endocrinology

Figure 11: 1.11
Hashimoto’s (autoimmune)
thyroiditis, with diffuse
thyroid enlargement (a)
and a grayish, fleshy cut
surface (b). Microscopy
shows extensive lymphoid
infiltrates with reactive
germinal centers (c). The
follicular cells are large and
contain granular,
eosinophilic cytoplasm (d,
Hürthle cells, arrow).
de Quervain’s thyroiditis is
similar but with
granulomatous infiltrates

Figure 13: 1.13 Follicular adenoma of the thyroid.
Note the sharp demarcation (encapsulation) and
colloid shine of this macrofollicular adenoma (a).
Microscopy (b, c) shows a follicular adenoma of the
thyroid with a well-developed, fibrous capsule

Figure 14: 1.14 (a) This well-circumscribed lesion mimics
adenoma, but a suspicious satellite nodule (arrow)
suggests malignancy. (b) Another view shows a formalin-
fixed (brownish) thyroid with poorly demarcated, diffuse,
and nodular cancerous infiltration (white parts). (c)
Microscopy confirms the diagnosis of papillary carcinoma

Figure 15: 1.15 Carcinomas
of the thyroid have various
histologic appearances,
including papillary
carcinoma with
characteristic ground glass
nuclei (“Orphan Annie eye”)
(a), follicular variant of a
papillary carcinoma (b), and
psammoma bodies of
papillary carcinoma (c)

Figure 16: 1.16 Papillary carcinoma of the thyroid. An
ultrasound image (a) shows a heterogeneous mass with
calcium. Doppler ultrasonography (b) shows
hypervascularity

Figure 17: 1.17 Follicular carcinoma of the thyroid. (a, b)
Note the irregular growth of well-differentiated follicles,
with signs of capsular and vascular invasion

Figure 18: 1.18
Anaplastic thyroid
carcinoma, showing
dense population of
undifferentiated,
pleomorphic cells with
multiple mitotic figures
(arrows)

Figure 19: 1.19
Medullary (C-cell)
carcinoma of the
thyroid.
(a) A gross specimen shows
poorly delimited, slightly
yellowish infiltration of the
gland (arrow). (b) Microscopy
shows small-cell infiltrates
with amyloid deposits (arrow)
in interstitial tissue. (c)
Amyloid shows characteristic
birefringence on polarization
of Congo red-stained sections.
(d) Immunohistochemistry
shows positive staining for
calcitonin

Figure 20: 1.20
Primary malignant non-
Hodgkin’s lymphoma of the
thyroid.
Note the diffuse, whitish enlargement of
the gland (a) caused by pronounced
interstitial infiltration by atypical lymphoid
cell populations (b)

Figure 21: 1.21
Parathyroid glands.
The gross picture (a),
showing the location,
is a view from the
posterior with the
esophagus removed.
The parathyroid
glands are shown on
the posterior surface
of the thyroid gland
(arrows). The normal
location may vary,
however, occasionally
reaching down into the
thymus. Microscopy
shows a normal
parathyroid gland with
abundant fat tissue (b)
and a hyperplastic
gland with extensive
replacement of fat
tissue by parathyroid
endocrine cells (c)

Figure 22: 1.22 Parathyroid adenoma and carcinoma
frequently are distinguishable only by microscopy.
Gross appearance (a) showing several nodular,
tumorous infiltrates of enlarged parathyroid gland
(original magnification ×3). Microscopy shows
parathyroid adenoma (b) and carcinoma with signs of
tumorous invasion of the capsule and adjacent
tissues and cellular polymorphism (c)

Figure 23: 1.23
Hyperparathyroidism—whether
primary (parathyroid adenoma,
carcinoma, or primary
hyperplasia) or secondary (due
to renal disease)—causes
increased bone resorption (such
as the lacunar osteoclastic
resorption shown in this image),
causing dissecting fibro-
osteoclasia and finally osteitis
fibrosa cystica (von
Recklinghausen’s disease).
Hypercalcemia also leads to
calcification of soft tissues and
mucosal surfaces, and to
nephrolithiasis (See also Chaps.
6 and 9 for renal and bone
diseases)

Figure 24: 1.24 Technetium (99mTc) sestamibi parathyroid scan (after 15 min
and 2 h) showing a left inferior parathyroid adenoma (Figure provided by
Bechara Y. Ghorayeb, M.D., Houston, Texas [www. ghorayeb. com])

Figure 25: 1.25 (a) A technetium (99mTc) sestamibi
scan at 15 min (immediate) and after a 3-h delay,
showing a large adenoma. (b, c), surgical pictures of
the same adenoma (Figure provided by Bechara Y.
Ghorayeb, M.D., Houston, Texas [www. ghorayeb.
com])

Figure 26: 1.26 Islet cell tumors of the pancreas
(a, b). These tumors form nodular masses, which
often appear solid and are yellow-tan to white

Figure 27: 1.27 Microscopy of a pancreatic adenoma
producing gastrin (gastrinoma) on hematoxylin-eosin stain
(a) and with immunohistochemistry for gastrin (b brown
cells)

Figure 31: 1.31 (a, b) Axial and coronal CT scans of the
pancreas head show prominent nodular alterations
indicative of neuroendocrine tumor

Figure 32: 1.32 Adrenal
hemorrhagic necrosis in
meningococcal septicemia,
causing hemorrhagic shock and
the death of the patient
(Waterhouse–Friderichsen
syndrome; see also Chap. 1).
Note the extensive necrosis and
hemorrhage of the adrenal
cortex (a) and diffuse petechial
and confluent hemorrhages of
the skin (b). The internal organs
show similar hemorrhages

Figure 33: 1.33 Adrenal cortical hypoplasia. (a) The
gross appearance is of a small, brownish, thin, and
soft gland (about 1.8 cm in length). (b), Microscopy
shows hypoplastic adrenal cortex (C) with poorly -
organized layers (arrows). (c), By comparison,
normal cortex has clearly identifiable zones (G
glomerulosa, F fasciculate, R reticularis, M adrenal
medulla)

Figure 2: 1.2 Atrophy of the
pituitary gland (“empty sella
syndrome”). Note the cavitation
of the sella turcica (arrows)
associated with shrinkage of the
pituitary gland

Figure 30: 1.30 This axial CT scan, performed with
contrast, shows a pancreas nodule (presumed to be an
islet cell tumor) in a patient with von Hippel–Lindau
syndrome

Figure 38: 1.38 Left adrenal primary adrenocortical
carcinoma. This postcontrast CT scan shows a large (4.4
cm), irregularly enhancing left adrenal mass. The
differential diagnosis must include metastasis

Figure 39: 1.39 Pheochromocytoma. (a) This axial CT
scan with contrast shows a left adrenal
pheochromocytoma immediately medial and superior to
the left kidney. (b), A coronal CT with contrast in the same
patient

Figure 40: 1.40 Pinealoma (pineal germinoma), shown in
midsagittal (a) and axial (b) postcontrast T1-weighted MR
images (arrows)

Figure 34: 1.34 (a) Diffuse adrenal cortical hyperplasia.
Note the yellowish thickening of poorly demarcated
adrenal cortex (arrows), as shown in this cross section of
the gland. (b) Adrenal cortical adenoma. Note the well-
demarcated yellow nodule (arrows) (F periadrenal fat
tissue, AG adrenal gland). (c) Typical microscopy of the
adenoma, with fairly uniform, pale polygonal cells with
small dark nuclei and no mitoses. Adrenal cortical
adenomas and carcinomas may be associated with
primary hyperaldosteronism (Conn’s syndrome),
Cushing’s syndrome, feminization, or virilization, or may
be nonfunctional

Figure 35: 1.35 Adrenal cortical
carcinomas. (a–c), Note the
irregular structure with yellowish,
partly necrotic, and hemorrhagic
tissues with pseudocystic
degeneration. (d) Microscopy
shows irregular growth of more
polymorphic, partially poorly
differentiated cells, including giant
cells

Figure 36: 1.36 Adrenal medullary
pheochromocytoma: gross
appearance on the surface (a)
and cut surface (b), with soft
yellowish red “medullary” tissue,
focal hemorrhage, and
pseudocystic degeneration.
Microscopy (c) shows a
population of polymorphic
“epithelioid” cells with giant cells

Figure 37: 1.37 Adrenal medullary neuroblastoma. (a)
Gross appearance shows a whitish, nodular infiltrate of
the gland with focal degeneration and hemorrhage. (b)
Microscopy shows a typical small cellular (“lymphoid”)
infiltration with characteristic neurofibrillary rosettes

Figure 41: 1.41 (a) Gross sagittal section from a brain with
a pineal tumor. (b) Microscopy shows the biphasic pattern
of the pinealoma, with areas composed of large primitive
spheroidal cells and stromal areas with a prominent
lymphocytic component. (c) Microscopy of a pineocytoma,
a tumor of pineal parenchymal cells with pineocytomatous
rosettes (large fibrillar zones)

Figure 1: 1.1 Normal pituitary gland: location at the
base of the skull in the sella turcica (a, arrow) with
cross section (b). Enlarged picture of a removed gland
(c) showing the adenohypophysis (A, pink part) and
the neurohypophysis (N, white part)

Figure 4: 1.4 This formalin-fixed specimen (reconstituted in alcohol) shows a large pituitary adenoma (a) expanding
to the optic nerve and the intracerebral part of the internal carotid artery (arrows). Microscopy shows a typical
chromophobe adenoma composed of small cells (b). Chromophobe adenomas generally contain small numbers of
secretory granules (sparsely granulated) but may produce a number of different hormones. A adenoma

Figure 3: 1.3 (a) MRI in sagittal view shows distinct pituitary enlargement representing an adenoma (arrow). (b), A CT
scan of the cranium shows a tumorous mass on the right between the optic chiasm and the base of the third ventricle
(arrow)

Figure 6: 1.6 Pituitary macroadenoma. This coronal
magnetic resonance (MR) image (T1-weighted,
postcontrast) reveals a large, homogenously enhancing
mass that extends above the diaphragma sellae, abuts
and deviates the optic chiasm, and invades the right
cavernous sinus

Figure 7: 1.7 Prolactinoma. This coronal MR image (T1-
weighted, postcontrast) shows the classic findings of a
hypoenhancing mass in the pituitary, deviation of the
infundibulum from the mass, and upward convexity of the
pituitary border

Figure 5: 1.5 Other types of adenoma are composed of
basophilic cells producing corticotropin (clinical, Cushing’s
disease or Nelson’s syndrome). Adenomas composed of
acidophilic cells are typically associated with the
production of growth hormone (somatotropin) or prolactin.
About 25 % of pituitary adenomas are nonfunctional,
without endocrine activity. Newer classifications use
endocrine activities rather than cellular-staining qualities;
shown here, for example, is an FSH-producing adenoma,
with immunohistochemistry showing brown, FSH-positive
cells. This figure shows an immunohistochemical stain for
somatotropin

Figure 8: 1.8 Thyroid hyperplasia
(nodular goiter), showing gross
enlargement with nodular and cystic
(degenerative) structures (a
removed gland, b gland in situ seen
from behind, with larynx and trachea
in the center). Microscopy (c) of a
hyperplastic (adenomatous) nodule
in a patient with a nodular goiter,
demonstrating that the nodule is
partially encapsulated and is
composed of large, colloid-filled
follicles

Figure 9: 1.9 Thyroid gland from a patient with
Graves’ disease (hyperthyroidism, also referred
to as Basedow’s disease). The cut surface
shows diffuse hyperplasia and has a fleshy
appearance (a). Microscopically (b), follicles are
lined by hyperplastic follicular cells with focal
papillary structure and areas of colloid
resorption vacuoles

Figure 10: 1.10 Right thyroid goiter. (a, b) Axial and
coronal postcontrast CT scans, show a large right low-
density cyst consistent with a colloid cyst of goiter

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