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Gout occurs when urate crystals accumulate in your joint, causing the inflammation and intense pain of a gout attack. Urate crystals can form when you have high levels of uric acid in your blood.
Pathogenesis of hyperuricemia:
- Normal values of uric acid in the blood is 7.0 mg/dl in men and 6.0 mg/dl in women
- Hyperuricemia can result from over production of uric acid, decreased urinary excretion of uric acid or a combination of both.
| Purines are also found in certain foods, including red meat and organ meats, such as liver. Purine-rich seafood includes anchovies, sardines, mussels, scallops, trout and tuna. Alcoholic beverages, especially beer, and drinks sweetened with fruit sugar (fructose) promote higher levels of uric acid. |
Classification:
| Primary (idiopathic) Gout | Secondary |
|
Most common cause of overproduction of uric acid is increased turn over of nucleic acids, as seen in leukemia and Lymphomas and after chemotherapy for,cancer.
The most common cause of decreased urinary excretion of uric acid is chronic renalmdiseases that lead to renal failure. In renal failure the clearance of uric acid is,decreased, and with a fall in the rate of Glomerular filtrates, hyperuricemia ensues. |
Risk factors
- Diet
- Weight
- Medical conditions
- Certain medications.
- Family history of gout.
- Age and sex.
- Recent surgery or trauma.
Morphology
- When a sodium urate crystal precipitates from super saturated body fluids, they absorb fibronectin, complement, and number of other proteins of their surfaces.
- In phagocytizing those protein coated crystals, Neutrophiles release inflammatory mediators resulting in local inflammatory reaction
- Uric acid crystals may be found intracellularly in leukocytes of the synovial fluid.
- Extra cellular soft tissue deposits of these crystals (tophi), are surrounded by foreign body giant cells and an associated inflammatory response of mononuclear cells.
- These granuloma like areas are found in the cartilages and in any soft tissue around the joints.
Macroscopically
- It appears as chalky, white deposits on the surfaces of extraarticular structures and soft tissues around joints.
- Uric acid crystals also deposit in the kidney.
Clinical features:
During an attack of gout, the affected joint becomes:
- very painful
- tender
- red
- hot
- swollen.
There are four steps in the clinical course of gout:
| 1. Asymptomatic hyperuricemia | Precedes clinically evident gout by many years |
| 2. Acute gouty arthritis | Initially there is a monoarticular involvement and later in the course of the disease, poly articular involvement with fever is common |
| 3. Intercritical period | This is Asymptomatic interval between attacks |
| 4. Tophaceous Gout | Develops in the untreated patient in the form of tophi in the cartilage, synovial membrane, tendons and soft tissue. Thophus is a chalky; yellow white deposit of monosodium urate crystals. |
Treatments
- Treating the acute attack
- Treatments to prevent future attacks.
The most common drug treatments for attacks of gout are:
- Non-steroidal anti-inflammatory drugs (nsaids)
- Steroids
- Colchicine.
Tips for managing an attack at home
- Keep the area cool – an ice pack, or a bag of frozen peas wrapped in a tea towel, can be particularly good at reducing some of the pain and swelling.
- Rest the affected joint.
- Think about getting yourself a bed cage. These support the bedsheets above your feet so that your affected joint can rest without the strain of the sheets.
Treatments to prevent gout attacks
There are drugs available that can lower urate levels, prevent new crystals from forming and dissolve away the crystals in your joints. They are called urate lowering therapies (ULTs).
