Crystal arthropathy Flashcards
What is gout?
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium.
What causes gout?
Gout is caused by chronic hyperuricaemia (uric acid > 0.45 mmol/l).
What are some drug causes of gout?
Diuretics (thiazides, furosemide), ciclosporin, alcohol, cytotoxic agents, pyrazinamide, and aspirin.
How does aspirin relate to gout?
It was previously thought that only high-dose aspirin could precipitate gout. However, low-dose (e.g. 75mg) also increases the risk of gout attacks.
What should be considered when prescribing aspirin for gout patients?
The risk of gout attacks needs to be balanced against the cardiovascular benefits of aspirin.
What did the study show regarding allopurinol and aspirin?
The study showed that patients coprescribed allopurinol were not at an increased risk of gout attacks.
What is gout?
Gout is a form of inflammatory arthritis characterized by episodes of intense pain, swelling, and erythema.
How long do gout flares typically last?
Patients typically have episodes lasting several days and are often symptom-free between episodes.
What is the time frame for maximal intensity of acute gout episodes?
The acute episodes typically develop maximal intensity within 12 hours.
What are the main features of gout?
The main features of gout include significant pain, swelling, and erythema.
Which joint is most commonly affected in first presentations of gout?
Around 70% of first presentations affect the 1st metatarsophalangeal (MTP) joint.
What is the historical term for gout attacks affecting the 1st MTP joint?
Attacks of gout affecting this area were historically called podagra.
What are other commonly affected joints in gout?
Other commonly affected joints include the ankle, wrist, and knee.
What can happen if gout is untreated?
If untreated, repeated acute episodes of gout can damage the joints, resulting in a more chronic joint problem.
What does NICE recommend for investigating suspected gout?
NICE recommends measuring uric acid levels in suspected gout during the acute setting.
What uric acid level supports a diagnosis of gout?
A uric acid level ≥ 360 umol/L is seen as supporting a diagnosis.
What should be done if uric acid level is < 360 umol/L during a flare?
If uric acid level < 360 umol/L during a flare and gout is strongly suspected, repeat the uric acid level measurement at least 2 weeks after the flare has settled.
What is observed in synovial fluid analysis for gout?
Needle shaped negatively birefringent monosodium urate crystals under polarised light.
What are the radiological features of gout?
Radiological features include joint effusion, well-defined ‘punched-out’ erosions, relative preservation of joint space until late disease, eccentric erosions, and no periarticular osteopenia.
What may be seen in soft tissues of patients with gout?
Soft tissue tophi may be seen.
What is gout?
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium due to chronic hyperuricaemia (uric acid > 450 µmol/l).
What are the first-line treatments for acute gout management?
NSAIDs or colchicine are first-line treatments.
What is the recommended maximum dose of NSAIDs for gout?
The maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled.
What gastroprotection may be indicated during acute gout management?
Gastroprotection, such as a proton pump inhibitor, may also be indicated.
How does colchicine work?
Colchicine inhibits microtubule polymerization by binding to tubulin, interfering with mitosis, and inhibits neutrophil motility and activity.
What is a key side effect of colchicine?
The main side effect of colchicine is diarrhoea.
What should be considered if NSAIDs and colchicine are contraindicated?
Oral steroids may be considered, typically a dose of prednisolone 15mg/day.
What should be done if the patient is already taking allopurinol?
If the patient is already taking allopurinol, it should be continued.
When should urate-lowering therapy (ULT) be offered?
ULT should be offered to all patients after their first attack of gout.
When is ULT particularly recommended?
ULT is particularly recommended if there are >= 2 attacks in 12 months, presence of tophi, renal disease, uric acid renal stones, or for prophylaxis if on cytotoxics or diuretics.
What has traditionally been taught about starting ULT after an acute attack?
It has traditionally been taught that ULT should not be started until 2 weeks after an acute attack.
What did the BSR update in 2017 regarding ULT?
The BSR updated their guidelines to support a delay in starting ULT until inflammation has settled.
What is the first-line ULT?
Allopurinol is the first-line urate-lowering therapy.
What is the initial dose of allopurinol?
The initial dose of allopurinol is 100 mg od, titrated to aim for a serum uric acid of < 360 µmol/l.
What should be considered when starting allopurinol?
Colchicine cover should be considered when starting allopurinol; NSAIDs can be used if colchicine cannot be tolerated.
What is the second-line agent when allopurinol is not tolerated?
The second-line agent is febuxostat, also a xanthine oxidase inhibitor.
What is uricase and its purpose?
Uricase is an enzyme that catalyzes the conversion of urate to allantoin, and it can be used in refractory cases of gout.
What is pegloticase used for?
Pegloticase can achieve rapid control of hyperuricemia in patients with persistent symptomatic and severe gout despite adequate ULT.
What lifestyle modifications can help manage gout?
Reduce alcohol intake, lose weight if obese, and avoid foods high in purines such as liver, kidneys, seafood, oily fish, and yeast products.
What should be considered regarding precipitating drugs?
Consideration should be given to stopping precipitating drugs, such as thiazides.
What is the effect of losartan in gout management?
Losartan has a specific uricosuric action and may be suitable for patients with coexistent hypertension.
How can increased vitamin C intake affect serum uric acid levels?
Increased vitamin C intake may decrease serum uric acid levels.
What is gout?
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium due to chronic hyperuricaemia (uric acid > 450 µmol/l).
What are the first-line treatments for acute gout management?
NSAIDs or colchicine are first-line treatments.
What is the recommended maximum dose of NSAIDs for gout?
The maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled.
What gastroprotection may be indicated during acute gout management?
Gastroprotection, such as a proton pump inhibitor, may also be indicated.
How does colchicine work?
Colchicine inhibits microtubule polymerization by binding to tubulin, interfering with mitosis, and inhibits neutrophil motility and activity.
What is a key side effect of colchicine?
The main side effect of colchicine is diarrhoea.
What should be considered if NSAIDs and colchicine are contraindicated?
Oral steroids may be considered, typically a dose of prednisolone 15mg/day.
What should be done if the patient is already taking allopurinol?
If the patient is already taking allopurinol, it should be continued.
When should urate-lowering therapy (ULT) be offered?
ULT should be offered to all patients after their first attack of gout.
When is ULT particularly recommended?
ULT is particularly recommended if there are >= 2 attacks in 12 months, presence of tophi, renal disease, uric acid renal stones, or for prophylaxis if on cytotoxics or diuretics.
What has traditionally been taught about starting ULT after an acute attack?
It has traditionally been taught that ULT should not be started until 2 weeks after an acute attack.
What did the BSR update in 2017 regarding ULT?
The BSR updated their guidelines to support a delay in starting ULT until inflammation has settled.
What is the first-line ULT?
Allopurinol is the first-line urate-lowering therapy.
What is the initial dose of allopurinol?
The initial dose of allopurinol is 100 mg od, titrated to aim for a serum uric acid of < 360 µmol/l.
What should be considered when starting allopurinol?
Colchicine cover should be considered when starting allopurinol; NSAIDs can be used if colchicine cannot be tolerated.
What is the second-line agent when allopurinol is not tolerated?
The second-line agent is febuxostat, also a xanthine oxidase inhibitor.
What is uricase and its purpose?
Uricase is an enzyme that catalyzes the conversion of urate to allantoin, and it can be used in refractory cases of gout.
What is pegloticase used for?
Pegloticase can achieve rapid control of hyperuricemia in patients with persistent symptomatic and severe gout despite adequate ULT.
What lifestyle modifications can help manage gout?
Reduce alcohol intake, lose weight if obese, and avoid foods high in purines such as liver, kidneys, seafood, oily fish, and yeast products.
What should be considered regarding precipitating drugs?
Consideration should be given to stopping precipitating drugs, such as thiazides.
What is the effect of losartan in gout management?
Losartan has a specific uricosuric action and may be suitable for patients with coexistent hypertension.
How can increased vitamin C intake affect serum uric acid levels?
Increased vitamin C intake may decrease serum uric acid levels.
What is gout?
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium.
What causes gout?
Gout is caused by chronic hyperuricaemia (uric acid > 0.45 mmol/l).
What are factors leading to decreased excretion of uric acid?
Factors include diuretics, chronic kidney disease, and lead toxicity.
What are factors leading to increased production of uric acid?
Factors include myeloproliferative/lymphoproliferative disorders, cytotoxic drugs, and severe psoriasis.
What is Lesch-Nyhan syndrome?
Lesch-Nyhan syndrome is caused by hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency.
Who is affected by Lesch-Nyhan syndrome?
It is x-linked recessive, therefore only seen in boys.
What are the features of Lesch-Nyhan syndrome?
Features include gout, renal failure, neurological deficits, learning difficulties, and self-mutilation.
What is the effect of aspirin on plasma urate levels?
Aspirin in a dose of 75-150mg is not thought to have a significant effect on plasma urate levels.
The British Society for Rheumatology recommends it should be continued if required for cardiovascular prophylaxis.
What is gout?
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium.
What causes gout?
Gout is caused by chronic hyperuricaemia (uric acid > 0.45 mmol/l).
What are factors leading to decreased excretion of uric acid?
Factors include diuretics, chronic kidney disease, and lead toxicity.
What are factors leading to increased production of uric acid?
Factors include myeloproliferative/lymphoproliferative disorders, cytotoxic drugs, and severe psoriasis.
What is Lesch-Nyhan syndrome?
Lesch-Nyhan syndrome is caused by hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency.
Who is affected by Lesch-Nyhan syndrome?
It is x-linked recessive, therefore only seen in boys.
What are the features of Lesch-Nyhan syndrome?
Features include gout, renal failure, neurological deficits, learning difficulties, and self-mutilation.
What is the effect of aspirin on plasma urate levels?
Aspirin in a dose of 75-150mg is not thought to have a significant effect on plasma urate levels.
The British Society for Rheumatology recommends it should be continued if required for cardiovascular prophylaxis.
What is hyperuricaemia?
Increased levels of uric acid in the blood, which may occur due to increased cell turnover or reduced renal excretion.
Can hyperuricaemia be asymptomatic?
Yes, hyperuricaemia may be found in asymptomatic patients who have not experienced attacks of gout.
What conditions may be associated with hyperuricaemia?
Hyperuricaemia may be associated with hyperlipidaemia, hypertension, and the metabolic syndrome.
What are some causes of increased uric acid synthesis?
Causes include Lesch-Nyhan disease, myeloproliferative disorders, a diet rich in purines, exercise, psoriasis, and cytotoxic drugs.
What are some causes of decreased uric acid excretion?
Causes include low-dose aspirin, diuretics, pyrazinamide, pre-eclampsia, alcohol, renal failure, and lead exposure.
What is pseudogout?
Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium. It is now more correctly termed acute calcium pyrophosphate crystal deposition disease.
What is the association of pseudogout with age?
Pseudogout is strongly associated with increasing age. Patients who develop pseudogout at a younger age (e.g. < 60 years) usually have some underlying risk factor.
What are some underlying risk factors for pseudogout in younger patients?
Underlying risk factors include haemochromatosis, hyperparathyroidism, low magnesium, low phosphate, acromegaly, and Wilson’s disease.
Which joints are most commonly affected by pseudogout?
The knee, wrist, and shoulders are most commonly affected.
What are the findings in joint aspiration for pseudogout?
Joint aspiration reveals weakly-positively birefringent rhomboid-shaped crystals.
What does an x-ray show in pseudogout?
X-ray shows chondrocalcinosis, which can be seen as linear calcifications of the meniscus and articular cartilage in the knee.
What is the management for pseudogout?
Management includes aspiration of joint fluid to exclude septic arthritis, and NSAIDs or intra-articular, intra-muscular or oral steroids as for gout.
