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Rheumatology

Rheumatology . What could this be?. Differential diagnosis. Gout Infection; septic arthritis, cellulitis Pseudogout Rheumatoid arthritis Reactive arthritis Osteoarthritis Psoriatic arthritis Seronegative spondyloarthropathy haemachromatosis. Gout- acute attack.

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Rheumatology

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  1. Rheumatology

  2. What could this be?

  3. Differential diagnosis • Gout • Infection; septic arthritis, cellulitis • Pseudogout • Rheumatoid arthritis • Reactive arthritis • Osteoarthritis • Psoriatic arthritis • Seronegative spondyloarthropathy • haemachromatosis

  4. Gout- acute attack • sudden onset of acute pain that lasts for 1 to 2 weeks • common sites: • metatarsophalangeal joint of the big toe (75%) • ankle joint • finger joints • olecranonbursae • features of joint: • overlying skin is red and shiny • swollen and hot • tender • During the attack fever, nausea and mood swings may be present. • In rare instances, monosodium urate may be deposited in the conjunctiva and cause sore eyes.

  5. More common in men than women( 3.6:1) • Prevalence is 1.4% • Incidence is 1-2/1000 in men • Rare <25yrs of age

  6. Gout- acute attack • A disorder of purine metabolism resulting in raised uric acid levels in the blood • Uric acid is a waste product from the breakdown of purine residues of nuclei acid • 2/3rds is excreted via the kidney and 1/3rd by the gut • Aetiology • Primary gout (95%) inherited disorder that causes over production or under-excretion of uric acid. Underlying defect not known • Secondary gout (5%) • Increased formation • Reduced excretion • Drugs/toxins that cause over-production or under-excretion of uric acid

  7. Increased formation: • increased nuclei acid turnover: • lymphoma, • psoriasis, • hameolysis, • myloproliferative disorder, • enzyme deficiencies such as glucose 6 phosphates • Increased production: • high dietary intake, • fructsoe , • lesch-Nyhan syndrome • Reduced excretion; • chronic renal failure, • hyperparatyrdoidism, • lactic acidosis ( e.g. alcohol, exercise)

  8. Drugs that can raise plasma urate levels, • aspirin (low-dose) • Ciclosporin • cytotoxic drugs • diuretics (thiazide and loop) • Ethambutol • nicotinic acid • pyrazinamide • tacrolimus. • Any exposure to lead

  9. Whilst taking Mr H’s history you realise he has a high dietary intake of purines. What foods can cause this?

  10. Alcohol; • Beer • Stout • Port • Fortified wines • Food • Liver • Kidneys • Red meat • Seafood (herring, shell fish and sardines) • Certain vegetables (asparagus, beans, cauliflower, lentils, mushrooms, and spinach)

  11. What investigations would you perform to aid Mr H’s digagnosis?

  12. No initial investigations are required when managing a patient with gout-like symptoms • The following may be considered • Joint aspiration • Serum uric acid or plasma urate • Joint radiography • bloods

  13. American College of Rheumatology criteria for the diagnosis of acute gouty arthritis • The 'gold standard' for diagnosing gout is demonstration by microscopy of urate crystals in synovial fluid or in a tophus. • However, testing for urate crystals in joint fluid or tophi is often not practical. • In 1977, the American College of Rheumatology (ACR) published classification criteria for the diagnosis of acute gouty arthritis [Wallace et al, 1977]. • The criteria supported a diagnosis of acute gouty arthritis if six or more of the following were met: • More than one attack of acute arthritis. • Maximal inflammation developing within 1 day of onset. • Monoarthritis attack (90% of initial attacks are monoarticular). • Redness over affected joint. • Unilateral attack on the first metatarsophalangeal (big toe) joint. • Unilateral attack on the tarsal joint. • Tophus (proven or suspected). • Hyperuricaemia. • Asymmetric swelling within a joint on radiography. Asymmetric swelling can also be found on examination, but the data from which the ACR criteria were derived did not include this. • Subcortical cysts without erosions on radiography. • No organisms found on culture of synovial fluid.

  14. How would you manage Mr H?

  15. Management of an acute attack • Rest • Increased fluid intake • Medication • NSAIDs until 48hrs after attack has settled (naproxone, diclofenac or indomethacin) • Colchicines if NASIDs contraindicated • If above two contraindicated consider oral steroids • If no improvement after 12-24hrs then review the diagnosis

  16. Indomethacin • initial dose 50-100 mg orally • continue with 50 mg every 4 to 6 hours until symptoms subside • continue then with lower doses at longer intervals for about one week, for example 25 mg tds

  17. Colchicine • Useful in the following • Peptic ulcer disease • In patients with hypertension • Can be used in combination with anticoagulants • Contraindictaed in the following • Sever heart failure • Lover or renal impairment • Blood dyscrasia/bone marrow disease • Dose • 1 mg, then 500 mcg every 2-3 hours until the pain resolves, or the patient develops diarrhoea, or a total dose of 6mg has been taken. Treatment with colchicine should no be repeated within 3 days. • However reports suggest that these common unwanted effects may be avoided, while maintaining a beneficial effect, by reducing the dose to 500mcg up to three times daily • Side effects • diarrhoea and gastric irritation. • Rare side effects include renal failure, myopathy, cardiac arrhythmia, respiratory failure and peripheral neuropathy.

  18. Mr H’s acute attack of gout settles but he presents 3 months later with another attack – when would you consider commencing medication to prevent further attacks?

  19. prominent tophi • urate renal calculi • renal impairment • two or more attacks of gout per year • evidence of joint damage such as radiological changes • in practice, the decision concerning whether to initiate prophylaxis is often left to patient preference

  20. Where possible, correct any exacerbating factors especially: • consider stopping or reducing diuretic treatment • reconsider aspirin therapy • reduce alcohol intake • reduce intake of purine-rich foods • Drug treatment • the xanthineoxidase inhibitor allopurinal reduces the synthesis of uric acid • drugs such as probenecid and sulfinpyrazone increase urinary excretion of uric acid (uricosuric) • Caution • initiation of prophylactic therapy may provoke an acute gout attack and so an NSAID or colchicine should be given concomitantly for at least the first 3 months • prophylactic therapy should not be started during an acute attack because it can prolong symptoms • if an acute attack occurs during prophylactic treatment, this should be continued at the same dose while the acute attack is treated with an NSAID or colchicine.

  21. Allopurinol • 100mg daily after food • Increasing by 100mg every 2 weeks until the serum uric acid <300nmmol/l • Doses over 300mg should be taken over 2-3 divided doses • Very rare to need doses over 900mg • Monitor with serum uric acid 3 monthly in first year and then annually thereafter aiming for level <300mmool/l • Caution in those with renal impairment • Probenecid • commenced at 250 mg twice daily after food. • dose is increased after a week to 500 mg twice daily. • The maximum dose is 2 g daily in divided doses, titrated according to the plasma uric acid concentration. • Sulfinpyrazone • initial dose is 100-200 mg daily with food. • Over 2-3 weeks the daily dose is increased to 600 mg. • As uric acid levels normalise the maintenance dose may be reduced to as low as 200 mg.

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