Gout and pseudogout are diseases that are characterized by attacks of pain and inflammation that is caused by the accumulation of crystals in the joints. Both can be very painful, but there are marked differences in the pathogenesis of each disease and its treatment.
Arthritis is defined as an inherited metabolic disease caused by hyperuricemia, which is a form of acute arthritis and is characterized by inflammation of joint (Thomas, 1997). In gout, monosodium urate crystals form in joints and / or organs in the body when the levels of uric acid is high (hyperuricemia). Attacks of gout can occur at any time without notice and are often painful. They can be initiated by injury or stress, as they may result in increased production of uric acid in the blood. With an attack of gout, they become joint swells and the skin on the red, swollen, hot and tight. The joint may be tender to palpation. The patient may also have fever, chills or other constitutional symptoms. There are certain risk factors that predispose individuals to gout, such as obesity, hypertension, cardiovascular disease and diabetes (Wikipedia, 2008).
Urate crystals are often formed at the distal ends because the ends are cooler than the central part of the body and uric acid tends to crystallize in the cooler temperatures. These crystals, when accumulated, can cause tophi, which are hard lumps of urate crystals. Gout usually affects the big toe joint, but these crystals can accumulate in the ears, elbows, or even other organs such as kidneys. Most of the size of tophi may decrease slowly when the level of uric acid in the blood decrease, but large tophi can be surgically removed (Berkow, et al., 1997). The deposits often increase in size and through the skin to form a breast that downloads a chalky white material (Wikipedia, 2008). These crystals accumulate and can cause visible deformation of the device (as in the ears), and cause deformation of the joints because they inhibit the movement of the joints and cause damage to the joint itself (Berkow, et al., 1997 ).
Uric acid is the product of cell / tissue collapse during normal cell turnover and are able to be detected in blood by a simple blood test (eMedicineHealth, 2008). It is also produced when the purine metabolism takes place, what happens after the purine consumed by the patient and processed by the body (Wikipedia, 2008). It is excreted from the body by the kidneys and intestine (Wikipedia, 2008). If the excessive uric acid is created, or if there is not enough to be eliminated, hyperuricemia develop (Berkow, et al., 1997). Hyperuricemia is defined as a plasma urate (uric acid) above 420 ¼ mol / L (7.0 mg / dl) in men (or 380 ¼ mol / L in women (Wikipedia, 2008).
Some patients with gout (10%) produces too much uric acid in the diet or increased cell division, while others (90%) can effectively eliminate enough uric acid in urine (eMedicineHealth, 2008). An unexpected rise in uric acid levels can be caused by many different things, such as:
1. Excessive alcohol and red meat. The protein is a crude proxy for purines; delegating specific muscle. Purine metabolism due to uric acid, which is normally excreted in the urine. The main source of dietary purines is DNA and RNA, adenine and guanine bases through. A diet low in purines reduces the serum levels of uric acid. The main dietary sources of purines are the beer (which is a high-guanosine, coffee, tea and other beverages containing caffeine and chocolate (theobromine content) (Wikipedia, 2008).
2. Trauma or disease. During infection or trauma, the immune system quickly breaks down the cells to repair, which releases excess uric acid in the blood.
3. Starvation / dehydration. During dehydration, increased levels of urate, and their removal has been reduced by the kidneys.
4. IV contrast dyes can affect the kidneys and reduces their ability to remove uric acid in the blood.
5. Chemotherapy. Some drugs are purine-based. Chemotherapeutic agents is important for this (purine analog antimetabolite drugs [Wikipedia, 2008]) and cell proliferation activities (such as cancer).
6th Other drugs
a. Diuretics (increases dehydration)
b. Aspirin (low-dose aspirin may affect uric acid excretion by the kidneys (Shiel, 2006).
C. Nicotinic acid. For example, the body's ability to eliminate uric acid may have a negative impact, the nicotinic acid intake (FootPhysicians.com, 2005).
7th diseases that cause rapid cell division as some cancers of the blood can cause high levels of uric acid to be present in the blood.
8. Kidney disease or certain medications can prevent the kidneys are able to properly excrete uric acid (Berkow, et al., 1997).
A definitive diagnosis of gout is made by light microscopy of fluid aspirated from the municipality. This fluid is necessary to examine whether it shows intracellular monosodium urate crystals in synovial fluid (Wikipedia, 2008).
Treatment
Treatment of patients with gout is to control pain / inflammation first and then the prevention of recurrent attacks. Once the diagnosis has been confirmed, the drugs of choice for pain control are indomethacin and other nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids orally or intra-articular glucocorticoids administered by intra-articular (Wikipedia , 2008).
Some drugs used to reduce uric acid in the blood are:
The first colchicine. Interfere with white blood cells in the initiation of maintenance of the inflammatory response to monosodium urate crystals (DEGLIN Valle and Rand, 2001).
2. Allopurinol (inhibits the production of uric acid).
3. Sulfinpyrazone (increased uric acid excretion in the urine).
4th Probenecid, a drug that promotes excretion of uric acid in urine are commonly prescribed often in collaboration with colchicine.
5. Sodium bicarbonate (soda) is an old remedy, believed to work by increasing blood pH (acidity pressure).
However, the added sodium be inappropriate for some people (Wikipedia, 2008).
Prevention
Reduce intake of purines in the diet by avoiding foods high in purines, such as those listed above. Other indirect methods to reduce risk factors include arthritis, such as reducing obesity, hypertension, cardiovascular disease and diabetes (Wikipedia, 2008).
Avoid dehydration by drinking plenty of fluids, especially water, helps to excrete uric acid in the blood. Also avoid diuretic foods or medications (such as caffeinated drinks, aspirin, alcohol, etc.) (Wikipedia, 2008).
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