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12 Head andNeck Pathology

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Fig. 12.64 Grave’s disease: hyperplastic papillary thyroid epithelium. Scalloping of colloid (arrow)

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• Cyst lined by squamous or respiratory epithelium.

• Presence of thyroid tissue variably reported (25–60%).

• Thyroid tissue may exhibit nodules, hyperplasia, or rarely neoplasia.

Graves’ Disease (Diffuse Hyperplasia) (Fig.12.64)

• Diffuse toxic form of goiter; autoimmune hyperthyroidism

• Hyperplasia affecting entire gland, formation of simple papillary projections observed

• Scalloping phenomenon of colloid (small vacuoles) but colloid may be absent

• Lymphocytic inltration not uncommon

• Ophthalmopathy:

– Accumulation of chronic inammatory cells, edema, and glycosaminogly-

cans in extraocular muscles and contributes to proptosis

Multinodular Goiter (Fig.12.65)

• Adenomatoid nodules with cystic degeneration.

• Enlarged follicles with abundance of colloid.

• Papillary fronds that extend into irregular thyroid follicles.

• No compression of surrounding gland, poor or no encapsulation of nodules.

• Cells comprising nodule have similar morphology to cells adjacent to nodule.

Amyloid Goiter (Fig.12.66)

• Thyroid enlargement secondary to intercellular amyloid deposition

• Pale, eosinophilic, acellular, amorphous material with peculiar “cracking” artifact

• Can accumulate around blood vessels

• Minimal normal thyroid tissue remains, amyloid overtakes gland in systemic amyloidosis

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Fig. 12.65 Multinodular goiter: low magnication view of multinodular appearance

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Fig. 12.66 Amyloid goiter: acellular, eosinophilic amyloid. Present around blood vessel

• May see focal amyloid deposition in association with medullary thyroid carcinoma

• Special stains:

– Congo red stain shows apple green birefringence under polarized light. – Crystal violet: amyloid metachromatic. – Thioavin T positive.

Hashimoto’s Thyroiditis (Fig.12.67)

• Autoimmune disease associated with enlargement of thyroid and eventual hypothyroidism

• Advanced: similar to Riedel’s thyroiditis (extensive brosis) but localized to the thyroid

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Fig. 12.67 Hashimoto’s thyroiditis: thyroid tissue with marked inammation and germinal center formation

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Fig. 12.68 Follicular adenoma: encapsulated, cellular benign thyroid neoplasm. The tumor has a complete thin capsule and shows a growth pattern distinct from that of the adjacent normal thyroid

• Lymphocytic thyroiditis: inltration with germinal center formation

• Follicular acinar atrophy, degenerative phenomenon, decreased colloid

• Hurthle cell metaplasia: oxyphilic/oncocytic cells, extensive eosinophilia, large polygonal follicular cells with granular cytoplasm

Follicular Adenoma (Fig.12.68)

• Benign, encapsulated, noninvasive neoplasm with thyroid follicular cell differentiation.

• Adenoma cells different from normal gland: more cellular, +/− larger follicles.

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C. J. Fan et al.

• Normal thyroid gland adjacent to adenoma may appear compressed.

• Well-dened capsule present around adenoma, no capsular invasion, no vascular invasion.

• Architectural and cytological features of tumor different from surrounding thyroid.

• Uniform small round nuclei and nuclear atypia may be seen.

• Hurthle cell/oxyphilic cells can be present.

• Stroma component is scant but can be edematous, hyalinized, or mucin-like.

• Secondary changes like cystic degeneration, calcication, and osseous metaplasia possible.

Follicular Carcinoma (Fig.12.69)

• Malignancy arising from thyroid follicular cells and absent papillary thyroid carcinoma-nuclear features.

• RAS family mutations are found in 30–50% of tumors.

• Diagnosis requires identication of capsular and/or vascular invasion.

• Three subtypes:

– Minimally invasive (capsular invasion only) – Encapsulated angioinvasive – Widely invasive

• Variable microscopic patterns of tumor cells (solid, trabecular, microfollicles).

• Signicant morphologic overlap with benign follicular adenoma.

• Hurthle cell subtype/oxyphilic type may have limited colloid.

• Most reliable indication of malignancy: capsular and/or vascular invasion.

Neoplastic cells penetrate the entire thickness of the tumor capsule to qualify

for capsular invasion.

Fig. 12.69 Follicular carcinoma: capsular invasion by malignant thyroid neoplasm (arrows)

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Papillary Thyroid Carcinoma (Fig.12.70)

• Malignant epithelial tumor with follicular cell differentiation

• Cardinal features: Formation of papillae and unique nuclear features

– Papillae: neoplastic epithelial cells surface a central brovascular stalk

• Psammoma body: Laminated microcalcication common in classic, tall cell and hobnail

b c

Fig. 12.70 Papillary thyroid carcinoma: (a) Papillary architecture of malignant neoplasm. (b) Nuclear pseudoinclusion (long arrow) and nuclear groove (short arrow). (c) Concentric lamination of psammoma body

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C. J. Fan et al.

– Thought to represent the presence of old, calcied tumor cells. – Presence of psammoma body alone in the lymph node is indicative of meta-

static disease and considered pN1a by the College of American Pathologists (2017).

• Select subtypes (includes conventional/classic):

– Classic: well-formed papillae, nuclear grooves, pseudo-inclusions, psam-

moma bodies

– Follicular variant: encapsulated, small follicles present, lacks architecture of

papillae, enlarged and pale nuclei, nuclear grooves, dense colloid

– Diffuse sclerosing variant: brosis, lymphocytic thyroiditis, psammoma bod-

ies, often involves the entire gland

– Tall cell variant: tall columnar cells present, tightly packed, nuclear grooves,

irregular nuclear membranes

– Columnar cell variant: columnar cells present, prominent papillae, parallel

follicles

– Unfavorable histologic forms: diffuse sclerosing, tall cell, columnar cell

variants

Medullary Thyroid Carcinoma (MTC) (Fig.12.71)

• Malignant thyroid neuroendocrine tumor arising from parafollicular C cells.

• Most MTC cases are sporadic (70–75%), with hereditary and syndromic forms in 25–30%.

Fig. 12.71 Medullary thyroid carcinoma: Nests and ribbons of monotonous tumor cells with nely stippled chromatin, brous bands (two arrows) and amyloid deposits (single arrow)

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265

– Most commonly encountered syndromes include:

MEN2A, MEN2B, and familial MTC (latter may be in spectrum of MEN2A) C-cell hyperplasia in inherited, with associated elevated calcitonin levels Characterized by gain-of-function germline mutations in the RET proto-oncogene

• Histologic appearance does not vary between sporadic and inherited MTC.

• Sporadic cases tend to be unifocal, familial cases multifocal and bilateral.

• Tumor cells organized into many patterns with lymphovascular invasion.

• Stippled “salt and pepper” nuclear chromatin present in individual cells.

• Amyloid present as amorphous pink material in stroma; Congo red stain and polarized light shows apple green birefringence.

Anaplastic Carcinoma (Fig.12.72)

• High-grade thyroid malignancy composed of undifferentiated follicular thyroid cells

• May arise de novo or from high-grade transformation of a well-differentiated carcinoma, usually a papillary thyroid carcinoma

• Necrosis, extensive extrathyroidal extension common and rapid

• Lymphovascular invasion usually present

• Signicant cell pleomorphism: markedly atypical spindle cell predominant and/ or giant cells with large hyperchromatic nuclei

• Must identify origin from thyroid, may appear to be a soft tissue sarcoma

Fig. 12.72 Anaplastic carcinoma: Sheet of pleomorphic tumor cells and giant cells and adjacent necrosis (arrow)

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Parathyroid Gland (Fig.12.73)

• Chief cells: round nuclei, pale eosinophilic cytoplasm.

• Oxyphil cells: larger than chief cells, densely pink cytoplasm (oncocytic).

• Mature fat.

• Glands normally weigh 30–40mg each.

Parathyroid Hyperplasia (Fig.12.74)

• Non-neoplastic

• Most commonly results of hyperparathyroidism, but can be idiopathic

• Increased number of chief and oncocytic cells in multiple parathyroid glands, with limited stromal fat

Fig. 12.73 Normal parathyroid: chief (pale), oxyphilic (densely pink), and mature adipose tissue

Fig. 12.74 Parathyroid hyperplasia showing a nodular proliferation of chief and oncocytic cells

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Fig. 12.75 Parathyroid adenoma: Demonstrates a rim of compressed normal tissue

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Parathyroid Adenoma (Fig.12.75)

• Benign parathyroid neoplasm of chief oncocytic cells or an admixture.

• Can arise in normally situated or ectopic glands.

• 85% of cases with single, enlarged, hypercellular gland.

• 15% of patients with “double adenomas” show predilection for superior glands.

• Adenoma can be sporadic or occur in patients with genetic susceptibility.

• Genetic susceptibility: MEN1, MEN2A, CDC73-related disorders (hyperparathyroidism- jaw tumor syndrome, familial isolated hyperparathyroidism).

• Microscopically adenoma shows parenchymal cell proliferation (oncocytic/ chief cells).

• Usually gland enlarged, encapsulated, absence of intraparenchymal fat.

• May or may not have rim of compressed normal parathyroid tissue.

Parathyroid Carcinoma (Fig.12.76)

• Rare malignant neoplasm of parathyroid parenchymal cells.

• Majority of tumors are functional tumors (hypercalcemia, hyperparathyroidism).

• Aggregate of microscopic and clinical features are supportive of diagnosis.

• Capsular, vascular, or perineural invasion (not commonly seen).

• Adherence or invasion of thyroid or other soft tissue extension.

• Formation of thick brous septae/bands.

• Metastasis.

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Fig. 12.76 Parathyroid carcinoma: Trabeculae and islands of parathyroid carcinoma inltrating the skeletal muscle

C. J. Fan et al.