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ANATOMY AND PHYSIOLOGY OF HEAD AND NECK ENDOCRINE GLANDS
Figure 77.1 Relationship of the thyroid gland, larynx, and trachea.
posterior two thirds of the tongue. is tract can persist, forming a thyroglossal duct cyst, a
midline swelling that may require excision.
Microscopic Anatomy
yroid cells are organised into functional lobules surrounding a lobular artery. Lobules
contain 20–40 spherical follicles lined by a single layer of follicular cells around a collection of colloid. e basal and apical layers of the follicular cells are bound by tight junctions to allow control of the release of thyroid hormones. In response to thyroid-stimulating
hormone (TSH), follicular cells adopt a columnar shape, and their apical surfaces protrude
microvilli to facilitate reabsorption of colloid.
Follicles are located within a loose connective tissue stroma containing extensive capillary networks arranged into angiofollicular units. Parafollicular C cells can be found either individually or
within small clusters throughout the stroma, and they are responsible for secretion of calcitonin.
Physiology of the Thyroid Gland
yroid hormones are vital to the regulation and stimulation of cell metabolism; thus, they
have a number of signicant systemic eects on bone, the cardiovascular system, and the
central nervous system.
Synthesis of Thyroid Hormones
e thyroid produces two thyroid hormones, tetraiodothyronine (T4) and triiodothyronine (T3).
Eighty percent of production comprises T4. T4 is converted to T3 in the peripheral circulation. T3 is
more biological ly active, with a vefold greater potency and a shorter ha lf-life (1.5 days for T3 vs 7 days
for T4). Serum T3 and T4 concentrations are maintained peripherally by plasma thyroxine-binding
globulins, with only a small volume of free hormones available to stimulate physiological eects.
Synthesis and release of thyroid hormones begin with absorption of iodine from the small
intestine. yroid cells actively concentrate iodine at a level 20–50 times higher than
plasma levels. Within the follicular cells, iodine is oxidised and bound to thyroglobulin.
yroglobulin forms the polypeptide framework from which T3 and T4 are synthesised.
Production of thyroglobulin is unique to the thyroid; it can therefore serve as a tumour
marker following total thyroidectomy and radioiodine treatment for thyroid cancer.
When stimulated, follicular cells reabsorb thyroglobulin, breaking it down into diiodotyrosine (DIT) and monoiodotyrosine (MIT) using lysosomal proteases. DIT and MIT are then
398 Head and Neck Endocrine Surgery
ANATOMY AND PHYSIOLOGY OF HEAD AND NECK ENDOCRINE GLANDS
kidneys
T4 T3 TRH
Hypothalamus
T4
Anterior
pituitary
Figure 77.2 Feedback inhibition of thyroid hormones.
T3
Thyroid
TSH
T4 T3
Liver and
Heart
Liver
Bone
CNS
oxidised into T3 and T4 in a process mediated by thyroid peroxidase (TPO). e presence of
TPO antibodies can result in autoimmune thyroiditis.
Control of Thyroid Hormone Synthesis
e negative feedback loop of the hypothalamic-pituitary axis (HPA) controls release of T3
and T4 (Fi g u re 77. 2). A low metabolic rate or a reduction in circulating T3 stimulates the
release of thyrotropin-releasing hormone (TRH) by the hypothalamus. TRH stimulates the
anterior pituitary gland, releasing TSH, which binds to TSH receptors on follicular cells.
is results in a cascade ending in release of T3. Conversely, a high serum concentration of T3
directly inhibits release of TRH and TSH.
Calcitonin
Calcitonin is produced by the parafollicular C cells. It counteracts parathyroid hormone
action by reducing calcium reabsorption from bones and kidney tubules in response to
hypercalcaemia and hypergastrinaemia. Its role in humans is thought to be negligible.
Anatomy of the Parathyroid Glands
Macroscopic Anatomy
e parathyroid glands are two small pairs of yellow-brown ovoid organs located posterior to
the thyroid gland. e glands are surrounded by a thin capsule that is frequently continuous
with the capsule of the thyroid, and they average 6 mm by 3–4 mm in size.
In 84% of patients, there are four parathyroid glands: two superior glands found 1 cm above the
inferior thyroid artery, and two inferior glands within approximately 1 cm of the lower pole of
the thyroid. e glands can have highly variable anatomy, and their number can vary between 2
and 12. e inferior parathyroid’s embryological development from the third branchial arch and
its descent with the thymus means they can have a variable location. Supernumerary and ectopic
gland s can be found with in the thymus, posterior neck, ret ropharyngea l space, and media stinum.
e inferior thyroid arteries supply blood to the parathyroid glands with anastomoses with
the superior thyroid arteries, the parathyroid veins drain into the thyroid’s venous plexus.
Lymphatic drainage occurs via the deep cervical and paratracheal chains.
Microscopic Anatomy
Parathyroid lobules contain clusters of parenchymal cells surrounded by a brovascular
stroma with a rich capillary network. e most prominent cell type is the chief (principal)
cell; chief cells are responsible for production of parathyroid hormone (PTH). Larger and less
prevalent are the oxyphil cells. e function of oxyphil cells is not well understood.
Physiology of the Parathyroid Glands
e parathyroid glands release PTH, which regulates calcium homeostasis. e concentration of PTH and calcium is governed by a negative feedback loop independent of the HPA.
Head and Neck Endocrine Surgery 399
ANATOMY AND PHYSIOLOGY OF HEAD AND NECK ENDOCRINE GLANDS
Bone resorption Calcium reabsorption PTH synthesis
Calcium Homeostasis
Over 99% of human calcium reserves (approximately 1.1 kg) are stored in bones and teeth.
Around 50% of the remaining free calcium is ionised and is essential to the cell signalling
pathways of the heart, blood, muscles, and central nervous system. e remainder is bound
to proteins, such as albumin, which can change depending on the pH of blood.
e parathyroid glands release PTH when calcium-sensing receptors (CaSR) detect a reduction in extracellular calcium concentration. PTH release is inversely proportional to serum
calcium levels. PTH acts via physiological eects on the bones and kidneys. PTH has a short
half-life of just 3 min, and concentrations change within 1 min, peak in 4–10 min, and decline
again within 60 min.
In the kidneys, PTH blocks the reabsorption of phosphate at the proximal tubule while
increasing reabsorption of calcium within the ascending loop of Henle and distal and collecting tubules. Within the proximal renal tubules, PTH activates the enzyme 1-hydroxylase,
which converts vitamin D to its active form calcitriol.
In bone, PTH stimulates calcium reabsorption in slow and fast phases. e slow phase results
in proliferation, dierentiation, and activation of osteoclasts over the course of several days.
e fast phase occurs over a period of minutes, but its physiological mechanism is not well
understood.
Vitamin D
Vitamin D regulates calcium homeostasis at a slower rate than PTH (F igure 77.3). Within
the skin, UVB light changes 7-dehydroxycholesterol into vitamin D3 (cholecalciferol),
which undergoes 25-hydroxylation in the liver and 1-hydroxylation in the kidneys to form
1,25-dihydroxycholecalciferol (calcitriol). Calcitriol raises serum calcium levels through
increased absorption from the small intestine and, in conjunction with PTH, increases the
rate of renal and bone calcium reabsorption.
Sunlight (UV-B)
Colecalciferol
(vitamin D3)
Liver 25-hydroxylase
Renal 1α-hydroxylase
Figure 77.3 Vitamin D metabolism and its effects on calcium homeostasis.
400 Head and Neck Endocrine Surgery
Skin
Vitamin D supplements
25-OH vitamin D3
‘active’ 1,25-(OH)
Diet
vitamin D3
2
Ergocalciferol
(vitamin D2)
α-calcidol
(1-OH vitamin D)
Calcitriol
[1,25-(OH)
Liver
vitamin D3]
2
THYROID AND PARATHYROID PATHOLOGY
Post-Operative Hypoparathyroidism
Post-operative hypoparathyroidism can result in life-threatening hypocalcaemia. It occurs
secondary to accidental devascularisation or excision of all four parathyroid glands. Early
symptoms include nger, toe, and peri-oral numbness or tingling, with more acute symptoms
including papilloedema, tetany, seizures, and death. Avoidance of life-threatening hypocalcaemia is achieved through monitoring of post-operative serum calcium and PTH, prompt
replacement of falling serum calcium levels, and correction of pre-operative vitamin D
deciency.
KEY POINTS
• TSH is the best parameter for assessing thyroid function and monitoring replacement
therapy.
• TSH reacts slowly to changes in hormone supply, especially after long-term dysfunction.
Here, T4 monitoring gives more timely information.
• Thyroid hormone replacement with levothyroxine (T4) is standard. Replacement with T3
is more likely to result in uctuations of thyroid function tests and side effects.
• PTH concentrations alter within 1 min, peak in 4–10 min, and decline in 60 min.
• PTH deciency after damage to the parathyroids can result in life-threatening
hypocalcaemia.
• Vitamin D deciency in patients with primary hypoparathyroidism may introduce
additional (secondary) stimulation to the parathyroid glands.
78. THYROID AND PARATHYROID PATHOLOGY
The Normal Thyroid Gland
e thyroid gland is a bilobate structure, typically weighing between 15 g and 25 g. It is comprised of lobules of colloid-containing follicles lined by a monolayer of bland follicular epithelia l cells, surrounded by a thin brous pseudocapsu le. A subpopulation of para follicular/C
cells are present within the stroma.
Fine-Needle Aspiration Cytology (FNAC)
FNAC is a useful rst-line investigation of a thyroid mass (see Chapter 80, Evaluation
•
and Investigation of yroid Disease).
Some lesions can be condently diagnosed (e.g. papillary thyroid carcinoma).
•
Distinction between hyperplastic nodules and follicular neoplasms may not always be
•
achievable on FNAC.
It is not possible to distinguish between a follicular adenoma and carcinoma on
•
FNAC.
FNAC can induce histological changes that may modulate or obscure underlying
•
pathology.
Thyroglossal Tract Abnormalities
yroglossal duct remnants (cysts, sinuses, and stulae) are common and can occur at almost
any site, from the base of the tongue to the suprasternal region.
Head and Neck Endocrine Surgery 401
THYROID AND PARATHYROID PATHOLOGY
Thyroid Gland Pathology
Thyroiditis
yroiditis can be autoimmune (e.g. Hashimoto’s thyroiditis and Graves’ disease) or nonautoimmune (e.g. subacute thyroiditis, drug-induced thyroiditis, infectious thyroiditis, and
Riedel’s thyroiditis). While there are recognised pathological features in each, the diagnosis
is usually dependent on clinical, radiological, and serological ndings.
Hyperplastic Nodules
Nodules in a multinodular goiter are designated hyperplastic nodules and are comprised of
numerous follicles, oen wit h a growth pattern simila r to that in the adjacent gland. Bland papillary structures may be seen. ey are sometimes surrounded by a thin capsule and oen show
secondary changes, such as brosclerosis, cystic degeneration, calcication, and haemorrhage.
Follicular Adenoma
Follicular adenoma classically occurs as a solitary, encapsulated tumour that shows follicular
epithelial dierentiation with no evidence of capsular/vascular invasion and no features of
papillary thyroid carcinoma. An adenoma can show a variety of growth patterns, although the
architecture tends to be uniform. Mitoses are few. Several distinct histological subtypes are
recognised, although they do not dier in biological behaviour from a conventional adenoma.
Follicular Thyroid Carcinoma
Follicular thyroid carcinoma is a malignant tumour showing follicular dierentiation,
with no features of papillary thyroid carcinoma. It can be minimally or widely invasive.
Meticulous examination of the tumour/capsule interface is required to make the diagnosis.
Minimally invasive follicular carcinoma is a follicular neoplasm showing capsular invasion
and/or pericapsular vascular invasion (Figure 78.1). e presence of angioinvasion is associated with aggressive behaviour.
Widely invasive follicular carcinoma is an aggressive neoplasm with a high risk of metastases. Characteristically, there is inltrative, destructive, or multinodular growth of tumour
cells through the capsule. Extrathyroidal extension and vascular invasion are common.
Oncocytic (Oxyphil) Cell Tumours
Oncocytic change (swelling, with granular, mitochondrial-rich cytoplasm)
Common in benign and malignant conditions in the thyroid.
•
Masses with 75% or more oncocytic cells are designated oncocytic tumours.
•
Oncocytic tumours are subclassied according to the same criteria as their non-onco-
•
cytic counterparts (e.g. oncocytic adenoma, carcinoma, etc.).
More oncocytic tumours are malignant than standard follicular lesions are.
•
Papillary Thyroid Carcinoma
Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy and has an
excellent prognosis.
Figure 78.1 Macroscopic (a) and microscopic (b) capsular invasion.
402 Head and Neck Endocrine Surger y
THYROID AND PARATHYROID PATHOLOGY
Figure 78.2 Characteristic nuclear features of PTC—nuclear crowding, overlap, and nuclear grooves.
e principal dening feature of PTC is its nuclear morphology. Distinctive appearances
may be localised; therefore, adequate sampling is essential.
Characteristic nuclear features of PTC (Figure 78.2) are:
Nuclear enlargement, crowding, and overlapping
•
Margination of chromatin (‘ground glass’ nuclei)
•
Longitudinal nuclear grooves and nuclear irregularity
•
Intranuclear cytoplasmic inclusions
•
Other non-nuclear features include a papillary architecture, multinucleate giant cells,
hypereosinophilic colloid, and psammoma bodies.
ere are a number of recognised variants of PTC, some of which have a more aggressive
behaviour (e.g. tall cell, diuse sclerosing, diuse follicular, solid, and trabecular variants). Other poor prognostic indicators are increased mitoses, necrosis, extrathyroidal
extension, increasing size, and nodal metastases.
Papillary microcarcinomas are less than 10 mm and oen an incidental nding. ey are
commonly multicentric, and while they may metastasise to local lymph nodes, they generally pursue an indolent clinical course.
Follicular-Patterned Tumours of Uncertain Malignant Potential
Encapsulated follicular-patterned lesions with equivocal capsular/vascular invasion
and no features of PTC are termed follicular tumours of uncertain malignant potential
(F T-UMP).
e follicular variant of papillary thyroid carcinoma (FVPTC) is the most common PTC
and can be classied into invasive and encapsulated variants. A group of tumours exist
that are classied as non-invasive follicular thyroid neoplasm with papillary-like nuclear
features (NIFTP). ese are associated with an excellent clinical outcome and can be managed more conservatively than malignant tumours. Stringent histological criteria are used
to dene a NIFTP, and they require careful assessment of the entire lesion.
Poorly Differentiated Thyroid Carcinoma
Poorly dierentiated thyroid carcinoma shows limited evidence of follicular dierentiation, with biological behaviour intermediate between dierentiated thyroid carcinoma
and undierentiated/anaplastic carcinoma. e diagnosis is based upon growth pattern
(typically insular), mitotic activity, and necrosis. Minor elements of classical PTC and/or
follicular carcinoma may be recognised.
Undifferentiated (Anaplastic) Thyroid Carcinoma
Anaplastic carcinoma is a highly malignant tumour typically seen in elderly patients that
has a high mortality. It can arise de novo or result from dedierentiation of an existing
neoplasm. It is usually widely invasive and inoperable at presentation. e pathology varies, with the two main patterns being epithelioid and sarcomatoid.
Head and Neck Endocrine Surgery 403
THYROID AND PARATHYROID PATHOLOGY
Medullary Thyroid Carcinoma (MTC)
MTC is a calcitonin-secreting malignant tumour arising from parafollicular/C cells. It
can occur sporadically or in the context of a mutation of the RET proto-oncogene (seen
in multiple endocrine neoplasia and familial MTC). Microscopically, tumours can be well
demarcated or inltrative and comprise solid sheets, nests, and trabecula of cells separated
by brovascular septa. ere is usually only modest nuclear pleomorphism, but necrosis may
be a feature. Amyloid protein deposition is present in around 80% of cases.
Other Neoplasms and Tumour-Like Lesions
e thyroid is commonly aected by metastases, most oen from the lung, breast, skin, and
kidney cancers.
ere are numerous other neoplasms that can occur in the thyroid, including hyalinizing
trabecular tumour, squamous cell carcinoma, and mucoepidermoid carcinoma.
Thyroid Cancer Staging
yroid carcinomas are staged using the UICC/TNM8 system (Table 78.1). Stage is depen-
dent upon tumour size and the amount of extrathyroidal extension. Anaplastic carcinomas
are by denition pT4.
Table 78.1 TNM8 staging of thyroid carcinoma
TNM clinical classication
T–primary tumour*
TX Primary tumour cannot be assessed
T0 No evidence of primary tumour
T1 Tumour 2 cm or less in greatest dimension, limited to the thyroid
T1a Tumour 1 cm or less in greatest dimension, limited to the thyroid
T1b Tumour more than 1 cm but not more than 2 cm in greatest dimension,
limited to the thyroid
T2 Tumour more than 2 cm but not more than 4 cm in greatest dimension, limited to
the thyroid
T3 Tumour more than 4 cm in greatest dimension, limited to the thyroid, with gross
extrathyroidal extension invading only strap muscles (sternohyoid, sternothyroid, or
omohyoid muscles)
T3a Tumour more than 4 cm in greatest dimension, limited to the thyroid
T3b Tumour of any size with gross extrathyroidal extension invading strap
muscles (sternohyoid, sternothyroid, or omohyoid muscles)
T4a Tumour extends beyond the thyroid capsule and invades any of the following:
subcutaneous soft tissues, larynx, trachea, oesophagus, recurrent laryngeal nerve
T4b Tumour invades prevertebral fascia or mediastinal vessels, or encases carotid artery
Note: *Including papillary, follicular, poorly differentiated, Hürthle cell, and anaplastic carcinomas.
N – regional lymph nodes
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Regional lymph node metastasis
N1a Metastasis in Level VI (pretracheal, paratracheal, and prelaryngeal/
Delphian lymph nodes) or upper/superior mediastinum
N1b Metastasis in other unilateral, bilateral, or contralateral cervical nodes
(Levels I, II, III, IV or V) or retropharyngeal nodes
M – distant metastasis
M0 No distant metastasis
M1 Distant metastasis
404 Head and Neck Endocrine Surgery
THYROID AND PARATHYROID PATHOLOGY
KEY POINTS
• Correlation of clinical, radiological, and serological ndings can aid the diagnosis of
neoplastic and non-neoplastic thyroid conditions.
• FNAC is useful in the evaluation of thyroid lesions, with some limitations.
• The capsule of any follicular-patterned neoplasm should be comprehensively sampled
to search for both capsular and vascular invasion.
• Papillary thyroid carcinoma accounts for the majority of thyroid malignancies and
generally has an excellent prognosis.
• The role of ancillary tests, including molecular and genetic studies, in the
determination of thyroid malignancy is evolving.
Normal Parathyroid Glands
Most individuals possess at least two pairs of parathyroid glands, AND each gland weighs
approximately 0.03 g. Microscopically, they have a lobulated appearance and are composed
of chief, oxyphil, and water-clear cells arranged in nests and trabeculae in a richly vascularised stroma interspersed with adipocytes.
Parathyroid Gland Pathology
Parathyroid Gland Adenoma
Parathyroid adenoma is the predominant cause of primary hyperparathyroidism. It can
occur spontaneously or within the context of various syndromes. Excision of the abnormal
gland is curative.
Pathological distinction between hyperplasia and adenoma can be dicult. Adenomas
typically aect one gland and are well circumscribed, with a mean weight of 0.55 g.
Microscopically, they are hypercellular, with a loss of intraglandular adipocytes and a
peripheral rim of normal tissue. Most are composed of chief cells, which can be arranged in
a number of patterns.
Several subtypes are recognised, including cystic adenoma, lipoadenoma, papillary variant,
water-clear adenoma, follicular variant, and oxyphil adenoma.
An atypical parathyroid adenoma is a descriptive term applied to a tumour that displays
suspicious/atypical features but falls short of a condent designation of malignancy.
Parathyroid Carcinoma
Parathyroid carcinoma is rare. It is slow-growing and tends to invade local structures and to
metastasise late. Complete excision at rst operation aords the best opportunity for cure,
although it relies upon early recognition of malignancy.
Carcinomas can be encapsulated or inltrative. Microscopically, the appearances can vary
from deceptively bland to overtly malignant. Biological behaviour ultimately distinguishes
carcinoma from adenoma.
Absolute histological criteria to diagnose carcinoma are local invasion and metastatic disease. In the absence of these, secondary criteria can be used, which include capsular/vascular
invasion, broad intralesional brous septae, coagulative necrosis, increased mitotic activity,
abundant macronuclei and diuse growth/cellular atypia.
e proposed staging classication for parathyroid carcinoma is shown in Table 78.2.
Other Parathyroid Gland Tumours
Parathyroid cysts, branchiogenic cysts, amyloidosis, paragangliomas, and secondary neoplasms can occur in the parathyroid glands.
Head and Neck Endocrine Surgery 405
ENDOCRINE IMAGING
Table 78.2 Proposed TNM staging for parathyroid carcinoma
T – primary tumour
TX Primary tumour cannot be assessed
T0 No evidence of primary tumour
Tis Atypical parathyroid neoplasm (neoplasm of uncertain malignant potential)
T1 Localised to the parathyroid gland with extension limited to soft tissue
T2 Direct invasion into the thyroid gland
T3 Direct invasion into laryngeal nerve, oesophagus, trachea, skeletal muscle,
adjacent lymph nodes, or thymus
T4 Direct invasion into major blood vessels or spine
N – regional lymph nodes
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Regional lymph node metastasis
N1a Metastasis to Level VI (pretracheal, paratracheal, and prelaryngeal/Delphian
lymph nodes) or upper/superior mediastinal lymph nodes
N1b Metastasis to unilateral, bilateral, or contralateral cervical nodes (Levels I, II, III,
IV, or V) or retropharyngeal nodes
M – distant metastasis
M0 No distant metastasis
M1 Distant metastasis
Stage
There are not enough data to propose a formal staging system at this time.
Source: Adapted from AJCC Cancer Staging Manual, 8
th
Edition, 2017.
KEY POINTS
• It can be difcult to distinguish primary parathyroid gland hyperplasia and a
parathyroid adenoma histologically.
• Parathyroid carcinoma is rare, and the diagnosis requires clinicopathological
correlation.
79. ENDOCRINE IMAGING
Introduction
In assessing patients with suspected endocrine pathology, imaging is a key investigative step
that provides details of anatomy, morphology, and function.
Ultrasound, in general, is the simplest and quickest investigative modality for the head and
neck and has the benet of dynamic vascular assessment as well as guiding ne-needle aspiration (FNA) and core biopsies. Computed tomography (CT), magnetic resonance imaging
(MRI), and nuclear medicine studies can provide additional anatomical or functional detail
prior to surgical intervention.
406 Head and Neck Endocrine Surgery
ENDOCRINE IMAGING
Table 79.1 Ultrasound (U) classication of thyroid nodules as recommended by the British
Thyroid Association
U classication Nodule type Ultrasound characteristics
U1 Normal
U2 Benign Vascularity, eggshell calcication, cystic change,
isoechoic or mildly hyperechoic
U3 Indeterminate/equivocal Homogeneous, hyperechoic, equivocal echogenic
foci, mixed or central vascularity, solid or halo
U4 Suspicious Solid, hypoechoic, peripheral calcication,
lobulated outline
U5 Malignant Solid, hypoechoic, lobulated outline, intranodular
vascularity, taller > wide, lymphadenopathy
Source: From Table 61.16 in Scott Brown.
Thyroid
Ultrasound is the primary imaging modality for the assessment of the thyroid gland. It is
key in identifying thyroid nodules and supports risk stratication in decision-making about
sampling concerning nodules.
yroid nodules are clinically palpable in up to 4% of patients.
•
60–70% of patients can be found to have nodules on imaging.
•
Various ultrasound features of nodules are indicative of a potential malignancy. e
•
U classication is recommended for assessment and reporting of ultrasound features
in the United Kingdom (Table 79.1).
Where an indeterminate/suspicious nodule is seen, FNA or core biopsy should be
•
undertaken.
While size of a nodule is oen suggested as a criterion, nodule size correlates poorly
•
with risk of malignancy.
In practice, only nodules >1 cm are sampled.
•
Thyroid Malignancy
Papillary thyroid cancer (PTC) demonstrates four cardinal signs on ultrasound:
1 Solid and hypoechoic
2 Ill-dened margins
3 Microcalcications
4 Taller than wide
If none of these four features is present, then the negative predictive value for PTC is more
than 97%.
Medullary thyroid cancers (MTC) appear quite similar to PTC on ultrasound, although calcications can be more globular.
Follicular carcinoma:
Cannot be dierentiated from adenoma on FNA or ultrasound and is diagnosed on
•
pathology aer excision.
Follicular lesions tend to appear hyperechoic, with a low echogenic halo and increased
•
internal blood ow.
Anaplastic thyroid cancer (ATC):
Presents more commonly in the elderly and demonstrates a rapid, inltrative progression.
•
Ultrasound features are that of a large, solid, hypoechoic, ill-dened mass with evi-
•
dence of extrathyroidal spread and nodal metastases.
Core biopsy is superior to ne-needle aspiration cytology (FNAC) for conrming the
•
diagnosis.
Head and Neck Endocrine Surgery 407
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