Rheumatology Rural Health West au


Osteoarthritis OA


Degenerative joint disease due mainly to life’s wear and tear.

Slow degeneration of the articular cartilage is accompanied by hypertrophy (overgrowth) of bone at its margin.

The clinical features of osteoarthritis are joint pain with activity, transient stiffness in the morning or after rest, reduced range of motion, joint crepitus or periarticular tenderness, and bony swelling.

In OA there is often little inflammation. OA is more common in joints which have been injured in the past or regularly over-stressed, e.g. the hips and knees of obese people and those with abnormal posture or gait.

On examination, the range of passive movement may be normal until later in the process.

Treatment Aims

The aim is to maintain function and relieve pain and minimise disability

Management of OA

physiotherapy to maintain joint mobility and muscular strength

regular (daily) exercise within patient’s limits. Swimming is particularly good, as it is non-weight-bearing

weight loss if the patient is obese, to reduce weight-bearing stress on the hips and knees

in more advanced OA, appliances such as walking aids, joint supports and modifications to home and car.

Topical NSAIDs are safer than oral NSAIDs for osteoarthritis of the knee.

Paracetamol should be offered first before resorting to other analgesics.


Glucosamine and non-drug options such as therapeutic taping, exercise, acupuncture are useful in some.


Exercise and physiotherapy

Exercise improves muscular tone and joint function, so should not be avoided.

Physiotherapy reduces pain, improves joint range and muscle strength as well as

improving mobility and independence

Intra-articular hyaluronic



Joint replacement





Topical NSAIDS


Glucosamine chondroitin

Now generally considered to be ineffective BMJ 2010;341:c4675


Rheumatoid arthritis


Systemic autoimmune inflammatory disease affecting joints and other tissues and organs.

1-2% of the population, women > men (ratio 3:1), and its onset is 20-40 years of age.

Two key features

1 Joint damage (erosion of cartilage and bone) begins within a few months of the onset of RA. Later, ligaments and tendons may be eroded.

2 Remission of RA occurs in fewer than 20% of patients and rarely lasts as long as a year. In most patients, the disease process continues and the treatment regimen must also continue.

Presenting Symptoms

Vague malaise, joint aches and stiffness particularly morning lasting several (>6) weeks. Unexplained weight loss.


Symmetrical swelling of the small joints of the hands (PIPs) wrists or feet (MTPS). The swollen joints are usually tender on compression. They may be slightly flexed, and straightening them may be uncomfortable.

Prompt referral to rheumatologist is essesntial as disease modifying drugs may be able to limit irreversible joint damage.


NSAIDS: different NSAIDs work for different patients, so it is worth trying a selection. About a third of patients derive considerable benefit from NSAIDs, a third experience a degree of improvement and a third do not respond. A long-acting NSAID such as modifiedrelease diclofenac may be helpful at night. If there has been no response to an NSAID within 3 weeks, it is worth switching to a different one.

Steroids: long-term steroids are rarely indicated and their most common use is in the short term, for treatment of acute exacerbations.


reduce joint inflammation and limit permanant damage. They can take up to 6 months to take full effect (although a beneficial effect is usually observed after 1-3 months) and may be used for several years.





Blood monitoring is usually necessary

eg Methotrexate FBC weekly for the first 6 weeks, then monthly Liver function tests (LFTs) 3-monthly FBC 1 week after any change in dosage


RhA Diagnostic Criteria

RhA Diagnostic Criteria American College of Rheumatology

Four out of the following seven criteria

Morning stiffness of at least 1 hour for >6 weeks

Arthritis with swelling of three or more joint areas for >6 weeks

Arthritis with swelling of hand (metacarpophalangeal (MCP) or proximal interphalangeal (PIP) joints) or wrist joints for >6 weeks

Symmetrical arthritis of at least one part of the body (eg elbows, wrists, knees) for >6 weeks

Subcutaneous nodules

Serum rheumatoid factor-positive (occurs in 70-80% of cases, but is also positive in other diseases, such as systemic lupus erythematosus (SLE) and polymyositis

Typical radiographic features of hand or wrist with erosions or peri-articular osteopenia (although X-rays are often normal in early disease),

Blood tests

1 rheumatoid factor

2 erythrocyte sedimentation rate (ESR) > 30 mm/hour

3 an autoimmune antibody screen


Interpreting Rheumatoid Factor Results

These results refer to the factor by which serum has to be diluted before the antibodies can no longer be detected, ie 1:40 means that the serum has to be diluted by a factor of 40 before detection can no longer take place, while a result of 1:160 means that the serum has to be diluted 160 times before the antibodies “disappear.

Therefore, the higher the second number, the more strongly positive the result is, and the worse the prognosis:

A value of <1 :40 is negative.

A value of between 1:40 and 1:80 is borderline.

A significantly raised rheumatoid factor is one of above 1:160.

The same applies when interpreting other autoantibody results, eg antinuclear antibody (ANA)



Management RhA (McGavock)

1 NSAIDs relieve both pain and inflammation. but do not affect disease progression

2 Disease-modifying anti-rheumatic drugs (DMARD). Relieve symptoms and also suppress the disease process gradually over a 6-month period.

DMARDs usually reduce the need for NSAIDs.


start 7.5 mg weekly PO and build up the dose gradually to a maintenance level of 10 mg to 25 mg once a week.

Methotrexate is an anti-metabolite which interrupts cell division, and it has been used for decades to treat a variety of cancers. It is potentially toxic, even

at this low dosage, and the rheumatologist and primary care clinician must actively seek signs of toxicity . Full blood counts and liver function tests must be repeated fortnightly at the start of treatment, then every month once the dose has been stabilized.

Folic acid


500 mg daily, increasing to 1 gram twice daily by stages.

Sulfasalazine is a combination of a sulphonamide with a salicylate. It is the sulphonamide moiety which acts as the disease-modifying agent in RA.

The sulphonamide element can rarely cause serious blood disorders, and blood counts (Hb, WCC and differential count) must be monitored at least monthly for the first 3 months of treatment. Liver function tests must also be done regularly.

Other second-line drugs for RA include leflunomide, hydroxychloroquine, gold injections and d-penicillamine.

A group of exciting new biologic agents (etanercept, infliximab and adalimumab) are now available to the rheumatologist.

No single anti-rheumatic drug is invariably successful, and several drugs or drug combinations may need to be tried in order to achieve adequate control.

The important message is that ongoing joint inflammation will inevitably lead to damage, and must be controlled.

Response to DMARD treatment is assessed as a reduction in the ESR or CRP. If these parameters do not return to normal, the disease must be treated more aggressively.

Steroids in RhA

The high-potency synthetic oral steroid, prednisolone, is sometimes given in the early management of RA, to reduce joint inflammation while the

DMARD is starting to work (this may take weeks or months). Relief of symptoms is quick and dramatic, and patients will often press for its ongoing

use. However, its long-term side-effects mean that it should only be used in the short term for acute flare-ups. An alternative to oral steroids is an intramuscular injection of triamcinolone, which may reduce the risk of a major relapse of joint pain and stiffness once the steroid effect wears off.

The other important use of steroids in RA is the intra-articular injection of a high-potency steroid such as methylprednisolone.

This relieves pain and stiffness within a few days, and the beneficial effect often lasts for weeks or even months.


@@@ Non-drug measures in RA management

The patient should be given a realistic understanding of RA and the need for lifelong co-operation with the various specialties involved in their treatment.

Individual joints should be rested when the disease is active.

Using adjustable supports intermittently and night-time splints is often found to be helpful.

Exercise is important, under a specialist physiotherapist when the RA is active, including:

passive movement of all joints

hydrotherapy with gentle active exercise when the disease process is improving

in remission, daily exercise within the limits of pain-free movement; an occupational therapist can contribute greatly to the patient’s quality of

life in the quiescent phase of RA weight loss is essential if the patient is obese.


Rheumatoid hands

Synovitis of MCP joints, with filling of the hollow between MCP heads when fingrs flexed, and syovial swelling of extensor tendon sheaths.

Swan meck and boutonniere deformity due to tendon tears.  Spindle-shaped swelling of PIPs (Haygarth nodes) . Ulnar deviation.



OA Hands

Heberdens nodes – osteophytes at DIPs

Bouchards Nodes – IP joints

MCP joints including thumb causing square hand deformity



Psoriatic Arthritis


Ankylosing Spondylitis



Seronegative spondyloarthropathies



Systemic sclerosis



Acute joint pain / swelling


Septic arthritis

Septic Arthritis






Acute attacks


Naproxen tablets 250mg, 500mg

Dose: Acute gout, 750mg initially, then 250mg every 8 hours until attack has passed.

Indometacin capsules 50mg suppositories 100mg

Dose: Acute gout, 150-200mg daily in divided doses.

If effective, continue the NSAID until 48 hours after the attack has finished (up to 1-2 weeks). As the pain resolves, the dose of the NSAID should be rapidly reduced.

Indometacin should be avoided and NSAIDs should be used with caution in elderly patients.


Colchicine tablets 500 micrograms

Dose: Treatment of gout, 500micrograms twice daily to four times daily (lower doses in elderly) for up to 72 hours only. Severe renal impairment (GFR < 10mL/min) 500micrograms three times daily; maximum total dose 3mg per course. Stop treatment if vomiting or diarrhoea occurs. The course should not be repeated within 3 days.

Colchicine can be given to patients with heart failure and those taking oral anticoagulants.


Oral prednisolone or methylprednisolone acetate injection may be used in the treatment of an acute attack of gout in those who cannot tolerate NSAIDs or colchicine. Intra-articular injection of methylprednisolone acetate can be used in acute mono-articular gout (unlicensed indication). Methylprednisolone acetate by intramuscular injection can be effective in podagra. See local protocol on the Management of Gout for further information. Contact the rheumatology service if further advice is required.


Allopurinol tablets 100mg, 300mg

Dose: Initially 100mg daily as a single dose after food, then titrated every 6 weeks to achieve a serum urate concentration of less than 0.3mmol/L (lower doses in elderly); Maximum dose is 900mg daily. Severe renal impairment (GFR < 10mL/min) 100mg on alternate days; moderate renal impairment (GFR = 10-20mL/min) 100-200mg daily; mild renal impairment (GFR = 20-50mL/min) 300mg daily.

Febuxostat?is a 2-arylthiazole derivative that selectively inhibits xanthine oxidase, thereby decreasing uric acid. It is restricted to use either in patients who had an inadequate response to allopurinol (at maximum tolerated dosage), or in whom allopurinol is contraindicated or not tolerated, under the direction of a rheumatologist. LFTs are recommended before initiating treatment and again after 1 month. LFTs are only required thereafter if clinically indicated. (NB: the incidence of LFT derangement is the same as for allopurinol). See SPC for further details on precautions for use and interactions.

Allopurinol or febuxostat?should never be initiated during an acute attack as they can prolong the episode. They can be started 1-2 weeks after recovery from an acute attack. The initiation of allopurinol or febuxostat?may precipitate an acute attack of gout, therefore NSAIDs (for 12 weeks) or low dose colchicine (500micrograms twice daily for 6 months) should be used as a prophylactic to cover the period of introduction.

Arthritis due to deposition of monosodium urate monohydrate crystals within joints causing acute inflammation and eventual tissue damage.

Risk factors

  • Male sex
  • Meat
  • Seafood
  • Alcohol
  • Diuretics
  • Obesity
  • Hypertension
  • Coronary heart disease
  • Diabetes mellitus
  • High triglycerides
  • Chronic renal failure



There is florid synovitis and swelling and extreme tenderness with overlying erythema. Untreated, the attack resolves spontaneously over 5-15 days, usually with itching and desquamation of overlying skin.

Sites affected:

50% of all attacks and 70% of first attacks affect the first metatarsophalangeal joint.

Other sites often affected are: Knee Midtarsal joints Wrists Ankles Small hand joints Elbows

Atypical attacks can occur with tenosynovitis, bursitis and cellulitis, with mild discomfort without swelling lasting a day or two.

Chronic tophaceous gout in this condition large crystal deposits produce irregular firm nodules mainly around extensor surfaces of fingers, hands, forearms, elbows, Achilles tendons and ear. Typically, tophi are asymmetrical with a chalky appearance beneath skin.

Differential diagnosis

Acute attacks sepsis and other forms of crystal-related synovitis.

Chronic tophaceous rheumatoid arthritis, generalised nodal osteoarthritis, xanthomatosis with arthropathy.


Demonstration of monosodium urate (MSU) crystals in synovial fluid or tophi confirms the diagnosis of gout.

Gram staining and culture of synovial fluid should be arranged, even if MSU crystals are found, since gout and sepsis can co-exist.

Fasting glucose and lipids should be performed to rule out hyperglycaemia and hyperlipidaemia as gout is commonly associated with metabolic syndrome.

General points

An ice pack may be useful, as may rest. The joint should be elevated and trauma avoided.

Pharmacological therapeutic options include:

Non-steroidal anti-inflammatory drugs. Diclofenac, naproxen and indometacin are generally preferred (NSAIDs)



The opportunity should also be taken to discuss lifestyle issues such as weight loss, exercise, diet, alcohol consumption and fluid intake.

Drink alcohol sensibly beer or spirits should be avoided (there is a particularly strong link with beer, stout and port wines), but wine in moderation is not associated with an increased risk.

There is a good evidence base that reducing alcohol intake to moderate levels is helpful.

Avoid dehydration.

Dietary intervention reduction of purine-based foods.

Highest purine levels are found in heart, herring, sardines and mussels.

Other foods which are very rich in purines include liver, kidneys, red meat, yeast extracts, seafood (herring, sardines, and shellfish) and asparagus, beans, cauliflower, lentils, mushrooms, oatmeal and spinach.

Soya foods are also high in purines but are less likely to lead to gout than meats and seafood.

It is the quantity of purine-rich food consumed that is more important than the absolute purine content in each food.

Soft drinks containing high levels of fructose can affect the levels of purines and should also be avoided.

There is no evidence to support a reduction in purine-rich vegetables such as peas, beans, mushrooms or cauliflower, unless intake is extreme.

Weight reduction

Take regular exercise.

Stop smoking.

Manage risk factors

These may include:

Drugs causing hyperuricaemia: Thiazides and loop diuretics

Low dose salicylates e.g. aspirin < 1 g/day, pyrazinamide, ethambutol, nicotinic acid, ciclosporin


Impaired renal function

Hyperlipidaemia, especially hypertriglyceridaemia

Vascular disease

Chemotherapy consider starting prophylaxis before treatment begins

Myeloproliferative disease

NB: Aspirin in low doses (75–150 mg/day) has insignificant effects on the plasma urate and should be used as required for cardiovascular prophylaxis.


Gout has a prevalence of about 1% in the UK and is most common in Caucasian men over the age of 45 (it is very rare in Black Africans). The big toe is the most common site to be affected, but other joints that may be involved include the knee, wrist and finger. Gout is more likely to occur in patients with raised serum uric acid levels (>0.42 mmol/l), but most patients with hyperuricaemia do not have gout and therefore do not need to be treated. Uric acid levels may return to normal during an acute attack.

Acute attacks of gout usually resolve within 1 or 2 weeks. Treatment is with either NSAIDs or colchicine in patients who cannot tolerate NSAIDs.

Colchicine commonly produces gastrointestinal side-effects when given at licensed doses (1 mg followed by 500 micrograms every 2-3 hours until pain relief is achieved, to a maximum of 6 mg/day). Some case reports (British Medical }ournaI2003; 327: 1275) have suggested that smaller doses of 500 micrograms tds are just as effective, but produce fewer side-effects.


Losing weight and reducing alcohol and red meat consumption tend to result in a lowering of serum uric acid concentrations, and should therefore be encouraged. Patients who have two or more attacks per year may wish to consider prophylactic treatment, particularly if they find it difficult to take NSAIDs or colchicine. Allopurinol is a xanthine oxidase inhibitor, and is thebmost commonly used prophylactic drug. It should usually be started at a low dose (eg 100 mg od, taken with food) and then gradually increased until the

serum uric acid concentration falls into the normal range. Allopurinol should never be initiated during an acute attack of gout (it may prolong the attack).

Cover with an NSAID or colchicine is necessary for at least the first 3 months of treatment. If the patient gets an acute attack while on allopurinol, the drug should be continued at the same dose, and concomitant treatment with an NSAID or colchicine should be started.

Urate Metabolism






Gout prophylaxis

Gout BMJ Dec 2011


After two or more attacks within a year


Renal insufficiency

Uric acid stones and gout

Need for continuing diuretic treatment


Advise the person that allopurinol may cause acute attacks of gout just after initiating treatment, and for some weeks afterwards and will usually have to cover the first few months with an NSAID or Colchicine

If they have an attack while on Allopurinol explain that they should start their anti-inflammatory/colchicine/corticosterod treatment as soon as possible and not stop their allopurinol during acute attacks.

Start with a low dose (50-100 mg) and increase in 50-100 mg increments every 2-4 weeks until serum uric acid (SUA) level is below 300 micromol/l


Polyarticular joint pain

Polyarticular Joint Pain AAFP 2003


Hypermobility syndrome

Hypermobility Beighton diagnostic criteria

  • Score one point if you can bend and place you hands flat on the floor without bending you knees.
  • Score one point for each knee that will bend backwards.
  • Score one point for each elbow that will bend backwards.
  • Score one point for each thumb that will bend backwards to touch the forearm.
  • Score one point for each hand when you can bend the little finger back beyond 90°.
  • If you are able to perform all of above manouevres then you have a maximum score of 9 points.

Major Criteria

  • A Beighton score of 4/9 or greater (either currently or historically)
  • Arthralgia for longer than 3 months in 4 or more joints

Minor Criteria

  • A Beighton score of 1, 2 or 3/9 (0, 1, 2 or 3 if aged 50+)
  • Arthralgia (> 3 months) in one to three joints or back pain (> 3 months), spondylosis, spondylolysis/spondylolisthesis.
  • Dislocation/subluxation in more than one joint, or in one joint on more than one occasion.
  • Soft tissue rheumatism. > 3 lesions (e.g. epicondylitis, tenosynovitis, bursitis).
  • Marfanoid habitus (tall, slim, span/height ratio >1.03, upper: lower segment ratio less than 0.89, arachnodactily [positive Steinberg/wrist signs].
  • Abnormal skin: striae, hyperextensibility, thin skin, papyraceous scarring.
  • Eye signs: drooping eyelids or myopia or antimongoloid slant.
  • Varicose veins or hernia or uterine/rectal prolapse.

BJHS is diagnosed in the presence two major criteria, or one major plus two minor criteria, or four minor criteria.

Two minor criteria will suffice where there is an unequivocally affected first-degree relative.

Brad Cheek Dec 2006

Polymyalgia rheumatica (rheumatology)


Myalgia and myositis

(this is something of a mixed-bag and needs editing)









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