bubble_chart Overview

Due to insufficient iodine intake, the low concentration of thyroid hormones in the blood causes the anterior pituitary gland to secrete excessive amounts of thyroid-stimulating hormone, leading to compensatory enlargement of the thyroid gland, commonly known as simple goiter. The enlarged thyroid tissue then undergoes irregular hyperplasia and regeneration, and when nodules appear, it is called nodular goiter.

bubble_chart Etiology

The disease causes of simple goiter can be divided into three categories: ①Deficiency of raw materials (iodine) for thyroid hormone synthesis; this is the main cause of simple goiter. In mountainous areas far from the sea in China, such as the Yunnan-Guizhou Plateau and regions like Shaanxi, Shanxi, and Ningxia, the iodine in the soil is washed away, leading to insufficient iodine in food and drinking water. As a result, the incidence of this disease is higher, and it is also known as "endemic goiter." When the raw material "iodine" is lacking, but thyroid function still needs to meet normal requirements, the secretion of thyroid-stimulating hormone (TSH) from the anterior pituitary increases, thereby promoting compensatory enlargement of the thyroid gland. ②Increased demand for thyroid hormone: During adolescence, {|###|}pregnancy{|###|}, lactation, and menopause, the body's metabolism is vigorous, and the demand for thyroid hormone increases. This leads to prolonged excessive secretion of TSH, which can also cause thyroid enlargement. This enlargement is a physiological phenomenon and often resolves on its own in adults or after {|###|}pregnancy{|###|} and lactation. ③Impaired biosynthesis and secretion of thyroid hormone: Some cases of simple goiter occur due to disruptions in a certain step of thyroid hormone biosynthesis and secretion. For example, substances like perchlorate, thiocyanate, and nitrate can interfere with the thyroid's uptake of inorganic iodide. Sulfonamides, thiourea drugs, and vegetables containing thiourea (such as radishes and cabbage) can inhibit thyroid hormone synthesis. This leads to a decrease in thyroid hormone levels in the blood, which in turn increases the secretion of TSH from the anterior pituitary, promoting thyroid enlargement. Similarly, recessive inherited congenital defects, such as deficiencies in peroxidase or proteolytic enzymes, can also impair thyroid hormone biosynthesis or secretion, leading to goiter.

bubble_chart Pathological Changes

The most significant pathological change in simple goiter is the marked dilation of follicles, filled with abundant colloid, while the follicular wall cells become flattened, indicating a state of thyroid hypofunction. Although localized hyperplastic states can be observed microscopically, manifested as papillary projections composed of columnar cells protruding into the follicular lumen, such hyperplasia is merely compensatory.

Morphologically, simple goiter can be divided into diffuse and nodular types. The former is more common in adolescence, with dilated follicles evenly scattered throughout the gland. The latter, more prevalent in endemic areas, consists of dilated follicles aggregated into one or several nodules of varying sizes, surrounded by an incomplete fibrous capsule.

After a considerable period, nodular goiter often undergoes degenerative changes due to poor blood circulation, leading to cyst formation (frequently complicated by intracystic hemorrhage), local fibrosis, and calcification. Prolonged compression of the inter-nodular tissue by large nodules can cause atrophy and degeneration of functional tissue, clinically manifesting as hypothyroidism. Another outcome of nodule progression is the development of a certain degree of autonomy, where the thyroid nodule's secretion of thyroid hormones no longer depends on thyroid-stimulating hormone (TSH) and is no longer suppressed by exogenous thyroid hormone administration. In such cases, treatment with large doses of iodine can easily induce secondary hyperthyroidism. Additionally, nodular goiter carries the potential for malignant transformation.

bubble_chart Clinical Manifestations

Simple goiter generally does not involve functional changes, so systemic symptoms are usually absent, and the basal metabolic rate remains normal. In the early stages, the thyroid gland exhibits diffuse enlargement on both sides, with a soft texture, smooth surface, and no nodules, moving up and down with swallowing. Gradually, multiple (or single) nodules may be palpated on one or both sides of the enlarged gland; cystic degeneration of nodules may be complicated by intracapsular hemorrhage, causing rapid enlargement of the nodules within a short period.

Larger nodular goiters can compress adjacent organs, leading to various symptoms. ① Tracheal compression: This is relatively common. When compressed from one side, the trachea shifts or bends toward the opposite side; when compressed from both sides, the trachea becomes flattened. Due to the narrowing of the tracheal lumen, breathing difficulties occur, especially with retrosternal goiters, which are more severe. Prolonged compression of the tracheal wall may lead to softening and cause suffocation. ② Esophageal compression is rare. Only retrosternal goiters may compress the esophagus, causing discomfort during swallowing, but they do not lead to obstructive symptoms. ③ Compression of the deep cervical veins can impede blood return from the head and neck, a condition more commonly seen with large goiters located at the thoracic inlet, particularly retrosternal goiters. Clinically, this manifests as facial cyanosis, swelling, and prominent dilation of superficial veins in the neck and chest. ④ Compression of the recurrent laryngeal nerve can lead to vocal cord paralysis and hoarseness. Compression of the cervical sympathetic ganglion chain may cause Horner's syndrome.

Nodular goiter may be complicated by secondary hyperthyroidism or malignant transformation.

bubble_chart Diagnosis

1. It is commonly seen in endemic goiter areas, with a long course that can last for several years or even decades.

2. Initially, there is diffuse enlargement of both thyroid glands, followed by the appearance of single or multiple nodules of varying sizes in one or both thyroid glands.

3. The nodules are firm or relatively soft, smooth, and move up and down with swallowing. They grow slowly and rarely cause compressive symptoms. Substernal goiter may present with symptoms of head and neck venous return obstruction. If cystic degeneration occurs in the nodules, they may rapidly enlarge in a short period, accompanied by pain.

4. Thyroid function is generally normal.

5. Some patients may develop hyperthyroidism, and a few may undergo malignant transformation, manifested by rapid recent growth of the mass and signs of malignancy.

bubble_chart Treatment Measures

1. Physiological goiter during adolescence or {|###|}pregnancy{|###|} may not require drug treatment. It is recommended to consume iodine-rich foods such as kelp and seaweed.

2. For young individuals under 20 years old with diffuse simple goiter, a small amount of thyroid hormone can be administered to inhibit the secretion of thyroid-stimulating hormone from the anterior pituitary. The usual {|###|}dose{|###|} is 15–30 mg, taken orally twice daily, with a treatment course of 3–6 months.

3. Surgical treatment should be promptly considered under the following conditions, with subtotal thyroidectomy performed:

① Development of nodular goiter.

② Clinical symptoms caused by compression of the trachea, esophagus, recurrent laryngeal nerve, or sympathetic ganglion.

③ Substernal goiter.

④ Large goiter affecting work or daily life.

⑤ Nodular goiter complicated by hyperfunction.

⑥ Suspected malignant transformation of nodular goiter. {|108|}