Rheumatology - Gout Flashcards

1
Q

What is gout?

A

-Inflammatory arthritis associated with hyperuricaemia and intra-articular Na+ urate crystals

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2
Q

What is the pathogenesis of gout

A
  • 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.
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3
Q

What are clinical features of gout?

A
  • 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
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4
Q

Ix for gout

A
  • 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
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5
Q

Rx: basic rx (not allopurinol) for gout

A
  • 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)
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6
Q

What is allopurinol MOA?

A

◦ Allopurinol MOA: blocks enzyme xanthine oxidase, which converts xanthine into uric acid.

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7
Q

What are the S/E of allopurinol

A

Most common: skin rashes and grastro-intestinal intolerance

Most serious: bone marrow suppression or hypersensitivity reaction (with rash, fever, eosinophilia, hepatitis)

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8
Q

What is the protocol for taking allopurinol?

A

◦ 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

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9
Q

What are the three types of calcium pyrophosphate deposition (CPPD)?

A

• 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

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10
Q

What are the risk factors for CPPD?

A
  • Old age
  • Hyperparathyroidism
  • Haemochromatosis
  • Hypophosphataaemia
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11
Q

What Ix do you do for CPPD?

A

• 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

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12
Q

What is the Mx for CPPD?

A
  • Cool packs
  • Rest
  • Aspiration: greatly reduces pain
  • Intra-articular steroids
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13
Q

What is the Rx for CPPD?

A
  • Intra-articular steroids
  • NSAIDs
  • Colchicine (used with caution)
  • Chronic CPPD: methotrexate and hydroxychloroquine can be used
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