Uremia causes other changes in the human body system2017-04-26 18:52
Uremia is water, electrolyte, acid-base balance disorders, can not be normal metabolism, is the body of toxins can not rule out a process, anemia, bleeding tendency, a series of changes in hypertension, but also the emergence of various organ dysfunction and substances Metabolic disorders caused by the clinical manifestations, as described below.
(1) nervous system symptoms
Symptoms of the nervous system are the main symptoms of uremia in the early stage of uremia, patients often have dizziness, headache, fatigue, understanding and memory loss and other symptoms.With the aggravation of the condition can be irritability, muscle fibrillation, convulsions; Can develop into the expression of indifference, drowsiness and coma.The occurrence of these symptoms related to the following factors: ① accumulation of certain toxic substances may cause nerve cell degeneration; ② electrolyte and acid-base balance disorders; ③ renal hypertension caused by cerebrovascular Spasm, hypoxia and increased capillary permeability, can cause brain neuronal degeneration and brain edema.
(2) digestive system symptoms
Uremic patients with the earliest symptoms of digestive system is loss of appetite or indigestion; exacerbations may occur when anorexia, nausea, vomiting or diarrhea.The incidence of these symptoms may be associated with intestinal bacteria urease will urea decomposition of ammonia, ammonia stimulation of the stomach Intestinal mucosa caused by inflammation and multiple superficial small ulcers, etc. Patients often complicated by gastrointestinal bleeding, in addition to nausea, vomiting and central nervous system dysfunction.
(3) cardiovascular system symptoms
Chronic renal failure due to renal hypertension, acidosis, hyperkalemia, sodium and water retention, anemia and toxic substances such as the role of heart failure, arrhythmia and myocardial damage, etc. As a result of urea (and possibly Uric acid) stimulating effect, but also the occurrence of aseptic pericarditis, patients with precordial pain, physical examination and pericardial fricative. Severe cases of pericardial cavity in the cellulose and bloody exudate appear.
(4) respiratory symptoms
Acid poisoning in patients with slow and deep breathing, severe acidosis can be seen when the specificity of Kussmaul breathing. Patients exhaled breath with urine, which is due to bacterial decomposition of saliva in the formation of urea in the urine of patients with severe pulmonary edema , Fibrous pleurisy or pulmonary calcification and other diseases, pulmonary edema and heart failure, hypoproteinemia, sodium and water retention and other factors related to the role of cellulose pleurisy is caused by urea stimulation of inflammation; pulmonary calcification is calcium phosphate in lung tissue Deposits.
(5) skin symptoms
Skin itching is a common symptom of uremic patients, which may be caused by the stimulation of the skin receptors; some people think that with the secondary hyperparathyroidism, because the removal of the parathyroid, can immediately lift the pain In addition, the patient's skin dry, scaling and brown. Skin color changes, previously considered to be increased urinary pigment, but with the absorption spectrophotometer to check the skin pigment mainly melanin in the skin exposed parts, Slight contusion can cause skin eczema.As the sweat contains a higher concentration of urea, so in the sweat glands have white urea crystals, known as urea cream.
(6) material metabolic disorders
1. Glucose tolerance Reduces tolerance to sugar in uremic patients, whose glucose tolerance curve is similar to that of mild diabetes, but this change is insensitive to exogenous insulin. The mechanism of impaired glucose tolerance may be: (1) reduced insulin secretion; ② uremia due to the level of growth hormone secretion increased, so the role of antagonism of insulin to strengthen; ③ insulin and target cell receptor binding disorders, so that the role of insulin has weakened; ④ liver glycogen synthase activity decreased Glycogen synthesis disorders. At present that the cause of the above changes may be the main reason for urea, creatinine and molecular weight toxic effects such as toxic.
2. Negative nitrogen balance Negative nitrogen balance can cause patients to lose weight, cachexia and hypoalbuminemia. Hypoalbuminemia is one of the important causes of renal edema caused by negative nitrogen balance factors are: ① patients into the protein Limited or due to anorexia, nausea and vomiting caused by reduced protein intake; ② some substances such as methyl guanidine can contribute to the decomposition of cathepsin; ③ infection can lead to increased protein decomposition; ④ due to bleeding caused by protein loss; ⑤ with the urine loss of a certain amount of protein and so on.
Uremia can be a lot of urea from the blood into the intestine. Intestinal bacteria can be decomposed and released ammonia urea, ammonia transported to the liver after the blood can be synthesized urea, but also the synthesis of non-essential amino acids, which is beneficial to the body Therefore, some people think that uremic patients with protein intake can be lower than normal, even lower than 20g per day to maintain nitrogen balance, but must be given higher nutritional value of the protein, that is essential amino acids rich in nutrients. In order to maintain the nitrogen balance of uremic patients, protein intake should not be significantly different from normal people; and that, in order to pursue the blood urea nitrogen reduction and excessive restrictions on protein intake, can make their own protein consumption Too much, and thus detrimental to the patient and no benefit
3. Hyperlipidemia uremic patients mainly due to liver synthesis of triglycerides required lipoprotein (pre-β-lipoprotein) increased, so the production of triglycerides increased; also may be due to lipoprotein lipase (lipoproteinlipase) activity Reduced triglyceride clearance rate caused by reduced, it is easy to form hypertriglyceridemia .This change may be related to the accumulation of methyl guanidine.