toxic nodular goiter

Introduction

Introduction to toxic nodular goiter The disease is a hyperthyroidism disease reported by Plummer in 1913 that is different from Graves' disease. It is called Plummer disease, which is caused by excess thyroid hormone secreted by nodular lesions in the thyroid gland. In the narrow sense, nodular lesions refer to hyperfunctioning adenoma (toxic adenoma toxicadenoma), and broadly include toxic nodular goiter (toxicnodulargoiter). In fact, most of the reported Plummer disease in the past is considered to be gland. Tumor-like hyperplasia. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific people Mode of infection: non-infectious Complications: atrial fibrillation toxic nodular goiter

Cause

Toxic nodular goiter

(1) Causes of the disease

Plummer disease is secondary to nodular goiter, or thyroid tumor (high-functioning adenoma or toxic thyroid tumor), accounting for about 10% to 30% of hyperthyroidism.

At present, the cause of the disease is unknown. There may be long-term thyroid nodules or adenomas. Autonomous secretion dysfunction occurs. Sometimes the onset of hyperthyroidism is sudden. As the intake of iodine increases, the secretion of autonomic thyroid hormone is increased, and the typical symptoms of hyperthyroidism are produced.

(two) pathogenesis

1. Mechanism of occurrence Plummer disease is a disease of follicular adenoma or adenomatous hyperplasia and exhibits hyperthyroidism. Some cells in the thyroid are resistant to TSH, insulin-like growth factor, fibroblast growth factor ( Fibroblast growth factor) and other thyroid stimulants are sensitive to nodular hyperplasia, develop into follicular adenoma or adenomatous hyperplasia, and then self-disciplined to produce thyroid hormone, causing hyperthyroidism, Plummer disease in areas with iodine deficiency See, often combined with endemic goiter, also indicates that the occurrence of this disease is related to long-term chronic stimulation of thyroid proliferative stimulating substances such as TSH.

In addition, some of the Plummer's disease have a TSH receptor gene mutation (somatic mutation). Such cases have no TSH stimulation and are caused by the continuous production of cAMP, resulting in excessive secretion of autonomic thyroid hormone. However, the TSH receptor gene involved in the Plummer disease. The mutation frequency varies greatly from 0 to 80%.

2. Pathological thyroid gland is nodular enlargement (one or more), the capsule is intact or no capsule, the follicular epithelial hyperplasia in the nodule can be seen under the microscope, the nipple is formed, and the gelatinous fluid in the follicle is small and thin ( This is different from simple nodular goiter. The nodules can also be adenoma-like changes. There may be hemorrhage, calcification, etc. in the nodules. The thyroid tissue around the nodules is atrophied and squeezed.

Immunohistochemical staining showed that the follicular epithelium at the nodules was T3, T4 was strongly positive, and the surrounding epithelial cells were negative or weakly positive.

Electron microscopy: Similar to the morphology of follicular epithelial cells such as Graves disease, the cytoplasmic mitochondria, endoplasmic reticulum and Golgi apparatus are increased.

Prevention

Toxic nodular goiter prevention Pay attention to proper rest, do not master the combination of movement and rest, rest well, is conducive to the recovery of the body; exercise can enhance physical strength and enhance disease resistance, and the combination of the two can better recover.

Complication

Toxic nodular goiter complications Complications, atrial fibrillation, toxic nodular goiter

Hyperthyroidism is a prominent clinical manifestation of toxic nodular goiter. It can also occur in Graves patients with long history and severe symptoms, especially in middle-aged and elderly patients, so it is discussed here.

1. Etiology and pathogenesis

Thyroid hormone has a direct excitatory effect on the myocardium, which can increase the activity of Ca-ATPase and myosin ATPase in Na-K-ATPase and sarcoplasmic reticulum in the myocardium, enhance myocardial contractility, and increase cardiac output. Cardiac load aggravated ventricular progressive compensatory hypertrophy, while thyroid hormone can increase the number of beta receptors and atrial stress, this effect is synergistic with the effect of catecholamines on the myocardium, such as patients with other organic In heart disease, the heart is heavier and more prone to heart failure.

2. Clinical manifestations

(1) Arrhythmia: Common premature contractions and atrial fibrillation, both of which may be episodic or persistent. The incidence of atrial fibrillation in hyperthyroid heart disease is reported to be 10% to 28% in the literature. After more self-recovery, Yuen et al reported a group of 165 patients with hyperthyroidism complicated with atrial fibrillation. 101 patients (61%) had atrial fibrillation disappearing after the symptoms of hyperthyroidism were controlled. All self-recovery time was using RIA or Within 4 months after antithyroid drug treatment.

(2) Heart enlargement: In patients with severe hyperthyroidism with a long course of disease, the heart is enlarged due to excessive stress in the heart for a long time. Due to the enlargement of the left ventricle, the mitral valve is relatively closed, and the apex can be heard in grades II to III. Systolic murmur, caused by hyperthyroidism alone, after the control of hyperthyroidism, the heart can return to normal, a small number of long courses, severe heart disease can leave a permanent heart enlargement.

(3) Heart failure: elderly patients with hyperthyroidism and hyperthyroidism with other organic heart disease are prone to heart failure, sometimes even masking the performance of hyperthyroidism and causing misdiagnosis or delay in treatment.

Symptom

Toxic nodular goiter symptoms common symptoms exophthalmia hot nodules fatigue hand tremor weakness

Symptoms are basically similar to primary hyperthyroidism, but they are characterized by mild symptoms of hyperthyroidism. Local hyperthyroidism and single or multiple nodules are harder than normal thyroid gland. Generally, there is no exophthalmia, hand tremor is rare, and nervousness is mild. There may be thyroid finger disease, local compression symptoms are more common, such as hoarseness, respiratory pressure, fatigue is weak, heart damage is more prominent.

Examine

Examination of toxic nodular goiter

1.131I absorption rate generally 131I absorption rate increased, but sometimes it can be normal, surgical removal of thyroid nodules, 131I absorption rate returned to normal.

2. The radionuclide scan shows one or more "hot nodule" of concentrated 131I. The thyroid tissue outside the nodule has low iodine absorption function. After T3 is used, it does not inhibit the accumulation of radioactive iodine in the nodules and blood. The concentration of TSH decreased, and the thyroid hormone was secreted by the nodule. The Plummer disease accounted for about 20% to 25% of the cases of autonomic thyroid nodules. Among them, the hyperthyroidism was mild, and the surgical resection was "hot." After the nodule, the thyroid tissue that is inhibited outside the nodule can restore iodine absorption.

3. Ultrasound examination B-ultrasound can show the size of nodules, color Doppler examination, nodules have abundant blood flow.

4. When the CT scan of the thyroid scan is a thermal nodule, it is necessary to use ultrasound or CT to confirm whether there is a morphological nodular lesion consistent with the thermal nodule.

Diagnosis

Diagnosis and diagnosis of toxic nodular goiter

Nodular goiter, with varying degrees of hyperthyroidism symptoms and signs, thyroid total 131I rate is high or normal, one or more concentrated 131I hot nodules can be seen during scanning, and not exogenous thyroxine Inhibition, thyroid tissue other than nodules, iodine absorption is low, but can be excited by TSH, can also be inhibited by exogenous thyroxine, can be diagnosed as toxic nodular goiter.

Differential diagnosis

1. Graves' disease is characterized by hyperthyroidism, diffuse goiter, and anti-TSH receptor antibodies in the blood, which can be differentiated from Plummer.

2. Marine-Lenhart syndrome is a state of functional nodules complicated with Graves disease. It is clinically difficult to distinguish from Plummer's disease. In this syndrome, the stimulation of TSH increases the absorption of radioactive iodine, but it is enhanced in the nodules. Inhibition around is a hallmark of disease.

3. Toxic multinodular goiter is synonymous with generalized Plummer disease when it is called functional adenoma-like hyperplasia.

4. Papillary thyroid carcinoma can be associated with papillary structure due to Plummer disease, and it needs to be differentiated from papillary carcinoma. P1ummer disease does not show the unique nuclear appearance of papillary carcinoma such as ground-glass nucleus and nucleus.

5. Other diseases showing hot nodules during thyroid scan should be differentiated from Plummer's disease, and can be differentiated according to whether the symptoms of hyperthyroidism exist and whether nodular lesions are consistent with the hot nodules.

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