inflammation definition
This is the physiological response to tissue damage and is accompanied by a characteristics series of local changes. Its purpose is protective: to isolate, inactivate and remove both the causative agent and damage tissue, so that healing can take place. The cardinal signs of inflammation are redness, heat, swelling and pain.
Inflammatory conditioner recognised by their Latin suffix-itits; for example, appendicitis is the inflammation of the appendix and laryngitis is inflammation of the larynx.
Cause of inflammation
Any form of tissue damage stimulates the inflammatory response, even in the absence of infection. The wide range of causative agents includes extreme of temperature, trauma, corrosive chemical including extreme of PH, abrasion and infection by pathogens.
Types of Inflammation
There are two types-
Acute inflammation
Acute inflammation is typically of short duration, e.g. days to a few weeks, and may range from mild to very severe, depending on the extent of the tissue damage. Most aspects of the inflammatory response are hugely beneficial, promoting removal of the harmful agent and setting the scene for healing to follow.
The acute inflammatory response is described here for convenience as a collection of separate events: increased blood flow, accumulation of tissue fluid, migration of leukocytes, increased core temperature , pain and suppuration. In reality, these events significantly overlap and develop together.
Increased blood flow
Following injury, both the arterioles supplying the damaged area and the local capillaries dilate, increasing blood flow to the site. This is caused mainly by the local release of a number of chemical mediators from damaged cells, e.g. histamine and serotonin. Increased blood flow to the area of tissue damage provides more oxygen and nutrients cellular activity that accompanies inflammation. Increased blood flow causes the increased temperature and reddening of an inflamed area, and contributes to the swelling associated with inflammation.
Increased tissue fluid formation
One of the cardinal sign of inflammation of swelling of the tissues involved, which is caused by fluid leaving local blood vessels and entering the interstitial spaces. This is partly due to increased capillary permeability caused by inflammatory mediators such as histamine, serotonin and prostaglandins, and partly due to elevated pressure inside the vessels because of increased blood flow. Most of the excess tissue fluid drains away in the lymphatic vessels taking damaged tissue, dead and dying cells and toxins with it.
Plasma proteins, normally retained within the bloodstream, also escape into the tissue through the leaky capillary walls; this increases the osmotic pressure of the tissue fluid out of the blood. These proteins include antibodies, which combat infection, and fibrinogen, a clotting protein. Fibrinogen in the tissues is covered by thromboplastin to fibrin, which forms an insoluble mesh within the intwrsirial space, walling off the inflamed area and helping to limit the spread of any infections. Some pathogens, e.g. streptococcus pyrogens, which causes throat and skin infections, release toxins that break down this fibrin network and promote spread of infection into adjacent healthy tissue.
Sometimes tissue oedema can be harmful . For instance, swelling around respiratory passages can obstruct breathing and insignificant swelling around a painful, inflamed joint cushions it and limits movements, which encourages healing.
Migration of leukocytes
Loss of fluid from the blood thickens it, slowing flow and allowing the normally fast-flowing white blood cells to make contact with, and adhere to, the vessel wall. In the acute stages, the most important leukocytes is the neutrophil, which adheres to the blood vessel lining, squeezes between the endothelial cells and enters the tissues, where its main function is in phagocytosis of antigen. Phagocyte activity is promoted the raised temperatures associated with inflammation. After about 24 hours, macrophages become the predominant cell type at the inflamed site, and they persist in the tissue if the situation is not resolved, leading to chronic inflammation. Macrophages are larger and longer lived than neutrophils. They phagocytose dead/dying tissue, microbes and other antigenic material, and dead/dying neutrophils. Some microbes resist digestion and provide a possible source of future infections, egg. Mycobacterium tuberculosis.
Chemotaxis
This is the chemical attraction of leukocytes, including neutrophils and macrophages, to an area of inflammation. It may be that chemoattractants act to remain passing leukocytes in the inflamed area, rather than activity attracting them from distal areas of the body. Chermoatractants include microbial toxins, chemical released from leukocytes, prostaglandins from damaged cells and complement proteins.
Increased temperature
The increased temperature of inflamed tissues has the twin benefits of inhibiting the growth and devision of microbes, whilst promoting the activity of phagocytes.
The inflammatory response may be accompanied by a rise in body temperature, especially if there is bacterial infection. Body temperature rises when an endogenous pyrogen is released from macrophages and granulocytes in response to microbial toxins or immune complexes. Interleukin 1 is a chemical mediator that rests the temperature thermostat in the hypothalamus at a higher level, causing pyrexia and other symptoms that may also accompany systemic inflammation, e.g. fatigue and loss of appetite. Pyrexia increases the metabolic rate of cells in the inflamed area and, consequently, there is an increased need for oxygen and nutrients.
Pain
This occurs when local swelling compresses sensory nerve endings. It is exacerbated by chemical mediators of the inflammatory process, e.g. bradykinin and prostaglandins which potentiate the sensitivity of the sensory nerve endings to painful stimuli. Although pain is an unpleasant experience, it may indirectly promote healing, because it encourages protection of the damaged site.
Suppuration (Pus formation)
Pus consists of dead phagocytes, dead cells, fibrin, inflammatory exudate and living and dead microbes. A localised collection of pus in the tissues is called an abscess. The most common pyogenic bacteria are staphylococcus aureus and streptococcus pyrogens.
Outcomes of acute inflammation
Resolution
This occurs when the cause has been successfully overcome. Damaged cells and residual fibrin are removed, being replaced with new healthy tissue, and repair is complete, with or without scar formation.
Chronic Inflammation
The processes involved are very similar to those of acute inflammation but, because the process is of longer durations, considerably more tissue damage is likely. The inflammatory cells are mainly lymphocytes instead of neutrophils and fibroblasts are activated, leading to the lying down of collagen, and fibrosis. If the body defences are unable to clear the infections, they may try to wall it off instead, forming nodules called granulomas, within which are collection of defensive cells. Tuberculosis is an example of an infection that frequently becomes chronic, leading to granuloma formation. The causative bacterium, mycobacterium tuberculosis, is resistant to body defences and so pockets of organisms are sealed up in granulomas within the lungs. Chronic inflammation may either be a complications of acute inflammation or follow chronic exposure to an irritant.
Development of chronic inflammation
Acute inflammation may become chronic if resolution is not complete, e.g. if live microbes remain at the site, as in some deep-seated abscess, wound infection and bone infections
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