Diabetes knowledge spectrograph speaker: date: table 02, basic awareness of major speculative characteristics 01 disease,03 clinical performance and integrated management strategy 05 for diagnosis of 04 emergency chronic complications 05 integrated management strategy for the prevention and monitoring of epidemics 04. Type 1 diabetes is absolutely free of insulin due to its own immune damage to beta-celled insulin; type 2 diabetes is sexually sterilised in conjunction with insulin resistance; and pregnancy diabetes is associated with hormonal change during pregnancy. Continued high blood sugar can cause microvascular disease (retina, kidneys) and large vascular disease (hardening of anorexia) and increase the risk of neuroses. The key indicator for blood sugar metabolism (fpg) 01 is a normal value of 3. 9 - 6. 1 mmol/l, and ≥7. 0mmol/l can assist in diabetic diagnosis, reflecting basic insulin inoculation. The normal value of 2 hours of blood sugar (2hpg)02 < 7. 8mmol/l, ≥11. 1mmol/l is the diabetes criterion for assessing post-eating insulin regulation. The sugared hemoglobin (hba1c)03, which reflects average blood sugar levels for nearly three months, and the diagnosis threshold for diabetes, which is 6. 5%, are important indicators for the prediction of complications. Oral glucose tolerance test (ogtt)04 is dynamically monitored for screening for early diabetes or sugar tolerance anomalies. Insulin physiological effects promote glucose ingestion of glucose, which accelerates the intake and use of glucose by skeletal muscles and fat cells through the activation of the glut4 trans-shipment body and reduces blood sugar concentrations. Inhibition of liver sugar output inhibits liver glucose hexalysis, reduces internal glucose generation and maintains an empty abdominal sugar stability. Regulating fat metabolism promotes fat synthesis and inhibits fat decomposition, reduces releases of free fatty acids and reduces the risk of ketone disease. Protein synthesis promotes enhanced amino acid transfer to cells, promotes protein synthesis, inhibits protein decomposition and maintains a nitrogen balance. The main stylistic characteristic, chapter 1, interacts with the genetic and environmental factors of the hla-dr3/dr4 genotype, with a significant increase in the risk for carriers, and viral infections, such as the kosage virus, can trigger their own immune response. Sudden diseases are common among adolescents, as shown by drinking, urine, a sharp decline in body weight, and acute metabolic disorders such as diabetic acid poisoning. Insulin is absolutely lacking and requires life-long insulin treatment. The multiple metabolic co-effects of type 012 diabetes onset mechanism 03 are often associated with obesity (especially internal fat accumulation), lipid metabolic disorders (high glycerine triester haemasis), chronic low inflammation state (tnf-α, il-6). The sexual decline in the β-cell function of insulin 02 accelerated the process with the progression of the pathology, the reduction in the number of β-cells and the impairment of their functioning, and insulin deposition and oxidation. Insulin resistance and retributive high-insulin haemorrhagic tissues (muscle, liver, fat) are less sensitive to insulin, with the early recovery of beta-cells through increased excretion and subsequent endocrine failure. The special screening and diagnostic criteria for the characteristics of diabetes during pregnancy are subject to a 75-gogtt test in the 24-28 week of pregnancy, which can be confirmed by any blood sugar overvalue (5. 1 mmol/l, 1h ≥10. 00 mmol/l, 2h ≥8. 5 mmol/l). The resistance to insulin in the late stages of pregnancy increases placenta hormonal hormones (e. G. Hpl, pregnancy ketone) is resistant to insulin, and normal pregnant women can be paid for by β cells, but there are abnormal sugar tolerances in high-risk groups. The double health risk for mothers and children increases the risk of high child, birth injury and low blood sugar for newborns, while the incidence of type 2 diabetes in the long term for mothers increases sevenfold, requiring a re-evaluation of sugar metabolism 6-12 weeks after delivery. Clinical performance and diagnosis of a typical "triple or less" of chapter's symptoms led to increased plasma penetration pressure due to an increase in blood sugar, irritation of the hypochondriatic centre, sustained and incalculable thirst, and daily drinking water of more than 3-5 l. Over01 insulin absolute or relative insufficiency has led to glucose use disorders, and the body has increased its intake in return for eating behaviour, as evidenced by a high appetite and a still evident sense of hunger after eating. Permeability is triggered by hyperuregic glucose states above the kidney sugar threshold (usually >10mmol/l), with a maximum of 2-3l urine per hour, and night-time urination can affect sleep in severe cases. Despite the increase in diets, the weight reduction was 5-10 per cent due to the accelerated use of glucose and the accelerated decomposition of fats, often due to unknown weight decreases within 1-3 months. 020304 diagnostic standards and detection methods, which operate easily but may leak after-eating patients with hyperglucose, after not receiving calorie for at least eight hours, are gill 7. 0mmol/l. An empty abdominal sugar test shows an average blood sugar level of nearly 2-3 months, with 6. 5% thorium of diagnostic value, but is disturbed by anaemia and haemoglobinism. Hba1c tested 75 g g g glucose for two hours, thalycol 11. 1 mmol/l, which is the gold standard for diabetic diagnosis, and is particularly applicable to people who suffer from abdominal sugar deficiency. The typical symptoms of glucose glucose tolerance test (ogtt) 010302 in abdominal form can be used as a basis for diagnosis, with attention to the identification of hyperglytic high blood sugar. The random blood sugar test 04 recommends systematic screening every three years, focusing on a combination of abdominal obesity (90 cm for males and 85 cm for females) or bmi≥24kg/m2. Including the population with abdominal sugar damage (6. 1-6. 9 mmol/l) and sugar tolerance abnormalities (ogt2 hour blood sugar 7. 8-11. 0 mmol/l), which require review every 6-12 months. After 6-12 weeks of delivery, a review of 75 gogtt is carried out, followed by screening at least every 3 years, with an early assessment of another pregnancy. For those who meet two or more criteria such as high blood pressure, high glycerine triester, low hdl-c, it is recommended that emptied abdominal sugar and hba1c be tested annually. Among the most-at-risk groups, the factors that are common to the chapter metabolic disorders mechanism for women with pre-diabetes mellitus 04 acute chronic complications are infections, interruptions in insulin treatment, stress (such as surgery or trauma). There is a need to monitor blood sugar and urine on a regular basis and to adjust insulin doses in a timely manner to avoid dehydration and high fat diets. Incentives and preventive emergency treatment process immediately remediate dehydration, intravenous insulin inhibits the formation of ketone, corrects electrolytic disorders (e. G. Low potassium haematosis) and provides anti-infection or other treatment for induction. Due to acute insulin insulin, the accelerated decomposition of fat produced a large quantity of ketone, resulting in a decrease in blood ph and metabolic acid poisoning, manifested in nausea, vomiting, abdominal pain, high breathing (kussmaul breathing) and cognitive disorders. The chronic high blood sugar poisoning of acute ketone acid causes damage to retina microvasculars, resulting in seepage, haemorrhage and even retina detached, divided into non-inflation and fertilisation periods, to be diagnosed through eye-to-eye fluorescent fluorescent, with laser condensation and anti-vegf treatment delaying progress。diabetes retinal disease manifests itself in the evolution of trace protein urine to a significant amount of protein urine and kidney failure to control blood pressure (target)
