Gout is also called " high ", disorders of purine metabolism, which belongs to a kind of arthritis. Gout is the body of purine material the new supersedes the old. Disorders, uric acid synthesis is increased or discharged is reduced, hyperuricemia, blood uric acid concentration is too high, uric acid with sodium in the form of deposits in joints, cartilage and kidneys, causing tissue foreign body inflammatory reaction, i.e. pain wind.
Western medicine: Gout
English Name: Gout
Subordinate departments: Surgery Department of orthopedics
Incidence of parts: systemic
The main symptoms: Arthritis
The main etiology: purine metabolic disorder
Multiple groups: all groups
Contagious: no infectious
Whether to enter the medical insurance : Yes
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Cause of disease
Pathological physiology
Pathogenesis
Clinical symptoms and signs
Laboratory examination
Classification of diseases
Complication
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Diagnosis of traditional Chinese Medicine
Differential diagnosis
Early detection
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The causes of death in patients with
Spread disease profile
Cause of disease
Pathological physiology
Pathogenesis
Clinical symptoms and signs
Laboratory examination
Classification of diseases
Complication
Diagnosis of Western medicine diagnosis
Diagnosis of traditional Chinese Medicine
Differential diagnosis
Early detection
High risk population
Disease treatment and early treatment
Medication
Traditional Chinese medicine treatment
Acupuncture therapy
Diet therapy
A cup of coffee to the treatment of gout
Matters needing attention
Error recognition
Related questions
The causes of death in patients with
Edit this paragraph of gout disease spread
Gout ( gout ) is a purine metabolic disorder caused by a metabolic disease, but the incidence is obvious heterogeneity, in addition to hyperuricemia may be manifested as acute arthritis, tophi, chronic arthritis, joint deformity, chronic interstitial nephritis and uric acid urolithiasis. Clinically divided into primary and secondary two categories, primary gout purine metabolism abnormalities caused by congenital, often associated with obesity, carbohydrate lipid metabolism disorders, hypertension, arteriosclerosis and coronary heart disease aggregation occurs, secondary gout consists of some systemic disorders or drug induced. [1] gout due to purine biosynthesis metabolism increases, an excess of uric acid or due to excretion of uric acid in blood of undesirable due to elevated uric acid, deposition of urate crystals in synovial joints, bursae, cartilage and other tissues caused by recurrent inflammatory disease. The disease to joint fluid and tophi may find a birefringence of monohydrate sodium urate crystal for its characteristic. More common in obese in older men and women after menopause. With the development of economy and the life style change, its prevalence is rising gradually. Multiple parts of the human body, joint pain, hardly wished to live. "Pain ", and soon 1-7 days pain as " wind" blown over, so called " gout ". 40+ in males than in females (95% ), a female general in postmenopausal common, because estrogen can inhibit the formation of uric acid; but after menopause increases the attack rate. Hyperuricemia and gout have no direct relationship, just high uric acid have higher incidence of hyperuricemia gout may be, some people will not cause gout, hyperuricemia and some people found in a week or a month occur first gout the first gout, generally will have 1-2 years of intermittent period, there are 10 during the rest period (5% ), during active treatment, prevention of tophi formation. Editor this paragraph 1 pathogenesis. The reason caused by high uric acid: nucleic acid oxidation decomposition of endogenous purine total purine 80%, food and other exogenous purine purine 20% total. Eating food containing excessive purine ingredients in food, and in the new supersedes the old. In the process, the body will not be further metabolism of purines from the kidney by the excretion of urine. Serum uric acid concentration if reaches saturation, these substances ultimately form crystals, accumulated in soft tissues. If have an incentive to cause deposition in soft tissues such as articular membrane or tendon in uric acid crystals release, it causes the body's immune system and cause inflammation allergy. If the blood concentration of uric acid in long term than the saturation point, medicine known as " hyperuricemia ". 2. High-purine ingredients in food: (1 ) animal viscera such as brain, liver, kidney, heart, stomach. And the deep color of meat, Western-style thick broth, ox, such as chicken. Seafood; sardines, herring fish store, ( Herring ), dental hairtail, spring fish, scallops, sea cucumber, dried scallops, oysters, Qingkou division, catfish, shrimp, dried fish, fish, fish eggs. Goose, wild animal. ( 2) nuts such as peanuts, cashew nuts, wine ( overdose) ( 3) part of plant sprouts containing moderate ingredients, can not eat, cauliflower, beans, bamboo shoots, beans. 3. Gout gout can cause: by diet, the weather changes such as temperature pressure mutation, etc. caused by trauma. Drinking is easy to cause gout, because alcohol in the liver tissue metabolism, absorb moisture, so that the blood concentration of strengthen, the original is close to saturation of uric acid, accelerated into the soft tissue to form a crystalline, causing the body to the immune system over-reacts ( sensitive ) caused by inflammation, pain in ancient times known as the "king of the wind. ", so in good in the high officials and noble lords who, as Kublai Khan later because of excessive alcohol and suffered from gout pain. Some food after metabolism after partial derivatives, which can cause the original savings in the soft tissue of the crystals of uric acid to dissolve, then can induce and aggravate arthritis. 4 male predisposition to causes of gout gout can occur at any age. But the most common is 40 years of age or older middle-aged man. According to the latest statistics, men and women the incidence proportion is 20: 1. Mental workers, body fat, high incidence rate. Gout preference for males with reason is: female hormones can promote the excretion of uric acid, and inhibit the onset of arthritis effect. Men like drinking, eating dinner, rich in purine, protein food, make uric acid increased, discharge reduction. The doctor statistics, feast constantly, the incidence was 30%, often eat hot pot incidence is much also. This is because the hot pot is the main raw material of animal offal, shrimp, seafood, shellfish, drink beer, nature is add fuel to the flames. Investigation showed: Rinse chaffy dish than a meal intake high purine 10 times, even dozens of times. A bottle of beer can make uric acid increased one times. Hypertensive patients with gout 10 times more likely to be. Gout and diabetes is a lifelong disease. The key is to control the diet, eat more contain " purine " low alkaline food, such as fruits, vegetables, less meat, fish and other acidic foods, be light diet, low in sugar and fat, drinking water, for the benefit of the uric acid excretion. Warning: man gout patients do not drink, dinner not to excess. Once the diagnosis of gout, meat, fish, seafood in food restriction list. Spicy, stimulating food also should not eat, but determined to stop drinking! 5 pseudo gout is a due to calcium pyrophosphate crystal deposition in the articular cartilage and surrounding tissue caused by arthritis as the main manifestations of the disease, because of similar symptoms of gout and its name, also known as calcium pyrophosphate deposition disease or cartilage calcification. In 50 years of age or older, the incidence increased with age increasing, the ratio of male to female was 1.4:1. Cause: the cause is unknown, may be related to genetic and metabolic disorders, trauma and other factors. The basic disease because of calcium pyrophosphate deposition. Editor this paragraph pathophysiology when blood uric acid of more than 7mg/dl or 0.41mmol/L plasma is saturated ( in pH7.4, temperature 37℃and serum sodium in normal circumstances ). At 30 ℃, uric acid salt solubility is 4mg/dl, so the needle of monosodium urate ( MSU ) will be no blood supply ( such as soft bone ) or blood supply relatively few organizations ( such as tendon, ligament ) deposition, the site includes a distal peripheral joints and like ear temperature low tissue. Prevalence of severe and long time of the patient, monosodium urate crystals in the central joint and parenchymal organs such as kidneys in deposition. Tophaceous gout is MSU crystal aggregates, initially to the joint X piece appears, " to create " lesions, a late manifestation of subcutaneous nodules, which can be observed by naked eye or hand feel. The result of urine pH acid, uric acid is easy to form crystals, and gathered stones, which can lead to obstructive diseases of urinary system. Persistent hyperuricemia common cause is due to renal urate clearance decreased, especially in patients receiving long-term diuretic therapy and decreased glomerular filtration rate of primary kidney disease patients. The higher the degree of hyperuricemia longer disease course, crystal deposition and acute gouty attack chances. However, there are still a lot of hyperuricemia gout did not occur. Purine synthesis is increased for the original pathogenesis of abnormal state, may also be due to blood diseases such as lymphoma, leukemia or hemolytic anemia caused by nucleic acid protein turnover acceleration, or such as psoriasis caused by white cell proliferation, death rate increases quickly. The majority of patients with gout uric acid synthesis is increased by the reason is unclear, a minority of patients are due to hypoxanthine guanine phosphoribosyl transferase deficiency or because of phosphoribosylpyrophosphate synthetase activity caused by elevated. One enzyme abnormalities in infancy cause kidney stones, kidney disease and severe gout, such as complete lack of this enzyme, can cause neurological abnormalities, athetosis, spasticity, mental retardation and compulsive autotomy ( Lesch-Nyhan syndrome ), dietary purine also affected the level of serum uric acid. Compulsive overeating purine rich in food, especially while drinking can obviously make uric acid levels. Alcohol can not only promote the nucleoside in the liver metabolism, and can inhibit renal tubular urate secretion, but strict low purine diet can lower blood uric acid of about 1mg/dl ( 0.06mmol/L ). Serum uric acid salt reflect extracellular can be mixed with uric acid salt volume, normally every 24 hours turnover 1; 1/3 uric acid salt from fecal excretion, 2/3 discharged from the urine. In 3 days of low purine diet after normal uric acid excretion in 24 hours for 300~600mg, 600~900mg. under the condition of normal dietary intake and food sources, uric acid every day about 450mg. hyperuricemia and gout following organ transplantation is receiving cyclosporine in the treatment of the most common complications in patients with. Premenopausal women uric acid levels than males in the low 1mg/dl ( 0.6mmol/L ), but after menopause male close level. Editor this paragraph pathogenesis of gout pathogenesis
Long term high uric acid in blood is the key reason of gout. Human uric acid mainly comes from two aspects: 1, the cells of the body protein catabolism derived nucleic acids and other purine compounds, by some enzymes and generate endogenous uric acid. In 2, the food contained in the purine compounds, nucleic acid and nuclear protein composition, after digestion and absorption, by some enzymes generating exogenous uric acid. The formation of uric acid is a very complex process, requiring some enzymes involved in the. These enzymes can be broadly divided into two categories: promotion of uric acid synthesis enzymes, mainly for the 5- phosphoric acid nucleic acid -1- pyrophosphate synthetase, adenine nucleotides transferase, phosphoribosylpyrophosphate amidotransferase and xanthine oxidase inhibition by uric acid; synthesis enzymes, mainly hypoxanthine - bird purine nucleoside transferase. Gout is due to various factors leading to the activity of these enzymes abnormalities, such as the promotion of uric acid synthetase activity, inhibiting the uric acid synthetase activity weakened, resulting in the formation of uric acid over. Or due to various causes renal excretion of uric acid to produce an obstacle, the accumulation of uric acid in the blood, resulting in hyperuricemia. Hyperuricemia as a long-standing, uric acid uric acid salt form will be deposited in the joints, the subcutaneous tissue and the kidney and other parts, cause arthritis, gout calculi, kidney stones or subcutaneous gouty nephropathy and a series of clinical manifestations. This disease of peripheral joint of recurrent acute or chronic arthritis, is due to supersaturation of hyperuricemia in body fluids by monosodium urate crystals in joints, tendons and its surrounding deposition induced by. Pathogenesis of gout patients and a ratio of 20 to 1, female gout incidence is low main reason is: the female hormones can promote the excretion of uric acid, and inhibit the onset of arthritis effect. If it is genetic of gout patients, because of incomplete metabolism of relationship, most and primary hypertension. Editor this paragraph clinical manifestations due to uric acid in human blood concentration is too high, in the soft tissues such as articular membrane or tendon in the formation of acicular crystal, causing the body to avoid
The immune system react ( sensitive ) and cause painful inflammation. The general attack positions as the thumb joint, ankle joint, knee joint. Chronic gout patients have seizures in the finger joints, and even parts of the ear with soft tissue case. Acute gouty attack site appears red, swollen, hot, severe pain, usually in the middle of the night attack, can make the person is awakened from sleep in. Early onset gout, more common in the lower limb. Gout can appear kidney damage. According to statistics, 20% - 25% of gout patients with uric acid nephropathy, and confirmed by autopsy, renal lesions of almost 100%. It includes gouty nephropathy, acute obstructive nephropathy and urinary stones.
Symptoms and signs
1 gouty nephropathy: persistent hyperuricemia, 20% in on clinical renal lesion was performed, after several years or longer may appear early or late renal tubular and glomerular damage, little part to uremia. Urate nephropathy incidence after gout arthritis injury, and has close relationship with the clinical course and treatment. Research shows, urate nephropathy and gouty arthritis severity was unrelated, i.e. mild arthritis patients may also have kidney disease, and severe arthritis patients do not have kidney abnormality. Early mild unilateral or bilateral flank pain, followed by mild edema and moderately elevated blood pressure. Urinary acidic, intermittent or persistent proteinuria, usually not more than + +. Almost all renal tubular concentration function decline, nocturia, polyuria, appear relatively low density of urine. About 5, 10 years after nephropathy aggravates, further development of uremia, about 17% - 25% died of renal failure. 2 urinary stones: gout patient urine acidic, and urinary uric acid concentration increased, the smaller stones in the urine, but often feel, urinary sediments visible in small brown sand; larger stones may be caused by obstruction of the ureter and renal colic hematuria, urinary flow is not smooth because of secondary infection become pyelonephritis. Large stones can cause renal pelvis deformation, hydronephrosis. Pure uric acid stones X line is not developing, when uric acid sodium and calcium salt of X online visible stone shadow. In 3 acute obstructive nephropathy: found in serum uric acid and urinary uric acid increased significantly, that is due to the large number of uric acid crystals in extensive obstruction caused by renal tubule. Gout and often have hypertension, hyperlipemia, arteriosclerosis, coronary heart disease and type 2 diabetes mellitus. In the cause of death in the elderly gout, cardiovascular factors than renal insufficiency. But the gout and cardiovascular disease is not a direct causal link, but both were associated with obesity, dietary factors. 4 tophi: also called gout nodules, is the human body due to excessive increase of blood uric acid, beyond its saturation in a part of the body of the white crystal precipitation. Like a cup of brine in salt content exceeds a certain limit, the bottom of the cup will appear white sediment. The separated crystal deposition in what place, on Tophus
Can what parts of the stones, gout patients in addition to the central nervous system, almost all tissues can form a tophus.
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