Inflammation part 1 Flashcards
Acute inflammation
-vascular and cellular inflammatory reactions are mediated by chemical mediators that are derived from plasma proteins or cells in response to inflammatory stimulus
Stimuli for acute inflammation
-microbes and toxins
-trauma
-physical and chemical agents
-tissue necrosis
-foreign bodies (eg.splinters)
-immune reactions (hypersensitivity reactions)
Sequence of inflammatory events
1.inflammatory stimulus
2.release of mediators (histamine and cytokines)
3.Vasodilation
4. increased blood flow and volume leading to heat/redness=hyperemia
5.increased permeability= loss of fluid= edema (swelling and pain)
6. Increased viscosity of blood results in slowed blood flow=stasis
7. Neutrophil margination, rolling, adhesion &migration into the interstitial tissue
8. Phagocytosis
Vascular changes during inflammation
-normal: plasma proteins and cells are kept in vessels and more in direction of blood flow
-inflammation: movement of plasma proteins and circulating cells move out of circulation and into site of infection
Vasodilation during inflammation
-caused by histamine, prostaglandins, and NO
-results in arteriolar dilation, and increase in blood volume and opens of new capillaries
Permeability vascular changes
-increased permeability (from increased endothelial gaps between cells)
- allows protein rich fluid to move into interstitium
How are gaps between endothelial cells formed?
1.Histamine, bradykinin, leukotrienes cause endothelial contraction by reorganizing the cytoskeleton resulting in endothelial gaps
2.direct endothelial injury (necrotic processes such as toxins, and leukocyte mediated through free radicals and proteases) causing necrosis an detachment
3.increased transcytosis in venules induced by VEGF
4.leakage of new blood vessels
Viscosity of blood
-loss of fluid results in concentration of cellular fraction of blood in capillaries and venules, which increases viscosity of blood and slower blood flow
Hypoproteinemia and vascular permeability
-loss of protein from the plasma through endothelial leakage
>due to decrease in intravascular osmotic pressure and an increased osmotic pressure of the interstitial fluid
Exudate
-same as high protein edema; cloudy
-always seen when you get gaps in endothelial cells
Transudate
-low protein; clear or light yellow
-move through changes in hydrostatic pressure
Ascites (transudate)
-low protein
-would not expect endothelial injury/gaps formed
Acute severe diffuse fibrinous pleuritis
-acute because fibrin can be pulled apart, not many cross links
Why does fluid exude?
-dilute injurious stimulus
-contain and isolate the process
-delivers antimicrobial substances (eg. Immunoglobulins)
-provides a meshwork for inflammation and repair