Crystal arthropathy (gout, pseudogout) Flashcards

1
Q

How long does a flare of gout last?

A

~5 days - this is less than most other forms of inflammatory arthritis

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2
Q

Who is most affected by pseudogout?

A

Older women

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3
Q

Which joints are most affected by pseudogout?

A

Wrists and knees

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4
Q

What dermatological side effect is associated with allopurinol use?

A

SJS - if any rash appears then start Febuxostat instead (XO inhibitor)

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5
Q

How do you manage an acute flare of pseudogout?

A

Intra-articular corticosteroid injection

NB: there is no role for allopurinol or hydroxychloroquine in management of calcium pyrophosphate dihydate deposition arthritis

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6
Q

What is the regimen for starting allopurinol?

A

Allopurinol 100mgs OD, escalating by 100mgs every two weeks to 300mgs OD

+ colchicine 500mcg BD (because allopurinol alone can precipitate flares)

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7
Q

What is the EULAR classification of CPPD?

A

They do not use the term ‘pseudoarthritis’

  • Type A - acute CPP arthritis usually mono-articular, affecting large joints
  • Type B - chronic CPP inflammatory arthritis, affecting large and small joints
  • Type C - OA with CPP attacks with inflammation
  • Type D - OA with CPP but no inflammation
  • Type E - ianthanic/asymptomatic
  • Type F - pseudo-neuropathic which is destructive
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8
Q

What is deposited in pseudogout? Which joints are affected?

A

Calcium pyrophosphate

Knees, wrists, shoulders, ankles, elbows, or hands can be affected typically in older people.

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9
Q

What is seen on a radiograph in pseudogout?

A

Chondrocalcinosis - although this alone will miss 60% of cases

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10
Q

What is calcium pyrophosphate produced by?

A

Chondrocytes

CPP crystals can be shed from cartilage into the articular space to cause an inflammatory response.

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11
Q

What are the risk factors for pseudogout?

A
  • Advanced age
  • Injury esp meniscal
  • Hyperparathyroidism
  • Haemochromatosis
  • FH
  • Hypomagnesaemia
  • Hypophosphatasia
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12
Q

What are the clinical features of pseudogout?

A
  • Painful and tender joints
  • OA-like involvement of joints (wrists, shoulders)
  • Sudden worsening of OA
  • Red and swollen joints
  • Joint effusion and fluctuance

Other:

  • Fever and malaise - uncommon
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13
Q

What investigations would you do for pseudogout?

A

Bloods/bedside:

  • Serum calcium
  • Serum parathyroid hormone
  • Iron studies
  • Serum magnesium
  • Serum ALP - to exclude hypophosphatasia

Imaging/invasive:

  • Arthrocentesis with synovial fluid analysis
  • XR joints
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14
Q

What is seen on synovial fluid analysis in pseudogout?

A

Intracellular or extracellular positively birefringent rhomboid-shaped crystals under polarised light confirms CPPD; fluids are often bloody

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15
Q

What is the mangement of pseudogout?

A

1st line:

  • Simple analgesia e.g. paracetamol
  • Intra-articular steroids - preferred for an acute attack ; triamcinolone hexacetonide is the longest-acting and most used.

2nd line: NSAIDs - COX-2 have lower GIT side-effects but same CVD risk

For those with polyarticular disease = systemic steroids

Surgery - in recurrent involvement associated with severe joint degeneration

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16
Q

What are the complications of pseudogout and its management?

A

Intra-articular corticosteroid-related adverse effects e.g. bleeding and bruising around injection site

17
Q

What is the prognosis in pseudogout?

A

Most will recover over days to weeks but many will relapse

18
Q

Define gout.

A

Gout is a syndrome characterised by:

  • hyperuricaemia and deposition of urate crystals causing attacks of acute inflammatory arthritis;
  • tophi around the joints and possible joint destruction;
  • renal glomerular, tubular, and interstitial disease;
  • and uric acid urolithiasis.
19
Q

Which joints are most affected in gout?

A
  • first toe (podagra),
  • foot,
  • ankle,
  • knee,
  • fingers,
  • wrist,
  • elbow;

However, it can affect any joint.

20
Q

How common is gout?

A

Affects 3% to 6% of men and 1% to 2% of women

Gout is rare in pre-menopausal women

21
Q

What are the risk factors for gout?

A
  • older age
  • male sex
  • use of drugs including aspirin, ciclosporin (cyclosporine), tacrolimus, or pyrazinamide
  • consumption of meat, seafood, or alcohol
  • genetic susceptibility
  • conditions with a high cell turnover rate
22
Q

What are the causes of gout?

A

Aetiology is hyperuricaemia

Hyperuricaemia is due to renal under-excretion of urate in 90% of cases and to over-production in 10%,

23
Q

What medications increase uric acid levels?

A

Increasing uric acid re-absorption:

  • aspirin
  • ciclosporin
  • tacrolimus
  • pyrazinamide

Reduced excretion of uric acid:

  • diuretics

Increased uric acid production:

  • chemotherapy
  • haematological cancers
24
Q

Why does gout commonly present as podagra?

A

Solubility of urate in the joints depends on temperature, pH, non-aggregated proteoglycans, and other factors.

1st MTP is a cool part of the body

25
What are the clinical features of gout?
* **Monoarticular/few affected joints** * **Sudden onset to maximum pain within 1 day** - patients can often indicate hour, most severe pain experienced * **Erythema and warmth** * **Redness over joints** * **Limited range of movement** - due to pain * **Joint stiffness-** morning * **Foot involvement** * **Tophi** - hard subcutaneous nodules (tophi) over extensor surface of elbows, knees, Achilles, hands, feet, helix of ears.
26
What is the management of acute gout?
**1st line:** * NSAIDs e.g. naproxen 500mg BD for 2 weeks * OR Corticosteroids - oral or injections * OR Colchicine - minimal effective dose **2nd line**: IL-1 inhibitors e.g. anakinra, canakinumab - only usefd in acute flare where patients are refractory/intolerant to other treatments.
27
What is the management of chronic gout?
_1st line:_ * **Allopurino**l + **NSAIDs/colchicine** - 100 mg orally once daily initially, increase by 100 mg/day increments every week according to serum urate level, maximum 800 mg/day;prophylactic NSAID/colchicine when initiating/tapering allopurinol, continued for 3-6 months _2nd line:_ * **Febuxostat + NSAID/colchicine** - XOi, should not be taken during acute attack; as above _3rd line:_ * **Probenecid/sulfinpyrazone + NSAID/colchicine -** uricosuric drugs _4th line_ * **Pegloticase +NSAID/colchicine** - pegylated recombinant mammalian uricase, if all else fails
28
What measures should be taken to prevent gout?
Avoid excessive alcohol consumption, diuretic use, and weight gain.
29
What investigations should be done for gout?
*Clinical diagnosis in those with reliable history of recurrent acute monoarthritis of the 1st MTP. Confirm with arthrocentesis.* * **Uric acid level** * **Arthrocentesis with synovial fluid analysis** - shows WCC \>2x10^9/L and strongly negatively birefringent needle-shaped crystals under polarised light * **XR** - not useful but may show periarticular erosions with overhanging edge or punched-out appearance
30
What are the complications of gout?
**Acute uric acid nephropathy** - usually only with very high levels of uric acid e.g. in those treated with cytotoxic agents **Nephrolithaisis** - may be over 10% prevalence
31
What is the prognosis with gout?
If not treated risk of recurrence after the first attack is 62%, 78%, and 84% during the first, second, and third year, respectively Untreated gout can cause tophi and severe debilitating arthritis (usually both 20yrs after first attack)
32
Which HLA is associated with risk of allopurinol hypersensitivity reaction?
HLA-B\*58:01 - common in Korea, Han Chinese, Thai