toe pain
Introduction
Introduction Gouty toe pain occurs mostly in middle-aged men, often acute onset, with toe, spasm and other joints redness and heat pain.
Cause
Cause
(1) Causes of the disease
The long-term increase of uric acid in the blood is the key cause of gout. Human uric acid mainly comes from two aspects:
(1) Nucleic acids and other terpenoids produced by protein catabolism in human cells produce endogenous uric acid by the action of some enzymes.
(2) The steroidal nucleic acid and nuclear protein components contained in the food are digested and absorbed, and then exogenous uric acid is produced by the action of some enzymes.
The production of uric acid is a very complicated process that requires the participation of some enzymes. These enzymes can be roughly divided into two categories: enzymes that promote uric acid synthesis are mainly 5-phosphate nucleic acid-1-pyrophosphate synthetase, adenine phosphate nucleotide transferase, phosphoribosyl pyrophosphate amide transferase and xanthine oxidase; The enzyme that inhibits uric acid synthesis is mainly hypoxanthine-guanosine transferase. Gout is caused by various factors, such as promoting the activity of uric acid synthase, inhibiting the activity of uric acid synthase, etc., resulting in uric acid. Excessive production or obstruction of uric acid in the kidney due to various factors causes uric acid to accumulate in the blood to produce hyperuricemia.
Hyperuricemia, such as long-term uric acid, will deposit in the form of urate in the subcutaneous tissues of the joints and kidneys, causing arthritis, subcutaneous gout stones, kidney stones or gouty nephropathy.
The disease is recurrent acute or chronic arthritis of the peripheral joint, which is caused by deposition of monosodium urate crystals in the supersaturated hyperuricemia body fluid in and around the joints and tendons.
(two) pathogenesis
Reduced uric acid breakdown as a mechanism leading to hyperuricemia has been ruled out during the normal conversion of nucleic acids and nucleotides, partially degraded into free sulfhydryl groups, mainly hypoxanthine and guanine, nucleic acids required for the synthesis of nucleotides. When it is excessive, it will degrade rapidly to hypoxanthine. The guanine will be deaminated to become jaundice under the action of guanine, and the hypoxanthine and astragalus will be oxidized to uric acid by the action of xanthine oxidase. Hypoxanthine nucleotides and guanine nucleotides are end products of purine biosynthesis. The above three purine nucleotides can be directly synthesized from a purine base such as guanine to a guanine nucleotide via one of two routes.
Hypoxanthine is converted into hypoxanthine nucleotides; adenine is converted to adenine nucleotides; or the first step of their re-synthesis of purine metabolism and its feedback inhibition is phosphoribosyl pyrophosphate (PRPP) + glutamine Amide + H2O phosphoribosyl ribose + glutamate + pyrophosphate (PPI), the reaction is catalyzed by phosphoribosyl pyrophosphate amide transferase (PRPPAT) to modulate this reaction to regulate the increase in runaway and increased synthesis of purines: PRPP glutamine concentration increased The amount or activity of the enzyme increases; the sensitivity of the enzyme to the feedback inhibition of purine nucleosides is reduced; the inhibition of the enzyme activity by the reduced concentration of adenosine or guanylate leads to a decrease in the inhibition of the enzyme in HPRT deficiency and PRPP synthesis. When the enzyme is overactive, the intracellular PRPP concentration is significantly increased. The synthesis is increased. In patients with increased uric acid production, the conversion of PRPP is accelerated. In addition, the cause of hyperuricemia is the deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT). When the enzyme is abnormal, the amount of PRPP increases, and the synthesis increases the production of uric acid. Others include any process that accelerates the decomposition of adenosine in the cells. The increased production of uric acid cause hyperuricemia.
For some patients with gout, the direct pathological mechanism of hyperuricemia is the decrease in renal tubular clearance of urate. The excretion of urate by the kidney is filtered by glomerulus, but the filtered urate is almost complete. The urate fraction secreted by the proximal convoluted tubules (reabsorbed before secretion) is also reabsorbed at the distal end of the proximal convoluted tubules, reabsorbed in Henry's sputum and collecting tubes (reabsorbed after secretion), thus urate Excretion is almost the secretion of uric acid from the renal tubules. The excretion of uric acid from the kidneys is 6% to 12% of the glomerular filtration excess. When glomerular urate filtration reduces the reabsorption of urate by the renal tubules or the secretion of urine from the renal tubules. Reduced acid salt, can cause a decrease in urate renal excretion leading to hyperuricemia. When blood uric acid increases beyond the supersaturated concentration of urate deposited in tissues in gout patients, the secretion of urate by nephron has been confirmed. It is falling.
Examine
an examination
Related inspection
Uric acid uric acid
First, clinical manifestations
There is no warning before the onset of acute gouty arthritis, mild traumatic gluttony sorghum food or excessive drinking surgery fatigue emotional stress medical emergency (such as infection of blood vessel obstruction) can induce gout, acute episodes often occur at night, acute single joint or more Joint pain is usually the first symptom of pain, progressive exacerbation is a symptom of severe pain, similar to acute infection, swelling, local fever, redness and obvious tenderness, local skin tension, fever, luster, appearance of dark red or purple red toe joints involving the toe joint The most common (foot gout) arch of the ankle, the wrist joint and the elbow joint are also common sites. Systemic manifestations include fever, chills, discomfort, and leukocytosis.
The first few episodes usually involve only one joint and only last for several days, but then multiple or more joints can be violated at the same time or in succession. If untreated for several weeks, the last local symptoms and signs will disappear. The joint function recovery is asymptomatic. As the disease progresses, the progress is getting shorter and shorter. If it is not prevented, there will be several occurrences of chronic joint symptoms and permanent destructive joint deformity every year. The hand and foot joints are often restricted in activities. In a few cases, the chest joints or the cervical vertebrae are jointed. Can also be affected by the common urate deposition in the mucus wall and the tendon sheath, the hand and foot can appear increased tophi and discharge the white urate-like urate crystal fragments of cyclosporin, causing gout to occur in the central large joints such as the hip Ankle joints can also be seen in the hands and even destroy the tubules.
1. Asymptomatic period: serum urate concentration increases with age and gender differences, this stage is mainly characterized by persistent or fluctuation of blood uric acid, from blood uric acid to symptoms can occur for several years to several Ten years, it is called gout only when arthritis occurs.
2. Acute arthritis episode: It is the most common first symptom of primary gout. It occurs in the lower extremity joint with the big toe and the first metatarsophalangeal joint. It is more common when the initial onset is a single joint inflammation recurrent, and the affected joints increase; The onset of gout indicates that the blood uric acid concentration is supersaturated over a long period of time resulting in the deposition of large amounts of urate in the tissue.
3. Intermittent period: Gout attacks last for several days to several weeks can be naturally relieved, without sequelae and completely recovered, and then the asymptomatic stage called acute exacerbation interval, after which about 60% of patients can relapse within 1 year. For more than 10 years.
4. Tophi and chronic arthritis: urate crystals are deposited in the cartilage sac fluid and soft tissue in untreated or poorly treated patients. Gout stone is common in this period. The performance often occurs in the forearm of the forearm, the elbow of the elbow, etc. The urate deposits in the joint and increases inflammation. The recurrent episode enters the chronic stage and cannot completely disappear, causing the joint bone erosion defect and the surrounding tissue fibrosis to cause the joint to be stiff and deformed. Restricted activity, with the repeated attacks of inflammation, the lesions become more and more serious, affecting joint function. Early prevention and treatment of hyperuricemia patients may have no current performance.
Second, diagnosis
Regarding the diagnosis of gout, there is no uniform standard in the country. Generally, the American College of Rheumatology standard American Holmes standard and the Japanese revised standard are introduced. The American College of Rheumatology classification standard for acute gouty arthritis (1977):
1. The specific urate crystals were found in the synovial fluid;
2. Gout stone is confirmed by chemical method or polarized light microscopy to contain sodium urate crystal;
3. With the following clinical laboratory and X-ray signs, 6 of 12 items:
(1) more than one episode of acute arthritis;
(2) Inflammation showed a peak within 1d;
(3) single arthritis episodes;
(4) The skin of the affected joint is dark red;
(5) pain or swelling of the first ankle joint;
(6) unilateral seizure involving the first metatarsophalangeal joint;
(7) unilateral seizure involving the tibial joint;
(8) There is a suspicious tophi;
(9) hyperuricemia;
(10) X-ray shows joint asymmetry swelling;
(11) X-ray film shows that the subcortical cyst is not accompanied by qualitative erosion;
(12) The microbial culture of joint fluid was negative during the onset of joint inflammation.
When the diagnosis of acute arthritis is difficult, you can try colchicine for diagnostic treatment. For the rapid relief of symptoms after gout colchicine, it is of diagnostic significance.
In conclusion, acute gout is not difficult to diagnose according to the typical clinical manifestations of laboratory tests and treatment response. The diagnosis of chronic gouty arthritis needs to be carefully identified and urate crystals should be obtained as much as possible.
Diagnosis
Differential diagnosis
Foot pain when the toe is flexed and flexed: common in the scaphoid fracture, symptoms, foot pain when the toe is flexed and flexed. The middle ankle joint, which is composed of the foot scaphoid, the wedge bone and the tibia, is also called the transverse joint, which is easy to cause dislocation due to trauma. Although the above-mentioned simple bone fractures are not frequent, they are not uncommon. About 0.3% of all body fractures should still be noticed.
The toes are cold and cold, showing pale or purple: the toes are cold and cold, and the pale or purple is the clinical manifestation of occlusive thromboangiitis. Thrombotic vasculitis is a different kind. In arteriosclerosis, vascular inflammation is distributed in segments, and the lesions mainly involve small and medium arteries and veins in the distal segment of the extremities. Pathologically, the main manifestations are characteristic inflammatory cell invasive thrombus, and less involvement of the vessel wall.
Toe flexion contracture: trauma to the foot due to flexion and contracture of the toes, such as soft tissue contusion, calcaneus and tibiofibular fractures can cause intrinsic ischemic necrosis of the foot, followed by a unique toe deformity.
