ENDOCRINE CONDITIONS
BY SBFL, MD
GENERAL AND CANCER SURGEON
BACKGROUND
Goiters (from the Latin guttur, throat), defined as an
enlargement of the thyroid, have been recognized since 2700
B.C.
thyroid gland (Greek thyreoeides, shield-shaped)
Embryology
The thyroid gland
arises as an outpouching of the primitive foregut around the
third week of gestation
originates at the base of the tongue in the vicinity of the
foramen cecum.
Endoderm cells in the floor of the pharyngeal anlage thicken
to form the medial thyroid anlage that descends in the neck
anterior to structures that form the hyoid bone and larynx.
During its descent, the anlage remains connected to the
foramen cecum via an epithelial-lined tube known as the
thyroglossal duct.
The epithelial cells making up the anlage give rise to the
thyroid follicular cells.
DEVELOPMENTAL ABNORMALITIES
Thyroglossal Duct Cyst and Sinus
most commonly encountered congenital cervical anomalies.
5th week of gestation, the thyroglossal duct lumen starts to
obliterate and the duct disappears by the eighth week of
gestation.
Rarely, the thyroglossal duct may persist in whole, or in part.
Thyroglossal duct cysts may occur anywhere along the
migratory path of the thyroid, although 80% are found in
juxtaposition to the hyoid bone.
They are usually asymptomatic, but occasionally become
infected by oral bacteria, prompting the patient to seek
medical advice.
Thyroglossal duct sinuses result from infection of the cyst
secondary to spontaneous or surgical drainage of the cyst
and are accompanied by minor inflammation of the
surrounding skin.
Histologically, thyroglossal duct cysts are lined by
pseudostratified ciliated columnar epithelium and squamous
epithelium with heterotopic thyroid tissue present in 20% of
cases.
The diagnosis is usually established by observing a 1- to 2-
cm, smooth, well-defined midline neck mass that moves
upward with protrusion of the tongue.
Routine thyroid imaging is not necessary, although thyroid
scintigraphy and ultrasound have been performed to
document the presence of normal thyroid tissue in the neck.
Treatment:
o "Sistrunk operation," which consists of en bloc
cystectomy and excision of the central hyoid
bone to minimize recurrence.
Approximately 1% of cysts are found to contain cancer that is
usually papillary (85%). Squamous, Hürthle cell, and
anaplastic cancers also have been reported, but are rare.
Medullary thyroid cancers are, however, not found in
thyroglossal duct cysts.
Lingual Thyroid
A lingual thyroid represents a failure of the median thyroid
anlage to descend normally and may be the only thyroid
tissue present.
Intervention becomes necessary for obstructive symptoms
such as choking, dysphagia, airway obstruction, and
hemorrhage.
Many of these patients develop hypothyroidism.
Medical treatment:
o administration of exogenous thyroid hormone
to suppress thyroid-stimulating hormone (TSH)
o radioactive iodine ablation followed by
hormone replacement.
o Surgical excision is rarely needed, but if
required, should be preceded by an evaluation
of normal thyroid tissue in the neck to avoid
inadvertently rendering the patient hypothyroid.
Ectopic Thyroid
Normal thyroid tissue may be found anywhere in the central
neck compartment, including the esophagus, trachea, and
anterior mediastinum.
Thyroid tissue has been observed adjacent to the aortic arch,
in the aortopulmonary window, within the upper pericardium,
and in the interventricular septum.
Thyroid tissue situated lateral to the carotid sheath and
jugular vein, previously termed "lateral aberrant thyroid,"
almost always represents metastatic thyroid cancer in lymph
nodes, and not remnants of the lateral anlage that had failed
to fuse with the main thyroid, as previously suggested by
Crile.
THYROID ANATOMY
brown in color and firm in consistency, and is located
posterior to the strap (sternothyroid and sternohyoid)
muscles.
weighs approximately 20 g, but gland weight varies with body
weight and iodine intake.
The thyroid lobes are located adjacent to the thyroid cartilage
and connected in the midline by an isthmus which is typically
located just inferior to the cricoid cartilage.
A pyramidal lobe, which represents the most caudal end of
the thyroglossal duct, is found in approximately 50% of
individuals having thyroid operations.
The thyroid lobes extend to mid-thyroid cartilage superiorly
and lie adjacent to the carotid sheaths and
sternocleidomastoid muscles laterally
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 The strap muscles (sternohyoid, sternothyroid and superior o Each follicle is lined by cuboidal epithelial cells
belly of the omohyoid) are located anteriorly and are and contains a central store of colloid secreted
innervated by the ansa cervicalis (ansa hypoglossi). from the epithelial cells under the influence of
The thyroid gland is enveloped by a loosely connecting fascia the pituitary hormone, TSH.
that is formed from the partition of the deep cervical fascia The second group of thyroid secretory cells is the C cells or
into anterior and posterior divisions. parafollicular cells, which contain and secrete the hormone
The true capsule of the thyroid is a thin, densely adherent calcitonin. T
fibrous layer that sends out septa that invaginate into the o They are found as individual cells or clumped
gland, forming pseudolobules. in small groups in the interfollicular stroma and
The thyroid capsule is condensed into the posterior located in the upper poles of the thyroid lobes.
suspensory or Berry's ligament near the cricoid cartilage and
upper tracheal rings. THYROID PHYSIOLOGY
Blood Supply Iodine Metabolism
The thyroid gland is well vascularized by two major sets The average daily iodine requirement is 0.1 mg, which can be
of arteries. derived from foods such as fish, milk, and eggs, or as
o superior thyroid arteries arise from the additives in bread or salt.
ipsilateral external carotid arteries and divide In the stomach and jejunum, iodine is rapidly converted to
into anterior and posterior branches at the iodide and absorbed into the bloodstream, from where it is
apices of the thyroid lobes. distributed uniformly throughout the extracellular space.
o inferior thyroid arteries are derived from the Iodide is actively transported into the thyroid follicular cells by
thyrocervical trunk shortly after their origin from an ATP-dependent process. T
the subclavian arteries. The inferior thyroid The thyroid is the storage site of greater than 90% of the
arteries travel upward in the neck posterior to body's iodine content and accounts for one-third of the
the carotid sheath to enter the thyroid lobes at plasma iodine loss.
their midpoint. The remaining plasma iodine is cleared via renal excretion.
o A thyroidea ima artery arises directly from the The synthesis of thyroid hormone consists of several steps4
aorta or innominate in 1 to 4% of individuals, to o Iodide trapping
enter the isthmus or replace a missing inferior  involves active (ATP-dependent)
thyroid artery. transport of iodide across the
Nerves basement membrane of the
o The left Reluctant laryngeal nerve (RLN) arises thyrocyte via an intrinsic membrane
from the vagus nerve where it crosses the protein, the Na+/I– symporter (NIS).
aortic arch, loops around the ligamentum  Thyroglobulin (Tg) is a large (660-
arteriosum and ascends medially in the neck kDa) glycoprotein, which is present
within the tracheoesophageal groove. in thyroid follicles and has four
o The right RLN arises from the vagus at its tyrosyl residues.
crossing with the right subclavian artery. o Oxidation of iodide to iodine
 iodination of tyrosine residues on Tg,
PARATHYROID GLANDS to form monoiodotyrosines (MITs)
Most individuals have four parathyroid glands, which derive and diiodotyrosines (DITs).
their blood supply primarily from branches of the inferior  Both processes are catalyzed by
thyroid artery. thyroid peroxidase.
Generally, parathyroid glands can be found within 1 cm of the o Coupling
junction of the inferior thyroid artery and the RLN. The  two DIT molecules to form
superior glands are usually located dorsal to the RLN, tetraiodothyronine or thyroxine (T4),
whereas the inferior glands are usually found ventral to the and one DIT molecule with one MIT
RLN molecule to form 3,5,3'-
triiodothyronine (T3) or reverse
THYROID HISTOLOGY 3,3',5'-triiodothyronine (rT3).
Microscopically, the thyroid is divided into lobules that contain  When stimulated by TSH, thyrocytes
20 to 40 follicles form pseudopodia, that encircle
There are roughly 3 x 106 follicles in the adult male thyroid portions of cell membrane containing
gland. thyroglobulin, which, in turn, fuse
o The follicles are spherical and average 30 m in with enzyme-containing lysosomes.
diameter. o Hydrolsis

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  thyroglobulin is hydrolyzed to
release free iodothyronines (T3 and
T4) and mono- and diiodotyrosines.
BENIGN THYROID DISORDERS
Hyperthyroidism
The clinical manifestations of hyperthyroidism result from an
excess of circulating thyroid hormone.
Graves' Disease
the most common cause of hyperthyroidism in North
America, accounting for 60 to 80% of cases.
It is an autoimmune disease of unknown cause with a
strong familial predisposition
female preponderance (5:1)
peak incidence between the ages of 40 and 60 years.
Graves' disease is characterized by thyrotoxicosis,
diffuse goiter, and extrathyroidal conditions, including
ophthalmopathy, dermopathy (pretibial myxedema),
thyroid acropachy, gynecomastia, and other
manifestations.
Etiology, Pathogenesis, and Pathology
o The exact etiology of the initiation of the
autoimmune process in Graves' disease is
unknown.
o conditions such as the postpartum state, iodine
excess, lithium therapy, and bacterial and viral
infections have been suggested as possible
triggers.
o Genetic factors also play a role, because
haplotyping studies indicate that Graves'
disease is associated with certain human
leukocyte antigen (HLA) haplotypes—HLA-B8
and HLA-DR3 and HLADQA1*0501 in white
patients—whereas HLA-DRB1*0701 is
protective.
o Polymorphisms of the cytotoxic T-lymphocyte
antigen 4 (CTLA-4) gene also have been
associated with Graves' disease development.
 Once initiated, the process causes
sensitized T-helper lymphocytes to
stimulate B lymphocytes, which
produce antibodies directed against
the thyroid hormone receptor
(TRAbs).
o TSI or antibodies (TSAbs) that stimulate the
TSH receptor, as well as TSH-binding
inhibiting immunoglobulins (TSIIs) or
antibodies (TBIAs) have been described
Graves' disease is also associated with other
autoimmune conditions such as type I diabetes mellitus,
Addison's disease, pernicious anemia, and myasthenia
gravis.
Macroscopically, the thyroid gland in patients with
Graves' disease is diffusely and smoothly enlarged, with
a concomitant increase in vascularity.
Microscopically, the gland is hyperplastic, and the
epithelium is columnar with minimal colloid present.
The nuclei exhibit mitosis, and papillary projections of
hyperplastic epithelium are common.
There may be aggregates of lymphoid tissue, and
vascularity is markedly increased.
Clinical Features
o The clinical manifestations of Graves' disease
can be divided into those occurring in any
patient with hyperthyroidism and those specific
to Graves' disease.
o Symptoms common to most patients with
hyperthyroidism include heat intolerance,
increased sweating and thirst, and weight loss
despite adequate caloric intake.
o Symptoms of increased adrenergic stimulation
include palpitations, nervousness, fatigue,
emotional lability, hyperkinesis, and tremors.
o The most common gastrointestinal symptoms
include increased frequency of bowel
movements and diarrhea.
o Female patients often develop amenorrhea,
decreased fertility, and an increased incidence
of miscarriages.
o Children experience rapid growth with early
bone maturation
o Older patients present with cardiovascular
complications such as atrial fibrillation and
congestive heart failure.
physical examination
o weight loss and facial flushing may be evident
o warm and moist skin ( African American
patients often note darkening of their skin)
o Tachycardia or atrial fibrillation is present, with
cutaneous vasodilation leading to a widening
of the pulse pressure and a rapid falloff in the
transmitted pulse wave (collapsing pulse).
o A fine tremor, muscle wasting, and proximal
muscle group weakness with hyperactive
tendon reflexes are often present.
o Clinical ophthalmopathy – 50%
o Eye symptoms :
 lid lag (von Graefe's sign)
 spasm of the upper eyelid revealing
the sclera above the corneoscleral
limbus (Dalrymple's sign)
 prominent stare as a consequence
of catecholamine excess.
 True infiltrative eye disease results in
periorbital edema, conjunctival
swelling and congestion (chemosis),
proptosis, limitation of upward and
lateral gaze (from involvement of the
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 inferior and medial recti muscles,
respectively), keratitis, and even
blindness as a result of optic nerve
involvement. T
 The etiology of Graves'
ophthalmopathy is not completely
known; however, orbital fibroblasts
and muscles are thought to share a
common antigen with thyrocytes, the
TSH receptor
o Ophthalmopathy results from inflammation
caused by cytokines released from sensitized
killer T lymphocytes and cytotoxic antibodies.
o Dermopathy occurs in 1 to 2% of patients and
is characterized by deposition of
glycosaminoglycans leading to thickened skin
in the pretibial region and dorsum of the foot .
o Gynecomastia is common in young men.
o Bony involvement leads to subperiosteal bone
formation and swelling in the metacarpals
(thyroid acropachy).
o Onycholysis or separation of fingernails from
their beds, is a more commonly observed
finding.
o On physical exam, the thyroid is usually
diffusely and symmetrically enlarged, as
evidenced by an enlarged pyramidal lobe.
o There may be an overlying bruit or thrill and
loud venous hum in the supraclavicular space.
Diagnostic Tests
o The diagnosis of hyperthyroidism is made by a
suppressed TSH with or without an elevated
free T4 or T3 level.
o Elevated thyroid-stimulating hormone receptor
(TSH-R) or TSAb are diagnostic of Graves'
disease and are increased in approximately
90% of patients.
o MRI scans of the orbits are useful in
evaluating Graves' ophthalmopathy.
Treatment
o antithyroid drugs
o thyroid ablation with radioactive 131I
o thyroidectomy.
o The choice of treatment depends upon
several factors, including the age of the
patient, the severity of the disease, the size of
the gland, any coexistent pathology,
associated ophthalmopathy, patient's
preferences, and desire for pregnancy.
Antithyroid Drugs
o Antithyroid medications are generally
administered in preparation for radioactive
iodine ablation or surgery. The medications
commonly used are propylthiouracil (PTU, 100
to 300 mg three times daily) and methimazole
(10 to 30 mg three times daily). Methimazole
has a longer half-life and can be dosed once
daily. Both drugs reduce thyroid hormone
production by inhibiting the organic binding of
iodine and the coupling of iodotyrosines
(mediated by thyroid peroxidase). In addition,
PTU also inhibits the peripheral conversion of
T4 to T3, making it useful for the treatment of
thyroid storm. Both drugs can cross the
placenta, inhibiting fetal thyroid function, and
are excreted in breast milk, although PTU has
a lower risk of transplacental transfer.
Methimazole is also associated with congenital
aplasia, therefore PTU is more preferred in
pregnant and breast-feeding women. Side
effects of treatment include reversible
granulocytopenia, skin rashes, fever,
peripheral neuritis, polyarteritis, vasculitis, and,
rarely, agranulocytosis and aplastic anemia.
Patients should be monitored for these
possible complications and should always be
warned to stop PTU or methimazole
immediately and to seek medical advice,
should they develop a sore throat or fever.
Treatment of agranulocytosis involves
admission to the hospital, discontinuing the
drug and broad-spectrum antibiotic therapy.
Surgery should be postponed until the
granulocyte count reaches 1000 cells/m3.
o The catecholamine response of thyrotoxicosis
can be alleviated by administering beta-
blocking agents.
o These drugs have the added effect of
decreasing the peripheral conversion of T4 to
T3.
o Propranolol is the most commonly prescribed
medication in doses of about 20 to 40 mg four
times daily.
o Higher doses are sometimes required
because of increased clearance of the
medication.
Radioactive Iodine Therapy
o Radioactive iodine (RAI; 131I) forms the
mainstay of Graves' disease treatment in North
America.
o The major advantages of this form of
treatment are the avoidance of a surgical
procedure and its concomitant risks, reduced
overall treatment costs, and ease of treatment.
o RAI therapy is most often used in older
patients with small or moderate-size goiters, in
patients who have relapsed after medical or
surgical therapy, and in patients in whom
antithyroid drugs or surgery are
contraindicated.
o Absolute contraindications to RAI include
women who are pregnant or breast-feeding.
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 o Relative contraindications include young
patients (especially children and adolescents),
patients with thyroid nodules, and patients with
ophthalmopathy.
Surgical Treatment
o have confirmed cancer or suspicious thyroid
nodules
o are young
o are pregnant or desire to conceive soon after
treatment (4) have allergies to antithyroid
medications
o have large goiters causing compressive
symptoms
o are reluctant to undergo RAI therap
Relative indications for thyroidectomy include patients,
particularly smokers, with moderate to severe Graves'
ophthalmopathy, patients who desire rapid control of
hyperthyroidism with a chance of being euthyroid, and
patients who demonstrate poor compliance with
antithyroid medications
TOXIC MULTINODULAR GOITER
occur in individuals older than 50 years of age,
who often have a prior history of a nontoxic multinodular
goiter.
The presentation is often insidious in that hyperthyroidism
may only become apparent when patients are placed on low
doses of thyroid hormone suppression for the goiter.
Symptoms and signs of hyperthyroidism are similar to Graves'
disease, but are less severe and extrathyroidal manifestations
are absent.
Diagnostic Studies
o Blood tests are similar to Graves' disease with
a suppressed TSH level and elevated free T4
or T3 levels. RAI uptake is also increased,
showing multiple nodules with increased
uptake and suppression of the remaining
gland.
Treatment
o Hyperthyroidism must be adequately controlled
as described above.
o Surgical resection is the preferred treatment
method for patients with toxic multinodular
goiter, with subtotal thyroidectomy being the
standard procedure.
o RAI therapy is reserved for elderly patients
who represent very poor operative risks,
provided there is no airway compression from
the goiter and thyroid cancer is not a concern
Plummer's Disease (Toxic Adenoma)
Hyperthyroidism from a single hyperfunctioning nodule
typically occurs in younger patients who note recent
growth of a long-standing nodule along with the
symptoms of hyperthyroidism.
Most toxic adenomas are characterized by somatic
mutations in the TSH receptor gene; G-protein-
stimulating gene (gsp) mutations occur less.
Thyroid Storm
Thyroid storm is a condition of hyperthyroidism
accompanied by fever, central nervous system agitation
or depression, cardiovascular dysfunction that may be
precipitated by infection, surgery, or trauma.
Beta blockers are given to reduce peripheral T4-to-T3
conversion and to decrease the hyperthyroid symptoms.
Oxygen supplementation and hemodynamic support
should be instituted.
Nonaspirin compounds can be used to treat pyrexia, and
Lugol's iodine or sodium ipodate (intravenously) should
be administered to decrease iodine uptake and thyroid
hormone secretion.
PTU therapy blocks the formation of new thyroid
hormone and reduces peripheral conversion of T4 to T3,
and corticosteroids help to prevent adrenal exhaustion.
Corticosteroids also block hepatic thyroid hormone
conversion.
Hypothyroidism
Deficiency in the circulating levels of thyroid hormone
leads to hypothyroidism, and, in neonates, to cretinism,
which is characterized by neurologic impairment and
mental retardation.
May also be associated with deafness (Pendred's
syndrome) and Turner's syndrome..
Causes of Hypothyroidism
o Primary (increased TSH levels)
 Hashimoto's thyroiditis
 RAI therapy for Graves'disease
 Postthyroidectomy
 Excessive iodine intake
 Subacute thyroiditis
o Medications: antithyroid drugs, lithium
o Rare: iodine deficiency, dyshormogenesis
o Secondary (decreased TSH levels)
 Pituitary tumor
 Pituitary resection or ablation
o Tertiary
 Hypothalamic insufficiency
 Resistance to thyroid hormone
Clinical Features
o Failure of thyroid gland development or
function in utero leads to cretinism and
characteristic facies similar to those of children
with Down syndrome and dwarfism.
o Failure to thrive and severe mental retardation
are often present.
o Hypothyroidism developing in childhood or
adolescence results in delayed development
and may also lead to abdominal distention,
umbilical hernia, and rectal prolapse.
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 o Mental performance tends to be diminished
with the onset of hypothyroidism after 6
months of age, but severe retardation is
uncommon.
o In adults, symptoms in general are nonspecific;
they include tiredness, weight gain, cold
intolerance, constipation, and menorrhagia.
o Patients with severe hypothyroidism or
myxedema develop characteristic facial
features as a consequence of the deposition of
glycosaminoglycans in the subcutaneous
tissues, leading to facial and periorbital
puffiness.
o The skin becomes rough and dry and often
develops a yellowish hue from reduced
conversion of carotene to vitamin A.
o Hair becomes dry and brittle, and severe hair
loss may occur. There also is a o via direct spread from persistent pyriform
characteristic loss of the outer two-thirds of the
eyebrows.
o An enlarged tongue may impair speech, which
is already slowed, in keeping with the
impairment of mental processes.
o Untreated dementia may lead to myxedema
madness.
o Patients may also have nonspecific abdominal
pain accompanied by distention and
constipation.
o Libido and fertility are impaired in both sexes.
o Cardiovascular changes in hypothyroidism
include bradycardia, cardiomegaly, pericardial
effusion, reduced cardiac output, and
pulmonary effusions.
o When hypothyroidism occurs as a result of
pituitary failure, features of hypopituitarism
such as pale, waxy skin, loss of body hair, and
atrophic genitalia may be present.
Laboratory Findings
o Hypothyroidism is characterized by low
circulating levels of T4 and T3. Raised TSH
levels are found in primary thyroid failure,
whereas secondary hypothyroidism is
characterized by low TSH levels that do not
increase following TRH stimulation.
o Thyroid autoantibodies are present and are
highest in patients with autoimmune disease
(Hashimoto's thyroiditis, Graves' disease),
although they are also elevated in patients with
nodular goiter and thyroid neoplasms.
o Other findings include anemia,
hypercholesterolemia, and decreased voltage
with flattening or inversion of T waves on
electrocardiogram.
o Comatose patients with myxedema also have
hyponatremia and CO2 retention.
Treatment
o Thyroxine is the treatment of choice and is
administered in dosages varying from 50 to
200 g per day, depending upon patient's size
and condition.
THYROIDITIS
an inflammatory disorder of the thyroid gland and is usually
classified into acute, subacute, and chronic forms.
Chronic and subacute thyroiditis is usually managed
medically, but surgical treatment is occasionally needed.
Acute (Suppurative) Thyroiditis
The thyroid gland is inherently resistant to infection as a
consequence of its extensive blood and lymphatic
supply, high iodide content, and fibrous capsule, but
infectious agents can seed it
o via the hematogenous or lymphatic route
sinus fistulae or thyroglossal duct cysts
o as a result of penetrating trauma to the thyroid
gland
o as a result of immunosuppression.
Streptococcus and anaerobes account for about 70% of
cases, but Escherichia coli, Pseudomonas aeruginosa,
Haemophilus influenzae, Eikenella corrodens,
Corynebacterium, and Coccidiomycosis species also
have been cultured
Subacute Thyroiditis
occur in either the painful or painless forms. etiology is
unknown, painful thyroiditis is thought to be viral in origin
or result from a postviral inflammatory response.
Genetic predisposition may also play a role, as
manifested by its strong association with the HLA-B35
haplotype
Painful thyroiditis most commonly occurs in 30- to 40-
year-old women and is characterized by the sudden or
gradual onset of neck pain, which may radiate toward
the mandible or ear.
History of a preceding upper respiratory tract infection
can often be elicited.
The gland is enlarged, exquisitely tender, and firm.
Chronic Thyroiditis
Lymphocytic (Hashimoto's) Thyroiditis
This disorder was first described by Hashimoto, in 1912,
as struma lymphomatosa—a transformation of thyroid
tissue to lymphoid tissue—and is the most common
inflammatory disorder of the thyroid and the leading
cause of hypothyroidism.
Hashimoto's thyroiditis is an autoimmune process that is
thought to be initiated by the activation of CD4+T
(helper) lymphocytes with specificity for thyroid antigens
Antibodies are directed against the three main
antigens—Tg (60%), TPO (95%), the TSH-R (60%)17—
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 and less commonly against the sodium/iodine symporter
(25%).
On gross examination, the thyroid gland is usually mildly
enlarged throughout and has a pale, gray-tan cut surface
that is granular, nodular, and firm.
On microscopic examination, the gland is diffusely
infiltrated by small lymphocytes and plasma cells, and
occasionally shows well-developed germinal centers.
Thyroid follicles are smaller than normal with reduced
amounts of colloid and increased interstitial connective
tissue.
o The follicles are lined by Hürthle or Askanazy
cells, which are characterized by abundant
eosinophilic, granular cytoplasm.
Clinical Presentation
o more common in women (male: female ratio
1:10 to 20) between the ages of 30 and 50
years
o The most common presentation is that of a
minimally or moderately enlarged firm gland
discovered on routine physical examination or
the awareness of a painless anterior neck
mass, although 20% of patients present with
hypothyroidism, and 5% present with
hyperthyroidism (hashitoxicosis
Diagnostic Studies
o When Hashimoto's thyroiditis is suspected
clinically, an elevated TSH, reduced T4 and T3
levels, and the presence of thyroid
autoantibodies confirm the diagnosis.
Treatment
o Thyroid hormone replacement therapy is
indicated in overtly hypothyroid patients, with a
goal of maintaining normal TSH levels.
Goiter
Any enlargement of the thyroid gland is referred to as a
goiter..
Most nontoxic goiters are thought to result from TSH
stimulation secondary to inadequate thyroid hormone
synthesis and other paracrine growth factors.
The thyroid gland enlarges in order to maintain the
patient in a euthyroid state.
Goiters may be diffuse, uninodular, or multinodular.
Familial goiters resulting from inherited deficiencies in
enzymes necessary for thyroid hormone synthesis may
be complete or partial.
Etiology of Nontoxic Goiter
o Endemic: iodine deficiency, dietary goitrogens
Medications: iodide, amiodarone, lithium
o Thyroiditis: subacute, chronic
o Familial: hormonal dysgenesis from enzyme
defects Resistance to thyroid hormone
o Neoplasm
Elevated TSH levels induce diffuse thyroid hyperplasia,
followed by focal hyperplasia resulting in nodules that
may or may not concentrate iodine, colloid nodules, or
microfollicular nodules.
Clinical Features
o Most patients with nontoxic goiters are
asymptomatic, although patients often
complain of a pressure sensation in the neck,
particularly with motion.
o As the goiters become very large
 compressive symptoms, such as
dyspnea and dysphagia, ensue.
 Patients also describe having to
clear their throats frequently
(catarrh).
 Dysphonia from recurrent laryngeal
nerve injury is rare, except when
malignancy is present.
 Obstruction of venous return at the
thoracic inlet from a substernal goiter
results in a positive Pemberton's
sign—facial flushing and dilatation of
cervical veins upon raising the arms
above the head
 Sudden enlargement of nodules or
cysts because of hemorrhage may
cause acute pain.
Physical examination may reveal a soft, diffusely
enlarged gland (simple goiter) or nodules of various size
and consistency in case of a multinodular goiter.
Deviation of the trachea may be apparent.
Diagnostic Tests
o Patients are usually euthyroid with normal TSH
and low-normal or normal free T4 levels.
Malignant Thyroid Disease
In the United States, thyroid cancer accounts for less
than 1% of all malignancies (2% of women and 0.5% of
men).
Thyroid cancer is responsible for six deaths per 1 million
persons annually.
Most patients present with a palpable swelling in the
neck, which initiates assessment through a combination
of history, physical examination, and FNA biopsy.
TYPES
o Follicular cancer
o Papillary cancer
o Medullary cancer
o Anaplastic cancer
o Lymphoma
Lymphomas account for less than 1% of thyroid
malignancies and most are of the non-Hodgkin's B-cell
type.
The disease can arise as part of a generalized
lymphomatous condition, most thyroid lymphomas
develop in patients with chronic lymphocytic thyroiditis
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Chronic antigenic lymphocyte stimulation has been
suggested to result in lymphocyte transformation.
Staging studies should be obtained to assess the extent
of extrathyroidal spread.
Prognosis depends on the histologic grade of the tumor
and whether the lymphoma is confined to the thyroid
gland or is disseminated.
The overall 5-year survival rate is about 50%; patients
with extrathyroidal disease have markedly lower survival
rates.
Treatment and Prognosis
o Patients with thyroid lymphoma respond
rapidly to chemotherapy (CHOP—
cyclophosphamide, doxorubicin, vincristine,
and prednisone), which is also associated with
improved survival.
o Combined treatment with radiotherapy and
chemotherapy is often recommended.
o Thyroidectomy and nodal resection are used to
alleviate symptoms of airway obstruction in
patients who do not respond quickly to the
above regimens, or in patients who have
completed the regimen prior to diagnosis. for
chemotherapy and radiotherapy for most
patients.