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Example research essay topic: Mycobacterium Tuberculosis Rheumatoid Arthritis - 1,983 words

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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), rumor (redness), calor (heat) and door (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, kinin's, 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. (3) Chronic inflammation occurs from unresolved or recurrent acute inflammation, or may follow exposure to insoluble agents, foreign bodies, intracellular pathogens such as Mycobacterium tuberculosis or M.

letras, or unknown a etiological factors, as in rheumatoid arthritis (RA). (2) It is this type of inflammation which tends to be involved in disease processes, and may last from weeks to years. In chronic inflammation the cellular infiltrate is made of a mixed cell population including macrophages which are derived from blood monocytes which migrated to the site of the inflammation, activated and proliferate. (2) The monocytes become wandering macrophages that are more powerful phagocytes than neutrophils. They consume damaged tissue, worn out neutrophils and any invading microbes. (3) Lymphocytes and plasma cells are also often present in chronic inflammation. Granulomas, which are collections of epithelioid (epithelial-like) macrophages and lymphocytes with necrotic tissue sometimes form, and often have the appearance of soft cheese. (2) This occurs in only a few disease processes: Causes of granulomatous inflammation Disease Cause Tuberculosis Mycobacterium tuberculosis Leprosy Mycobacterium letras Syphilis Treponema pallidum Schistosomiasis Schistoma Fungal infections Cryptococcus, etc. Foreign body reaction Suture material, silica, etc.

Sarcoidosis Unknown Crohn's disease Unknown (4) Rheumatoid arthritis (RA) is a common inflammatory joint disease due to an immune response, with destruction where the bones of a joint are in contact. It is a good example of when the bodies immune reaction, including the inflammatory process acts to harm the tissues, involving chronic inflammation. Normally combining Antibody (Ab) with antigen (Ag) has an important physiological role deactivating foreign bodies (Ag), but in RA the local concentrations of Ag become too great, and excess immune complexes form, leading to local tissue damage as effector cells and Fc receptors engage sensitive target cells (normal, self cells) and activation of C 3 (complement) causes lysis. It is characterised by non-specific, usually symmetrical inflammation of the peripheral joints. In the inflammation CD 4 T-helper cells are found, along with activated B lymphocytes and plasma cells.

There is also mixed inflammatory cell infiltrate in which lymphocytes, plasma cells and macrophages predominate, along with numerous cytokines including interleukin- 1 (IL- 1), Tumour necrosis factor (TNF) and Interferon-c which prolong inflammation. Tissue necrosis often occurs in fibrous connective tissues. Inflammation also occurs of the sclera (white of the eye) (scleritis), pleural membranes of the lungs (pleuritic) and the alveoli (alveoli tis), as blood-borne immune complexes cause complement and phagocyte activation, causing discomfort and difficulty breathing. Pericarditis also occurs, which is inflammation of the membranous sac surrounding the heart, as well as inflammation of the heart valves (valvulitis). (6, 11) In recent years inflammation has been linked to heart disease, with evidence that inflammation in the bloodstream can be useful in predicting heart disease in people with no other predisposing factors such as high cholesterol or high blood pressure. It is found that levels of the enzyme myeloperoxidase (MPO) (usually found in white blood cells) are elevated in people who have had heart attacks, and that IL- 6 is linked to an increased risk of death in heart patients, both of which are involved in inflammation.

It is suspected that smouldering inflammation can damage the walls of heart arteries, making them more prone to atherosclerosis (fatty build ups) that can lead to heart attacks. (7) C-reactive protein (CRP) is a protein whose level also increases with inflammation of blood vessels. It has been found that preventative aspirin therapy has greatest benefit among high-inflammation patients, which with aspirin being anti-inflammatory as well as blood thinning suggests that anti-inflammatory treatment may also help to prevent heart disease. It is thought that the initial inflammation which can lead to atherosclerosis could be caused by bacteria or virus infection, as well as other conditions. (8) Crohn's disease (also called ileitis or enteritis) is a disease in which inflammation extends deep into the lining of the small intestine, which causes pain and makes the intestines empty frequently, as diarrhoea. Crohn's disease can be difficult to distinguish from other inflammatory bowel diseases (IBD), such as ulcerative colitis, in which inflammation and ulcers occur of the top layer of the large intestine.

It is thought that the body's immune system reacts to a viral or bacterial infection in the intestine by causing an ongoing inflammatory reaction. Sufferers of Crohn's disease often have abnormalities of their immune system, but this may not be linked. Other complications associated with Crohn's disease include arthritis, skin problems and inflammation of the eyes or mouth. Research has found the cytokine tumour necrosis factor (TNF) has been found in the cells affected by Crohn's disease.

This may be responsible for the inflammation of Crohn's disease. Anti-TNF binds to TNF and removes it from the blood stream before it can reach the intestines and cause inflammation. (9, 13) In research to see whether lactase deficiency is related to IBD it was found that 1 / 3 of patients with IBD have lactase deficiency, which is not very different from non-IBD patients with chronic abdominal pain. Therefore this does not seem the case. (5) In both Parkinson's disease (PD) and Alzheimer's disease (AD) research has suggested that chronic inflammation occurs in infected brain regions. Chronic inflammation can damage host cells, and there is epidemiological evidence that it contributes to the progressive neuronal loss in Alzheimer's disease.

This inflammation is silent because the brain has no pain fibres. Also the local immune reaction does not involve the peripheral immune system. It occurs without Abs and without much involvement of T cells. Instead the reaction depends upon the synthesis of inflammatory components by the local neurones, glia and micro glia (phagocytes resident in the brain). The complement system, micro glia and inflammatory cytokines appear to play key roles. Therefore it seems possible that treatment with anti-inflammatory agents might slow the process of dopaminergic cell death in PD and AD, as well as possibly slowing the onset of dementia which PD sufferers seem more prone to than the general population. (10) Tuberculosis (TB) is one of the commonest and most important causes of granulomatous inflammation.

It is mainly caused by Mycobacterium tuberculosis, an anaerobic, slow growing bacteria of whose infection is acquired by inhalation and contact with infected individuals. Primary TB is observed in patients not exposed to mycobacteria. Post-primary, or secondary TB is observed in individuals who have been exposed to mycobacterial Ag. In pulmonary TB (also called consumption or phthisis) the bacteria is inhaled into the lungs where it sets up a primary tubercle (nodular lesion) and spreads to the nearest lymph nodes (the primary complex).

At this stage the immune system may heal the TB, or it may smoulder for months or years. The patient may show no symptoms or may develop a chronic infection and transmit the bacillus by coughing and sneezing. The bacilli may spread from the lungs into the bloodstream, setting up millions of tiny tubercles through the body, as miliary TB, or spread to the meninges to cause TB meningitis. TB causes an acute inflammatory response leading to granulomatous inflammation. (4) Another disease caused by mycobacteria is Leprosy, a chronic, slowly progressive destructive process involving peripheral nerves, skin and mucous membrane and caused by the mycobacterium letras There are two forms; Lepromatous Leprosy - macrophages filled with M. Leprae form nodules in the skin, eyes, testes, nerves, lymph nodes and spleen; and Tuberculoid - occurs in infected persons who manifest an effective granulomatous inflammatory response. Usually a single lesion, it is termed Tuberculoid as the lesions resemble those of TB, but lack the central caseous necrosis.

Bacilli are rarely found in those lesions. (12) Conclusion Inflammation plays a large part in many diseases, often caused by other factors, such as infection, but causing symptoms which whilst trying to aid healing can cause further pain and tissue damage of a serious nature. Therefore in many diseases the use of anti-inflammatory drugs might be a possible relief of discomfort and prevent further damage from occurring. Bibliography 1) Previous lecture notes, BIOM 3002 2) PHILLIPS Jonathan, MURRAY Paul, CROCKER John (1995) The Biology of Disease, UK, Blackwell Science, Pp 22 - 24 3) TORTORA J. , GRABOWSKI Sandra Reynolds, (2000) Principles of Anatomy and Physiology Ninth edition, New York, John Wiley & Sons Ltd. , Pp 750 - 751 4) WWW, web Chronic inflammation and tuberculosis, accessed 20 / 10 / 02 5) PFEFFERKORN MD, FITZGERALD JF, CROFFIE JM, GUPTA SK, CORKINS MR, MOLLESTON JP, (2002) Lactase deficiency: not more common in pediatric patients with inflammatory bowel disease than in patients with chronic abdominal pain, Journal of Pediatric Gastroenterol Nutrition, 35 (3) Pp 339 - 343 6) MARTIN Elizabeth A. (2002) Concise Medical Dictionary Sixth edition, Oxford, Oxford university press, P 710 7) WWW, web Studies bolster inflammation-heart disease linked, accessed 20 / 10 / 02 8) WWW, web Inflammation, Heart Disease and Stroke: The Role of C-Reactive Protein, accessed 20 / 10 / 02 9) WWW, web Crohn's disease, accessed 20 / 10 / 02 10) MCGEER Edith, YOSOJIMA Koji, MCGEER Patrick L. (2001) Inflammation in the pathogenesis of Parkinson's disease, BC Medical Journal, Volume 43, No. 3, Pp 138 - 141 11) Previous course work, BIOM 2004 12) WWW, web Leprosy, accessed 20 / 10 / 02 13) ASPLUND Sheryl, GRAMLICH Terry, FAZIO Victor, PETRAS Robert, (2002) Histological Changes in De functioned Rectums in Patients With Inflammatory Bowel Disease: A Clinicopathological Study of 82 patients With Long-Term Follow-Up, Diseases of the Colon & Rectum, 45 (9), Pp 1206 - 1213


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Research essay sample on Mycobacterium Tuberculosis Rheumatoid Arthritis

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