Excess fat

Introduction Obesity refers to obesity when the body's excess fat content is caused by various reasons and significantly exceeds the normal average amount of normal people. The fat stored under the skin accounts for about 50% of the total fat. Obesity can occur at any age, is more common in middle-aged people, and more women than men. The weight gain of obese people is due to the increase of adipose tissue, while the muscle tissue does not increase or decline, but the athletes' muscles are particularly developed, or the weight gain of edema is not included. When the calorie intake exceeds the body's consumption, the excess calories are stored in the body in the form of fat, so that those who weigh more than 20% of the standard weight are obese, more than 10% are overweight; and according to height and weight, the body mass index (weight team) Kg / height (m2) is calculated, more than 24 is obese. The World Health Organization (WH0) standards are: men>27, and women>25 are obesity.

Cause

The causes are divided into two categories: simple obesity and secondary obesity:

(1) Simple obesity

No obvious endocrine, metabolic diseases can be found.

1. Constitutional obesity is also known as juvenile onset obesity.

2. Acquired obesity is also known as adult onset obesity.

(two) secondary obesity

There are obvious causes such as endocrine and metabolic diseases.

Hypothalamic encephalopathy

(1) Hypothalamic syndrome: various causes such as sequelae of inflammation, trauma, tumor, granuloma, etc. can lead to hypothalamic syndrome obesity.

(2) Obesity reproductive incompetence: also known as Frohlich syndrome.

2. Pituitary disease

(1) pituitary ACTH cell tumor: also known as Cushing's disease.

(2) pituitary growth hormone (GH) cell tumor: also known as acromegaly.

(3) Pituitary prolactin (PRL) cell tumor.

3. Hypothyroidism

(1) Primary (thyroid) hypothyroidism.

(2) hypothalamic-pituitary hypothyroidism.

4. Islet disease

(1) Non-insulin-dependent (NIDDM, type 2) early diabetes.

(2) insulinoma: also known as islet B cell tumor.

(3) Functional spontaneous hypoglycemia.

5. Adrenal hyperfunction is also known as hypercortisolism, Cushing's syndrome.

6. Hypogonadism

(1) Female menopausal obesity.

(2) Polycystic ovary syndrome.

(3) Men have no testis or no testicular disease.

7. Other

(1) Painful obesity (Dercum disease).

(2) Sodium hydroxide retention obesity.

(3) Intracranial plate hyperplasia (Morgagni-Stewart-Morel syndrome).

(4) Sexual naive-retinal retinitis-multi-finger (toe) malformation syndrome (Laurence-Moon-Biedl syndrome).

8. Drug-induced obesity: long-term use of chlorpromazine in patients with mental illness, long-term use of insulin in certain diseases, promotion of protein synthesis preparations, glucocorticoids, and cisplatin may cause appetite and lead to obesity.

an examination

Related inspection

Ultrasound diagnosis of hepatic disease glycosylated hemoglobin component (GHb, HbA1c) urine 17-hydroxy-corticosteroid (17-OH-CS)

First, medical history

1. Ask the patient's eating habits and exercise situation to roughly calculate the daily calorie intake, too much diet and too little activity is the main external cause of simple obesity.

2. Ask about family history

Simple obesity patients often have parental obesity. Their brethren and patients are also obese at first age. Family habits are more like sweets, more food intake and frequency, and more snacks.

3. Understand personal birth history and physical development status, secondary sexual development and sexual function status. Simple obesity patients have no secondary sexual development disorder, sexual function is more normal, and secondary obesity patients have second. Sexual developmental disorders and sexual dysfunction. In addition, should ask about the past health conditions, with or without meningitis, encephalitis, craniocerebral trauma, history of cancer, because of secondary obesity have a clear cause, obesity is only one of its clinical manifestations, especially pay attention to the presence or absence of nerves History of mental illness, endocrine and metabolic diseases, such as hypothyroidism, hypercortisolism, giant disease and acromegaly, hirsutism, hypothalamic syndrome, and other history.

Second, physical examination

1. Measure the patient's height (m), weight (kg), body temperature, blood pressure, abdominal circumference and hip circumference to understand whether the patient is obese or not, and whether there is abnormal temperature regulation (hypotial dysregulation during hypothalamic syndrome) And blood pressure is elevated.

2. Observe the body shape and fat distribution. In simple obesity patients, male fat is distributed in the neck and head. The trunk is the main part; the female is mainly the abdomen, lower abdomen, chest breasts and buttocks. Secondary obesity varies with different diseases, such as heart-to-heart obesity, full moon face, buffalo back, multi-blood appearance, purple pattern. Acne is characteristic of hypercortisolism; females are obese and hairy. Amenorrhea infertility may be caused by polycystic ovary. Obesity, facial swelling, dry and rough skin, and unresponsiveness are characteristic of hypothyroidism. The extremities of the extremities are fat and the face is ugly and characterized by acromegaly.

3. Vision and visual field examination of hypothalamic and pituitary obesity, especially in this part of the tumor can cause visual impairment, hemianopia and so on. Detailed physical examination is the main clue for the diagnosis of the cause of secondary obesity.

Third, buy a laboratory inspection

(1) Laboratory testing of hypothalamic and pituitary functions

1. Hormone determination ACTH, FSH, LH, TSH, GH, PRL measurement, in order to understand the hypothalamic and pituitary function, the diagnosis of hypothalamic and pituitary obesity.

2.TRH, LH-RH excitation test

(1) TRH stimulation test: Intravenous injection of TRH200~500 g in the morning, and TSH levels were measured before injection and at 15, 30, 60, and 90 min after injection. Serum TSH peaked in normal people 30 min after injection, reaching 10~30 g /L. There is no increase in TSH in hyperthyroidism (no response). The baseline value of serum TSH is increased in primary hypothyroidism. The TSH value is significantly increased after intravenous injection of TRH (significant excitability); secondary hypothyroidism such as lesions in the hypothalamus, TRH TSH was significantly increased after stimulation; if the lesion was in the pituitary gland after TRH stimulation, TS H did not increase. Pituitary tumor, Xihan syndrome, advanced acromegaly and other pituitary diseases caused insufficient secretion of TSH, serum TSH levels were low, and the response after TRH stimulation was poor, suggesting that the pituitary TSH reserve function was poor.

(2) LH-RN (LRH) stimulation test: differential hypogonadism is primary or secondary. At 8 o'clock in the morning, LRH 100 g was injected intravenously, and LH was taken before injection and at 15, 30, 60 min after injection; then, LRH 100 g was intravenously injected (or intramuscularly) every other day for 3 times, and the above test was repeated. In normal women, the peak of LH appeared 15 minutes after injection, which increased to more than 3 times of the baseline value, and the absolute value increased by 7.5 nmol/L or more, which was twice as low as that of females. In patients with low primary dysfunction, the LH base value is increased. The peak value of LH after injection of LRH is 4-5 times higher than the baseline value. (The reaction is obvious in humans with pituitary lesions. The LH base value is low. After LRH injection, the response is poor or no reaction. In the thalamus, the LH has a low baseline value and a normal or delayed response after LRH injection (peak occurs 60 or 9 min after LRH injection)

(B) Determination of peripheral gland hormones

1. Thyroid hormone determination TT3, TT4, FT3, FT4 determination to understand thyroid function.

2. Determination of adrenocortical hormone: blood cortisol, 24h urine 17-hydroxysteroids and 17-ketosteroids, 24 h urinary free cortisol determination, the diagnosis of cortisol-induced obesity. In the early stage of hypercortisolism and simple obesity identified by the above-mentioned tests, a small dose of dexamethasone (2mg / d) inhibition test should be performed, the former is not inhibited.

3. Islet function test

(1) Fasting and postprandial 2h blood glucose measurement: It is necessary to do oral glucose (75 g) tolerance test (OGTT) to help diagnose diabetes (DM) and impaired glucose tolerance (IGT).

(2) Determination of insulin and C peptide: it is helpful for the diagnosis of pancreatic obesity. In particular, the insulin release test can reflect the reserve function of islet B cells (in OGTT) while measuring plasma insulin concentration).

4. Determination of blood lipids.

5. Vertical position water test: shows that the patient has water retention when standing. After urinating in the morning on an empty stomach, the patient drank 1000 ml of water within 20 minutes, and then urinated once every hour for 4 hours to record the urine volume. On the first day, take the lying position (without the pillow), and take the standing position for the next day, such as the activity or the normal person's standing position, the drainage rate is 81.8+ 3.7% of the drinking water, and the urine output in the lying position is equal to the drinking water or even the drinking water. In the case of water retention obesity, the urine volume in the standing position is lower than the urine volume in the lying position by more than 50%.

Fourth, equipment inspection

(1) Inspection of obesity diagnosis methods

1. Diagnosis according to height and weight: firstly find the standard weight according to the patient's age (see the standard body weight scale), or calculate the following formula: standard weight = "height (cm) - 100" x 0.9, if the actual weight of the patient exceeds the standard 20% of body weight can be diagnosed as obesity. However, factors due to muscle development or water retention must be excluded.

2. Skin wrinkle calipers measure subcutaneous fat thickness: 25-year-old normal shoulder swelling subcutaneous fat thickness averaged 12.4?, more than 14? for obesity; deltoid muscle sebum thickness male average price. 4mm, female 17.5? (normal person 25 years old value).

3. X-ray soft tissue filming calculation of skin fat thickness, ultrasonic reflection imaging method to estimate subcutaneous fat thickness and other methods (standard with caliper method).

4. Calculate body weight (kg) / body 2 (?) > 24 according to body mass index. World Health Organization standards: men > 27, women > 25 for obesity.

(2) CT, MRI

Diagnosis of hypothalamic, pituitary tumors, vacuolar sella, adrenal tumors, and insulinoma.

(3) B-mode ultrasound

It is helpful for the diagnosis of adrenal hyperplasia, tumor and islet cell tumor.

(d) 131I-19-Iodocholinol and computer program for adrenal scanning

It is helpful for the diagnosis of adrenal hyperplasia or tumor.

Differential diagnosis

First, simple obesity

(1) Constitutional obesity (young onset obesity)

From childhood obesity to adulthood, there is a family history of obesity, good appetite, uniform distribution of body fat, hypertrophy of fat cells, poor diet and enhanced exercise, and less sensitive to insulin. No obesity can be found.

(2) Acquired obesity (adult onset obesity) is more than 20 to 25 years old, due to overnutrition, decreased activity and genetic factors, obesity, fat cell hypertrophy, no proliferation, diet control and exercise weight loss Well, the sensitivity of insulin can be restored after weight loss.

Second, secondary obesity

(a) hypothalamic obesity

Various causes of hypothalamic syndrome involve diseases caused by the hypothalamus.

(two) pituitary obesity

Diagnosis basis: Skull X-ray film shows that the saddle enlargement is spherical or oval, and the saddle bone can be absorbed; the skull CT can show the expansion of the pituitary fossa, the pituitary atrophy, and the fossa is filled with low-density brain effusion; MRI can show The pituitary tissue is compressed and flattened, clinging to the bottom of the saddle, and the saddle is filled with water-like signals. Saddle bottom subsided.

(C) Cushing's syndrome

Clinical manifestations: Typical clinical manifestations are often known, but the early stages of the disease are often atypical and require laboratory testing.

(4) Islet disease obesity

Insulinoma, also known as islet B cell tumor, is caused by repeated hypoglycemia due to the secretion of large amounts of insulin from the tumor. Hypoglycemia is more frequent than morning fasting or after exercise, and blood sugar and hypoglycemia at the time of onset.

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