Rheumatology - Gout Flashcards
What is gout?
-Inflammatory arthritis associated with hyperuricaemia and intra-articular Na+ urate crystals
What is the pathogenesis of gout
- Many patients there is no obvious cause
- Impaired excretion of uric acid: CKD, drugs (thiazidess, low dose aspirin, HTN, hypothyroidism, G6PD deficiency, increased lactic acid production)
- Increased production of uric acid: very weird diseases due to de novo mutations
- Acute gout precipitation: ingestion of polymorpholeucocytes of Na-Urate crystals causing the release of pro-inflammatory cytokines from phagosomes and complement activation.
What are clinical features of gout?
- Typically middle-aged male with sudden onset of agonising pain, swelling and redness of the first MTP joint
- Attacks can occur any time but may be precipitated by too much food/alcohol/dehydration/new diuretic rx
- Attacks last approx 7 days, in 25% there is another joint affected as well.
- Severe attacks: difficult to distinguish clinically from infective cellulitis
Ix for gout
- Clinical picture often diagnostic + rapid response to NSAIDs or colchicine
- Joint fluid microscopy: most specific test - will show needle-shaped monosodium urate crystals displaying negative birefringence under polarised light
- Serum uric acid: usually raised (>600 micro-mol/L) - if not recheck after few weeks b/c level falls immediately after acute attack.
- Serum urea and creatinine: monitored for signs of renal impairment
Rx: basic rx (not allopurinol) for gout
- NSAIDs/coxibs at high doses rapidly reduce pain/swelling
- analgesia: Naproxen and diclofenac
- Dietary advice: advice pts to reduce alcohol intake (esp beer), total calorie and cholesterol intake and avoid purine rich food (shellfish/spinach)
What is allopurinol MOA?
◦ Allopurinol MOA: blocks enzyme xanthine oxidase, which converts xanthine into uric acid.
What are the S/E of allopurinol
Most common: skin rashes and grastro-intestinal intolerance
Most serious: bone marrow suppression or hypersensitivity reaction (with rash, fever, eosinophilia, hepatitis)
What is the protocol for taking allopurinol?
◦ Can only use Allopurinol when attacks are frequent and severe or have renal impairment/tophi or when pt can’t tolerate NSAIDs or colchicine.
◦ Cannot start within 1 month of acute attack
◦ Need NSAIDs/Colchicine cover 2-4 weeks before starting Allopurinol and can stop them 4 weeks after.
◦ Start at 100mg/24h and titration increasing every 4 weeks until plasma urate levels are <300 micromol/L
*once people start allopurinol they will normally take it lifelong and cannot stop it during attacks
What are the three types of calcium pyrophosphate deposition (CPPD)?
• Acute CPP crystal arthritis: like gout, causes acute monoarthropathy of typically larger joints in elderly patients (knee and wrist)
◦ Usually spontaneous and self limiting
◦ Can be provoked by illness, surgery or trauma
• Chronic CPPD: inflammatory RA like (symmetrical) polyarthritis and synovitis
• Osteoarthritis with CPPD: chronic poly articular osteoarthritis with superimposed acute CPP attacks
What are the risk factors for CPPD?
- Old age
- Hyperparathyroidism
- Haemochromatosis
- Hypophosphataaemia
What Ix do you do for CPPD?
• Polarised light microscopy of synovial fluid shows weakly birefringent crystals.
• X-ray: soft tissue calcium deposition
*Must exclude septic arthritis and send joint fluid for culture
What is the Mx for CPPD?
- Cool packs
- Rest
- Aspiration: greatly reduces pain
- Intra-articular steroids
What is the Rx for CPPD?
- Intra-articular steroids
- NSAIDs
- Colchicine (used with caution)
- Chronic CPPD: methotrexate and hydroxychloroquine can be used