Crystal arthropathy (MSK) Flashcards
Define gout.
Acute inflammatory monoarthritis, caused by precipitation of monosodium urate crystals in joints
What is gout characterised by? (4)
- 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
- uric acid urolithiasis
Which joints are commonly affected in gout?
- first toe (podagra)
- foot
- ankle
- knee
- fingers
- wrist
- elbow
- however, it can affect any joint
What are the primary sources of uric acid?
Purine + pyrimidine (nitrogen-containing heterocycles, DNA components) - released when cells broken down
What is the strongest risk factor for crystal arthropathy?
Hyperuricaemia
What are the causes of hyperuricaemia (crystal arthropathy)?
- increased urate intake/production:
- overproduction - tumour lysis syndrome
- increased nucleic acid turnover e.g. lymphoma, leukaemia, psoriasis
- increased dietary intake of purines - shellfish, anchovies, red meat
- decreased renal excretion of uric acid:
- renal failure / CKD
- thiazide/loop diuretics (and other drugs e.g. ciclosporin)
- alcohol excess
- dehydration
- idiopathic
Describe the pathophysiology of gout.
- hyperuricaemia –> deposition of monosodium urate crystals in joint + soft tissues + kidneys –> acute inflammation and pain –> areas of slower blood flow + poorer solubility of uric acid –> precipitation e.g. joints and kidney tubules
- overtime repeated gout attacks can cause destruction of joint tissue = arthritis –> chronic gout
What is chronic gout?
Repeated gout attacks –> chronic gout - permanent deposits of urate crystals (tophi) which form along the bones below the skin
A type of arthritis with joint tissue destruction + permanent joint deformity + tophi
What is pseudogout?
Deposition of calcium pyrophosphate crystals within the joint space (articular cartilage), often secondary to joint damage (e.g. OA, trauma)
Name a risk factor for pseudogout.
Hyperparathyroidism - due to increased serum calcium
What are the clinical features of gout? (6)
- sudden severe monoarticular pain
- stiff, red, swollen, warm joint
- asymmetrical joint distribution (can be polyarticular)
- podagra - painful big toe MTP
- tophi - over extensor surface joints e.g. elbows, knees, Achilles tendon
- acute attacks after large meal with purine-rich foods e.g. red meat, seafood, alcohol
Describe the disease course of gout.
- symptoms peak at 24h and resolve over 7-10 days
- acute attacks (with cellulitis, polyarticular or periarticular involvement) after large meals containing purine-rich foods e.g. red meat, seafood, alcohol
- attacks often recurrent + symptom-free between acute attacks
- intercritical gout = asymptomatic period between acute attacks
- repeat acute attacks –> chronic tophaceous gout
What are the features of chronic tophaceous gout? (4)
- persistent low-grade fever
- polyarticular pain with painful tophi (urate deposits)
- best seen on tendons and pinna of ear
- symptoms of urate urolithiasis (renal calculi symptoms)
Where are tophi found in gout?
Present over extensor surface joints:
- elbows
- knees
- Achilles tendons
What are the clinical features of pseudogout? (4)
- pain and swelling
- knee common, ankle, shoulder, elbow, wrist
- longer duration of acute attacks than gout (several days to weeks)
- chronic: pain, stiffness, functional impairment
What do you see on examination in gout/pseudogout?
Acute episodic arthritis: painful, warm, erythematous + swollen joint –> decreased range of motion –> disability
What are the risk factors for gout? (7)
- older age
- male
- meat and seafood
- alcohol
- drugs: diuretics, ciclosporin, tacrolimus, pyrazinamide, aspirin
- genetic susceptibility
- high cell turnover rate
What are the risk factors for pseudogout? (8)
- advanced age
- injury
- hyperparathyroidism
- haemochromatosis
- Fx CPPD
- hypomagnesaemia
- hypophosphatasia
- gout
What is the 1st-line investigation in crystal arthropathy?
Arthrocentesis with synovial fluid analysis
What does arthrocentesis with synovial fluid analysis show in gout vs pseudogout?
- gout: monosodium urate crystals, needle-shaped, negatively birefringent, (yellow under parallel light and blue under perpendicular light)
- pseudogout: calcium pyrophosphate crystals, rhomboid/brick-shaped, positively birefringent, (blue under parallel light and yellow under perpendicular light)
Following an acute episode, what should be checked in gout?
- once settled down, serum urate levels checked 2 weeks later (if falsely normal/low uric acid levels at time of flare)
- uric acid levels may be high, or falsely normal/low during the attack
- raised in gout: >420micromol/L in men; >360micromol/L in women
What would an X-ray show in gout vs pseudogout?
- gout: rat-bite erosions (may have overhanging edge or punched-out appearance), tophi in chronic
- pseudogout: chondrocalcinosis (CPPD deposition –> cartilage calcification), maybe signs of OA (LOSS)
What must you exclude in crystal arthropathy and how?
Septic arthritis - by gram stain and culture
What might you see on abdominal XR/KUB in gout?
Uric acid renal stones may be seen
What would FBC show in an acute attack of crystal arthropathy?
High WCC
What are some differential diagnoses for crystal arthropathy? (6)
- septic arthritis
- trauma
- rheumatoid arthritis
- reactive arthritis
- osteoarthritis
- polymyalgia rheumatica (prolonged morning stiffness involving hips and shoulders, symmetrical, synovial fluid analysis negative)
What is the first-line management for an acute attack of gout?
Choose out of NSAIDs, colchicine, corticosteroids:
- NSAIDs (naproxen)
- if NSAIDs contraindicated (e.g. peptic ulcers, CKD): colchicine
- intra-articular corticosteroids (prednisolone)
- 2nd line: IL-1 inhibitor (anakira, canakinumab)
- intramuscular ACTH in difficult cases
What is the first-line management for recurrent gout (prophylaxis)?
- allopurinol - lowers uric acid levels via inhibition of xanthine oxidase
- PLUS suppressive therapy with long term colchicine/NSAIDs/corticosteroids
What medication can allopurinol (gout) have a bad interaction with?
Azathioprine - can cause bone marrow suppression
What do we do with allopurinol during acute flares of gout?
Allopurinol should be continued during an acute attack in patients who are already established on treatment
What lifestyle changes are needed for management of gout? (3)
- increase fluid intake to lower risk of renal calculi
- weight loss
- diet (avoid purines) - reduce meat (liver), seafood, oily fish, alcohol
When is surgery considered for gout?
If large or ulcerating tophus
What is the first-line management for acute pseudogout (mono/oligoarticular disease)?
Intra-articular corticosteroids (dexamethasone)
If not possible: NSAIDs or colchicine
If this fails/CI: systemic corticosteroids (prednisolone)
What is the first-line management for acute pseudogout (polyarticular disease)?
NSAIDs or colchicine
If this fails/CI: systemic corticosteroids (prednisolone) or intra-articular corticosteroids (dexamethasone)
What analgesic can we give for pseudogout?
Paracetamol
What is the first-line management for chronic recurrent pseudogout (knee, hip or shoulder with severe degeneration)?
Joint replacement surgery
What is the first-line management for chronic pseudogout with osteoarthritis/rheumatoid-like disease OR 3+ attacks annually?
Maintenance therapy with colchicine
What are some complications of gout? (4)
- nephrolithiasis
- urate nephropathy - urate crystals deposit in the interstitium of kidney
- renal failure
- secondary infection/ulceration of tophi
What are some complications of pseudogout? (3)
- chronic pyrophosphate arthropathy
- GI haemorrhage secondary to NSAID use
- rare - destructive arthropathy with Charcot’s joint features, recurrent haemarthrosis + joint capsular rupture (in very elderly women)
