Classification of obesity According to the etiology is generally divided into primary and secondary two categories. A, primary obesity (a) simple obesity obesity is the main clinical performance, no obvious neurological, endocrine system morphological and functional changes, but accompanied by fat, sugar metabolism regulation process disorders. Such obesity is the most common. 1.Somatic obesity. Is due to the adipocyte proliferation, with 25 years of age before the over nutrition related. Most of them have a family history of heredity. Overweight children usually become overweight adults. It is reported that 42% of women and 18% of men who were overweight at the age of 0 to 13 became obese at the age of 31. From the 30th week of fetal life to 1.5 years after birth, fat cells have an extremely active proliferation period, called the “sensitive period”. In this period, such as excessive nutrition, can lead to increased fat cells. Therefore, the childhood period, especially within 10 years old, to maintain a normal weight is very important. 2.Nutritional obesity. Also known as acquired (exogenous) obesity, mostly due to 20 to 25 years of age after excessive nutrition, calorie intake more than the body’s various metabolic activities required; or due to physical activity too little or for some reason need more long-term bed rest, calorie consumption less and cause obesity. This type of obesity is mainly caused by adipocyte hypertrophy and adipocyte hyperplasia. Physical obesity, can also occur again acquired obesity, and become mixed type. The above two kinds of obesity, collectively called simple obesity, especially in the city 20 ~ 30 years old women are common, after middle age men and women also have spontaneous obesity tendency, menopausal women are more likely to occur. (B) water, sodium retention obesity also called idiopathic swelling. This type of obesity is mostly seen in reproductive and menopausal women. Its occurrence may be related to estrogen increase caused by capillary permeability increase, aldosterone secretion increase and venous reflux slowdown and other factors. Fat distribution is uneven, mainly in the lower legs, femur, buttocks, abdomen and breast. Weight gain is rapid and closely related to body position, with weight gain after exertion and standing and weight loss after rest and lying down. The weight change in the morning and evening is 0.4 kg in normal people, but the weight change in the morning and evening is more than 1 kg in patients with this disease. The change of swelling in this disease is often cyclic, with swelling of the face and eyelids in the morning, activity after waking up, gradual swelling of the lower limbs and trunk, and weight increase of 1.2 to 4.5 kg before dinner compared with that before breakfast, with an average of 2.4 ± 0.7 kg. Standing water test shows that the patient has water and sodium retention. Second, secondary obesity is a disease as the primary cause of symptomatic obesity. Clinically rare or rare, only accounted for less than 5% of obese patients. (A) endocrine disorder obesity 1, mesencephalic obesity. Mainly including hypothalamic syndrome and obesity reproductive incompetence. (1) hypothalamic syndrome: can be caused by hypothalamic lesion itself or pituitary lesion affecting hypothalamus, or midbrain, third ventricle lesion. The nature of the lesion can be inflammation, tumor, injury, etc. In some patients, the cause is unknown, and the main manifestations are central neurological symptoms, vegetative and endocrine metabolic dysfunction. Obesity is caused by damage to the appetite center of the hypothalamus, resulting in abnormal appetite, such as overeating. Abnormal secretion of hormones from the hypothalamus leads to target gland dysfunction, such as abnormal sexual function or precocious puberty, abnormal thyroid function, hyperadrenocorticism, amenorrhea and lactation, and uremia. Neurological disorders may include somnolence or insomnia, episodic sleeping sickness, deep sleep disorder or episodic sleepiness and anorexia; fever or hypothermia; mental disorders such as hyperexcitability, crying and laughing erratically, hallucinations and irritability; mesencephalic epilepsy; hyperhidrosis or sweating shutdown; cyanosis of the hands and feet; sphincter dysfunction. Underdeveloped or diminished intelligence. (2) Obesity reproductive incompetence: caused by pituitary and stalk lesions, partly affecting hypothalamic function, the obesity of the pre-developmental children is under the jaw, neck, hip and upper thighs and abdomen; upper limbs are also fat, long and gradually sharp fingers, but plump and fat; boys often have breast hypertrophy, small external genitalia, partly sunk in the congested fat, then more reduced; bone development is late, may be combined with urogenital disorders. If the onset is after development, the secondary sexual characteristics are poorly developed, and the genitalia of juveniles with the onset are not developed and mentally retarded. It must be distinguished from juvenile somatic obesity with delayed sexual development. In the latter case, the fat distribution is uniform, there is no organic lesion of the nervous system, the intelligence is normal, and the sexual organs eventually develop completely. When this disease occurs in adults, there may be loss of sexual function, lack of sperm, menopause and other manifestations of infertility. 2.Pituitary obesity. Anterior pituitary secretion ACTH cell tumor, secrete too much ACTH, make bilateral adrenal cortex hyperplasia, produce too much cortisol, lead to centripetal obesity, called Koxin disease. Pituitary tumors that secrete other hormones may produce secondary gonadal and hypothyroidism due to the enlargement of the tumor and compression of extra-tumoral tissues, leading to obesity. In addition to obesity, there are often symptoms of peripituitary tissue compression, such as headache, visual impairment and visual field defects. Imaging examination can find the butterfly saddle change. 3.Thyroidal obesity. See in hypothyroidism patients. More obvious symptoms than obesity are bloated face, pale skin, weakness, hair loss, slow reaction, indifferent expression. Serum T3, T4 is reduced, TSH is increased, TRH excitation test response is enhanced. 4.Adrenal obesity. Commonly in adrenal cortical adenoma or adenocarcinoma, autonomous secretion of excessive cortisol, causing secondary obesity, known as Coxin syndrome. Characterized by centripetal obesity, full-moon face, buffalo back, polycystic appearance, purple skin, hypertension and hypoglycemic tolerance or diabetes. Blood and urine cortisol are elevated and ACTH is decreased. Imaging examination shows adrenal tumor. 5. Islet obesity. Commonly seen in early stage of mild type II diabetes, islet beta cell tumor and functional spontaneous hypoglycemia. Obesity is often due to overeating. Islet β-cell tumor is mainly due to excessive insulin secretion. Recurrent episodes of hypoglycemia with fasting blood glucose below 2.8 mmol/L (50 mg/dL), which rapidly improves after injection or oral glucose. Spontaneous functional hypoglycemia is reactive (i.e. postprandial) hypoglycemia, caused by imbalance of vegetative nerves, especially high excitability of vagus nerve, mostly seen in middle-aged women, often occurs after certain mental stimulation, usually seen about 3 hours after meal, feeling hungry, panic, weakness, sweating, anxiety and nervousness, pale, tachycardia, high blood pressure, tremor, blackout, etc. Cerebral hypoglycemia symptoms are rare, with occasional fainting. Each attack lasts 15 to 20 minutes. Generally, the symptoms can recover on their own or disappear with a little food. The physical signs are often only obesity because of good hunger and eating. The glucose tolerance test is reactive hypoglycemia in the 3rd to 4th hour, and the blood sugar returns to normal in the 4th to 5th hour, while islet beta cell tumor remains low in the 4th to 5th hour. Fasting test helps to differentiate the two. The disease can last 10 to 20 years without signs of deterioration. Diabetics with polyuria, polyphagia, polyphagia, etc., fasting blood glucose ≥ 7.8 mmol/L (140 mg/dL), or 75g glucose oral method glucose tolerance test 2 hours blood glucose ≥ 11 mmol/L (200 mg/dL). 6, hypogonadal obesity. Mostly seen in women after menopause and men with testicular dysplasia and other cases. Most are obese due to hypogonadism. After the male go to the potential or female after the menopause obesity, that is such. Male hypogonadism obesity is generally not as significant as female menopause fat. Gonadal obesity whole body fat accumulation is more proportional, to chest abdomen, femur, back is obvious. It may be accompanied by hypertension, purple lines, and a reduced glucose tolerance curve. 24-hour urinary 17-hydroxy or 17-keto is consistently high, and the dexamethasone suppression test is often positive. Urinary gonadotropins are elevated. A small number of cases belong to Stein-Leventhal syndrome, which is characterized by obesity, amenorrhea, anovulation, infertility, masculinization, and polycystic ovaries. Its absence of masculinization is called polycystic ovaries (PCO). The ovaries are hyperandrogenic, with increased urinary 17 ketones, increased blood testosterone, increased LH, and normal or decreased FSH. the LHRH excitation test is overreactive. (B) congenital abnormal obesity Mostly due to genetic genes and chromosomal abnormalities. Commonly found in the following diseases. 1, congenital ovarian insufficiency individual manifestation type is female, primary amenorrhea, infantile reproductive organs, short stature, mental retardation, webbed neck, elbow valgus, short fourth metacarpal bone. Low blood estrogen level, increased LH and FSH, and XO sex chromosome karyotype. 2. Congenital testicular hypoplasia Primary hypogonadism in males, aphthous body type (tall, long limbs, finger spacing greater than body length, pubic symphysis to ground distance greater than 1/2 of height), secondary sex characteristics are not developed, genitalia infantile, male breast feminization, low blood testosterone level, increased LH and FSH, and sex chromosomes mostly XO. The sex chromosomes are mostly XXY. Laurence-Moun-Biedl syndrome has six main signs: obesity, mental retardation, retinitis pigmentosa, polydactyly, juxtaposition of fingers (toes), and genital hypoplasia. Urine 17 ketones and blood LH were below normal. LHRH excitation test is unresponsive; LHRH excitation test has increased LH response with one or more injections. 4, glycogen accumulation disease type I The child is obese body, the face and trunk subcutaneous fat is especially rich. There are also growth retardation, short stature dwarf state; hypoglycemia, up to 0.56 mmol/L, (10 mg/dL); liver and kidney enlargement; muscle weakness; hyperlipidemia; hyperlactatemia and ketosis. The disease is a recessive genetic disorder. 5.Cranial plate hyperplasia The main manifestations are obesity, headache, cranial plate hyperplasia, masculinity and mental disorder. Obesity is more obvious in the trunk and proximal extremities. Skull X-ray shows that there is frontal bone and (or) other intracranial plate hyperplasia. Most of the patients are female, and most of the symptoms appear after menopause. (C) other 1, painful obesity also known as neurological adiposity. The cause is unknown. Women are more frequent, and appear after menopause, often have premature menopause, hypogonadism and other symptoms. Clinical manifestations on the basis of obesity appear multiple painful fat nodules or painful fat mass. The fat is mostly deposited on the trunk, neck, axillae, waist and arms. The fat nodules are soft in the early stage and become hard in the late stage. As the fatty nodules increase in size, the pain increases and numbness and weakness and sweating disorders occur. The pain is sharp, paroxysmal or continuous, and there is pressure along the nerve trunk. There is often arthralgia. There may be psychiatric symptoms, such as depression, mental retardation, etc. 2.Progressive fat atrophy Patients with this disease have progressive atrophy of the upper body subcutaneous fat and normal or abnormal increase of the lower body subcutaneous fat. There is also lower body fat atrophy and upper body fat deposition. It may be accompanied by hyperthyroidism, hepatosplenomegaly, muscle hypertrophy, hyperlipidemia, diabetes, etc. Secondary obesity with a certain disease as the primary disease, their obesity is only one of the manifestations of the primary disease, often not the main manifestation of the disease, moreover, not the only manifestation of the disease. Through the treatment of the primary disease, obesity can be mostly cured.