Acute Inflammation

AcuteInflammation

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AcuteInflammation

Physicalinjury results in the destruction of cells and blood supply to anarea. The damaged tissue cells become activated and start releasingchemical mediators – histamine and bradykinin. These chemicalmediators are also released from white blood cells, platelets and theendothelial cells of blood vessels. The released chemical mediatorsrelax the vascular smooth muscles causing vasodilation. Vasodilationresults in increased blood flow to the injured area causing the areato become red and warm. Apart from causing vasodilation, chemicalmediators also act on the blood vessel walls resulting in increasedvascular permeability. The increased vascular permeability allowsplasma proteins, leukocytes and water to exude from blood vesselsinto the interstitial space. As fluid accumulates in the interstitialspace, the tissues start increasing in size and this is visualized asa swelling at the site of injury. The accumulating fluid also exertspressure on nerve endings resulting in pain at the area of injury. Inaddition, persistent irritation of nerve endings by the chemicalmediators is also perceived as pain at the injured site (Szalay,2015). Although warmth, redness, swelling and pain are the cardinalsigns of acute inflammation involving surface injuries, both pain andwarmth are not manifested in the acute inflammation of internalorgans. This is because internal organs lack nerve endings and theirtemperature is always similar to the body’s core temperature(Kumar, Abbas, &amp Aster 2012).

Theexuded leukocytes are mostly made up of neutrophils and monocytes.They are attracted from the blood vessels into the surroundingtissues through chemotaxis. In the tissues, the leukocytes increasein number and proliferate. Neutrophils are the majority cells in thefirst 6 to 24 hours and they are later replaced by monocytes. Whenleukocytes encounter bacteria in the tissues, they attach and engulfthem through a process known as phagocytosis. The engulfed microbesare then killed or degraded (Samikhsa, n.d.).

References

Kumar,V., Abbas, A., &amp Aster, J. (2012). , RobbinsBasic Pathology(9th ed.), (pp. 31-44). Philadelphia, PA: Elsevier Saunders.

Samikhsa,S. (n.d.). 4 Sequences of Events of Acute Inflammatory Response |Immunology. Retrieved fromhttp://www.yourarticlelibrary.com/immunology/4-sequences-of-events-of-acute-inflammatory-response-immunology-2/28037/

Szalay,J. (2015, September 30). Inflammation: Causes, Symptoms &ampAnti-Inflammatory Diet, LiveScience. Retrievedfrom http://www.livescience.com/52344-inflammation.html