Inflammation :: science

Inflammation Inflammation is the bodies normal response to injured tissues, although it can sometimes lead to further tissue damage. It was first described around 30 BC by Celsius, as tumour (swelling), rubor (redness), calor (heat) and dolour (pain); although excess secretion and loss of function are now commonly added. Inflammation is a response which has evolved to try and put things right in a damaged tissue, for example the pain and loss of function allow the tissue to heal easier whilst the heat and redness are caused by an increased blood flow to the tissue. (1) Inflammation occurs to control infection or injury, to eliminate pathogens, and to initiate healing and tissue repair. (2) An inflammatory pathology is usually indicated by the suffix '-itis', such as in bronchitis, dermatitis, orchitis and enteritis, and can be either acute or chronic. (1) It is a non-specific defence and so the response of the body to a cut, burn, radiation, bacteria or virus are all very similar. There are three basic stages to inflammation: 1) Vasodilation and increased permeability of blood vessels, 2) Phagocyte emigration, and 3) Tissue repair (3) Unfortunately, sometimes inflammation can be the cause of, or increase the symptom severity of a disease, such as in: Tuberculosis, leprosy and syphilis, which are persistent infections with low virulence micro-organisms Silicosis, atherosclerosis and radiation, prolonged exposure to potentially toxic agents. Rheumatoid arthritis and Hashimoto's thyroiditis, autoimmune diseases (4) Body Acute inflammation occurs rapidly, within a few hours after the injury or infection occurs to which the inflammation is acting. Initially venules and arterioles dilate, causing hyperaemia. This then decreases and the vessels increase their permeability, allowing blood plasma and platelets into the tissue as serous exudate. this causes an oedema (excess fluid in the tissue). Fibrinogen in the exudate is converted to fibrin, which deposits itself to help to localise tissue damage and control bleeding. (2) Within an hour of the inflammation starting neutrophils, and then hours later monocytes, arrive on the scene. They leave the bloodstream by emigration (also known as diapedesis), dependent on chemotaxis; they are attracted by microbes, kinins, complement and other neutrophils. These neutrophils attempt to destroy the foreign bodies by phagocytosis. Any remaining dead phagocytes or damaged tissue after a few days becomes purulent exudate, or pus. This may be broken down in the body or may reach the surface of the body, but if it cannot be an abscess may be formed.