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Rheumatoid arthritis is the second most common arthritis which the exact cause is unknown. Friesen, H. (2009) states that unlike osteoarthritis it isn't a disorder of wear and tear, rheumatoid arthritus is typified by widespread persisting synovitus. It is thought to be a cell mediated autoimmune disease of the synovial lining of the joints, causing polyarthritus and systemic complaints. Typically involving the joints of the fingers, wrists, feet, shoulders and neck.
Most patients have the presence of rheumatoid factor in their serum. Rhematoid factor is:
As the disease progresses the ligaments supporting the joints are damaged and there is an erosion of the bone, leading to deformity of the joints.
Increased permeability of blood vessels and the synovial lining layer leads to joint effusions and contain lymphocytes and drying polymorphs.
Hyperplasic synovium spreads from joint margins on to the cartilage surface. It damages and breaks down nutritional route for cartilage. This cases the cartridge to thin and over time the underlying bone becomes unprotected by it and exposed. Erosions lead to a variety of deformities and contribute to long-term disability.
Fibroblasts from the synovium also grow along the blood vessels and the bone cavity.
Chronic synovial inflammation is caused by ongoing T cell activation
The presence of activated t cells and macrophages and local production of rheumatoid factor autoantibodies in the joint in RA suggests that immune deregulation plays a fundamental role in pathogenesis.
Activated mast cells which release histamine and TNF-Î± may also play a role.
Synovium is usually thin and comprises of a layer of a few cells thick containing fibroblast like synocytes and macrophages overlying loose connective tissue.(kumar and clark) in rheumatoid arthritis the synovium between joints is greatly thickened to the extent that it is palpable as boggy swelling around joints and tendons. Thickened also by white blood cells that have entered via new blood vessels, these produce substances such as histamine that cause inflammation more specifically:
Dolor - Vasodilation (redness, heat)
Calor - Vascular permeability (swelling)
Tumor - White cell movement to and infiltration of affected area (pus)
Rubor - Nerve ending stimulation (pain)
The body produces dolor, calor, tumor, rubor primarily to confine injurious agents that have been produced in the synovium.
But in rheumatoid arthritis the body over produces this inflammatory reaction and the presence of these in the joints produces symptoms of tender joints, pain and eventually deformity. When these chemicals are released into the blood stream they cause the sufferer fatigue, disequilibrium.
Many factors are thought to play a part in rheumatoid arthritis it could be:
An immunological disorder that causes chronic synoivial inflammation by t cells. The presence of activated t cells and local cell production in the joints suggest immune dyregulation. T cells are a cell mediated response also found in bone marrow, these are educated via the thymus and directly attach cell to cell. They seek antigens around the body, once they recognise antigens they differentiate. There are three types of T cell, these are:
Killer T cells role is to recognise & kill
Helper T cells role is to coordinate response
Memory T cells are classed as left over killer cells ready for next time
It could also be that B cell production is over stimulated and produce too many antibodies to protect the body and end up having a destructive affect on the joints. B cells are a humeral response produced in bone marrow. They stay in the lymphatic tissues and produce antibodies to protect the body.
Or it could be that this abnormal B and T cell interaction stimulates the release of rheumatoid factor which then causes inflammation in the synovium.
The body produces increased blood cells and moves plasma movement to injured areas to enhance immune response. This should have the effect of destroying injurious agents in a 'healthy' human, but sufferers of rheumatoid arthritis the body over produces white blood cells. The role of white blood cells is: to control inflammatory reaction, release inflammatory chemicals such as histamine, attack antigens, produce antibodies and phagocytosis.
Production of Rheumatoid factor by plasma cells in the synovium and local immune complexes are thought to play a part.
IgM autoantibodies (rheumatoid factors) against IgG form complexes in joint, leading to inflammation and cartilage damage
Epidemiology - distribution
Onset can be at any age with ranges of severity, most commonly it will occur in women ages 30-50.
0.5% of the population, lower in black Africans and Chinese people.
Genetic factors - 60% of sufferers are genetically predisposed to RA.
Association between RA and certain HLa halotypes. Genetic and environmental factors (Kumar and Clark)
Ra affects three times more premenopausal women than men this suggests a hormonal link for the disease.
RF isn't found in everyone with Ra but a high precencxe of RA in early bllod tests imples that the disease will be more aggressive and hearder to treat.
Aetiology and pathogenesis
Inflammation of the synovial lining of the joints, tendon sheaths and bursa.
Rheumatoid arthritis is a particularly unpredictable disease that can compromises many aspects of life.
Improvements in drug therapy my RA is now fairly well managed.
Criticism and lack of understanding in the workplace
Hartman L states, ligamentous laxity will affect not just the peripheral joints but the body as a whole.
Ligamentous laxity in the cervical spine is common; support for the dens of the axis against the atlas can become disrupted.
Long-term use of steroids can produce osteoporosis and a disorganisation effect on the ligamentous structures particularly of the cervical spine.
Joints are initially swollen and stiff and are usually affected symmetrically.
70%of cases start as a slow progressive, symmetrical, peripheral Polyarthritus, evolving over a period of a few weeks or months.
Less commonly symptoms can occur over a few days; these patients have a better prognosis
Palindromic - monoarticular attacks last 24-48 hrs- 50% progress to other types of RA.
Transient - self limiting disease, lasting less than 12 months, leaves no permanent joint damage.
Remitting - a period of several years during which the arthritis is active but then remits leaves minimal damage.
Chronic persistent - most common, relapsing and remitting course over many years. Develops greater joint damage and long term disability. Warranting earlier and more aggressive treatment with disease modifying agents.
Rapidly progressive - the disease progresses over a few years and rapidly leads to severe joint damage and disability. High incidence of systemic complications and difficult to treat.
Clinical manifestation/ Symptoms
sufferers of rheumatoid arthritis have many varying complaints due to the unpredictability of teh disease. Many have muscle wasting, atrophy this is found particularly in the forearms, hands and thighs, this will give the patient problems opening jars and trouble getting out of chairs
It is difficult for work colleagues to be continually supportive when your illness directly affects them and can possibly increase their workload.
Other symptoms include; flu like symptoms and joint swelling and pain eventually causing immobility
hands are deformed and contain cutaneous nodules
Fibrous or bony ankylosis or soft tissue contracture most commonly in the small joints, Metacarpophangeal, proximal and distal interphangeal and feet.
10% also suffer carpal tunnel syndrome
Disturbed sleep, fatigue , disequilibrium
Pain worse in morning (for more than 30 mins) and may improve with gentle activity
Sleep is disturbed
Joints warm and tender
General complications for suffers may be ruptures tendons or joints, such as Bakers cysts, Joint infection, Amyloidosis, Septic arthritis - hot and inflamed, fever.
Hands and fingers can be affected as tendon sheaths become inflamed, ulnar deviation occurs, Boutonniere deformity - fixed flexion, Swan neck deformity - fixed hyperextension
Swelling and dorsal subluxication of the ulnar styloid leads to wrist pain and may cause rupture of the finger extensor tendons, leading to finger drop this needs surgical repair to regain mobility.
In the Shoulders Painful arc syndrome, similar to rotator cuff tears, tears are common complications with RA. This Immobility of the shoulder may interfere with dressing, feeding and personal hygiene.
In the Elbows Swelling and painful flexed deformity are common complaints.
In the feet; Walking and weight bearing may be painful and limited, the foot becomes broader, ulcers and calluses may develop under the metatarsal heads and the dorsum of the toes, hammer toes may develop. Due to the protective posture the Ankle may develop a Valgus position.
In the Knees there is an increased risk of poetical cyst formation and rupture. Erosion of the cartilage and bones decreased the space between joint, Secondary OA may follow. Depending on progression may develop valgus or varus deformity.
Hips are less commonly affected than the knees but the symptoms are similar as there may be loss of joint space and OA causing Medial movement of the acetabulum
In the Cervical spine the pain is often muscular and due to muscle guarding of the cervical tissues to stabilise the neck ligaments may be lax or damaged. But may be due to synovitus affecting the synovial joints and destructing the bone. This can compress onto the spinal cord most commonly the atlantoaxial joint, causing loss of bladder or bowel control this is a neurosurgical emergency
Smoking is a risk factor for RA and gives greater risk to the sufferer of developing serosis of the lungs which causes pleural effusion, pleural nodules, fibrosing alveolitis, obstructive bronchiolitis, infective lesions. Vasculitus of the lungs caused by autoimmune deposits in arterial walls
Heart and peripheral vessels can be affected; athelscleoris of arteries or eventually myocardial infarction
In the nervous system there can be sensory loss in a glove and stocking distribution and carpal tunnel symptoms can develop.
In the eyes scleritis and episcleritis occur in severe, red lesions around the eye, sicca syndrome (dry)
Kidneys - renal failure
Spleen, lymph nodes and blood - leg ulcers, palpable nodes.
Communication and early referral to a rheumatologist is vital. 25% recover completely.
First years of the disease are hardest but people encouraged to carry on as normal.
Advice from physiotherapists about keeping mobile
Exercises to maintain joint range and muscle power is essential.
Exercise in a hydrotherapy pool
Family and friends involvement.
Once the patient had learnt to adapt to the deformities and control the pain, function may not be so restricted.
socioeconomic cost for suffers as the discomfort means that they are unable to perform daily tasks, some may need bath hoists in order to clean themselves, raisers for furniture, raised toilet frame, mobility cars, stair lifts and wheelchairs
There is no no cure for rheumatoid arthritis only control of the symtoms can be provided at the moment. In the early stages there are soft tissue changes, swelling and periarticular osteoporosis.
Later stages are characterised by boney erosions, narrowing of the articular surface, articular destruction and joint deformity. These characteristic changes can be detected on xrays.
The condition may resolve spontaneously, but is usually relapsing and remitting with steady progression, it may end but the boney deformities remain.
The symptoms treated with anti-inflammatory and immunosuppressive drugs that are closely monitored as they can give side affects that make the patent feel quite unwell. Physical therapy and hydrotherapy keeps joints movable. Surgical replacement of joints may be necessary in the end due to the erosion.
Any patient taking over 10mg per day over a period of more than 6 months should be treated with caution.
HVT's or use of excessive force may not be suitable for sufferers of RA.
Gentle short treatment may be helpful, excessive mobilisation is not wise.
Thrust techniques are not always suitable for patients suffering from RA, even of the peripheral joints.
Anti inflammatory analgesics, steroids and disease modifying antirheumatic drugs.
Surgical treatment is by the excision of the synovium in early cases or by fusion or joint replacement once boney changes have occurred.
Clark, M. Kumar, P (2009). Clinical Medicine. 7th Ed. Edinburgh: Saunders Elsevier.
Fischbach, M. (1991) Rheumatoid arthritis. 1st Ed. USA. Churchill Livingstone.
Friesen, H. (2009) illuminting discourse through lived experience of rheumatoid arthritis. PH.D. Thesis, University of British Columbia
Lahita, R. (2001)Rheumatoid arthritis. Everything you need to know.1st Ed. New York. Avery.