Toxic diffuse goiter
Introduction
Introduction to toxic diffuse goiter Toxic diffuse goiter (toxicdiffusegoiter) is an autoimmune disease. The clinical manifestations are not limited to the thyroid gland, but a multi-system syndrome, including: high metabolic syndrome, diffuse goiter, eye signs, skin lesions and Thyroid extremity disease, because most patients have high metabolic syndrome and thyroid enlargement, it is called toxic diffuse goiter, also known as Graves disease, also has diffuse goiter with hyperthyroidism, exophthalmia, original A goiter with hyperthyroidism, known as Basedow disease. In addition to the thyroid gland, it is characterized by invasive endocrine exophthalmos, which can exist alone without hypermetabolic disease. basic knowledge The proportion of illness: 0.03%--0.08% Susceptible people: no special people Mode of infection: non-infectious Complications: eye movement disorders diabetes dysphagia
Cause
Toxic diffuse goiter
(1) Causes of the disease
Although Graves' disease has been continuously explored in recent decades, including clinical and experimental research, its occurrence has not been positively explained, but there are some clear explanations.
1. Genetic factors: Genetic factors are the causes recognized by most people, indicating that there is a close relationship between Graves' disease and genetics. It is a case in which a family is often seen, and most of them are women, about 15% of patients. There are obvious genetic factors. About half of the relatives of Graves patients have thyroid autoantibodies. The occurrence of onychomycosis is significantly related to human leukocyte antigen (HLA class II antigen). The detection rate varies according to ethnic groups. HLA-H46 is clearly associated with a non-HLA gene in addition to the HLA gene.
2. Trauma: Excessive excitement caused by various causes, or excessive depression, can lead to excessive secretion of thyroid hormone. The mechanism may be that when the stress is high, the secretion of adrenocortical hormone is sharply increased, thereby changing the inhibitory T lymphocyte. The function of cells (Ts) or helper T lymphocytes (Th) enhances the immune response.
3. Abnormal immune system: T lymphocytes are sensitized to antigens in the thyroid gland, stimulate B lymphocytes, and synthesize antibodies against these antigens. T cells play an important role in hyperthyroidism, and average T cells in peripheral blood lymphocytes of normal people. 63.6% of the untreated Graves patients had 93.1% of T cells. The T cells of Graves patients were significantly higher than those of normal people. After treatment with antithyroid drugs, the proportion of T cells returned to normal and was not relieved. It is still similar to untreated patients. The blood thyroid stimulating hormone receptor antibody (TRAb) is a human-specific antibody that is only detected in patients with autoimmune thyroid disease and is considered to be the main and direct cause of Graves' disease. s reason.
(two) pathogenesis
1. Pathogenesis: Volpe proposes that the pathogenesis of Graves disease is: Graves disease patients with HLA-related genetic factors caused by Ts function-specific defects, environmental factors, infection, drugs, trauma or other stress reactions, etc., can also induce Ts Reduced function, reduced number, increased organ-specific T cell deficiency, thereby reducing Th inhibition of the thyroid, specific Th in the presence of monocytes and specific antigens, IFN-, stimulation specificity B lymphocyte activation produces thyroid stimulating antibody (TSAb). TSAb is similar to TSH, stimulates TSH receptor, increases thyroid hormone production, and enhances thyroid antigen expression. Interferon- (IFN-) is on the surface of thyroid cells. It causes the expression of HLA-DR antigen, which can be enhanced by TSAb and TSH. The thyroid cells become surface antigen cells due to the stimulation and continuous action of this specific Th, and the currently recognized pathogenesis is as follows.
Recent studies have shown that the development of Graves disease is the result of thyroid stimulation by stimulating antibodies such as TRAb. TRAb can directly act on TSH receptors on thyroid cells, intensify cAMP pathway, proliferate thyroid cells, activate thyroid cell metabolism, and synthesize. The increase of thyroid hormone, the positive rate of this autoantibodies in the serum of patients with Graves disease is 83% to 100%. In the untreated Graves patients, the positive rate of TRAb can be as high as 88.2%. These antibodies are only in the autoimmune thyroid gland. Patients with disease (AITD) are found in the blood. Non-AITD patients, such as simple goiter, thyroid tumors, etc., cannot detect TRAb in the blood, or can only detect very low concentrations of TRAb.
2. Pathology
(1) Gross morphology: The thyroid gland is usually diffusely symmetrical, with a weight ranging from 50 to 200 g. The surface of the thyroid is slightly uneven, the blood vessels are clearly visible, and the thyroid gland is slightly shiny red. The leaf shape is obvious, lacking the luster of the gum, showing a dark red meat, and the cut surface of the lymphoid follicle is sometimes spotted.
(2) Histomorphology: Hyperplasia of follicular epithelium is the basic image of Graves' disease. There are lobular structures composed of follicles of different sizes, but the shape remains. Untreated cases contain small follicles and the lumen is reduced. And the gelatin is reduced. In the gelatinous follicle, a vacuole called scalloping can be seen in the vicinity of the follicular epithelium. This scalloping is actually an artificial phenomenon. In addition, the hyperproliferative epithelium is often arranged in a nipple or serrated shape. Structure, cells are high columnar, cytoplasm is lightly stained, sometimes scattered polyploid large nuclei, interstitial mostly mild fibrosis with lymphocytic infiltration and increased dendritic cells, also visible lymphatic filtration In the formation of vesicles, lymphoid follicles are mainly B cells, which are surrounded by T lymphocytes. Cases with strong lymphocytic infiltration may also show changes in follicular destruction and follicular epithelial eosinophilic changes similar to Hashimoto's thyroiditis. A case similar to the pathological changes of Hashimoto's thyroiditis can also be called Hashimoto's poisoning, and it is very likely that it will develop into hypothyroidism in the future. In addition, cases with granules can be seen, Graves. The histological changes of the disease are not singular, and the morphological changes of different parts and even different parts of the same case are diverse.
Histological images of Graves' disease can be divided into several types:
1 non-colloidal follicle diffuse presence;
2 gel-free follicles are limited in existence;
3 Most follicles contain gelatinous, and the follicular epithelium is marked with papillary projections;
4 Similar to the normal thyroid tissue type, as a combined lesion, 2% to 9% of Graves' disease can be seen as adenoma, papillary carcinoma or follicular carcinoma and other tumorous lesions, and papillary carcinoma is mostly microcarcinoma.
The histopathological changes of Graves' disease may vary widely depending on the treatment method and treatment stage. After using anti-thyroid drugs such as propyl oxypyrimidine or methimazole, TSH secretion can be promoted, and excessive hyperplasia can be seen. Foam and gelatinous expanded follicles, after using inorganic iodine, the follicular epithelial volume becomes smaller, the hyperproliferative changes are reduced, and the secretion of thyroglobulin is inhibited, causing the gelatin to concentrate, using a large amount of radioactive iodine. After the destruction of the thyroid gland, as a reaction after the destruction, eosinophilic changes occur in the follicular epithelium, the nucleus is polyploidized, and interstitial fibrosis occurs. In addition, the -receptor blocking drug and thyroxine production and secretion There is no direct relationship, so the thyroid morphology has little effect. The nodular changes in the cases of recurrent thyroid resection are more common than the proliferative changes.
Cytological examination, can be found in paving stone-like cell clusters, sometimes visible small follicular structure, large nuclear nucleus, nuclear ovate bias, marginal vacuoles visible in the cytoplasm, small follicles as the main case There are often less gums. In some cases, a large number of lymphocytes can appear in the background. In the case of no therapeutic effect, the cell edge vacuoles are more common, and in the case of therapeutic effect, the cell edge vacuoles are not obvious.
(3) Immunohistochemistry: Immunohistochemical staining revealed that thyroid-specific proteins such as thyroglobulin, T3, and T4 were strongly positively stained in follicles and epithelium due to hyperthyroidism. In addition, HLA in follicular epithelium -DR and CD45 positive, increased CD4 positive T lymphocytes in the stroma.
Electron microscopy showed that the cytoplasmic mitochondria, endoplasmic reticulum and Golgi apparatus increased in organelles, and the cell follicle surface was slightly microfilamented. These findings showed that the follicular epithelial hyperfunction was observed. In addition, the electron density in the basement membrane was also high. Immune complex-like sediment.
(4) Changes in organs outside the thyroid: Graves' disease is caused by edema in the muscles and connective tissues, inflammatory cell infiltration or increased adipose tissue, which causes an increase in the volume of the posterior part of the eyeball, muscles and connective tissue in the eyelids. The deposition of medium glass acid and chondroitin sulfate is increased. The edema is caused by the hydrophilicity of aminodextran produced by fibroblasts. The histological swelling of the muscles in the eyelids, the disappearance of transverse stripes, lymphocytic infiltration, local mucous edema Lymphocytes infiltrating into the dermis can be seen on the skin, and mucopolysaccharide deposits.
Pathophysiology The pathophysiological effects of excessive thyroid hormone secretion are various, but the principle of action has not been fully elucidated. In the past, excessive thyroid hormone was thought to act on mitochondria, which has a decoupling effect on oxidative phosphorylation, resulting in oxidation. The free energy generated by the process cannot be stored in the form of ATP and is depleted. Therefore, the oxidation rate increases and the energy supply is insufficient, which causes clinical symptoms. In recent years, there has been no evidence of decoupling in patients with hyperthyroidism. Hormones can promote phosphorylation, mainly by stimulating the cell membrane Na+-K+-ATPase (ie, Na+-+K pump), which requires a large amount of energy to promote the active transfer of Na+ during the process of maintaining the Na+-K+ gradient inside and outside the cell. As a result, the hydrolysis of ATP increases, which promotes mitochondrial oxidative phosphorylation. As a result, both oxygen consumption and heat production increase. Although the role of thyroid hormone is multifaceted, it mainly promotes protein synthesis, promotes heat production, and has mutual interaction with catecholamines. Promote the effects of various metabolic and organ functions, such as thyroid hormones increase the basal metabolic rate, plus The consumption of various nutrients, muscles are also easy to consume, the synergistic effect of thyroid hormone and catecholamines strengthens the excitement and stimulation of the latter in organs such as nerves, cardiovascular and gastrointestinal tract, in addition, thyroid hormones on the liver, heart and intestines There is also a direct stimulating effect. Non-invasive exophthalmos may be caused by increased sympathetic excitability. The cause of infiltrative exophthalmos is unknown. It may be related to autoimmunity (thyroglobulin-anti-thyroglobulin immune complex and extra-muscle muscle binding). After, causing muscle lesions), lymphocyte infiltration after the ball, and the presence of exophthalmos antibodies in the blood is a strong testimony to this statement.
Prevention
Toxic diffuse goiter prevention
The key to preventing recurrence after hyperthyroidism is not to keep too much thyroid tissue during surgery.
Complication
Toxic diffuse goiter complications Complications, eye movement disorder, diabetes, dysphagia
1. Endocrine infiltrative exophthalmia: also known as malignant exophthalmia Graves disease, invasive eye disease, no hypermetabolism, also known as normal thyroid function Graves disease, the incidence of 6% to 10% of the original hyperthyroidism %, more men than women, older than 40 years old.
(1) Etiology and pathogenesis: It has not yet been fully elucidated. Although it is often associated with Graves disease, it can also occur in patients with hypothyroidism or Hashimoto's thyroiditis, and even in patients without thyroid disease. It is thought to be related to autoimmune factors, and there are two opinions on the relationship with Graves' disease. One is that infiltrative exophthalmos is an independent autoimmune disease, it has nothing to do with Graves' disease, and the other is that eye disease and Graves disease are Interrelated, thyroid stimulating antibodies (TsAb) are associated with the occurrence of exophthalmos. Recent studies have shown that both cellular and humoral immunity are associated with the development of exophthalmos. Using the MIF test for leukocyte migration inhibitory factors, it is found that patients with malignant exophthalmos have targeted Sensitized T lymphocytes of the posterior muscle antigen; in addition to TSAb, the secretory antibody (EPAb) and the pituitary-induced exophthalmia (EPS) are involved in the process of exophthalmos, wherein EPS may be a hydrolysate of TSH, animal experiment It was found to bind to receptors on the cell membrane of guinea pig eyeballs. The thyroglobulin antigen-antibody complex acts on the extraocular muscle cell membrane to cause edema and lymphoid Infiltration, causing exophthalmos and external ophthalmoplegia, in addition, lymphocytes, infiltrate the fat tissue and the ball mucopolysaccharide, hyaluronic acid is deposited in the plasma cells also retrobulbar tissue, edema, increased volume.
(2) clinical manifestations: onset can be acute and slow, bilateral eyeballs can be symmetrical or asymmetrical, a few can be unilateral exophthalmos, eyeball protrusions are more than 19 ~ 20 mm, patients with eyelid edema, eyeball pain , fear of light and tears, vision loss and other symptoms, ocular palsy may appear strabismus and diplopia, due to diaphragmatic contraction, eyeballs are highly prominent, eyelids can not be closed, can cause corneal dryness, and even secondary ulcers, perforation, a small number of patients due to paralysis Increased internal pressure affects the blood supply to the optic nerve, which can cause edema of one or both optic discs, optic neuritis and even optic atrophy, loss of vision. Most patients have goiter and hyperthyroidism. The degree of exophthalmos is not related to the severity of hyperthyroidism. Some patients may be associated with localized mucinous edema lesions. The incidence of this disease is usually 1 to 2 years. It is also prolonged to 5 years. After the disease is relieved, the eyes are congested and the swelling is gradually reduced. Disappeared, the symptoms are relieved, but most patients can not fully return to normal, still left different degrees of eyelid contraction, eyeballs, extraocular muscle fibrosis, etc. If the treatment is not appropriate, such as excessive dose of anti-thyroid drugs, excessive control of symptoms, or excessive hypothyroidism, it may increase the exophthalmos, so attention should be paid to the treatment of radionuclide 131I or surgery. There are also exacerbations after surgery. This may be due to thyroid damage and increased antigen release. Therefore, patients with Graves' disease with malignant exophthalmos should be treated with caution and 131I treatment.
2. Localized mucinous edema: It is a special skin lesion of Graves disease, which can occur alone or simultaneously with invasive exophthalmos. Patients may or may not be accompanied by hyperthyroidism.
(1) Etiology and pathogenesis: It is generally considered that similar to invasive exophthalmos, the detection rate and concentration of TSI in patients' blood are higher, and the content of acid mucopolysaccharide in skin is significantly increased.
(2) Clinical manifestations: skin lesions are mostly symmetrical, slightly higher than the skin, dark red or reddish brown, slightly shiny surface, thin and tense skin, sometimes with desquamation, clear boundary with normal skin, generally no symptoms Occasionally itching or slight pain, which occurs in front of the sputum, can also be found in the back of the hands and feet, ranging in size and sometimes wide, and often merges with each other in the later stage, so that the two calves are thickened, and the skin is easily merged after being scratched or bruised. Infection, a small number of patients with mucous edema can be combined with clubbing and bone and joint lesions.
3.Graves disease with myopathy
(1) acute hyperthyroid myopathy: also known as hyperthyroidism with acute thyrotoxic myopathy, clinically rare, rapid onset, often develops into severe conditions within a few weeks, dysphagia, inaccurate pronunciation, and can cause Respiratory muscle paralysis, endangering the lives of patients.
(2) chronic thyrotoxic myopathy (chronic thyrotoxic myopathy): more common, the cause is unknown, may be due to excessive thyroid hormone on the mitochondria of muscle cells, causing swelling and degeneration, energy metabolism disorders, research found that the human body The proximal muscle group is mainly composed of mitochondria-rich red muscle. Therefore, in the early stage of the disease, the proximal muscle group is often the earliest affected, and the lesion is also the heaviest. It is characterized by progressive muscle weakness, muscle atrophy, and patients often complain of going upstairs. It is difficult to stand up and comb the head, and the excretion of creatine in the urine is often increased in the laboratory. The application of neostigmine is generally ineffective.
(3) thyrotoxicosis associated with periodic paralysis: more common in the eastern countries, the mechanism is not very clear, may be related to the increase of potassium ions into the intracellular transfer, Japan reported that hyperthyroidism with periodic sputum accounted for 1.6% of hyperthyroidism, May be related to high levels of carbohydrates in the diet. These carbohydrates cause more potassium ions to enter the cells when synthesizing glycogen, which is mainly caused by young males. Most of them appear when the symptoms of hyperthyroidism are obvious or the symptoms are controlled. Before the typical hyperthyroidism, the symptoms are similar to familial periodic paralysis, often accompanied by hypokalemia. Intravenous infusion of glucose and insulin can induce this disease.
(4) Hyperthyroidism associated with myasthenia gravis: primary hyperthyroidism and myasthenia gravis are autoimmune diseases. Hyperthyroidism does not directly cause muscle weakness. It may occur in patients with genetic defects at the same time or at the same time. According to the literature, nearly 3% of patients with myasthenia gravis suffer from hyperthyroidism, which is much higher than the incidence of hyperthyroidism in the general population. The lesions mainly involve the eye muscles, which are characterized by ptosis, eye movement disorders and diplopia. It is light and heavy.
4. Hyperthyroidism with diabetes: Glucose metabolism is affected during hyperthyroidism. Increased thyroid hormone levels can promote glycogenolysis and gluconeogenesis, and increase intestinal glucose absorption. Therefore, non-diabetic patients can also express food at this time. After the increase of blood sugar and impaired glucose tolerance, it is generally believed that hyperthyroidism does not cause diabetes, but it can aggravate the condition of the original diabetes, and even induce ketoacidosis. Studies have found that some hyperthyroidism with diabetes may have genetic immunity related to autoimmunity. The basis, such as: 1 in the close relatives of patients with hyperthyroidism, the incidence of diabetes is higher; 2 hyperthyroidism and diabetes can occur in identical twins; 3 the positive rate of serum anti-thyroglobulin antibody in diabetic patients is higher than the control group; 4 insulin dependence Type 2 diabetes, diffuse goiter with hyperthyroidism and adrenal insufficiency in patients with HLA (human leukocyte antigen) are more common.
5. Hyperthyroidism with diabetes: treatment should be treated with hyperthyroidism and diabetes, respectively, because both are consumptive diseases, should pay attention to strengthen supportive care, eat more high-calorie, high-protein and vitamin-rich foods, Before the symptoms of hyperthyroidism are controlled, the amount of insulin should be more than that of normal diabetic patients.
Symptom
Symptoms of toxic diffuse goiter Common symptoms Psychosis is easy to be anxious Anxiety Diabetes depression
The onset of this disease is slow, in the typical performance, high metabolic syndrome, goiter and eye signs are more obvious, but if the condition is mild, it can be confused with neurosis, and some patients can be special (some) Symptoms such as exophthalmos, cachexia or myopathy are the main manifestations. The performance of elderly and children is often atypical. In recent years, due to the gradual improvement of the diagnostic level, the findings of mild and atypical patients have increased. Typical cases often have the following which performed.
1. Nervous system: patients are prone to excitement, mental allergies, tongue and second-hand flatness when there is fine tremor, excessive speech, insomnia, insomnia, anxiety, irritability, suspicion, etc., sometimes hallucinations, even Asian mania, but also taciturn, depressed, patients with active reflexes, shortened reflection time.
2. Hypermetabolic syndrome: patients are afraid of heat and sweat, skin, palm, face, neck, underarm skin rosy and sweaty, often low fever, high fever can occur when crisis occurs, patients often have tachycardia, palpitations, stomach Na is obviously aggressive, but the weight is declining and fatigue is weak.
3. Goiter: Most patients with thyroid enlargement as the main complaint, diffuse symmetrical swelling, soft, swallowing up and down movement, a small number of patients with thyroid asymmetry, or swollen, due to increased thyroid blood flow Therefore, vascular murmurs and convulsions and tremors can be heard on the outside of the upper and lower leaves, especially in the upper part of the gland. The diffuse symmetry of the thyroid with murmur and tremor is a special sign of the disease, which is of great significance in diagnosis, but should be Note the difference between venous and carotid murmurs.
4. Eye signs: There are two special eye signs in this disease.
(1) Non-invasive exophthalmos: also known as benign exophthalmos, accounting for the majority, generally symmetry, sometimes one side of the eye before the other side, mainly due to sympathetic excitation of the extraocular muscles and upper diaphragm (Miiller Increased muscle tension, mainly changed to the appearance of the eyelids and the outside of the eye, the tissue changes little after the ball, the eye signs have the following: 1 eye crack widening (Darymple sign), less instant and gaze (Stellwag sign), 2 The inner side of the eyeball can not be aggregated or poorly (Mbius sign). When the eyes are down, the upper eyelid can not follow the eyeball drop due to retraction (Von Graefe sign). When the 4 eyes look up, the forehead skin cannot be wrinkled (Joffroy sign) ).
(2) invasive exophthalmos: also known as endocrine exophthalmia, ophthalmoplegia ocular eye disease or malignant exophthalmos, less common, more serious, can be seen in patients with hyperthyroidism or no hypermetabolic disease, mainly Due to increased extracorporeal muscle and post-balloon tissue volume, lymphocytic infiltration and edema.
The American Thyroid Association classifies the eye of Graves' disease into 7 levels:
Level 0: asymptomatic signs;
Grade I: non-invasive exophthalmos, asymptomatic only signs, unobtrusive eyes, eye signs can gradually recover with the control of hyperthyroidism;
Grades II to IV: Invasive exophthalmos, with obvious symptoms, progressive development, serious nature, can be alleviated by treatment, but generally can not return to normal.
5. Cardiovascular system complains of heart palpitations, shortness of breath, slight activity is obviously aggravated, severe cases often have arrhythmia, heart enlargement, heart failure and other serious manifestations.
(1) tachycardia: often sinus, general heart rate 100 ~ 120 times / min, heart rate is still fast at rest or sleep, is one of the characteristics of this disease, is an important parameter in the diagnosis and treatment.
(2) arrhythmia: pre-systolic contraction is the most common, paroxysmal or persistent atrial fibrillation and flutter and atrioventricular block and other arrhythmias can also occur.
(3) Heart sounds and murmurs: The heart beats powerfully, the first sound in the apical area is hyperthyroidism, the common smell and systolic murmur, similar to the murmur when the mitral regurgitation is incomplete, and the apex area can be heard and diastolic murmur.
(4) cardiac hypertrophy, enlargement and congestive heart failure, more common in elderly men with severe disease, combined with infection or the use of -blockers can easily induce heart failure.
(5) systolic arterial blood pressure increased, diastolic blood pressure was slightly lower or normal, pulse pressure increased, due to this disease, thyroid blood flow is rich, arterial anastomotic branch increased, cardiac output and output per minute increased.
6. Digestive system: The appetite is hyperthyroidism, but the weight is obviously decreased. The two are often accompanied by the possibility of the disease or diabetes. Excessive thyroxine can excite the peristalsis and increase the frequency of stools, sometimes due to fat malabsorption. It can also have direct toxic effects on the liver, resulting in hepatomegaly and BSP retention, and increased GPT.
7. Blood and hematopoietic system: The total number of white blood cells in the blood around the disease is low, the percentage and absolute value of lymphocytes and mononuclear cells increase, platelet life is also short, sometimes purpura may occur, due to increased consumption, malnutrition and iron The use of obstacles can cause anemia.
8. Exercise system: The main manifestation is that the muscles are weak and weak, and a few can be manifested as hyperthyroidism.
9. Reproductive system: Female patients often have menstrual reduction, prolonged period, and even amenorrhea, but some patients can still be pregnant, fertility, male impotence, and occasionally breast development.
10. Skin and acromegaly: A small number of patients have typical symmetrical mucinous edema, but not hypothyroidism, which is more common in the lower front part of the calf, sometimes in the back and knees, face, upper limbs, and even the head. Dark pink-red skin lesions at the beginning, thick and thick skin, later flaky or nodular folds, hair follicles become thicker, the skin is orange-like, and finally bark-like, with secondary Infection and hyperpigmentation, and even the appearance of flaky vitiligo in the skin, in a few patients, the soft tissue of the fingertips is swollen, showing a sacral shape, the new bone formation of the metacarpal subperiosteum, and the finger or toenail are thinned, forming a concave shape. Spoon A (Plummer A), the separation of the free edge of the nail near the end of the nail and the nail bed separation phenomenon, called the fingertip thick.
11. Endocrine system: Excessive thyroid hormone can affect gonadal function, adrenal cortical function is often active in the early stage of the disease, but in patients with severe disease (such as crisis), its function is relatively reduced, or even incomplete; pituitary secretion of ACTH Increased, plasma cortisol concentration is normal, but its clearance rate is accelerated, indicating that its operation and utilization increase.
Examine
Examination of toxic diffuse goiter
Laboratory tests are important for a definitive diagnosis, especially in cases with atypical clinical manifestations.
1. Basal metabolic rate (BMR): It is one of the commonly used diagnostic methods in the past. However, due to excessive factors, including technology, environment, patient's mental state and the influence of some chronic diseases, it is no longer a diagnostic criterion. However, there is still a certain reference value for patient self-test, the patient can self-test blood pressure, pulse, and then use the formula to calculate.
2. Serum thyroid hormone
(1) Total thyroxine (TT4): is the sum of T4 and free T4 in blood. When serum thyroid hormone binding protein (TBG) is normal, TT4 is greater than the normal reference value.
(2) Total triiodothyronine (TT3): It is the sum of T3 and free T3 in blood. When serum TBG is normal, if the TT3 result is higher than the normal reference value, it can be diagnosed as hyperthyroidism.
(3) T3 uptake test (T3U): reflects the saturation degree of TBG, the normal reference value is 24% to 35%, or 0.8 to 1.2, when the serum TBG is normal, the measured value is greater than 35%, or 1.3 to support the diagnosis of hyperthyroidism.
(4) Free T4 (FT4): It is the part of the blood where thyroid hormone does not bind to TBG. It is elevated when hyperthyroidism, and the normal reference value is 10.3 to 25.8 mol/L or 0.8 to 2.0 ng/dl.
(5) Free T3 (FT3): is a part that does not bind to thyroid hormone, and hyperthyroidism is elevated (normal reference value for adults is 2.2 to 6.8 pmal/L or 1.4 to 4.4 pg/ml).
3. Serum TSH determination and TRH stimulation test
(1) Serum thyroid stimulating hormone (TSH): In the case of Graves' disease, serum TSH decreases, and the normal reference value is 3.8 to 7.5 mU/L (RIA method) or 0.4 to 5.0 mU/L (ICLA method).
(2) TRH stimulation test: Under normal circumstances, the thyroid-stimulating hormone releasing hormone (TRH) secreted by the hypothalamus promotes the secretion of pituitary TSH, TSH promotes the secretion of thyroid hormone, and in Graves' disease, the patient does not respond to TSH after the injection of TRH, and a few patients respond. reduce.
4.131I uptake rate and inhibition test
(1) 131I uptake rate: when hyperthyroidism is elevated, or there is a peak shift, but some factors, such as foods and drugs rich in iodine, can affect the determination of 131I uptake rate.
(2) Inhibition test: The 131I uptake rate before and after taking thyroid was compared, and the 131I uptake rate was not inhibited, or <50%, in Graevs disease.
5. Serum biochemical examination
(1) Blood lipids can be reduced.
(2) blood sugar and glucose tolerance: due to increased sugar absorption, diabetes can occur, manifested by elevated blood sugar, or impaired glucose tolerance.
(3) Serum phosphorus, alkaline phosphatase and osteocalcin: elevated, serum parathyroid hormone and 1,25-dihydroxyvitamin D3 decreased, urinary calcium and hydroxyproline emissions increased.
6. Radionuclide scanning: The thyroid gland exhibits diffuse radioactive iodine absorption (Figure 12).
7. Ultrasound examination: B-mode ultrasonography has little help in the diagnosis of Graves' disease. Color Doppler ultrasonography has certain value. The thyroid gland is diffusely enlarged, and the focal echo is reduced. The typical "fire-sea sign" can be seen. "The blood flow velocity of the thyroid artery, especially the upper artery, is significantly accelerated, and the vascular resistance is reduced.
8. X-ray examination: X-ray examination can help determine whether the trachea is under pressure, whether the thyroid gland falls into the chest, CT scan helps to understand the position of the thyroid, the relationship between the thyroid and blood vessels and esophagus.
9. MRI examination: diffuse thyroid enlargement, T1WI, T2WI showed high signal, uniform signal, which is characteristic of MRI signal changes (Fig. 14). This T1WI high signal and serum high thyroxine level, 24h iodine Related to increased function, on the high-resolution MRI map, a large number of rough filamentous fibrous interstitial and dilated vascular shadows are seen in the enlarged glandular parenchyma.
Diagnosis
Diagnosis and diagnosis of toxic diffuse goiter
Diagnostic criteria
After medical history, physical examination and laboratory examination, the diagnosis of hyperthyroidism is mostly not difficult, and the following should be noted during the diagnosis.
1. Symptoms and signs of pediatric and elderly patients are not typical: under normal circumstances, children's T3 is higher than that of adults. The elderly's T4 is lower than that of young adults and adults. Older men have lower T3 and slightly higher women, and older people have TSH. Adults are high, the pulse of elderly patients may not be fast, and the thyroid may not be swollen.
2. Apathetic hyperthyroidism: the patient is extremely tired and weak, with a lack of expression, lack of language, lack of vision, slow response, no obvious goiter, or small, palpable nodules when palpation, pulse rate is not fast, occasional limbs Cool, dry skin, less eye marks, older patients, may be associated with atrial fibrillation, heart failure, and even thyroid crisis, other manifestations include unexplained myopathy, diarrhea, loss of appetite or vomiting These more serious situations are actually caused by abnormal body reaction caused by hyperthyroidism. It should be used to make a comprehensive test of multiple thyroid functions to avoid delay in diagnosis.
3. T3 and T4 type hyperthyroidism: with its unique laboratory results, the clinical manifestations of T3 type hyperthyroidism are mild, only T3 is elevated, serum T4 and FT4 are normal or low, and T4 and FT4 are increased in T3 type hyperthyroidism patients. And T3 is normal or reduced.
4. Neurosis: Although there is goiter, it is not hyperthyroidism, but nervousness and anxiety. It is common in menopausal women. Although the palm of the patient is moist, it is cold, because the blood circulation of the surrounding tissues does not increase, and the appetite is not obvious. Increased, tremors on the extremities but thicker, and irregular, and different from the tremor of hyperthyroidism, can be further diagnosed as a thyroid function test.
5. Simple goiter: thyroid enlargement, but no hyperthyroidism, 131I absorption rate is iodine deficiency curve, absorption 131I rate is increased, but the peak does not move forward, determination of T3, T4, TSH, or inhibition test can help diagnosis.
Differential diagnosis
1. Rheumatic heart disease and coronary heart disease: atrial fibrillation occurs in patients with hyperthyroidism, and heart failure should be noted.
2. Malignant tumors: Lymphomas may have neck masses, fever, weight loss, fatigue, weakness, and patients with malignant tumors have weight loss, diarrhea, and apprehension of appetite should be noted.
3. Addison's disease: Hyperthyroidism with skin pigmentation may be confused with Addison's disease, because of fatigue, weight loss, diarrhea, but no hyperpigmentation of the oral mucosa, goiter, thyroid function changes.
4. Unilateral ocular protrusion should be differentiated from intraorbital tumor. Children's bilateral exophthalmos should be differentiated from narrow cranial disease.
