Diabetes

Introduction Generally refers to glucose and urine. Normal people have a small amount of glucose in the urine, and the daily urine sugar content is 0.7~0.52 mmo1 (31-93 mg), and the qualitative test is negative. Daily urine sugar exceeds 0.83 IIUnol door p) is positive by qualitative test, called diabetes. The previous qualitative test of diabetes used copper sulfate reagent (Ban's L is based on the reduction of sugar, urine contains glucose, fructose sugar, maltose, pentose, non-sugar substances with reducing effect (some drugs can be positive) In recent years, glucose oxidase paper method has been used to measure urine sugar, which is specific to glucose, but it can also be positive when ascorbic acid or salicylate is present.

Cause

mechanism

First, blood sugar increased diabetes

The normal human insulin excretion threshold is 8.9 mmol/L (160 mg/dl), and the appearance of diabetes is related to the following factors:

1 circulating blood glucose concentration> 8.g mmol / L (160mg / dl);

2 glomerular swimming through the glucose rate;

3 The rate of reabsorption of glucose by the renal proximal convoluted tubules. The normal human glomerular filtration rate is 125ml/min. If the blood glucose is normal 5.6 mmol/L (100 mg/dl), the glucose is filtered from the glomerulus by 125 mg, while the normal human renal proximal tubule reabsorbs glucose. 250-300mg/min, the glucose filtered from the glomerulus was completely reabsorbed in the first battle without sugar; for example, the blood glucose concentration was 16.7 mmol/L (300 mg/dl), and the glomerular glucose was 375. Mg / min, after the absorption of renal tubules, the remaining 75 ~ 125mg with the urine excretion, the emergence of diabetes. The stability of blood glucose levels in normal people depends on the coordination of central sleeves, endocrine glands, liver, gastrointestinal and kidneys. The endocrine glands and liver are the most important. The only hormone that lowers blood sugar in insulin county. When the insulin secretion is absolutely or relatively insufficient or the target cells are less sensitive to insulin, the blood level rises, and when the renal sugar threshold is exceeded, diabetes occurs.

The most common clinical manifestations are primary diabetes and impaired glucose tolerance with hyperglycemia. There are more hormones in the body that have elevated blood sugar, mainly:

1 Glucagon: Secreted by the islet A cells, it can activate liver phosphorylase, promote the decomposition of liver glycogen into glucose, promote gluconeogenesis, and thus increase blood sugar. In normal people, when glucagon is too high, glucagon secretion is inhibited, but it is not inhibited in diabetes. Especially in acidosis, glucagon is 2-4 times higher than normal. In the islet A cell tumor (glucagonoma), the glucagon concentration is absolutely too high, causing hyperglycemia and diabetes.

2 Adrenal gland promotes the release of glucagon, inhibits insulin secretion, reduces the utilization of sugar by peripheral tissues, causes hepatic glycogen decomposition and increased gluconeogenesis, and increases blood sugar. In pheochromocytoma, tumor tissue secretes polyphenols (adrenalin and norepinephrine) to cause hyperglycemia and diabetes.

3 growth hormone promotes lipolysis and gluconeogenesis, inhibits insulin's role in promoting glucose permeation through the cell membrane, inhibits intracellular glucose phosphorylation, raises blood sugar and occurs in diabetes. Acromegaly, giant disease, excessive growth hormone in the body, resulting in high blood sugar and diabetes.

4 Adrenal cortex hormone (mainly cortisol) inhibits the uptake and utilization of glucose by peripheral tissues, promotes protein decomposition and causes a large amount of amino acids to enter the liver, and promotes gluconeogenesis, such as hypercortisolism (Cushing's syndrome), when blood sugar is increased And there is diabetes.

5 thyroid hormone accelerates the absorption of sugar in the intestine, enhances the decomposition of glycogen and muscle glycogen, accelerates gluconeogenesis, accelerates the degradation of insulin, and causes hyperglycemia and diabetes. For example, hyperthyroidism is often accompanied by impaired glucose tolerance or diabetes.

Hyperglycemia causes hyperglycemia, and pancreatic cancer, acute or chronic pancreatitis, and pancreatic resection can cause hyperglycemia and diabetes due to insulin deficiency. Intravenous injection of glucose or eating a large amount of sugar causes the intestine to absorb too much sugar and can cause hyperglycemia and diabetes. Liver function damage causes blood sugar to be converted to hepatic glycogen, resulting in postprandial hyperglycemia and diabetes. In some stress states (acute myocardial infarction, cerebrovascular accident, etc.), hyperglycemia can increase stress and hyperglycemia and diabetes.

Second, normal blood sugar, diabetes

Normal blood sugar, normal glucose tolerance, due to the ability of the renal tubular to reabsorb sugar, resulting in diabetes, called renal diabetes. When the ability of the renal tubular re-absorbs sugar to fall below 150 mg/min (normally 250 mg/min), glycemicity occurs when blood glucose exceeds 6.7 mmol/L and the ability of human glomerular filtration of glucose is normal (150 mg filtered per minute). Found in familial renal diabetes, renal tubular acidosis, Fanconi syndrome. During pregnancy, due to increased extracellular fluid volume, glomerular filtration rate increases, the function of re-absorption of sugar in the proximal convoluted tubule is inhibited, and the renal sugar threshold is lowered to cause diabetes, which is called gestational diabetes.

Diabetes is found in many diseases, and the causes are classified as follows:

First, glucose urine

(a) blood sugar increased diabetes

1. Primary diabetes: 1 insulin-dependent (type I) diabetes; 2 non-insulin-dependent (type 2) diabetes; 3 malnutrition-associated diabetes.

2. Gestational diabetes.

3. Secondary diabetes (with a clear cause) 1 Pancreatic diabetes: pancreatitis, pancreatic cancer, pancreatectomy. 2 endocrine: hyperthyroidism, Cushing's syndrome. Glucagonoma, pancreatic somatostatin, vasopressin, pheochromocytoma, primary aldosteronism, hypoparathyroidism (hypocalcemia), acromegaly, and giant disease Wait. 3 drugs and chemicals caused by diabetes: streptozotocin, alloxan, rodenticide vacor; diuretic antihypertensive drugs in thiazide diuretics, furosemide, etalic acid, chlorpromone, cola Ding, chlorobenzyl dioxazide; analgesic antipyretics such as aspirin, indomethacin; ACTH in hormonal drugs, glucocorticoids, growth hormone, glucagon, thyroid hormone, catecholamines, female oral contraceptives In the neuropsychiatric drugs, phenytoin, levodopa, isoproterenol, propranolol, chlorpromazine, perphenazine, bicarbonate, chloropyrazine, and tricyclic anti-inhibitors Ping, amitriptyline, normic acid, imipramine; other morphine, cyclic phosphate, aspartame, isoniazid, EDTA, cimetidine, heparin; cadmium, aluminum in heavy metals , mercury poisoning, etc. 4 Insulin receptor abnormalities such as con-genital lipodystrophy, acanthosis nigricans with female masculinization, and insulin-resistant drug-induced diabetes caused by receptor antibodies. 5 hereditary syndrome with diabetes, such as type 1 hepatic glycogenosis, acute paroxysmal porphyria, hyperlipidemia, diabetic optic atrophy with diabetes insipidus and deafness, insulin resistance syndrome such as lipoatrophy syndrome , early and old syndrome.

4. Others: 1 stressive diabetes; 2 hepatogenic diabetes; 3 nourishing diabetic; 4 hemochromatosis.

(two) normal blood sugar diabetes

Renal glucosuria, pregnancy, tubular lesions, certain nephrotoxic chemicals such as carbon monoxide, lead, mercury, etc.

Second, non-glucose urine

Lactoseuria, fructoseuria, galactoseuria, pentoseuria, non-sugar substances Benedict qualitative false positive diabetes such as vitamin C, uric acid, glucuronic acid, salicylic acid, hypochlorite (oxidation of pigments), hydrogen peroxide (oxidized pigment), isoniazid, tetracycline. Streptomycin, rhubarb, scutellaria, and phellodendron in traditional Chinese medicine, and gynecological external use of furazolidone powder (including sugar).

an examination

Related inspection

Serum already urinary sediment apolipoprotein AI glycated serum protein (GSP) placental lactogen

First, medical history

(1) Family history

Hyperglycemia is more common in diabetes (type 1 and type 2), which is related to genetic factors, and has a positive family history such as diabetes and hypertension.

(2) Eating and living habits

Typical diabetic patients have three syndromes, namely polydipsia, polydipsia, polyuria, and polyphagia. In mild cases, the trisomy is inconspicuous or asymptomatic, but usually eats a lot or eats sweets, nightingales, etc. Overweight or obese, less activity, etc. Many patients first found complications such as prone to swollen edema, urinary tract infection, and genital itching. Diabetes is found in cholecystitis, tuberculosis, cataracts, and the like. In renal glucosuria, due to impaired renal tubular function, the urine concentration function is low, and a large amount of hypotonic urine is discharged to cause polyuria and polydipsia.

(3) Asking about past medical history and medication history

History of liver disease, history of gastrointestinal disease (acute and chronic pancreatitis), history of gastrointestinal surgery (history of major gastrectomy, history of pancreatic resection), history of kidney disease, history of endocrine disease (history of secondary diabetes) should also be asked about medication history. Such as the history of diuretic antihypertensive drugs (thiazide diuretics, furosemide, ethenic acid, clonidine, etc.), phenytoin, propidolol, glucocorticoids, cyclic phosphate and so on.

(4) Personal history, menstrual history, childbirth history and many other endocrine diseases caused by hyperglycemia and diabetes often accompanied by menstrual disorders. Women who give birth to a large fetus are often at high risk for diabetes.

Second, physical examination

Detailed examination is another important clue to diabetes in addition to medical history. Body obesity, uniform fat distribution or above-mentioned half-body obesity, more common in diabetes type 2. Many secondary hyperglycemia and diabetes have special postures, such as acromegaly or giant disease, hypercortisolism (Cushing's syndrome), hyperthyroidism, glucagonoma, pheochromocytoma, severe Liver disease, etc.

Third, laboratory inspection

(1) Urine sugar qualitative and quantitative

1. Urine sugar qualitative test: generally use copper reduction method (Bene-dict) and glucose oxidase test paper method, the former is less specific, urine can be pentose, lactose, galactose, fructose, etc. can be positive, urine Some substances such as vitamin C, salicylate, etc. may also be positive; the latter is highly specific.

2. Urine sugar quantification: to understand the total amount of sugar excreted in the patient's 24h urine, in order to judge the improvement or deterioration of the patient's metabolic condition. In general, the amount of urine glucose is parallel to the blood glucose level, but when the glomerular filtration rate of the patient is reduced due to glomerular lesions, and the renal tubular function is normal, the blood sugar may be high but the amount of urine sugar does not increase. The urine sugar can be quantified by the o-toluidine method or the copper reduction method, and the method for measuring blood sugar is also applicable to the urine sugar amount.

(two) blood glucose measurement (plasma true method)

The fasting blood glucose concentration of normal people was 3.9-6.1 mmol/L (70-110 mg/dl). The fasting blood glucose was 7.8 mmol/L (140 mg/dl) in diabetes, and the blood glucose was 11.1 mmol/L (200 mg/dl) 2 hours after meal.

(3) Oral Glucose Tolerance Test (OGTT)

Applicable to diabetes positive, fasting blood glucose > 5.9-106 ~ <140mg / dl), clinically suspected of diabetes. If the diagnosis of fasting blood glucose 7.8 mmol / L diabetes can be determined, then taking a large amount of glucose can increase the islet burden, should be exempted. The most common clinical use is oral 75 g glucose (or 1.75 g per kg body weight). Rest for 30 minutes before the test, the subjects were fasted for 10-12 h. After taking empty blood, 75 g of glucose solution dissolved in 250-350 ml of water was consumed in 5 min, then blood was collected at 30, 60, 120, and 18 min. Blood glucose measurement (if necessary, it can be extended to 4-5h people at the same time, urine is collected every time to measure urine sugar (qualitative). Normal people are almost completely absorbed by the intestine after taking sugar, the peak is 30 to 60 minutes after taking sugar, below the peak abdominal level Urine sugar is negative. After the age of more than 50 years old, the glucose tolerance is physiologically reduced, and the blood glucose increases by 0.56 mmol/L (10 mg/dl) every 10 years of age at the peak of lh. Low glucose diet or starvation can reduce glucose tolerance before the test. 3d should adjust the diet so that the daily sugar is not less than 250 g to get reliable results.

(D) Cortisol glucose tolerance test.

For suspicious cases that have not been diagnosed by OGTT, this method can be used: oral cortisone 50 mg at 8 h and 2 h before the test, or 10 mg prednisone 2 h before the test, according to the OGTT method, and the results are the same as OGTT.

(5) Other inspections

1. Determination of blood and urine endocrine hormones: AC TT, TSH, GH. Cortisol, T3, T4 catecholamines, glucagon, etc. are helpful for the diagnosis of endocrine hyperglycemia and diabetes.

2. Renal function measurement, hematuria osmotic pressure measurement, hematuria pH value measurement, urine relative density, blood gas analysis, etc., can help the diagnosis of renal diabetes.

3. Determination of liver function: meaningful for the diagnosis of hepatic hyperglycemia and diabetes. Fructose and galactose are used abnormally when liver dysfunction, and fructose or galactose can occur in the blood.

4. Blood electrolyte analysis is useful for the diagnosis of the cause of diabetes.

Fourth, equipment inspection

For pancreatitis, pancreatic cancer, pheochromocytoma, acromegaly or giant disease, Cushing's syndrome and other diseases that cause hyperglycemia and diabetes, it is often necessary to use B-mode ultrasound, X-ray (CT, MRI, etc.) .

Differential diagnosis

Renal glucosuria refers to a disease of diabetes caused by a decrease in glucose function in the proximal tubules when the blood glucose concentration is normal or lower than the normal renal sugar threshold. First, we should rule out the overflowing diabetes and non-glucose glucosuria caused by hyperglycemia. The urinary succinol test is positive in fructose, the urinary urinary dihydroxytoluene hydrochloride is positive, the lactoseuria, galactose and mannose glucosuria use urine. Paper chromatography can be determined.

Keto-urine: severely starved or untreated diabetics with low blood glucose levels lead to increased gluconeogenesis, fatty acid oxidation accelerates the production of large amounts of acetyl-CoA, while gluconeogenesis causes oxaloacetate to be depleted, while the latter is acetyl-CoA into the lemon Essential for the acid cycle, whereby acetyl-CoA is directed to the direction of the ketone body. A large number of ketone bodies appear in the blood and urine.

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