodate ↑ BF)
• Increased capillary permeability/ BM loosens to allow cells to injured tissue
• Acute inflammation is triggered by tissue injury (damage = alteration to cells and tissues-
invasion by microorganisms, cellular mutations, hypoxia, nutritional deficiencies,
physical or chemical damage)
Increased BF needed:
1. Phagocytosis/ promote healing
2. Dilute harmful substances
- Response at the blood vessel near the site of injury; blood vessels dilate or widen to
accommodate increased blood flow to the site;
- the lining of the blood vessel is more permeable to allow cells to move from the vessel into the
-This loosening occurs at the basement membrane of the blood vessel and adjacent endothelial
cells; the vessel is separated from the tissues of the body. The vessel walls are needed to confine
blood cells and plasma, but the injury must be loosened to allow for movement of healing fluids
and cells into damaged tissues.
- Watery exudate that accumulates at the site of injury has a high protein and leukocyte
sign that the vessels are more permeable and that cells active in phagocytosis (engulfing
and removing harmful agents) and ready to fend off microorganisms.
The whole process is caused by inflammatory mediators:
- specifically vasoactive inflammatory mediators
- facilitate the process of widening and loosening of blood vessels at the site.
- located in the blood plasma and in many cells, including platelets, mast cells, basophils,
neutrophils, endothelial cells, macrophages and monocytes.
-white blood cells
-endothelial or damaged tissue cells
- Some inflammatory mediators are formed within blood plasma and some are formed within
cells (most in cell plasma membrane or made up of proteins in the cell).
- Most commonly it is the WBC that produce and release inflammatory mediators, platelets,
endothelial cells and injured cells are also potential sources.
Mast cell / Basophil
- They are leukocytes that are housed in the connective tissues of the body and near all blood
vessels. (their placement allows for rapid response)
- Responsible for the production and immediate release of inflammatory mediators through the
process of degranulation: where mast cell breaks apart and releases inflammatory mediators in
the form of grain like particles
Inflammatory mediators released by mast cells: histamine, leukotrienes and prostaglandins
Signals to trigger, enhance and discontinue the inflammatory response are also generated by
lymphocytes, monocytes, macrophages.
Cytokines: more than 100 distinct proteins found in white blood cells that have a role in
- active through the whole process
-examples: interleukins, growth factors, interferons, chemokines
Platelets: active in generating and releasing inflammatory mediators to promote vasodilation,
clotting, attraction of WBC and healing of injured tissues
- Serotonin/Histamine is a mediator found in platelets (vasodilation and increased vascular
Endothelial cells or injured tissue cells- can release inflammatory mediators:
1. Platelet activating factor: in the cell membrane- vasodilation, clotting, attracting
WBC to site of injury
2. Arachidonic acid: from plasma membrane of injured cell
- Stimilates inflammatory mediators through chemical conversion.
- Includes: prostaglandins, lipoxins, leukotrienes and thromboxane
- Processes of vasodilation and vasoconstriction, increased vascular permeability,
bronchodilation and bronchoconstriction and attraction of leukocytes
- Corticosteroids block this acid (therefore decrease the inflammatory response)