Crystal Arthritis Flashcards

1
Q

What two crystals account for the majority of crystal induced arthritis?

A

Sodium urate: gout

Calcium pyrophosphate: pseudogout

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2
Q

What is gout?

A

An inflammatory arthritis caused by hyperuricaemia and intra-articular sodium urate crystals. Hyperuricaemia and sodium urate deposition is also often asymptomatic

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3
Q

What are the risk factors for gout?

A
Older age
Male sex
Menopausal status
Family history
Drugs:
- Low dose aspirin
- Cyclosporine or tacrolimus
- Pyrazinamide
- Diuretics
Consumption of meat, seafood or alcohol
Genetic susceptibility
Conditions with a high cell turnover rate i.e. high endogenous purine metabolism e.g. haematological malignancies, psoriasis, chemotherapy induced cell death
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4
Q

Describe the epidemiology of gout

A

10 times more common in men
Occurs rarely before young adulthood (early onset gout suggests a specific enzyme defect)
Seldom seen in premenopausal women

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5
Q

What are the two broad categories of causes of hyperuricaemia?

A

Impaired excretion of uric acid

Increased production of uric acid

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6
Q

What may cause impaired excretion of uric acid?

A

Chronic kidney disease
Drug therapy e.g. thiazide diuretics; low dose aspirin
Hypertension
Lead toxicity
Primary hyperparathyroidism
Hypothyroidism
Increased lactic acid production from alcohol, exercise or starvation

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7
Q

What may cause increased production of uric acid?

A

Increased de-bove purine synthesis (rare)
Increased turnover of purines
Myeloproliferative disorders
Lymphoproliferative disorderes e.g. leukaemia
Carcinoma
Severe psoriasis

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8
Q

What is urate derived from?

A

Breakdown of purines- adenine and guanine- in DNA and RNA

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9
Q

What are the four clinical syndromes that may result from hyperuricaemia and deposition of sodium urate crystals?

A
  • Acute sodium urate synovitis- acute gout
  • Chronic polyarticular gout
  • Chronic tophaceous gout
  • Urate renal stone formation
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10
Q

What is the typical presentation of acute gout?

A

Middle aged male presents with sudden onset of severe pain, swelling and redness of the MTP joint of the big toe. The joint is often inflamed and hot to touch.

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11
Q

What might precipitate an attack of acute gout?

A

Dietary or alcohol excess
Dehydration
Starting a diuretic

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12
Q

How commonly is a joint other than the big toe affected in acute gout?

A

25% of cases

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13
Q

How might an elderly woman on long-term diuretics present with gout?

A

May present with a polyarticular inflammatory arthritis

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14
Q

How does chronic tophaceous gout present?

A

Large, smooth, white deposits (tophi) in the skin and around the joints, particularly on the ear, the fingers and on the Achilles’ tendon

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15
Q

What is the most specific and diagnostic test for gout?

A

Joint fluid microscopy which reveals long, needle shaped crystals which are negatively birefringent under polarized light.

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16
Q

How is gout differentiated from pseudogout?

A
  • Psuedogout is less common in people younger than 50 years of age
  • Pseudogout is more likely to affect wrist and knee joints
  • In pseudogout, chondrocalcinosis (radiographic calcification of cartilage in certain joints) is usually present
  • The definitive diagnosis is finding calcium pyrophosphate crystals in the synovial fluid. These are positively birefringent
17
Q

What is the first line treatment in acute gout?

A

NSAIDs

18
Q

What is the second line treatment in acute gout?

A

Colchicine

19
Q

What is the third line treatment in acute gout?

A

Corticosteroid

20
Q

When is colchicine used to treat gout?

A

Only in patients unable to tolerate NSAIDs due to history of GI bleeding or comorbidities

21
Q

What is the risk of using colchicine?

A

Narrow therapeutic index and extremely toxic in overdose- thus minimal dose should be used

22
Q

What are the side effects of colchicine?

A

Common side effects: diarrhoea, nausea and vomiting

In overdose may cause multi-organ failure

23
Q

How does colchicine work?

A

It inhibits leukocyte micro-tubular formation and migration i.e. reduces the number of white blood cells which travel into the inflamed areas. This helps break the cycle of inflammation and reduces swelling and pain

24
Q

When is allopurinol used to treat gout?

A

Patients who have frequent attacks (>2 per year) despite dietary changes or with gouty tophi or renal impairment

Should not be started during an acute attack as it may prelong the attack or precipitate more attacks. Should not be started for 1 months following an acute attack and NSAIDs or colchicine are given for 4 weeks before and after starting allopurinol to reduce risk of attack being induced

25
Q

How does allopurinol work?

A

Competitively inhibits xanthine oxidase which converts adenine & guanine (purines) to uric acid, thereby lowering serum urate

26
Q

Why should allopurinol not be used acutely?

A

The rapid fall in serum uric acid causes mobilisation of uric acid stores which will prolong the acute attack

27
Q

What is pseudogout?

A

A crystal arthritis caused by calcium pyrophosphate deposition in articular cartilage, which gives the radiological appearance of chondrocalcinosis (linear calcification parallel to the articular surfaces). Shedding of crystals into the joint causes an acute synovitis that can resemble acute gout

28
Q

How does pseudogout present differently from gout?

A

More common in elderly women

Usually affects the knee or the wrist

29
Q

What conditions might pseudogout be associated with in young people?

A

Haemochromatosis

Hyperparathyroidism

30
Q

Describe the pathophysiology of pseudogout?

A

CPP crystals can be shed from cartilage into the articular space, where they may induce an inflammatory response and cause acute CPP arthritis.

However, the conditions under which they elicit inflammation remain unknown as they can also be found in non-inflamed joints between attacks.

31
Q

How is pseudogout diagnosed?

A

Joint fluid microscopy demonstrating small, brick-shaped pyrophosphate crystals which are positively birefringent under polarized light.
OR
Deduced from presence of chrondrocalcinosis on X-ray

32
Q

How is mono- or oligo-articular pseudogout treated?

A

First line: intra-articular steroids + paracetamol for analgesia

If joints are inaccessible to injection or patient declines injection, prescribe NSAIDs (first line) or colchicine (second line) also with paracetamol

If intra-articular steroids fail or are not tolerated and NSAIDs and colchicine are contraindicated, systemic corticosteroids may be used. Due to side effects, a combination of analgesia/joint aspiration/splinting may be preferable in some patients