Gout Flashcards

1
Q

How should you dose allopurinol in CKD?

A

Smaller initial dose (e.g. 50 mg daily or 2nd daily) and slower increments to reach maximal dose

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2
Q

What is the reason for increased flares when starting allopurinol?

A

Allopurinol lowers serum uric acid . This causes movement of precipitated MSU crystals which makes it more prone to immune recognition, leading to a flare

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3
Q

Gout is rare in men < 25 and pre-menopausal women. True or false?

A

True.
Common in older men, Pacific Islanders and SE Asians. Estogren is uricoseric and hence lower incidence in pre-menopausal women.

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4
Q

What are the causes of hyperuricaemia ?

A

Urate overproduction: dietary purines, accelerated ATP degradation in heavy alcohol use, increased nucleotide turnover in haem disease

Urate under-excretion 90% caused by this
CKD, medications (HCT, diuretics)

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5
Q

What is immune pathway that causes gout?

A

MSU crystals detected by TLR 2 and TLR 4 –> pro-inflammatory cytokines —> inflammatory response.

Coated with IgG –> inflammatory response
Coated with apolipoprotein –> undergo phagocytosis –> induce less inflammation

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6
Q

What are the risk factors for gout?

A

Renal impairment, alcohol, medications (diuretics, tacrolimus, cyclosporin, low dose aspirin) diet, male gender, older age, family history, ethnic background

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7
Q

What is the most commonly affected joint in gout?

A

1st MTP (50% cases)

Following that, ankles and knees
Involvement of hands, wrist and elbows - suggests severity

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8
Q

What are clinical features of gout?

A

Rapid onset of painful, warm, erythematous and swollen joint with fevers
Presence of tophi is a sign of chronicity and severity

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9
Q

How does gout cause renal disease?

A

Urate nephropathy
1) MSU in interstitial tissues (slower decline in renal function)
2) MSU in collecting ducts and ureters (usually TLS) –> AKI and CKD

Uric acid nephrolithiasis - uric acid stones (10-25% gout patients)

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10
Q

How is gout diagnosed?

A

Gold standard is joint aspiration showing MSU crystals - needle shaped and neg birefringent

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11
Q

Why is serum uric acid often normal during a flare?

A

Flare causes inflammation involving IL-6 which is uricosuric - paradoxically low or normal uric acid

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12
Q

What is seen on imaging with gout?

A

X ray changes are late
- tophi cause soft-tissue shadowing
- periarticular “rat-bite” erosions

US: double contour sign around articular margin

DECT: allows urate crystals to be identified, only validated for feet

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13
Q

How is gout managed?

A

Aim is to reduce serum uric acid
Saturation point is 0.40
Targets:
- no tophi/erosions aim <0.36
- tophi or erosions < 0.30

Urate-lowering therapy
Flare prophylaxis
Flare management
Metabolic management
Dietary suggestions

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14
Q

What are management options for flares?

A

NSAIDS (indomethacin, shorter acting - ibuprofen, diclofenac)
Colchicine - 0.5 mg daily or BD- most effective in first 36 hours
Prednisone 0.25-0.5 mg/kg for 5 days then wean
IA steroids
IL-1 antagonist (anakinra) and ACTH

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15
Q

Medications with mild uricosuric effects

A

amlodipine , losartan, fenofibrate, leflunomide, atorvastatin, rosuvastsatin

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16
Q

What can be used for flare prophylaxis?

A

Low dose NSAIDs
Colchicine 0.5 mg daily or BD
Low dose prednisone

17
Q

What are indications for urate lowering therapy ?

A

Indications: tophi, recurrent flares

  1. Xanthine oxidase inhibitors - stops conversion of purines to uric acid e.g. allopurinol and febuxostat .
  2. Uricosuric : reduce tubular reabsorption of uric acid e.g. probenecid

Look at eTG for dose suggestions

18
Q

What are drug interactions to be aware of ?

A

Azathioprine and mercaptopurine is metabolised by xanthine oxidase –> can cause azathioprine toxicity

19
Q

What genetic test requested before allopurinol?

A

HLAB5801 - allopurinol
Screen Asian patients - Chinese, Thai and Korean

20
Q
A