In terms of MRCP, you need to expand the above knowledge to include the following...
Gout usually presents as a single, swollen, hot, painful joint. If the joint affected is the big toe, it is called a podagra.
Microscopy of joint fluid would reveal negatively birefrigent needle-shaped monosodium urate crystals.
Uric acid may be >450micromols - but equally may be normal in an acute attack.
CRP is usually raised, but if the question shows a raised WCC too start thinking about different diagnoses, for example septic arthritis.
Gout may be either primary or secondary.
Primary gout may be:
- idiopathic - usually due to decreased excretion of uric acid
- associated with Lesch-Nyhan Syndrome (to be covered in a very brief battle tomorrow)
Secondary gout can broadly be divided into things which cause increased production/intake of urate, and things which decrease its excretion.
Causes of increased production/intake include:
- myeloproliferative/lymphoproliferative disorders
- psoriasis
- cytotoxic drugs
- food - beer, yeast, seafood, liver, kidney
- exercise
- fits
- acidosis
Causes of decreased excretion include:
- renal failure
- diuretics
- low dose aspirin
- alcohol
- lead poisoning
XR should show a normal joint space (may be decreased in late disease) and large punched-out erosions distant from the joint margins.
Treatment is NSAIDs - if these are contraindicated, colchine can be used.
Prophylaxis is with allopurinol (a xanthine oxidase inhibitor). It should be started 2 to 3 weeks after an acute attack if:
- >1 attack
- tophi present
- renal disease
- urate stones
- Lesch-Nyhan syndrome
- cytotoxic drugs used (in which case it should be given before any episodes of gout)
So after that quick whizz through gout, lets embrace is near-cousin pseudo-gout...
