Gout Flashcards

1
Q

What crystal is deposited in gout?

A

Monosodium urate (MSU)

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2
Q

What causes gout? What is the threshold that defines this?

A

Hyperuricaemia

Urate > 0.41 mmol/L

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3
Q

What is the source of urate?

A

Degradation product of purines:

  • cell turnover
  • dietary intake
  • de novo synthesis
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4
Q

What joints are most commonly affected?

A

Metatarsophalangeal joint
Mid-foot
Knee
Less commonly can cause oligo/polyarthropathy

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5
Q

Clinical presentation:

  1. time course
  2. symptoms
A
  1. acute onset, lasting 7-10 days before spontaneous resolution (if no treatment used)
  2. Intensely painful arthropathy
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6
Q

What are gouty tophi? Why to they form and what made from?

A

Nodules consisting of MSU crystals and chronic granulomatous inflammatory tissue

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7
Q

What is the prevalence of gout?

What countries have particularly high rates of gout?

A

2.7 - 6.7% in countries with a western lifestyle

Taiwan and Maori people

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8
Q

What are the risk factors for Gout?

A

Hyperuricaemic and the things that cause it:

  1. increased production: high cell turnover (psoriasis, myeloproliferative disorders)
  2. High dietary intake: (alcohol), (fructose), beer, meats, seafood
  3. Reduced excretion: CKD, metabolic syndrome, diuretic use
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9
Q

Other than hyperuricaemia, what other factors predispose to gout?

A

Joint trauma, medical illness, surgery, dehydration, advancing age, male sex

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10
Q

What proportion of people with hyperuricaemia develop gout?

A

The minority of people with hyperuricaemia develop gout - it is necessary but not sufficient.

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11
Q

Do dietary or genetic effects have a greater impact on hyperuricaemia?

A

Genetic

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12
Q

What are the steps in pathophysiology of gout?

A
  1. Hyperuricaemia
  2. Crystal formation (reduced solubility, nucleation, crystal growth)
  3. Crystals interact with macrophages to activate NLRP3 inflammasome resulting in release of IL-1beta and inflammatory infiltration along with cardinal signs
  4. Resolution when dying neutrophils result in NETs, sequestration of pro-inflammatory cytokines
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13
Q

What are the microscopy findings consistent with gout?

A

negative birefringent, needle-shaped crystals

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14
Q

Typical clinical manifestations

Atypical clinical manifestations

A
  1. acute episodes involving joint structures, asymmetric, self-limiting
  2. development of tophi without flares (people taking corticosteroids), multiple joints involved (more common with chronic hyperuricaemia), persistent symptoms (not self-limiting), proximal large joints
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15
Q

Diagnosis

A

Gold-standard is microscopy based

classification criteria based diagnosis is less accurate

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16
Q

Differential diagnoses

A
  1. CCP crystal arthropathy
  2. psoriatic arthritis
  3. reactive arthritis
  4. Lyme disease
  5. septic arthritis
17
Q

What imaging can be useful in the diagnosis of gout?

A
  1. Ultrasonography - “double-contour” sign

2. Dual energy CT

18
Q

Is uric acid always elevated during a gout flare?

A

No, can be normal, especially in post-surgical flares

Consider rechecking after resolution of flare.

19
Q

What effect does bariatric surgery have on uric acid levels in the obese?

A

reduces serum levels

reduces incidence of gout by 34%

20
Q

Management:

1. Gout flares

A
1. NSAIDs (naproxen 500mg BD), colchicine (1mg followed by 0.5mg 1 hour after), corticosteroids - alone or in combination, 
##canakinumab (IL-1beta MAB, rarely used due to cost but it is effective)
# Anakinra non-inferior to NSAIDs, colchicine, prednisolone
21
Q

Management

  1. Urate lowering therapy
    - medication classes
    - practice points
A
  • xanthine oxidase inhibitors (allopurinol, febuxostat)
  • uricosuric drugs (probenecid)
  • recombinant uricase (pegloticase)
    -Recommended to treat to target (<0.36 mmol/L) to prevent progressive joint damage and further acute flares (consider lower target <0.3 mmol/L in tophaceous gout)
    Commence if there is an established diagnosis of gout with more than one flare per year, tophi, CKD or urolithiasis
    Can be safely started during a flare but start at low dose
    Monitor serum urate levels
22
Q

Management

3. Anti-inflammatory prophylaxis

A

Can be used (colchicine or low dose NSAIDs)

23
Q

Management

4. Lifestyle modification

A

Little data, however, rheumatology guidelines recommend the following:
- weight loss, reduced intake of purine rich foods, avoidance of EtOH and fructose, low-fat dairy

24
Q

Management

5. Nurse led care

A

Comprehensive nurse led care has been found to be superior to GP care

25
Q

What are some AEs for xanthine oxidase inhibitors?

A

Allopurinol:

  1. allopurinol hypersensitivity syndrome (AHS)
    - first few months post commencement, associated with HLA-B*5801 (Asian, esp. Chinese populations), CKD, concomitant diuretic use
  2. Febuxostat
    - may be associated with increased cardiovascular events