Clinical Methods: The History, Physical, and

Laboratory Examinations. 3rd edition.

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Chapter 138Neck and Thyroid

Examination
Terry J. Smith.

Definition
The thyroid gland normally lies just caudal to the thyroid cartilage in the anterior
neck. This location allows an examiner to inspect and palpate this bilobed structure,
which in the adult human being weighs from 15 to 25 g. Physical examination of the
thyroid gland enables the experienced clinician to construct a rather narrow
differential of its anatomical pathology, whereas diagnostic testing (Chapter 142) is
frequently necessary to establish the thyroid's functional status.

Technique
The patient should hold a glass of water and be seated. There should be room for the
examiner on all sides of the seated patient. Place the patient's head in slight
hyperextension with good crosslight falling on the anterior neck and then ask the
patient to swallow. The outline of the thyroid gland in thin individuals can be
observed frequently as a protuberance on both sides of the trachea moving cephalad in
tandem with but 2 cm below the crest of the thyroid cartilage (Figure 138.1). Look for
abnormal enlargement, contour, asymmetry, and masses while the patient swallows
repeatedly. The neck should also be inspected for abnormal masses and prominent
pulsations.

Figure 138.1

The deep structures of the anterior neck. These anatomic landmarks properly orient
the examiner.
The art of thyroid gland palpation has spawned a number of distinct attitudes, and
each examiner should, through practice, adopt a comfortable technique. Frequently it
is advantageous to examine the gland while you stand behind as well as on each side
of the patient. Identify the thyroid cartilage, the thyrocricoid membrane, and the
cricoid cartilage, a horizontal structure 5 mm wide that marks the superior border of
the isthmus. Palpate the isthmus (frequently impalpable unless enlarged), and if
standing to the side of the patient, slide the tips of your fingers so that their palmar
surfaces rest on the trachea with the dorsal surface medial to the sternocleidomastoid
muscle. A frequent mistake is to move the fingers too laterally and trap the body of
the muscle between your fingers and the trachea. The ipsilateral lobe can be palpated
simultaneously with your thumb or with the other hand from the opposite direction.
When you stand behind the patient, identify the landmarks and isthmus with one
hand, and when in position to feel the thyroid lobe on that side, place the fingers of
your other hand symmetrically on the other side of the trachea. Again identify each
lobe while the patient swallows. Feel the gland's surface, note any asymmetry,
texture, and estimate the size of each lobe (normally 7 to 10 g). When goiter is
present, measure any discrete masses as well as the neck's greatest circumference. A
penciled tracing of the goiter's outline provides a reliable record for future
comparison. One should also palpate the neck for lymphadenopathy and search for
masses (especially in the midline for abnormalities of the thyroglossal duct) and
surgical scars.

Transillumination is helpful only in confirming the nature of a superficial thin-walled

cyst. Occasional patients with Graves" disease present with an auscultable bruit and
palpable thrill over a diffusely enlarged goiter.

Basic Science
The anlage of the thyroid gland, recognizable by the third week of gestation, develops
from an endodermal thickening at the base of the tongue and migrates caudally, with
the ultimobranchial bodies from the fourth pharyngeal pouch. This fusion accounts for
the two distinct cell types that constitute the mature gland and possess quite distinct
functions: the follicular cells, which concentrate and organify iodine and are involved
in thyroid hormone synthesis; and the parafollicular, or "c," cells, which secrete
calcitonin, a polypeptide that has a minor role in the regulation of serum calcium
concentrations. The gland is first able to concentrate iodine by week 12 of gestation.

The substance of the gland is arranged into secretory units called follicles, which are
surrounded by epithelial cells participating in thyroid hormone synthesis. The
follicular lumens are filled with colloid-storing thyroglobulin, the macromolecular
glvcoprotein precursor of the circulating hormones.

The fully developed thyroid has the shape of a butterfly with two lobes connected by
a thin isthmus overlying the trachea. The body is encompassed by a thin fibrous
capsule and normally moves cephalad with deglutition. The parathyroid glands
usually lie posterolateral to the thyroid lobes, whereas the recurrent laryngeal nerves
run down grooves between the trachea and esophagus. These anatomic relationships
are crucial to thyroid surgeons, since the major complications of thyroidectomy
involve the accidental disturbance of these two structures. The pyramidal lobe, an
embryonic vestige of the thyroglossal duct, usually arises from the medial aspect of
the right lobe and extends cephalad as a small, fingerlike projection. Occasionally, the
thyroid gland can be found in ectopic locations (e.g., behind the sternum and at the
base of the tongue).

The gland elaborates two major hormones, thyroxine (T4) and triiodothyronine (T3) in
a molar ratio of approximately 10 : 1. The major thyromimetic activity belongs to T3,
the 5′-monodeiodinated product of T4. The latter compound may function mainly as a
prohormone, and whether it has intrinsic activity remains controversial. Once released
from the gland, T4 arid T3 circulate in the serum bound in large part to proteins:
thyroid binding globulin (TBG), prealbumin, and albumin. Over 99% of each is
bound, and most of the evidence to date suggests that the free hormone is the
biologically available portion. Once delivered to the target tissue, T4 apparently enters
the cell, is deiodinated to T3, and translocates to the cell nucleus where it binds to
endogenous proteinaceous receptors. The nature of these receptors has recently been
elucidated. They are apparently encoded by isoforms of the c-erb A proto-oncogene
and are related to nuclear receptors for steroid hormones and retinoic acid. Through
its interaction with the cell nucleus, thyroid hormone is an important regulator of
protein synthesis and may have direct actions on the mitochondrion and the plasma
membrane. One important effect of thyroid hormone is to stimulate cellular
respiration, a process that apparently derives from the induction of Na+-K+-ATPase,
the sodium pump.

A major determinant of thyroid gland function is thyrotropin (TSH), a glycoprotein

synthesized and released from thyrotropic cells in the anterior pituitary. TSH is
regulated in turn by the hypothalamus through its elaboration of thyrotropin-releasing
hormone (TRH), a tripeptide. TSH stimulates the thyroid gland to increase iodine
uptake and thyroid hormone synthesis and release. Thyroid hormone then feeds back
on the pituitary and provides negative modulation of TSH production.

Clinical Significance
Enlargement of the thyroid most commonly results from increased pituitary secretion
of TSH or lymphocyte production of TSH-like immunoglobulins. In addition, a
number of inflammatory, infiltrative, and neoplastic diseases can cause goiter.
Physical examination enables the clinician to differentiate among these possibilities.

The pituitary most commonly secretes an excess amount of TSH to compensate for a
deficiency in thyroid hormone biosynthesis. Initially TSH causes a symmetrical
enlargement of the thyroid gland. With time the gland can become asymmetrical and
multinodular. A dominant nodule in a multinodular gland can resemble a neoplastic
process. Immunoglobulins that mimic TSH stimulation also cause a symmetrical
goiter, but because hormone biosynthesis is not defective, thyrotoxicosis can result.
These goiters become quite vascular and can manifest a bruit and thrill. When
"destructive" immunoglobulin predominates in autoimmune thyroid disease, one can
feel a characteristic finely nodular ("cobblestone") texture. Autoimmune thyroid
disease can also produce uninodular or multinodular lesions indistinguishable from
neoplasia. Although autoimmune goiter is rarely painful, inflammatory diseases
characteristically present with a tender goiter. Subacute thyroiditis, the most common
inflammatory thyroid disease, usually enlarges the whole gland, but can also present
with a dominant mass. Acute bacterial infections, while more focal, are easily
distinguishable by their exquisite tenderness and the warmth and redness of the
overlying skin.

Although a dominant nodule in a diffusely abnormal gland can harbor a malignancy,

the physician most frequently entertains this diagnostic possibility with a solitary
nodule in an otherwise normal gland. These palpable abnormalities mandate further
evaluation, which might include sonography, radionuclide scanning, or, preferably,
microscopic tissue examination. The relative merits of each of these diagnostic
maneuvers have been described in detail elsewhere.

The finding of goiter per se does not necessarily imply that the gland is supplying the
body with a disordered amount of thyroid hormone. When thyroid function is so
altered, the patient presents with systemic manifestations as a result of excessive or
deficient peripheral actions of thyroid hormone. Table 138.1 lists the common
symptoms and signs resulting from excessive amounts of circulating thyroid hormone.
Many patients will have several of these symptoms, and it is rare for all to be absent
in clinically significant thyrotoxicosis. Hyperthyroidism most commonly results from
autoimmune production of thyroid-stimulating immunoglobulins and is known in
America as Graves" disease. Nodular goiters can also cause hyperthyroidism as a
result of an excessive "autonomous" production of thyroid hormone. A solitary toxic
nodule typically suppresses the remainder of the gland and appears as a unilateral
goiter, often with no palpable gland contralaterally. The ingestion of pharmacologic
amounts of exogenous thyroid hormone suppresses the entire gland, leaving no
palpable tissue in the face of thyrotoxicosis. Granulomatous and lymphocytic
thyroiditis can disrupt the thyroid's follicular architecture, releasing sufficient
amounts of stored hormone to cause transient thyrotoxicosis.

Table 138.1

Symptoms and Physical Signs of Hyperthyroidism.

Hypothyroidism occurs when the gland is unable to produce enough hormone to

satisfy the metabolic requirements of the body. Primary hypothyroidism in association
with goiter is caused by iodine deficiency, enzymatic defects in thyroid hormone
biosynthesis, autoimmune destruction of the glandular parenchyma, as in Hashimoto's
thyroiditis, and in individuals with underlying thyroid disease by the ingestion of
goitrogens such as lithium, sulfonamides, and large quantities of iodine. Nongoitrous
hypothyroidism results from idiopathic thyroid atrophy, iatrogenic ablation, and
dysfunction of the pituitary or hypothalamus. The latter secondary and tertiary forms
of hypothyroidism are important to recognize and distinguish from primary
hypothyroidism because concomitant dysfunction of the hypothalamic—pituitary—
adrenal axis is commonly present. The symptoms and signs of hypothyroidism are
listed in Table 138.2. They may be quite subtle when hypothyroidism is mild and of
short duration. Conversely, these manifestations may be flagrant and profound in
patients who have gone undiagnosed for several years. Severe, long-standing
hypothyroidism is characterized by the deposition of glycosaminoglycans in the skin
and other organs, a process known as myxedema.

Table 138.2

Symptoms and Physical Signs of Hypothyroidism.

References
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