Musculoskeletal Medicine E-book Flashcards
(34 cards)
Hyperuricaemia and Gout
Gout is a disease from history that lives on in the early 21st century. Hippocrates himself noted that gout only presented in men after puberty and in women following the menopause. Van Leeuwenhoek (1632-1723) described the appearance of microscopic crystals in a tophus, and in 1847 Garrod discovered that gout was associated with hyperuricaemia.
Symptoms
Gout
Gout is one of the most painful conditions known to man. A classical presentation of acute gout would involve a middle aged man presenting with sudden onset extreme pain in the great toe at night, although any joint can be affected. The joint will be swollen and inflamed; sometimes patients will not even be able to stand the bed sheet touching the joint. Normally only one joint is affected and an attack will last around 7-14 days without treatment. Following the initial attack patients may suffer a similar event within the next 12 months. Other symptoms of gout include renal colic and gouty nephropathy
Causes - gout
In the past gout was considered to be a disease of the
rich. Both alcohol and a high consumption of red meat
do contribute to the development of gout, however one of the main risk factors for the development of the disease is hyperuricaemia (increased levels of uric acid in the blood). Hyperuricaemia is caused by a disorder of purine metabolism. When the levels of uric acid reach a critical concentration in the blood, it tends to precipitate. Specifically this occurs in the joints, causing uric acid crystals to be deposited. These lead to the classic symptoms of pain and inflammation. After an extended period of hyperuricaemia, tophi may develop, these are hard aggregates of uric acid crystals which tend to form in the ears or joints.
Summary of factors contributing to hyperuricaemia
Overproduction
- Myeloproliferative disorders
- Chemotherapy
- Trauma
Diet
- Alcohol (especially beer)
- Red meat
Under excretion
- Thiazide diuretics
- Alcohol
- Renal impairment
- Genetic factors e.g. male Maori
Gout can be classified according to four phases:
asymptomatic hyperuricaemia, acute gout, interval or intercritical gout and chronic tophaceous gout.
Diagnosis and Treatment - gout
Any patient presenting with severe pain, swelling and inflammation in one joint with a history of alcohol consumption should be considered for a diagnosis of gout. A careful history should be taken as previous injuries to the affected joint and a systemic temperature
could suggest septic arthritis. There are diagnostic criteria that can be used. The definitive diagnostic test will show uric acid crystals in the fluid that has been aspirated from the affected joint. Serum uric acid levels can also be measured. Treatment involves two main approaches: reduction of uric acid levels, by diet or pharmacological means, and pain relief.
Summary of lifestyle changes recommended for a patient with acute gout
- Optimise weight - Slow weight loss
- Reduce alcohol intake
- Modify diet - avoid high purine foods
- Adequate fluid intake
- Withdraw drugs that may precipitate an attack e.g. thiazide diuretics
Medicines used in an acute attack of gout
NSAIDs provide the cornerstone of pain relief. A patient should also be prescribed a gastroprotective agent as per relevant guidance. Aspirin is not indicated in gout as it can reduce uric acid excretion. Colchicine can be given but toxicity can develop at higher doses e.g. vomiting, diarrhoea and abdominal pain. Dose adjustments may be necessary due to drug interactions. There is a maximum dose of 6mg per course and the course should not be repeated within 3 days. Canakinumab and oral, parenteral or intra-articular corticosteroids can also be used.
Long-term treatment of gout
Allopurinol is widely used for the long-term (interval) treatment of gout. It inhibits the enzyme xanthine-oxidase which catalyses purine metabolism. The starting dose is
dependent on the severity of the condition and doses can be adjusted according to uric acid concentrations. If renal impairment is present then dose reductions may be necessary. Side effects include skin rashes and hypersensitivity. Febuxostat is also a xanthine-oxidase
inhibitor, it is only recommended by NICE for patients who have contra-indications to or are intolerant of allopurinol. It can cause serious hypersensitivity reactions.
Sulfinpyrazone is a uricosuric drug that can also be used. Allopurinol, febuxostat and sulfinpyrazone should never be started during an acute attack; they are usually started 1–2 weeks after the attack has settled. They can precipitate an acute attack, therefore an anti-inflammatory analgesic or colchicine should be used prophylactically for at least one month after the hyperuricaemia has been corrected. Other drugs used for the long term control of gout include colchicine and benzbromarone.
Main Clinical Features - Rheumatoid arthritis
Systemic involvement, MCPs, PIPs
Main Clinical Features - Systemic Lupus Erythematous
Malar Rash, psychological symptoms, renal involvement
Main Clinical Features - Reactive arthritis
Often follows infection
Main Clinical Features - Enteropathic arthritis
Associated with Crohn’s and Ulcerative Colitis
Main Clinical Features - Ankylosing spondylitis
“Bamboo spine” tends to affect men < 40 years old
Main Clinical Features - Psoriatic arthritis
DIP involvement, nail changes
Main Clinical Features - Juvenile idiopathic arthritis
Patient <16 years old
Rheumatoid Arthritis (RA)
Rheumatoid Arthritis (RA) is an inflammatory autoimmune disease which primarily affects the synovial joints. It is characterised by joint swelling, tenderness and eventually destruction of the synovial joint. It typically affects the small joints of the hands and feet especially the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints of the hand and the metatarsophalangeal (MTP) joints of the feet. It is a systemic disease so other tissues such as the heart, eyes and lungs can also be affected.
Rheumatoid arthritis patients have a reduced life expectancy and have an increased risk of heart disease, osteoporosis and opportunistic infections.
Aetiology
Rheumatoid Arthritis
Rheumatoid Arthritis affects approximately 400,000 adults aged 16 and over in the UK. As with many autoimmune diseases, the specific reason why the body starts to attack itself is unknown. The HLA-DR1, 4 and 10 alleles are associated with the disease, pregnancy
alleviates symptoms and smoking slightly increases the risk of developing RA.
Physical Symptoms
RA
RA is a systemic progressive polyarthritis. Classical symptoms include inflammation of the small joints of the hands and feet, causing pain and stiffness. Larger joints can also be affected and the pattern of joint involvement tends to follow a symmetrical course. The stiffness in RA tends to be worse in the morning and is termed ‘early morning stiffness’, this can confine patients to their beds for hours.
Other signs include raised inflammatory markers such as ESR and CRP, and raised autoantibodies such as anti-CCP and Rheumatoid Factor. In later disease, the characteristic changes of joint destruction can be seen with ulnar deviation of the fingers and boutonnière and swan neck deformities.
Diagnosis
RA
RA is becoming more difficult to diagnose as healthcare professionals have become more aware of the destructive nature of the disease. In fact, some medics now believe that it will be a disease of the past in 15-20 years as cytokines and autoantibodies can be detected in
the bloodstream before any joint damage occurs. Referral from primary care for a specialist opinion is indicated for any adult with suspected persistent synovitis of undetermined cause and urgent referral if the small joints of the hands or feet are affected, more than one joint
is affected or there has been a delay of 3 months or longer between onset of symptoms and seeking medical advice
Classical symptoms of RA
- Symmetrical polyarthropathy
- Early morning stiffness (may last for hours)
- Tender and swollen joints
- Arthritis of MCP, PIP joints
- Increased CRP and ESR
- Fatigue, weight loss and myalgia
- May have a positive rheumatoid factor
- May have positive anti-cyclic citrullinated peptide (anti-CCP) years before diagnosis
- Joint damage visible on X-ray
Treatment for RA
Treatment for RA has greatly improved over the last 20 years as our understanding of the disease has progressed. It is now widely recognised that aggressive treatment is required in early disease to prevent the progression to joint destruction.
Summary of treatments available for RA
- Non-steroidal anti-inflammatory drugs (NSAIDs) - Anti-inflammatory, pain relief
- Analgesics (Not NSAIDs) - Symptomatic pain relief
- Corticosteroids (oral, intra-muscular or intra-articular) -
Anti-inflammatory - Disease Modifying Anti-Rheumatic Drugs (DMARDs) -
Prevention/attenuation of disease progression - Biological agents e.g. anti-TNFs - Prevention/attenuation of disease progression
DMARDs
Previously DMARDs were reserved only for patients in the later stages of RA who had joint deformity, now newly diagnosed patients will ideally be commenced on a conventional DMARD (cDMARD) of oral once weekly methotrexate, leflunomide or sulfasalazine. Hydroxychloroquine can be considered in some cases. cDMARDs can cause bone marrow suppression and thus require regular blood test monitoring. Specific tests are also required for some e.g. patients treated with hydroxychloroquine should be tested for visual acuity at specific intervals.
DMARDs are not pain killers and only slow down the
progression of the disease. It may take some months
before any benefit is seen with treatment, it is therefore important that patients with RA receive adequate relief from pain and inflammation
