Crystal Arthritis Flashcards
What two crystals account for the majority of crystal induced arthritis?
Sodium urate: gout
Calcium pyrophosphate: pseudogout
What is gout?
An inflammatory arthritis caused by hyperuricaemia and intra-articular sodium urate crystals. Hyperuricaemia and sodium urate deposition is also often asymptomatic
What are the risk factors for gout?
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
Describe the epidemiology of gout
10 times more common in men
Occurs rarely before young adulthood (early onset gout suggests a specific enzyme defect)
Seldom seen in premenopausal women
What are the two broad categories of causes of hyperuricaemia?
Impaired excretion of uric acid
Increased production of uric acid
What may cause impaired excretion of uric acid?
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
What may cause increased production of uric acid?
Increased de-bove purine synthesis (rare)
Increased turnover of purines
Myeloproliferative disorders
Lymphoproliferative disorderes e.g. leukaemia
Carcinoma
Severe psoriasis
What is urate derived from?
Breakdown of purines- adenine and guanine- in DNA and RNA
What are the four clinical syndromes that may result from hyperuricaemia and deposition of sodium urate crystals?
- Acute sodium urate synovitis- acute gout
- Chronic polyarticular gout
- Chronic tophaceous gout
- Urate renal stone formation
What is the typical presentation of acute gout?
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.
What might precipitate an attack of acute gout?
Dietary or alcohol excess
Dehydration
Starting a diuretic
How commonly is a joint other than the big toe affected in acute gout?
25% of cases
How might an elderly woman on long-term diuretics present with gout?
May present with a polyarticular inflammatory arthritis
How does chronic tophaceous gout present?
Large, smooth, white deposits (tophi) in the skin and around the joints, particularly on the ear, the fingers and on the Achilles’ tendon
What is the most specific and diagnostic test for gout?
Joint fluid microscopy which reveals long, needle shaped crystals which are negatively birefringent under polarized light.
How is gout differentiated from pseudogout?
- 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
What is the first line treatment in acute gout?
NSAIDs
What is the second line treatment in acute gout?
Colchicine
What is the third line treatment in acute gout?
Corticosteroid
When is colchicine used to treat gout?
Only in patients unable to tolerate NSAIDs due to history of GI bleeding or comorbidities
What is the risk of using colchicine?
Narrow therapeutic index and extremely toxic in overdose- thus minimal dose should be used
What are the side effects of colchicine?
Common side effects: diarrhoea, nausea and vomiting
In overdose may cause multi-organ failure
How does colchicine work?
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
When is allopurinol used to treat gout?
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
