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What is inflammation? 5 Cardinal Signs of Inflammation

Five Cardinal Signs of Inflammation

Inflammation is defined as the body’s response to an injury. It manifests as 5 cardinal signs of inflammation that include tumor (swelling), calor (heat), dolor (pain), rubor (redness), and functio-laesa (loss of function) (Serhan et al, 2010). Once inflammation initiates, a number of cellular and humoral factors play their role to develop the complete constellation of signs that are collectively referred to as inflammation. The primary purpose of inflammatory response is to restore the body’s condition to the pre-injury state i.e. the state of health (Yanoff et al, 1996). The underlying mechanisms of cardinal signs of inflammation are discussed below:


Swelling

Under physiological conditions, osmotic pressure within a blood vessel acts to retain fluid within the vessel while the hydrostatic pressure works to force the fluid out of the blood vessel. An intricate balance between the osmotic and hydrostatic forces is essential to prevent accumulation of fluid in the extravascular compartment of a tissue. Certain inflammatory mediators like histamine, leukotrienes and bradykinin act to make blood vessels leaky; thereby permitting extravasation (Holm, 2016). Since blood vessels become leaky during inflammation, proteins which are responsible for the osmotic pressure start leaking into the extravascular compartment. As a result the equilibrium between opposing forces gets disturbed and fluid starts to accumulate within the tissue i.e. edema ensues. The condition worsens when the lymphatic drainage of the tissue also gets affected due to inflammation. Cellular factors that play a role in persistent swelling include macrophages and lymphocytes. Humoral factors that contribute to swelling include nitric oxide, neuropeptides and cytokines (Reisner, 2013).

Heat - a sign of inflammation

Heat

Inflammatory response is associated with arteriolar dilatation which directly increases blood flow through the inflamed tissue. Due to a 7 – 10 folds increase in blood flow, the inflamed tissue appears warmer than the normal tissues. An indirect consequence of increased blood flow is the increased metabolic rate that ensues during inflammation (Marieb and Hoehn, 2007). This heightened metabolic rate also contributes to the warmth that is witnessed in an inflamed tissue. Heat may be thought of as a protective mechanism, since leukocytes have been demonstrated to exhibit thermotropism in inflammatory tissues (Koenigsberg, 1990).

Pain

Immediately following an insult, the body responds by delivering the message of pain to the central nervous system. This stimulation serves to warn the nervous tissue about an ongoing pathological change at the site of inflammation. Although various mediators of pain have been identified, the role of bradykinin is most prominent in this regard. Bradykinin starts appearing within an inflamed tissue once inflammation begins (Goodman and Fuller, 2011). Bradykinin is 50 times more potent than histamine or serotonin in eliciting a hyperalgesic state. The role of other mediators like nerve-growth factor, proteases and cytokines has also been suggested (Bonica, 1990).


Redness

The arteriolar dilatation and the resulting increase in blood flow also contribute to the redness that is characteristic of an acutely inflamed tissue. In cases of chronic inflammation however, redness may not be a characteristic sign (Roy et al, 2012).

Loss of function

Loss of function is secondary to the pathological changes that take place at inflammation site. In some cases, functional loss may be permanent due to the loss of functioning parenchyma whereas in others it may be temporary (Murakami, 2012). Swelling may limit the movement due to its physical impact. Pain on the other hand may restrict movement due to conscious control or reflexively.


References

Bonica, J.J., 1990. The management of pain (Vol. 1). Lippincott Williams & Wilkins. Goodman, C.C. and Fuller, K.S., 2011. Pathology for the physical therapist assistant. Elsevier Health Sciences. Holm, A., 2016. Aquaporins in Infection and Inflammation. Koenigsberg, R. ed., 1990. Medical Dictionary: Churchill's Illustrated Medical Dictionary. Churchill Livingstone. Marieb, E.N. and Hoehn, K., 2007. Human anatomy & physiology. Pearson Education. Murakami, M., 2012. The molecular mechanisms of chronic inflammation development. Frontiers E-books. Reisner, H., 2013, Essentials of Rubin's Pathology, Lippincott Williams & Wilkins. Roy, S., Bagchi, D. and Raychaudhuri, S.P. eds., 2012. Chronic Inflammation: Molecular Pathophysiology, Nutritional and Therapeutic Interventions. CRC Press. Serhan, C.N., Ward, P.A. and Gilroy, D.W., 2010.Fundamentals of inflammation. Cambridge University Press. Yanoff, M., Fine, B.S. and Gass, J.D.M., 1996.Ocular pathology (pp. 67-68). London: Mosby-Wolfe.


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