M10.042

Clinical Causes: Overproduction of uric acid by the body Impaired excretion of uric acid through the kidneys Diet high in purine-rich foods such as red meats, shellfish, and alcohol Certain medications that increase uric acid levels Genetic predisposition to uric acid metabolism abnormalities Dehydration, which can concentrate uric acid in the bloodstream Obesity, increasing uric acid production and reducing its excretion Chronic conditions such as hypertension or metabolic syndrome

Key Symptoms: Sudden onset of sharp, intense joint pain Swelling and redness in the affected joint Warmth and tenderness around the joint Limited range of motion in the affected hand Podlike lumps called tophi in chronic cases Pain episodes often occur at night, waking the individual from sleep Possible fever and feeling generally unwell during acute attacks

Diagnosis Path: Joint aspiration to detect uric acid crystals under a microscope Blood tests to measure serum uric acid levels, noting that levels can be normal during attacks Imaging studies such as X-rays, ultrasound, or dual-energy CT scans to identify joint damage or uric acid deposits

Treatment Protocols: Nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation and pain Colchicine, which can decrease joint inflammation if taken early during an attack Corticosteroids, administered orally or via injection, for severe cases or when NSAIDs are contraindicated Lifestyle modifications such as dietary changes to reduce purine intake Adequate hydration to help eliminate uric acid from the body Medications to lower uric acid levels, such as allopurinol or febuxostat, especially for recurrent gout cases Regular monitoring of uric acid levels to adjust treatment plans Weight management strategies to reduce overall uric acid burden