1 type diabetes mellitus
Among them, 1 type diabetes mostly occurs in teenagers. Because of insufficient insulin secretion, they rely on exogenous insulin to maintain their lives. Childhood diabetes is also a common target of 1 type diabetes. Most children with 1 type diabetes have a sudden onset, and can suddenly show obvious polydipsia and polyuria within a few days. Drinking water and urine are as high as several liters per day, and their stomach intake is increased but their weight is reduced. The common phenomenon of enuresis and emaciation among teenagers has attracted the attention of parents. Inducing factors are often due to infection and improper diet. Infants and young children are often characterized by enuresis. Drinking too much urine is easy to be ignored, and some do not come to see a doctor until ketoacidosis occurs.
Type 2 diabetes mellitus
Insulin is the only hypoglycemic hormone secreted by human pancreatic B cells. Insulin resistance refers to the decrease of the sensitivity of peripheral tissues to insulin, and the resistance of peripheral tissues such as muscle and fat to insulin to promote the absorption, transformation and utilization of glucose. Clinical observation shows that insulin resistance is very common in type 2 diabetes, up to about 90%. Diabetes can lead to infection, heart disease, cerebrovascular disease, renal failure, blindness and gangrene of lower limbs, and become the main cause of death and disability. Hypertonic syndrome of diabetes mellitus is a serious acute complication of diabetes mellitus. At the initial stage, it can be manifested as polyuria, polydipsia, fatigue and slow response. With the increase of water loss, the disease develops rapidly, with symptoms similar to stroke such as drowsiness, disorientation, epileptic convulsion, hemiplegia and even coma.
Edit this paragraph of secondary diabetes
Complications caused by pancreatitis, cancer and subtotal pancreatectomy should be considered in combination with medical history analysis. Patients with hyperpigmentation, hepatosplenomegaly, diabetes and iron metabolism disorder should be differentiated, but this situation is rare. Stress hyperglycemia or gestational diabetes should be determined through follow-up. Generally, stress can be recovered within 2 weeks after it disappears, ... or it can be identified by follow-up after delivery. ....
Edit this paragraph of symptom analysis
omnivorous
Due to a large loss of urine sugar, such as losing more than 500 grams of sugar every day, the body is in the environmental factors of semi-starvation diabetes.
State, lack of energy needs to be supplemented, leading to excessive appetite and increased food intake. At the same time, because hyperglycemia stimulates insulin secretion, patients are prone to hunger, overeating and always feel inadequate. Even if they eat it five or six times a day, the staple food reaches 1 ~ 1.5 Jin, and the amount of non-staple food is obviously higher than that of normal people, which can't satisfy their appetite.
polydipsia
Because of polyuria and excessive water loss, dehydration occurs in cells, which stimulates the thirst center, leading to drinking more and drinking more, increasing the amount and frequency of drinking water, thus supplementing water. The more you urinate, the more you drink, which is in direct proportion.
be diuretic
The urine volume increases, reaching 3000 ~ 5000 ml per day and night, and the highest can reach more than 10000 ml. The frequency of urination has also increased, and it is possible to urinate 1 time in an hour or two, and some patients even reach more than 30 times every day and night. The blood sugar concentration of diabetic patients is increased, which can not be fully utilized in the body, especially glomerular filtration can not be completely reabsorbed by renal tubules, resulting in osmotic diuresis and polyuria. The higher the blood sugar, the more urine sugar is excreted, and the more urine is excreted.
lose weight
Weight loss: Due to insufficient insulin, the body can't make full use of glucose and accelerate the decomposition of fat and protein to supplement energy and calories. In this way, carbohydrates, fat and protein in the body are consumed in large quantities, and the patient loses weight and gains weight, and in severe cases, the weight can drop by dozens of pounds, resulting in fatigue and listlessness. Similarly, the longer the course of disease, the higher the blood sugar; The more serious the illness, the more obvious the weight loss. ...
Early symptoms of diabetes
1. Eye fatigue, decreased vision, eye fatigue, decreased vision. When you feel that your eyes are easily tired, you can't see clearly, your eyes are black when you stand up, your eyelids are drooping, your vision is narrowed, your vision is blurred, and your eyes suddenly change from hyperopia to myopia or presbyopia that you didn't have before, you should have an eye examination immediately. 2. Hunger and Overeating Because the sugar in the body is excreted in the form of urine sugar, it can't absorb enough calories to maintain the basic needs of the body. I often feel extremely hungry and eat a lot, but I am still very hungry. 3. Paralysis and trembling of hands and feet Diabetic patients will have intractable paralysis of hands and feet, trembling of hands and feet, poor finger movement and pain, severe inflammatory foot pain, lower limb paralysis, low back pain, unwillingness to walk, leg cramps at night, eye motor nerve paralysis, poor attention and autonomic nerve disorder. Once found, you should go to the hospital for examination immediately.
Common etiology
1, which is related to 1 type diabetes:
Autoimmune system defects: Because many autoimmune antibodies can be found in the blood of 1 type diabetic patients, such as glutamic acid decarboxylase antibody (GAD antibody) and islet cell antibody (ICA antibody). These abnormal autoantibodies can damage the pancreatic structure.
Damage the insulin-secreting human islet B cells, making them unable to secrete insulin normally.
2. Factors related to type 2 diabetes mellitus
Genetic factors: Similar to 1 type diabetes, type 2 diabetes also has the characteristics of familial disease. So it is probably related to genetic inheritance. This genetic feature is more obvious in type 2 diabetes than in 1 type diabetes. For example, one twin has 1 type diabetes, and the other has a 40% chance of suffering from this disease; But if it is type 2 diabetes, another person has a 70% chance of developing type 2 diabetes. Obesity: Obesity may be an important factor in type 2 diabetes. Genetic causes can lead to obesity and type 2 diabetes. Body-centered obese patients have excess fat concentrated in the abdomen, and they are more likely to develop type 2 diabetes than those who have fat concentrated in the buttocks and thighs. Age: Age is also a risk factor for type 2 diabetes. More than half of patients with type 2 diabetes develop symptoms after the age of 55. Elderly patients are prone to diabetes, which is also related to the overweight of the elderly. Modern lifestyle: Eating high-calorie food and reducing exercise can also cause diabetes, which some people think is also caused by obesity. Like type 2 diabetes, obesity is more common among Asian Americans and Latin American businessmen whose diet and activity habits have been "westernized".
3. Related factors of gestational diabetes mellitus.
Hormone abnormality: During pregnancy, the placenta will produce a variety of hormones for fetal development and growth. These hormones are very important for the healthy growth of the fetus, but they will block the insulin action in the mother's body, thus causing diabetes. The 24th week to 28th cycle of pregnancy is the peak of these hormones, and it is also the frequent period of gestational diabetes. Genetic basis: Patients with gestational diabetes are at great risk of developing type 2 diabetes in the future (but it has nothing to do with 1 diabetes). Therefore, some people think that the genes that cause gestational diabetes and those that cause type 2 diabetes may be related to each other. Obesity: Obesity is not only easy to cause type 2 diabetes, but also can cause gestational diabetes.
Pathogenesis of type 2 diabetes mellitus
A large number of studies show that under the stimulation of hyperglycemia and high free fatty acid (FFA), a large number of free radicals are produced in the human body, which in turn initiates oxidative stress. Activation of oxidative stress signal pathway will lead to insulin resistance (IR), impaired insulin secretion and diabetic angiopathy. It can be seen that oxidative stress not only participates in the pathogenesis of type 2 diabetes, but also constitutes the pathogenesis of late complications of diabetes. Oxidative stress and diabetes promote each other, forming an unbreakable vicious circle. Insulin resistance can appear before diabetes, and under its action, the compensatory secretion of insulin increases in the early stage of the disease to maintain normal glucose tolerance. When insulin resistance increases, the compensatory secretion of insulin decreases or both appear at the same time, the disease gradually progresses to impaired glucose tolerance and diabetes, and blood sugar begins to rise. Hyperglycemia and high FFA*** both lead to a large number of ROS production and oxidative stress, and also activate stress-sensitive signaling pathways, thus aggravating insulin resistance, which is clinically manifested as the continuous progress and deterioration of diabetes. In vitro studies have shown that ROS and oxidative stress can cause a cascade of activation of various serine kinases. Recent experiments on improving blood sugar control by antioxidants also confirmed that ROS and oxidative stress can cause insulin resistance. Oxidative stress has become the core of diabetes.
Beta cells are also important targets of oxidative stress, and their antioxidant enzyme levels are low, so they are sensitive to ROS. ROS can directly damage islet β cells, promote β cell apoptosis, and indirectly inhibit β cell function by affecting insulin signal transduction pathway. Beta cells are damaged, the insulin secretion level is reduced, the secretion peak is delayed, and the blood sugar fluctuation is intensified, so it is difficult to control the rapid rise of blood sugar after meals, which causes more significant damage to cells. In 2004, Professor Ceriello put forward the theory of * * * and soil, that is, oxidative stress is the basis of * * * and insulin resistance (IR), diabetes and cardiovascular diseases. 2004 is a theory, and 2009 has become an indisputable fact.
Edit the lesion in this paragraph.
(a) islet pathology
The pathological changes of type ⅰ and type ⅱ are different. Most type I cases are insulitis. The number of islets and β cells decreased greatly, suggesting absolute insulin deficiency. Type ⅱ, especially obese people, has larger islets and more β cells than normal in the early stage; Special staining was shown, and the section showed the decrease of β cell granules. When diabetes occurs for more than 5 years, the number and size of islets and the number of β cells decrease until several typical changes are observed after death. According to Warren et al.' s research, the pathological results of pancreatic islets in 81kloc-0/diabetic patients of all ages are as follows: normal 33%, hyaline degeneration 4 1%, fibrosis 23%, edema degeneration 4%, lymphocyte infiltration 1%. Histochemistry of islet hyaline degeneration is a glycoprotein, which is stained by transparent substances and distributed in β cells. Under electron microscope, its submicroscopic properties are the same as those of amyloid deposits, so it is called islet amyloidosis and may be amylin. This kind of lesion is more common in patients with type II diseases over 40 years old and those who have been ill for 10 years or more. Fibrosis can be seen in patients with type I and type II diabetes, especially in the elderly. In adolescent patients, some people think that this is the result of islet inflammation, and eventually the islet is completely fibrotic, and β cells often
(ii) Vascular diseases, diabetic retinopathy
1. More than half of patients have atherosclerosis, and its onset is not limited by age. It mainly involves aorta, coronary artery and cerebral artery, which often causes serious cardiac, cerebral and renal complications and leads to death. Sclerosis of peripheral arteries, especially the dorsal arteries of lower limbs, can cause gangrene. 2. Microvessels include capillaries, arterioles and venules. It was found by light microscope and electron microscope that diabetic microangiopathy is characterized by thickening of capillary basement membrane: the thickness of normal basement membrane is about 80 ~ 250 nm, and the thickness of diabetic basement membrane can reach 500 ~ 800 nm. There is sugar deposition in the basement membrane, in which hydroxylysine is mainly reduced in proportion, suggesting that lysine is hydroxylated into hydroxylysine. This microangiopathy is often accompanied by abnormal microcirculation, which is the pathological basis of many organ diseases. Widely distributed, especially the capillaries of glomerulus, fundus, nerve, myocardium and muscle, cause kidney diseases, fundus diseases, neuropathy and myocardial diseases, and become the main factors that determine the prognosis of patients. Diabetes treatment
There are two theories about the pathogenesis of basement membrane thickening: metabolic disorder theory: according to recent biochemical tests, this basement membrane thickening is due to the deposition of glycoprotein, and the most definite one is glomerular basement membrane, which is also found in glomerular mesangium. Glomerular endothelial cells, epithelial cells and mesangial cells can synthesize the substances in this basement membrane. In diabetic patients with microalbuminuria, the content of negatively charged HS-PG in glomerular basement membrane (GBM) decreased significantly during glomerulosclerosis, and there were similar changes in coronary artery. The decrease of HS-PG in ECM or GBM leads to the decrease of negative charge of GBM, albumin is easy to leak from GBM, and arteries are easy to harden. Therefore, microalbuminuria is not only a diabetic nephropathy, but also a risk factor for cardiovascular disease. Thickening of capillary basement membrane is closely related to hyperglycemia and vigorous auxin, which promotes the synthesis of glycated protein and slows down its decomposition. Hereditary theory: Thickening of capillary basement membrane can be seen in pre-diabetes, but metabolic disorder is not obvious at this time, so it is considered to be caused by genetic factors. The main function of basement membrane or ECM is to maintain structural integrity and anti-proliferation. When the basement membrane thickens, the degree of crosslinking changes, the negative charge decreases, the permeability increases, and small molecular proteins leak out, forming microalbuminuria, resulting in proteinuria and advanced nephropathy. And fundus retinopathy and arteriosclerosis will occur.
(III) Kidney
Diabetic glomerulosclerosis accounts for 25% ~ 44%, which can be divided into nodular type, diffuse type and exudative type. Especially in type I diabetes, pyelonephritis and renal arteriosclerosis are also common, and necrotizing renal mastoiditis is rare. People who die of diabetic coma may suffer from acute renal failure with tubular necrosis.
(4) Liver
Often swollen, accompanied by fat infiltration, edema degeneration and glycogen reduction, fatty liver is common.
(5) Heart
In addition to the coronary artery inside and outside the heart wall and its intramural branches showing extensive atherosclerosis with myocardial infarction, myocardial lesions have also been confirmed, including autopsy and various animal models (including BB mouse diabetes) and other evidence. Myofibrils in myocardial cells decreased obviously, and a large number of myofibrils were lost under electron microscope, and focal necrosis of myocardial fibers occurred in severe cases. There are many lipid droplets and glycogen particles deposited in myocardial cells. Mitochondrial swelling, crista rupture, matrix cavitation, myocardial cell membrane rupture, and the formation of medullary corpuscles and lipofuscin particles can be seen. The intercellular space of intercalated disc mucosa was enlarged, and microvascular lesions, basement membrane thickening, endothelial cell proliferation, vascular wall thickening, PAS positive glycoprotein and vitreous substance deposition only occurred in BB rats with diabetes 16 weeks or more. Perivascular myocardial interstitial fibrosis.
(6) nervous system
All nerves can participate. Peripheral neuropathy is the most common, showing edema, degeneration, fracture and sheath shedding; Axonal degeneration, fibrosis and swelling of motor endplate. The vegetative nerve showed chromatin dissolution, vacuolar degeneration and nuclear necrosis, and cholinesterase activity decreased or lacked. Tissue sections showed that the vegetative nerve showed rosary or spindle fracture, vacuolar degeneration and so on. Spinal cord and its nerve roots showed atrophy and rubbery degeneration, myelin membrane became thinner, axial mutation became thinner, severe glial fibrosis accompanied with vacuolar degeneration, anterior horn cells shrank and were replaced by adipose tissue. Diabetic coma is common with brain edema and ganglion cell edema and degeneration.