In uremia, in addition to water, electrolyte, acid-base balance disorders, anemia, bleeding tendency, hypertension aggravated, but also clinical manifestations of each organ system dysfunction, and metabolic disorders caused by substance, it is described as follows.
(A) neurological symptoms
Neurological symptoms are the main symptoms of uremia. In the early uremia, patients often have dizziness, headache, fatigue, comprehension and memory loss and other symptoms. As the disease worsens, there may be irritability, muscle tremor, convulsions; may eventually develop into apathy, lethargy and coma. These symptoms occur with the following factors: ① some accumulation of toxic substances may cause nerve cell degeneration; ② electrolyte and acid-base balance disorders; ③ renal hypertension caused by cerebral vasospasm, hypoxia and capillary permeability increased, which can cause degeneration of brain cells and brain edema.
(B) digestive symptoms
The earliest symptoms of uremia patients with digestive system is loss of appetite or indigestion; exacerbations can occur when anorexia, nausea, vomiting or diarrhea. These symptoms may occur within the intestinal bacterial urease urea decomposition of ammonia, ammonia stimulate gastrointestinal mucosa causing inflammation and multiple superficial small ulcers and so on. Patients often complicated by gastrointestinal bleeding. Also nausea, vomiting, and also related to the central nervous system dysfunction.
(C) the cardiovascular system symptoms
Chronic renal failure due to renal hypertension, acidosis, hyperkalemia, sodium and water retention, anemia and toxic substances can be heart failure, arrhythmias, and myocardial damage and so on. Since urea (possibly uric acid) of stimulation effect, but also aseptic pericarditis, patients determined before the pain, smell and pericardial friction rub physical examination. Severe pericardial cavity cellulose and bloody exudate appears.
(D) respiratory symptoms
Acidosis in patients with slow and deep breathing, severe acidosis can be seen particularity Kussmaul breathing. The off gas exhaled by the patient with Niaowei, which is due to bacterial decomposition of urea solution formed sleeping ammonia sake. Can occur in patients with severe pulmonary edema, or pulmonary calcification cellulose pleurisy and other diseases, pulmonary edema and heart failure, hypoalbuminemia, sodium and water retention and other factors related to the role of stay. Cellulose pleurisy is caused by inflammation of urea stimulation; lung calcification calcium phosphate deposition in the lung tissue caused.
(E) skin symptoms
Uremic pruritus is common in patients with symptoms that may be toxic products stimulate receptors on the skin caused; others believe and secondary hyperparathyroidism related, because the removal of the parathyroid, can relieve the pain immediately symptoms. In addition, patients with dry skin, scaling and was brown. Changes in skin color, previously thought to be an increase in the urinary pigment so, but check with the absorption spectrophotometer proved mainly for skin pigment melanin. Exposed parts of the skin, can cause slight contusion skin ecchymosis. Since sweat contains high concentrations of urea, and therefore the opening of the sweat glands in the white crystals of urea, known as urea cream.
(F) metabolism disorders
1. Uremic patients with impaired glucose tolerance reduces the amount of glucose tolerance, the glucose tolerance curve and mild diabetes are similar, but this change is not sensitive to exogenous insulin. Mechanisms may cause impaired glucose tolerance as follows: ① reduced insulin secretion; ② When uremia due to elevated basal levels of growth hormone secretion, so antagonistic to strengthen the role of insulin; ③ insulin receptor binding to target cells obstacles to insulin's effects vary weakened; ④ related glycogen synthase activity decreased glycogen synthesis caused the disorder. Now that the main cause of these changes may be urea, creatinine, and the molecular weight of poisons and other toxic effects.
2. Negative nitrogen balance negative nitrogen balance can cause the patient weight loss, cachexia and hypoalbuminemia. Hypoalbuminemia is one of the important causes of renal edema. Factors that cause negative nitrogen balance are: ① patients restricted intake of protein or because anorexia, nausea and vomiting caused reduced intake of protein; ② certain substances such as methyl guanidine can strengthen tissue protein catabolism; ③ infection when available resulting in enhanced protein breakdown; ④ protein loss caused by bleeding; ⑤ with urine lost a certain amount of proteins.
Uremia lot of blood urea may penetrate the intestine. Intestine bacteria can be released from the decomposition of urea and ammonia, the blood is transported to the liver, the urea can be synthesized, non-essential amino acids can also be synthesized, which is beneficial to the body. So some people think that protein intake uremic patients may be less than the normal person, even less than 20g a day to maintain nitrogen balance, but it must be given a higher nutritional value of protein, essential amino acids that contain abundant nutrients. In recent years, some people think.
Uremic patients in order to maintain nitrogen balance, protein intake should be no significant difference between normal; but think simply in order to pursue lower blood urea nitrogen and unduly limit protein intake, consume too much protein can make their own, and thus harmful to the patient. 3. Uremic patients with hyperlipidemia mainly due to hepatic triglyceride synthesis required for lipoprotein (former β- lipoprotein) increased, so increased production of triglycerides; but also may be due to lipoprotein lipase (lipoprotein lipase) activity decreased caused by decreased clearance of triglycerides, it is easy to form hypertriglyceridemia. Such changes may be related to the accumulation of methyl guanidine.
(A) neurological symptoms
Neurological symptoms are the main symptoms of uremia. In the early uremia, patients often have dizziness, headache, fatigue, comprehension and memory loss and other symptoms. As the disease worsens, there may be irritability, muscle tremor, convulsions; may eventually develop into apathy, lethargy and coma. These symptoms occur with the following factors: ① some accumulation of toxic substances may cause nerve cell degeneration; ② electrolyte and acid-base balance disorders; ③ renal hypertension caused by cerebral vasospasm, hypoxia and capillary permeability increased, which can cause degeneration of brain cells and brain edema.
(B) digestive symptoms
The earliest symptoms of uremia patients with digestive system is loss of appetite or indigestion; exacerbations can occur when anorexia, nausea, vomiting or diarrhea. These symptoms may occur within the intestinal bacterial urease urea decomposition of ammonia, ammonia stimulate gastrointestinal mucosa causing inflammation and multiple superficial small ulcers and so on. Patients often complicated by gastrointestinal bleeding. Also nausea, vomiting, and also related to the central nervous system dysfunction.
(C) the cardiovascular system symptoms
Chronic renal failure due to renal hypertension, acidosis, hyperkalemia, sodium and water retention, anemia and toxic substances can be heart failure, arrhythmias, and myocardial damage and so on. Since urea (possibly uric acid) of stimulation effect, but also aseptic pericarditis, patients determined before the pain, smell and pericardial friction rub physical examination. Severe pericardial cavity cellulose and bloody exudate appears.
(D) respiratory symptoms
Acidosis in patients with slow and deep breathing, severe acidosis can be seen particularity Kussmaul breathing. The off gas exhaled by the patient with Niaowei, which is due to bacterial decomposition of urea solution formed sleeping ammonia sake. Can occur in patients with severe pulmonary edema, or pulmonary calcification cellulose pleurisy and other diseases, pulmonary edema and heart failure, hypoalbuminemia, sodium and water retention and other factors related to the role of stay. Cellulose pleurisy is caused by inflammation of urea stimulation; lung calcification calcium phosphate deposition in the lung tissue caused.
(E) skin symptoms
Uremic pruritus is common in patients with symptoms that may be toxic products stimulate receptors on the skin caused; others believe and secondary hyperparathyroidism related, because the removal of the parathyroid, can relieve the pain immediately symptoms. In addition, patients with dry skin, scaling and was brown. Changes in skin color, previously thought to be an increase in the urinary pigment so, but check with the absorption spectrophotometer proved mainly for skin pigment melanin. Exposed parts of the skin, can cause slight contusion skin ecchymosis. Since sweat contains high concentrations of urea, and therefore the opening of the sweat glands in the white crystals of urea, known as urea cream.
(F) metabolism disorders
1. Uremic patients with impaired glucose tolerance reduces the amount of glucose tolerance, the glucose tolerance curve and mild diabetes are similar, but this change is not sensitive to exogenous insulin. Mechanisms may cause impaired glucose tolerance as follows: ① reduced insulin secretion; ② When uremia due to elevated basal levels of growth hormone secretion, so antagonistic to strengthen the role of insulin; ③ insulin receptor binding to target cells obstacles to insulin's effects vary weakened; ④ related glycogen synthase activity decreased glycogen synthesis caused the disorder. Now that the main cause of these changes may be urea, creatinine, and the molecular weight of poisons and other toxic effects.
2. Negative nitrogen balance negative nitrogen balance can cause the patient weight loss, cachexia and hypoalbuminemia. Hypoalbuminemia is one of the important causes of renal edema. Factors that cause negative nitrogen balance are: ① patients restricted intake of protein or because anorexia, nausea and vomiting caused reduced intake of protein; ② certain substances such as methyl guanidine can strengthen tissue protein catabolism; ③ infection when available resulting in enhanced protein breakdown; ④ protein loss caused by bleeding; ⑤ with urine lost a certain amount of proteins.
Uremia lot of blood urea may penetrate the intestine. Intestine bacteria can be released from the decomposition of urea and ammonia, the blood is transported to the liver, the urea can be synthesized, non-essential amino acids can also be synthesized, which is beneficial to the body. So some people think that protein intake uremic patients may be less than the normal person, even less than 20g a day to maintain nitrogen balance, but it must be given a higher nutritional value of protein, essential amino acids that contain abundant nutrients. In recent years, some people think.
Uremic patients in order to maintain nitrogen balance, protein intake should be no significant difference between normal; but think simply in order to pursue lower blood urea nitrogen and unduly limit protein intake, consume too much protein can make their own, and thus harmful to the patient. 3. Uremic patients with hyperlipidemia mainly due to hepatic triglyceride synthesis required for lipoprotein (former β- lipoprotein) increased, so increased production of triglycerides; but also may be due to lipoprotein lipase (lipoprotein lipase) activity decreased caused by decreased clearance of triglycerides, it is easy to form hypertriglyceridemia. Such changes may be related to the accumulation of methyl guanidine.
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