The Thyroid and Parathyroid Glands

Embryology of the Thyroid Gland

The thyroid gland is the first endocrine gland to develop in the human embryo. It develops at the floor of the primitive pharynx at the same location of the base of the tongue. The developing thyroid gland will migrate inferiorly along the anterior neck region to the lower neck anteriorly to the trachea. The migration may leave behind embryonic remnants or ectopic thyroid tissue that should atrophy but may form developmental cysts.

Anatomy of the Thyroid Gland

The thyroid gland is located inferior to the thyroid cartilage (Adam’s apple) in the anteroinferior neck. The gland has an “H” or a “U” configuration and consists of right and left lobes that consist of upper, middle, and lower poles that are connected across the midline by a thin bridge of thyroid tissue called the isthmus . The isthmus straddles the trachea anteriorly, whereas the paired lobes extend on either side of the trachea, bounded laterally by the common carotid arteries and internal jugular veins. When present, the pyramidal lobe arises from the isthmus and tapers superiorly just anterior to the thyroid cartilage and may be seen in 15% to 30% of patients ( Fig. 22.1A ). The pyramidal lobe is most commonly visualized in pediatric patients and usually atrophies with age. A fascia surrounds the thyroid, trachea, esophagus, and parathyroid glands (see Fig. 22.1B ).

The thyroid gland is made up of two types of cells: follicular and parafollicular cells. Follicular cells make up the majority of thyroid tissue and secrete the main thyroid hormones T ₃ and T ₄ . The follicular cells require an adequate supply of iodine to produce the correct amount of thyroid hormones. The parafollicular cells (also called C cells) secrete calcitonin.

Thyroid Physiology and Laboratory Data

The role of the thyroid is to maintain normal body metabolism, physical and mental growth, and development by the synthesis, storage, and secretion of thyroid hormones. Every cell in the body depends on thyroid hormones for regulation of its metabolism. The mechanism for producing thyroid hormones is through iodine metabolism. The thyroid follicular cells are the only cells in the body that can absorb iodine. Through a series of chemical reactions, the thyroid produces T ₃ and T ₄ . Most endocrine glands do not store their hormones, but thyroid hormones are stored in the colloid material of the gland to be secreted when needed into the blood. In terms of amount of hormone secretion, T ₄ is more abundant at 80%, whereas T ₃ is 20% of secretion; however, T ₃ is more potent.

When thyroid hormones are needed in the body, they are released into the bloodstream by the action of thyrotropin, or thyroid-stimulating hormone (TSH) , which is produced by the pituitary gland. The secretion of TSH is regulated by thyrotropin-releasing hormone (TRH) , which is produced by the hypothalamus. The level of TRH is controlled by the basal metabolic rate in a negative feedback system. Low concentration of thyroid hormones causes a decrease in the basal metabolic rate, which results in an increase in TRH. This causes an increased secretion of TSH and a subsequent increase in the release of thyroid hormones. When the blood level of thyroid hormones is returned to normal, the basal metabolic rate returns to normal and TSH secretion stops. In summary, the hypothalamus signals the pituitary gland to tell the thyroid gland to produce more or less thyroid hormones.

Calcitonin decreases the concentration of calcium in the blood by first acting on bone to inhibit its breakdown of calcium. When less calcium is being resorbed into the blood, less calcium moves out of the bone into the blood with a decrease in blood calcium levels. Calcitonin secretion will increase after any concentration of blood calcium increases.

Tests of Thyroid Function

Laboratory Tests

The most common laboratory test to evaluate thyroid function is serum T ₄ . This test reflects the amount of T ₄ in the blood and is considered a good screening test of thyroid function. Serum T ₃ reflects the amount of T ₃ in the blood. Measurements of both thyroid hormones may be used to give a more accurate picture of thyroid function. The TSH (serum thyrotropin) laboratory test will also indicate thyroid function and may be the first to elevate as an indication of hypothyroidism. Often the TSH level is opposite the T ₄ and T ₃ levels with thyroid dysfunction (i.e., low TSH with elevated T ₄ and T ₃ indicates hyperthyroidism). If the TSH, T ₃ , and T ₄ levels are all low, this could indicate pituitary dysfunction or pituitary mass from secondary hypothyroidism. The laboratory findings associated with common thyroid disorders are listed in Table 22.2 .

Table 22.2

Laboratory Findings With Common Thyroid Disorders

Laboratory Test	Normal Thyroid (Euthyroid)	Hyperthyroidism	Primary Hypothyroidism	Secondary Hypothyroidism (Possible Pituitary Dysfunction or Mass)
T 4 , T 3	Normal	High	Low	Low
TSH	Normal	Low	High	Low

Calcitonin helps to maintain homeostasis of blood calcium levels and helps to prevent increased amounts of calcium in the blood (hypercalcemia). In addition, calcitonin is not a common indicator of thyroid function but can be a laboratory test for medullary carcinoma with elevated calcitonin used as a tumor marker.

Nuclear Medicine or Scintigraphy

Scintigraphy can be used to determine the thyroid function with two tests that can be performed together: iodine uptake scan and thyroid scan. For an iodine uptake scan, a capsule containing a small amount of radioactive iodine (called a radiotracer) is ingested by mouth. The amount of radioactivity accumulated in the thyroid gland is measured at multiple time points for up to 24 hours by a gamma camera. In comparison with normal thyroid uptake, patients with hyperthyroidism have a higher percentage of radioactivity in the thyroid gland; a lower percentage of radioactivity is present with hypothyroidism.

The thyroid scan will detect the amount of radioactive tracer to image the thyroid gland and demonstrate the thyroid size, shape, and position. In addition, if the thyroid has a concentrated amount of radioactivity, this will be imaged as a “hot” (hyperfunctioning) nodule (see Fig. 22.2A ). An area of the thyroid with lower concentration of the radioactive tracer will demonstrate absence of uptake as a “cold” (nonfunctioning) nodule (see Fig. 22.2B ). The majority (80% to 85%) of nodules in a thyroid scan are demonstrated as a cold nodule, with the remaining (15% to 20%) seen as a hot nodule. Hot nodules are considered to be benign. Cold nodules have the potential to be malignant, but only 10% to 15% of cold nodules are shown to be malignant with FNA biopsy.

Other imaging modalities for thyroid include computed tomography (CT) and magnetic resonance imaging (MRI) to determine thyroid size, shape, position, and imaging characteristics of masses within the gland and neck area.

Sonographic Evaluation of the Thyroid Gland

No patient preparation is required for thyroid sonography. The sonographer should review the examination indication and the available imaging results (i.e., previous thyroid sonography, scintigraphy, CT, or MRI). A thorough patient clinical history should be obtained before the sonographic examination. Pertinent information includes results of the physician’s physical examination (e.g., palpable nodule or goiter), pain/duration, history of hyperthyroidism, hypothyroidism, thyroiditis and symptoms related to thyroid disorders, thyroid medications, or surgery. If the patient has a previous history of cancer, along with prior history of radiation or surgery to the neck and upper chest, this should be noted in the examination record. If the patient has a palpable mass, ask the patient to indicate the location or obtain a description of the palpable area from the ordering physician.

The examination procedure should always be explained to the patient before scanning. The patient is placed in the supine position with a pillow or pad under both shoulders to provide moderate hyperextension of the neck with chin elevated to place the thyroid more horizontal and bring the inferior portion of the gland more superior for visualization ( Fig. 22.3 ). If the lower pole of the thyroid is still difficult to view, having the patient swallow will move the entire gland superiorly. Having the patient elevate the chin superiorly and turn to the opposite side will enable better visualizing of each lobe. It is important to be conscious of elderly patients or those who may experience dizziness or neck strain and make positioning adjustments as needed.

A high-frequency (7 to 15 MHz) linear array transducer should be used, selecting the highest frequency to penetrate the entire thyroid and surrounding musculature. Each lobe and isthmus should be carefully surveyed in transverse and longitudinal planes. The survey should also extend superior, inferior, and lateral of the thyroid gland to identify and document any enlarged cervical lymph nodes ( Fig. 22.4 ). The transverse survey is completed scanning from above to below the thyroid to note gland symmetry. Multiple transverse images of the superior, mid, and inferior levels of each lobe are imaged and labeled accordingly ( Fig. 22.5 ). Virtual convex, split screen, or panoramic features may provide imaging of larger glands ( Fig. 22.6 ).

Transverse and longitudinal survey of the isthmus is completed with images recorded and labeled. Transverse imaging landmarks include the trachea, common carotid artery, and internal jugular vein. The trachea is noted in the midline posterior to the isthmus with posterior shadowing. The common carotid artery is a circular, pulsatile structure directly lateral and adjacent to the gland. The oval-shaped internal jugular vein lies lateral to the common carotid artery ( Fig. 22.7 ).

To locate the longitudinal scan plane of the thyroid gland, it is helpful to align the longitudinal axis of the common carotid artery and slide medially. Longitudinal survey is completed by scanning from the lateral to internal jugular vein to the midline isthmus. Multiple longitudinal images of the lateral, mid, and medial portions of each lobe are imaged individually and labeled accordingly (see Fig. 22.4 ). On longitudinal scans, landmarks include the recurrent laryngeal nerve and inferior thyroid artery, which may be seen between the thyroid lobe and esophagus on the left and between the thyroid lobe and longus colli muscle on the right.

During the examination, obtain three measurements of each lobe for volume calculations at maximum length, AP, and width of gland. The AP measurement of isthmus should be imaged in the transverse plane ( Fig. 22.8 ). Examination protocol should also include color Doppler images of both transverse and longitudinal planes of the middle portion of the thyroid demonstrating gland vascularity (see Fig. 22.6B ). A low pulse repetition frequency is chosen for the color Doppler scale to distinguish all vascular structures. Power Doppler or pulsed wave Doppler may also contribute information on vascular hemodynamics and should be obtained as needed.

Normal sonographic appearance of the thyroid gland is fine homogeneous echotexture that is slightly more echogenic than the surrounding musculature. The thyroid capsule is imaged as a thin, hyperechoic line that outlines the gland from surrounding relational anatomy. The air-filled trachea is demonstrated as a curvilinear structure with acoustic shadowing. Multiple, tiny vascular structures may be seen as tubular anechoic structures more apparent at the periphery and upper and lower poles within the gland representing the superior and inferior thyroid arteries and veins. Normal pulsed Doppler spectrum will demonstrate peak systole velocities of 20 to 40 cm/sec in the major thyroid arteries and 15 to 30 cm/sec in intraparenchymal arteries.

The surrounding musculature of the thyroid gland is hypoechoic compared with the normal thyroid parenchyma. The strap muscles are anterior to the gland with the larger sternocleidomastoid muscle imaged more anterolateral to the gland. The hypoechoic longus colli muscle is found posterior to each lobe of the thyroid (see Fig. 22.5 ). The recurrent laryngeal nerve and the inferior thyroid artery pass in the angle between the trachea, esophagus, and thyroid lobe. The esophagus is adjacent to the trachea, with a hypoechoic rim surrounding an echogenic center more commonly visualized slightly to the left of the midline, next to the trachea, with peristalsis noted in real time with patient swallowing ( Fig. 22.9 ).

Congenital Abnormalities of the Thyroid Gland

Congenital abnormalities of the thyroid gland include aplasia, hypoplasia, and ectopic locations of the thyroid gland. Aplasia is congenital absence of gland and may affect one lobe, the isthmus, or the entire gland. Complete absence of the thyroid gland has a severe impact on physical and mental development. Hypoplasia refers to underdevelopment of any part of the gland and may be associated with congenital hypothyroidism.

Ectopic locations may be present along the path of embryonic descent if the thyroid migrates too little or too far. Most commonly, ectopic tissue may be present posterior to the tongue (sublingual or lingual thyroid). Other ectopic locations include larynx (prelaryngeal thyroid) or mediastinum (substernal thyroid). Scintigraphy is best for visualization of ectopic thyroid tissue.

Pathology of the Thyroid Gland

Pathology identified in the thyroid and adjacent neck structures should always be documented in both longitudinal and transverse scan planes. The gland measurements and volume should be obtained and parenchyma defined as homogeneous or heterogeneous. If a nodule is visualized, the location should be noted in relationship to gland (e.g., right thyroid transverse upper; left thyroid long lateral) and also measured in three dimensions. The sonographic appearance should be demonstrated and echogenicity described (e.g., hypoechoic, hyperechoic, and whether cystic, complex cystic, solid, and/or presence and type of calcifications). In addition, the nodule borders should be described as ill defined or well defined and whether a hypoechoic halo is surrounding the nodule. It is not uncommon for sonography to demonstrate multiple nodules (MNG) in a gland. Vascularity should also be demonstrated with color or power Doppler and possibly pulsed wave Doppler.

Nodular Thyroid Disease

Nodular Hyperplasia, Multinodular Goiter, and Adenomatous Hyperplasia

Approximately 80% of nodular thyroid disease is due to hyperplasia or compensatory hypertrophy forming micronodules and macronodules of the gland. This can lead to overall enlargement (goiter) or MNG that may be unilateral or bilateral; it is seen more commonly in women with increasing age. When evaluated microscopically, most benign nodules are classified as hyperplastic, adenomatous, and colloid type nodules.

The most common cause of thyroid disorders worldwide is iodine deficiency, which leads to nodule and goiter formation. Often the gland is able to keep up with the demand and provide normal release of thyroid hormones. However, in some cases, the gland lags behind the demand and the patient develops hypothyroidism. In the first stage, hyperplasia occurs; in the second stage, colloid involution occurs. Progression of this process leads to an asymmetric and multinodular gland with areas of hemorrhage and calcification ( Fig. 22.10 ).

An endemic goiter may affect large groups of people in a specific geographic area where iodine levels in the soil, food, and water are low (e.g., mountainous areas or the Great Lakes region). Certain types of food (cabbage, turnips, and other related vegetables) when ingested in large quantities may increase blood synthesis of T ₃ and T ₄ but increase TSH secretion from the pituitary gland. This dietary deficiency can cause hyperplasia and hypertrophy and can promote goiter formation in the thyroid gland. Iodized salt as a dietary supplement usually corrects the iodine deficiency. In areas not deficient in iodine, autoimmune processes (Graves disease or Hashimoto thyroiditis) are believed to be the basis for most cases of thyroid disease.

A toxic goiter is a condition in which nodular enlargement causes hyperactivity of the thyroid gland and hyperthyroidism. Nontoxic (simple) goiter occurs when nodular enlargement is not associated with thyroid dysfunction (hypothyroidism or hyperthyroidism).

Clinical Findings

A goiter may first present visibly as an anterior protrusion on the neck on thin patients. The clinician may palpate an enlarged thyroid during a physical examination. A goiter may become very large, compressing the esophagus with difficulty swallowing (dysphagia), pressure on the trachea (inspiratory stridor) or neck veins (venous distention), or laryngeal nerve (hoarseness). Patients may also present with clinical symptoms of hypothyroidism or hyperthyroidism. Table 22.3 lists the common findings, sonographic appearances, and differential considerations for nodule thyroid disease.

Table 22.3

Thyroid Findings: Nodular Thyroid Disease

Clinical Findings	Sonographic Appearances	Differential Considerations
Nontoxic Simple Goiter
Thyroid enlargement	Sometimes smooth, sometimes nodular; possible compression of surrounding structures	Thyroiditis Hypothyroidism Neoplasm
Toxic Multinodular Goiter
Thyroid enlargement	Enlarged inhomogeneous gland; can have focal scarring, focal ischemia, necrosis, and cyst formation	Neoplasm Cyst
Graves Disease
Diffuse toxic goiter	Diffusely homogeneous and enlarged	Neoplasm Ophthalmopathy Cutaneous manifestations Hyperthyroidism
Thyroiditis
Swelling and tenderness of the thyroid; later, hypothyroidism	Homogeneous enlargement with nodularity; later, inhomogeneous	Neoplasm
Benign Lesions
Cysts
Solitary nodules or multiple nodules	Anechoic areas, echogenic fluid, or moving fluid levels	Toxic multinodular goiter
Adenoma
Usually euthyroid or hyper-thyroidism	Compression of adjacent structures; fibrous encapsulation; ranges from anechoic to hyperechoic; may have halo	Graves disease

Sonographic Findings

Sonographic appearance of nodular thyroid disease will vary. There can be diffuse symmetric gland enlargement ( Fig. 22.11 ) or localized discrete nodule(s). Enlargement can involve both lobes and isthmus with several nodules, described as an MNG ( Fig. 22.12 ), or one lobe. Nodules can also vary in echogenicity (i.e., isoechoic, hyperechoic, and complex cystic) due to fibrosis, colloid, focal scarring, ischemia, cystic degeneration, or calcification formation. Nodules may present as poorly circumscribed or well defined and encapsulated by a thin, peripheral hypoechoic halo due to surrounding compressed tissue and should be documented ( Fig. 22.13 ). Hyperfunctioning nodules usually demonstrate increased perinodular and intranodular vascularity on color or power Doppler as seen in Fig. 22.12B .