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Pathophysiology: Urate crystals form due to high levels of uric acid. Symptoms: Sudden onset of joint pain, redness, and swelling, often in the big toe. Treatment: Medications like NSAIDs, colchicine, and allopurinol; dietary changes.

Pathophysiology: BCP crystals accumulate in the joint cartilage. Symptoms: Joint pain, stiffness, and sometimes acute pseudogout attacks. Treatment: Analgesics, joint lavage, and possibly surgical debridement.

Pathophysiology: Formation of calcium pyrophosphate dihydrate (CPPD) crystals in the joint. Symptoms: Joint pain and swelling, resembling gout but typically affecting the knee. Treatment: NSAIDs, colchicine for acute attacks, and corticosteroid injections.

Pathophysiology: Characterized by CPPD crystal deposition in cartilage. Symptoms: Joint stiffness, pain, and sometimes a pseudogout attack. Treatment: Symptom management with NSAIDs, corticosteroids, and colchicine.

Pathophysiology: Inflammatory disorder caused by mutations in the MEFV gene. Symptoms: Recurrent fevers and serositis, acute arthritis episodes. Treatment: Colchicine to prevent attacks and reduce symptoms.

Pathophysiology: Deposition of calcium oxalate crystals due to high oxalate levels. Symptoms: Joint pain and swelling. Treatment: Dietary oxalate restriction, hydration, and removal of the source of oxalate, if known.

Pathophysiology: Deposition of monosodium urate and calcium phosphate crystals due to hyperglycemia. Symptoms: Joint pain, swelling, and stiffness. Treatment: Glycemic control, NSAIDs, and potentially colchicine.

Pathophysiology: Deposition of hydroxyapatite crystals within tendons, bursae, and joints. Symptoms: Joint pain, tenderness, decreased range of motion. Treatment: Rest, NSAIDs, corticosteroid injections, and physiotherapy.

Pathophysiology: Progressive urate crystal accumulation due to long-standing hyperuricemia. Symptoms: Chronic joint pain, tophi formation, joint damage. Treatment: Urate-lowering therapy, surgery for tophi removal, chronic pain management.

Pathophysiology: Deposition of apatite crystals (a form of calcium phosphate) in the joint, causing destruction. Symptoms: Destructive arthritis with erosive changes. Treatment: Anti-inflammatory medications, joint injections, and surgery for severe cases.

Pathophysiology: Rapid deposition of calcium phosphate crystals in the joint. Symptoms: Severe joint pain and inflammation. Treatment: Treatment with NSAIDs, colchicine, corticosteroids, and joint aspiration.

Pathophysiology: CPPD crystals form secondary to metabolic or endocrine disorders. Symptoms: Similar to primary CPPD, with joint pain and swelling. Treatment: Address the underlying disorder, symptomatic treatment with NSAIDs, colchicine, and corticosteroids.

Pathophysiology: Joint degeneration due to loss of sensation and abnormal stress distribution. Symptoms: Progressive joint destruction, lack of inflammation. Treatment: Offloading the joint, surgery in advanced cases, and tight control of the underlying disease.

Pathophysiology: Deposition of calcium hydroxyapatite crystals in tendons or joints. Symptoms: Joint pain, may lead to 'calcific tendinitis'. Treatment: NSAIDs, physiotherapy, extracorporeal shock wave therapy (ESWT), and surgery in refractory cases.