Bursae Health Dictionary

Bursae: From 1 Different Sources


Natural hollows in the ?brous tissues, lined by smooth cells and containing a little ?uid. They are situated at points where there is much pressure or friction, and their purpose is to allow free movement without stretching or straining the tissues: for example, on the knee-cap or the point of the elbow, and, generally speaking, where one muscle rubs against another or against a bone. They develop also beneath corns and bunions, or where a bone presses on the skin.
Health Source: Medical Dictionary
Author: Health Dictionary

Bursa

A fluid-filled sac that acts as a cushion at a pressure point in the body, often near a joint, where a tendon or muscle crosses bone or other muscles. The important bursae are around the knee, elbow, and shoulder.... bursa

Arthritis

Arthritis refers to any condition of joints of the limbs or spine associated with in?ammatory or structural change. It is distinguished from ARTHRALGIA which simply implies joint pain with or without any in?ammatory or structural change. The two main categories of arthritis are osteoarthritis, in which the primary change is thought of as mechanical failure of articular cartilage; and rheumatoid arthritis, in which the primary problem is a chronic in?ammation of the synovial lining of joints, tendon sheaths and bursae. Other, less common forms of in?ammatory arthritis include psoriatic arthritis, Reiter’s syndrome, colitic arthritis and Behçet’s syndrome. Spondarthritis refers to an in?ammatory arthritis with involvement of the spine and is often associated with the HLA B27 tissue type. (See OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; RHEUMATIC FEVER.)... arthritis

Bursitis

In?ammation within a bursa (see BURSAE). Acute bursitis is usually the result of injury, especially on the knee or elbow, when the prominent part of the joint becomes swollen, hot, painful and red.

Chronic bursitis is due to too much movement of, or pressure on, a bursa, with ?uid building up therein. Fluid may need to be drained and the affected area rested. Excision of a chronically in?amed bursa is sometimes necessary. For example, the condition of housemaid’s knee is a chronic in?ammation of the patellar bursa in front of the knee, due to too much kneeling.

Chronic bursitis affecting ligaments round the wrist and ankle is generally called a GANGLION.... bursitis

Rheumatoid Arthritis

A chronic in?ammation of the synovial lining (see SYNOVIAL MEMBRANE) of several joints, tendon sheaths or bursae which is not due to SEPSIS or a reaction to URIC ACID crystals. It is distinguished from other patterns of in?ammatory arthritis by the symmetrical involvement of a large number of peripheral joints; by the common blood-?nding of rheumatoid factor antibody; by the presence of bony erosions around joints; and, in a few, by the presence of subcutaneous nodules with necrobiotic (decaying) centres.

Causes There is a major immunogenetic predisposition to rheumatoid arthritis in people carrying the HLA-DR4 antigen (see HLA SYSTEM). Other minor immunogenetic factors have also been implicated. In addition, there is a degree of familial clustering which suggests other unidenti?ed genetic factors. Genetic factors cannot alone explain aetiology, and environmental and chance factors must be important, but these have yet to be identi?ed.

Epidemiology Rheumatoid arthritis more commonly occurs in women from the age of 30 onwards, the sex ratio being approximately 4:1. Typical rheumatoid arthritis may occur in adolescence, but in childhood chronic SYNOVITIS usually takes one of a number of di?erent patterns, classi?ed under juvenile chronic arthritis.

Pathology The primary lesion is an in?ammation of the synovial membrane of joints. The synovial ?uid becomes diluted with in?ammatory exudate: if this persists for months it leads to progressive destruction of articular CARTILAGE and BONE. Cartilage is replaced by in?ammatory tissue known as pannus; a similar tissue invades bone to form erosions. Synovitis also affects tendon sheaths, and may lead to adhesion ?brosis or attrition and rupture of tendons. Subcutaneous and other bursae may be involved. Necrobiotic nodules also occur at sites outside synovium, including the subcutaneous tissues, the lungs, the pericardium and the pleura.

Clinical features Rheumatoid arthritis varies from the very mild to the severely disabling. Many mild cases probably go undiagnosed. At least 50 per cent of patients continue to lead a reasonably normal life; around 25 per cent are signi?cantly disabled in terms of work and leisure activities; and a minority become markedly disabled and are limited in their independence. There is often an early acute phase, followed by substantial remission, but in other patients gradual step-wise deterioration may occur, with progressive involvement of an increasing number of joints.

The diagnosis of rheumatoid arthritis is largely based on clinical symptoms and signs. Approximately 70 per cent of patients have rheumatoid factor ANTIBODIES in the SERUM but, because of the large number of false positives and false negatives, this test has very little value in clinical practice. It may be a useful pointer to a worse prognosis in early cases if the level is high. X-RAYS may help in diagnosing early cases and are particularly helpful when considering surgery or possible complications such as pathological fracture. Patients commonly develop ANAEMIA, which may be partly due to gastrointestinal blood loss from antiin?ammatory drug treatment (see below).

Treatment involves physical, pharmacological, and surgical measures, together with psychological and social support tailored to the individual patient’s needs. Regular activity should be maintained. Resting of certain joints such as the wrist with splints may be helpful at night or to assist prolonged manual activities. Sound footwear is important. Early use of antirheumatic drugs reduces long-term disability. Drug treatment includes simple ANALGESICS, NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS), and slow-acting drugs including GOLD SALTS (in the form of SODIUM AUROTHIOMALATE), PENICILLAMINE, SULFASALAZINE, METHOTREXATE and AZATHIOPRINE.

The non-steroidal agents are largely e?ective in reducing pain and early-morning sti?ness, and have no e?ect on the chronic in?ammatory process. It is important, especially in the elderly, to explain to patients the adverse effects of NSAIDs, the dosage of which can be cut by prescribing paracetamol at the same time. Combinations of anti-rheumatic drugs seem better than single agents. The slow-acting drugs take approximately three months to act but have a more global e?ect on chronic in?ammation, with a greater reduction in swelling and an associated fall in erythrocyte sedimentation rate (ESR) and rise in the level of HAEMOGLOBIN. Local CORTICOSTEROIDS are useful, given into individual joints. Systemic corticosteroids carry serious problems if continued long term, but may be useful under special circumstances. Much research is currently going on into the use of tumour necrosis factor antagonists such as INFLIXIMAB and etanercept, but their precise role remains uncertain.... rheumatoid arthritis

Periarthritis

n. inflammation of tissues around a joint capsule, including tendons and *bursae. Chronic periarthritis, which may be spontaneous or follow injury, is a common cause of pain and stiffness of the shoulder; it usually responds to local steroid injections or physiotherapy.... periarthritis

Sports Medicine

The ?eld of medicine concerned with physical ?tness and the diagnosis and treatment of both acute and chronic sports injuries sustained during training and competition. Acute injuries are extremely common in contact sports, and their initial treatment is similar to that of those sustained in other ways, such as falls and road traf?c incidents. Tears of the muscles (see MUSCLES, DISORDERS OF), CONNECTIVE TISSUE and LIGAMENTS which are partial (sprains) are initially treated with rest, ice, compression, and elevation (RICE) of the affected part. Complete tears (rupture) of ligaments (see diagrams) or muscles, or fractures (see BONE, DISORDERS OF – Bone fractures) require more prolonged immobilisation, often in plaster, or surgical intervention may be considered. The rehabilitation of injured athletes requires special expertise

– an early graded return to activity gives the best long-term results, but doing too much too soon runs the risk of exacerbating the original injury.

Chronic (overuse) injuries affecting the bones (see BONE), tendons (see TENDON) or BURSAE of the JOINTS are common in many sports. Examples include chronic INFLAMMATION of the common extensor tendon where it

attaches to the later EPICONDYLE of the humerus – common in throwers and racquet sportspeople – and stress fractures of the TIBIA or METATARSAL BONES of the foot in runners. After an initial period of rest, management often involves coaching that enables the athlete to perform the repetitive movement in a less injury-susceptible manner.

Exercise physiology is the science of measuring athletic performance and physical ?tness for exercise. This knowledge is applied to devising and supervising training regimens based on scienti?c principles. Physical ?tness depends upon the rate at which the body can deliver oxygen to the muscles, known as the VO2max, which is technically di?cult to measure. The PULSE rate during and after a bout of exercise serves as a good proxy of this measurement.

Regulation of sport Sports medicine’s role is to minimise hazards for participants by, for example, framing rule-changes which forbid collapsing the scrum, which has reduced the risk of neck injury in rugby; and in the detection of the use of drugs taken to enhance athletic performance. Such attempts to gain an edge in competition undermine the sporting ideal and are banned by leading sports regulatory bodies. The Olympic Movement Anti-Doping Code lists prohibited substances and methods that could be used to enhance performance. These include some prohibited in certain circumstances as well as those completely banned. The latter include:

stimulants such as AMPHETAMINES, bromantan, ca?eine, carphedon, COCAINE, EPHEDRINE and certain beta-2 agonists.

NARCOTICS such as DIAMORPHINE (heroin), MORPHINE, METHADONE HYDROCHLORIDE and PETHIDINE HYDROCHLORIDE.

ANABOLIC STEROIDS such as methandione, NANDROLONE, stanazol, TESTOSTERONE, clenbuterol, androstenedone and certain beta-2 agonists.

peptide HORMONES, mimetics and analogues such as GROWTH HORMONE, CORTICOTROPHIN, CHORIONIC GONADOTROPHIC HORMONE, pituitary and synthetic GONADOTROPHINS, ERYTHROPOIETIN and INSULIN. (The list produced above is not comprehen

sive: full details are available from the governing bodies of relevant sports.) Among banned methods are blood doping (pre-competition administration of an athlete’s own previously provided and stored blood), administration of arti?cial oxygen carriers or plasma expanders. Also forbidden is any pharmacological, chemical or physical manipulation to affect the results of authorised testing.

Drug use can be detected by analysis of the URINE, but testing only at the time of competition is unlikely to detect drug use designed to enhance early-season training; hence random testing of competitive athletes is also used.

The increasing professionalism and competitiveness (among amateurs and juveniles as well as professionals) in sports sometimes results in pressures on participants to get ?t quickly after injury or illness. This can lead to

players returning to their activity before they are properly ?t – sometimes by using physical or pharmaceutical aids. This practice can adversely affect their long-term physical capabilities and perhaps their general health.... sports medicine




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