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Cholesterol
0%
0/20
Calcium phosphate
Calcium oxalate
Monosodium urate
100%
20/20
Copper
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This clinical vignette is most consistent with gouty arthritis, which is caused by deposition of monosodium urate crystals. In the pathogenesis of gout, hyperuricemia occurs either due to increased production or decreased excretion of uric acid. Monosodium urate crystals accumulate in bones, joints, and soft tissues, causing acute and chronic inflammation with bone and cartilage breakdown. Acute attacks most commonly affect a single joint, most often the at first metatarsophalangeal joint of the greater toe or knee. Longstanding gout can lead to chronic arthritis, bony erosions known as tophi, uric acid nephrolithiasis, and chronic nephropathy. While the initial differential for unilateral joint pain is broad, the answer choices point towards some type of joint deposition disease. Gout due to uric acid deposition is the most likely choice, given the involvement of a single joint, especially in the great toe (known as podagra). Additionally, the patient's diabetes and chronic kidney disease predispose to hyperuricemia and gout. Incorrect Answers: Answer 1: Cholesterol deposition in the tendons and joints are known as tendinous and tuberous xanthomas. They are generally non-painful nodules, which may be associated with underlying genetic hypercholesterolemia. Answer 2: Calcium pyrophosphate deposition disease (CPPD) may have similar symptoms, but more commonly presents in the knee or wrist. CPPD crystals are rhomboid shaped with weakly positive birefringence, while gout crystals are needle shaped with strong negative birefringence. Answer 3: Calcium oxalate deposition can occur due to genetic oxalate overproduction or chronic kidney disease, and can lead to arthritis and pathological fractures, most commonly affecting the hands. Answer 5: Copper deposition may occur in Wilson's disease and most commonly affects the large joints like the knees. For an acute gout attack, non-steroidal anti-inflammatory medication and corticosteroids are first-line agents. Prophylaxis against future attacks includes urate lowering medications such as allopurinol, colchicine, or probenecid, and avoidance of purine-rich foods and alcohol (1).
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