Keterangan
Gout is a form of inflammatory arthritis caused by the accumulation of uric acid crystals in the joints. Uric acid is a byproduct of the breakdown of purines, which are found in certain foods and naturally occur in the body. When there is an excess of uric acid, it can form crystals in the joints, leading to inflammation and intense pain.
Ringkasan
- Gout is a monosodium urate crystal deposition disease, becoming increasingly prevalent worldwide and predominantly affecting adult men and postmenopausal women. Hyperuricemia, while common, is only a risk factor and does not automatically equate to gout; elevated uric acid levels must coincide with other factors to warrant treatment. The level of uric acid that warrants treatment is typically above 9, not just 7 or 8 flagged as abnormal by labs.
- Uric acid, the end product of purine degradation, needs a serum concentration above 6.8 for crystals to form. The pathogenesis involves macrophages engulfing these crystals, triggering an inflammatory cytokine cascade. Risk factors include both non-modifiable factors like gender and ethnicity, and modifiable factors such as alcohol consumption and diuretic use.
- Gout progresses through stages, starting with hyperuricemia, then acute flares, recurrent flares, and finally chronic gout. Early gout presents with abrupt onset of intense pain, warmth, swelling, and inflammation, typically in the big toe. The diagnosis can be confirmed with joint aspiration and visualized with crystal fluroscopy.
- The ULCratology and European specification criteria can assist in diagnosis when aspiration is not possible. Imaging, particularly ultrasound, helps identify signs like the double contour sign. Late-stage gout manifests with tophi and erosions detectable on X-rays.
- Management focuses on confirming the diagnosis, managing flares, preventing future flares, and lowering uric acid levels to target. Acute flares are treated with anti-inflammatories and colchicine, administered early for optimal effect. Prophylaxis with colchicine, NSAIDs, or low-dose prednisone is crucial for those starting urate-lowering therapy.
- Urate-lowering therapy, such as allopurinol or febuxostat, requires titration to achieve a target serum uric acid level of less than 6 mg/dL (or <5 for tophi). Allopurinol is generally the preferred first-line agent due to safety concerns associated with febuxostat and increased cardiovascular risks. Prophylaxis should continue until the patient is attack-free, tophi are resolved, and target uric acid levels are maintained for 3-6 months.
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