Rheum - Gout Flashcards
describe the pathophysiology of gout
Arthritis due to deposition of MONOSODIUM URATE crystals within joints, causing acute inflammation and eventual tissue damage.
Often involves HYPERURICAEMIA (although can occur in pts with normal plasma urate levels), usually due to impaired renal excretion of urate (e.g. CKD, HTN, hyperparathyroidism, alcoholism, drugs, obesity). 10% over-produce rate, e.g. myeloproliferative disorders, haemolysis, extreme exercise…
suggest possible risk factors for gout
- male gender
- age (30-60 yrs)
- purine-rich food: meat and seafood
- alcohol
- diuretics (loop and thiazide)
- obesity, DM, high triglycerides
- HTN, CHD, HF and CKD
- psoriasis and chemotherapy
describe the typical presentation of crystal arthropathies
- acute joint pain - reaches crescendo over 6-12 hrs (untreated, resolves spontaneously over 5-15 days)
- swollen, extremely tender and erythematous joint
- inflammation reaches peak within 24 hrs, often with fever and malaise
Often more severe in gout than pseudogout.
what is the most common site for gout attacks? what are the other possible sites?
Most common = 1st MTP joint (podagra).
Other sites:
- knee
- midtarsal joints
- wrists
- ankles
- small hand joints
- elbows
what is chronic tophaceous gout?
In some pts, large crystal deposits produce irregular firm nodules, mainly around extensor surface of fingers, hands, forearms, elbows, Achilles tendons and ears.
Tophi are typically asymmetrical with a chalky appearance beneath skin.
which Ix would you request for a pt with suspected acute gout?
- synovial joint aspirate: demonstration of MSU crystals (needle-shaped, negatively birefringent) in synovial fluid confirms Dx
- Bloods:
- serum uric acid: often raised (>360 umol/L) but can be normal
- fasting glucose and lipids: as gout commonly associated with metabolic syndrome - 24 hr urine sample: renal uric acid secretion can be helpful in Dx (esp. if onset <25 yo or with renal stones - likely over-excreters of urate)
describe the X-ray features of chronic gout
- joint effusion (earliest sign)
- eccentric erosions: well-defined, ‘punched out’ with sclerotic margins in marginal and juxta-articular distribution
- tophi (pathognomonic)
- preserved joint space until late stages and absence of periarticular osteopenia
how would you manage a pt with acute gout attack
- NSAIDS, e.g. diclofenac, naproxen: 1st line option, use for min. time due to CVD and GI risk (+/- PPI)
- colchicine: 500 ug 2-4x/day until symptoms relieved. Max. 6 mg per course. Effective, esp. when NSAIDs poorly tolerated, in HF or in pts on anti-coagulation.
- corticosteroids (PO, IM, IV or intra-articular): when NSAIDs or colchicine contra-indicated.
- regular simple analgesics, e.g. paracetamol + codeine: when all other drugs contra-indicated, or as adjunct.
- canakinumab (IL-1 inhibitor): for pts with no response to above after 2-3 days or who are intolerant.
describe the MOA of a common drug used in gout prophylaxis. how is Tx initiated and maintained?
ALLOPURINOL: xanthine-oxidase inhibitor that reduces formation of uric acid from purines.
- should not be started during acute attack; wait until 1-2 wks after resoltion
- start with lose dose (50-100 mg) and titrate up every 2-4 wks until SUA level <300 umol/L
- co-prescribe colchicine or low-dose NSAID to prevent gout attack whilst initiating Tx (causes increased risk of attack)
- life-long Tx, should not be stopped during an attack
describe a drug that can be used instead of or as adjunct to allopurinol
Uricosurics, e.g. SULFINPYRAZONE: increases renal urate excretion (increased risk of urate stone precipitation)
suggest possible complications of gout
- chronic urate nephropathy: widespread deposition of urate crystals in medulla and pyramids causing inflammation and fibrosis
- urate and oxalate kidney stones
- severe degenerative arthritis
- secondary infections
- recurrent, painful episodes
- carpal tunnel syndrome (rare), nerve or spinal cord impingement
what is pseudogout?
Acute onset, self-limiting joint inflammation caused by deposition of calcium pyrophosphate crystals in articular and periarticular tissues.
Is one possible manifestation of calcium pyrophosphate dehydrate crystal deposition disease.
which Ix confirm Dx of pseudogout?
- Synovial joint aspirate:
- joint fluid looks purulent
- intracellular and extracellular weakly positive birefringent CPP crystals
- raised WCC (esp neutrophils) - Imaging:
- X-ray: linear opacification of articular cartilage (chondrocalcinosis)
how would you manage a pt with acute pseudogout attack?
- ice packs, temporary rest
- NSAIDs (caution in elderly)
- intra-articular steroid injection or systemic steroids
- colchicine - if NSAIDs or steroids are contra-indicated
