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49 Cards in this Set

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Hx of radiation exposure
Think cancer, specifically Papillary carcinoma of thyroid
cold, warm, hot thyroid nodules def.?
Warm = functional, avidity for isotope in the lesion same as surrounding glands (normal)

Hot = hyperfunctional, traps more isotope than surrounding glands

Cold = hypofunctional, less isotope is trapped than in surrounding glands
Hot vs Cold nodules
“Hot” nodules are almost always benign.
80% of “cold” nodules are benign.
solid thyroid lesions vs. cystic lesions
Solid lesions are more worrisome than cystic lesions (which usually are adenomatous nodules umdergoing cystic degeneration).
Papillary Carcinoma of thyroid
Papillary carcinoma
a. Epidemiology
i. Account for 80% of malignant thyroid tumors
ii. Females> males; age 20-50
iii. Risk factor: radiation exposure
b. Micro
i. The tumor typically exhibits a papillary pattern
ii. Occasional psammoma bodies
iii. Characteristic nuclear features
. Clear "Orphan Annie eye" nuclei . Nuclear grooves
. Intranuclear cytoplasmic inclusions
c. Lymphatic spread to cervical nodes is common
d. Treatment
1. Resection is curative in most cases
11. Radiotherapy with iodine 131is effective for metastases
e. Prognosis: excellent; 20-year survival =90%
Papillary Carcinoma of thyroid: histo
Papillary structures w/ enlarged nuclei
Optically clear “Orphan Annie” nuclei (A)
Nuclear grooves (B)

Also, psamomma bodies
What diseases have psammoma bodies?
Dystrophic Calcification
Meningioma
Cysadenocarcinoma of the Ovary
Papillary Carcinoma of the Thyroid
What are risk factors for papillary carcinoma of the thyroid?
Irradiation of the head and neck areas during the first two decades of life
There is also a slightly increased risk of carcinoma in patients with Hashimoto thyroiditis
What is an encapsulated tumor likely to be?
The presence of a thick and irregular capsule tends to favor a follicular carcinoma over an adenoma on gross examination.
Follicular carcinoma
a. Accounts for 15% of malignant thyroid tumors
b. Females> males; age 40-60
c. Hematogenous metastasis to the bones or lungs is common
Follicular carcinoma: Histology
Small, closely packed neoplastic follicles containing colloid.
No well-formed papillae or psammoma bodies are present.
Medullary carcinoma
a. Accounts for 5% of malignant thyroid tumors
b. Arises from C cells(parafollicular cells) and secretes calcitonin
c. Micro: nests of polygonal cells in an amyloid stroma
d. Minority (25%) are associated with MEN II and MEN III syndromes (see Multiple
Endocrine Neoplasia Syndromes)
Medullary carcinoma: gross and histo
Round/polygonal tumor cells with abundant amphophilic granular cytoplasm; some cells have clear cytoplasm.
Stromal amyloid deposits, derived from calcitonin or its precursor molecules, is also present. //

The tumor is nodular and well circumscribed.
Familial Medullary carcinoma
May present with:

MENII (IIa or sipple): along with pheochromocytoma and parathyroid adenoma.//

MENIII (IIb): along with pheochromocytomas and neurofibromas.//
What gene is involved in MEN II and MEN III?
RET proto-onco gene
Thyroid cancer frequency
Papillary cancer ~70%
Follicular carcinoma ~20%
Medullary ~5%
Anaplastic ~5%.

ALSO SEE SLIDE 22 FOR COMPARISON
Hashimoto thyroiditis
a. Definition: chronic autoimmune disease characterized by immune destruction of
the thyroid gland and hypothyroidism
b. Most common noniatrogenic/nonidiopathic cause of hypothyroidism in the
United States
c. Clinical presentation
i. Females> males; age 40-65
ii. Painless goiter
iii. Hypothyroidism
iv. Initial inflammation may cause transient hyperthyroidism (hashitoxicosis)
d. Gross: pale enlarged thyroid gland .
e. Micro
i. Lymphocytic inflammation with germinal centers
ii. Epithelial "Hiirthle cell" changes
f. May be associated with other autoimmune diseases (SLE,RA, SS [Sjogren syndrome],
etc.)
g. Complication: increased risk of non-Hodgkin lymphoma (NHL) B-celllymphoma
Hashimoto thyroiditis: Histo
Histologic features:
Destruction and atrophy of thyroid follicles
Lymphocytic and plasmacytic infiltration of the thyroid stroma with lymphoid follicles; germinal centers can also be seen.
Discuss the pathogenesis of Hashimoto disease.
CD4+ T cells targeted at thyroid antigens are activated after an
infection or following exposure of sequestered thyroid antigens.
Activated CD4+ T cells stimulate B cells to produce antibodies
and CD8+ T cells to destroy the gland parenchyma.
Hashimoto thyroiditis: More Histo features
Oxyphilic cell metaplasia of follicular epithelium (Hürthle cells), with pink, slightly granular cytoplasm.
Why does the cytoplasm of Hürthle cells looks granular?
Increased number of mitochondria
What autoantibodies are present Hashimoto thyroiditis?
High titers of thyroid peroxidase, antithyroglobulin antibodies and TSH receptor antibodies
Iodine transporter antibodies may also be seen
What is the effect of the anti-TSH receptor antibodies in
Hashimoto thyroiditis? …in Graves disease?
In Hashimoto thyroiditis they block the action of TSH and contribute to hypothyroidism.
//
In Graves disease they mimic TSH and result in hyperthyroidism.
In what population is Hashimoto thyroiditis most prevalent?
Women, between 45 - 65 years old, often presenting with some degree of hypothyroidism.
Patient with Hashimoto thyroiditis are at increased risk to develop what malignancy?
B-cell lymphomas
Cushing syndrome
a. Definition: diseasecharacterized by increased levels of glucocorticoids
b. Etiology
i. Iatrogenic (exogenous corticosteroids)
ii. Pituitary corticotroph adenoma (Cushing disease) . Adenoma produces ACTH . ElevatedACTH
. Cortisol suppression with high-dose dexamethasone
iii. Adrenocortical adenoma
. Adenoma produces cortisol . DecreasedACTH . No cortisol suppression with dexamethasone
IV. Paraneoplastic syndrome . Small-cell lung cancer producing ACTH
ElevatedACTH
. No cortisol suppression with dexamethasone
Cushing syndrome etiologies
Adrenal adenomas account for 5-10% of cases of Cushing syndrome in adults and are the most common cause in children <8 years old.
Other etiologies include ectopic ACTH production and pituitary adenomas. Most common cause is exogenous glucocorticoids.
dexamethasone suppression test
High dose dexamethasone suppression test (suppression
would rule out pituitary cases) and plasma ACTH levels
(low in adrenal neoplasia, high in ACTH secreting tumors).
Adrenal Cortical Adenoma
Clear tumor cells adjacent to a rim of non-tumorous adrenal
Regular uniform large cells with ample clear cytoplasm, filled with lipid.
 Neoplastic cells form sheets, nests or cords.
Conn Syndrome
Primary hyperaldosteronism (Conn syndrome)
a. Definition: adrenocortical adenoma producing aldosterone
b. Clinical feature: hypertension
c. Lab:hypokalemia, elevated aldosterone, and decreased renin
How does hypokalemia
manifest?
Muscle weakness and
fatigue.
This photograph suggests a cortical adenoma associated with Conn syndrome, not with Cushing syndrome. Why?
The adjacent adrenal cortex is not atrophic, as would be expected in Cushing syndrome. Adenomas associated with hyperaldosteronism do not usually suppress ACTH secretion.
What are some some causes of hypercalcemia?
Parathyroid-related: adenomas, hyperplasias, lithium, MEN
Malignancy-related: SCC, bone metastases, leukemia,
Vitamin D-related: vitamin D intoxication
High bone turnover: hyperthyroidism, immobilization
Renal failure
What would you expect the serum levels of PTH to be like if you suspected hypercalcemia from a squamous cell cancer?
PTH should be very low or undetectable, PTHrP should be high.
What are the clinical manifestations of primary hyperparathyroidism?
Osteitis fibrosa cystica, kidney stones (“stone and bone” disease), mental status and mood changes, hyperactive reflexes, chronic pancreatitis and constipation are among the frequent manifestations.
Hypercalcemia and hypophosphatemia are the characteristic serum abnormalities.
Parathyroid Adenoma
 Parathyroid adenoma is typically an encapsulated, ovoid to round, soft tissue mass with homogeneous cut surface. About 10% occur in anomalous locations (mediastinum, pericardium, etc).
What is the most common bone
disease associated with parathyroid
adenoma?
Osteopenia
Parathyroid Adenoma: Histo
Chief cells (versus oxyphilic cells) are the dominant cell type in most adenomas and are often arranged in sheets, cords, nests, or glandular formations
Stromal fat cells are absent within an adenoma (in normal parathyroid glands, 50% of the gland is constituted by adipocytes)
Early bone changes in hyperparathyroidism
Abnormal cavities of osteoclastic resorption in the bone trabeculae accompanied by patchy marrow fibrosis.
Burrowing of an overzealous osteoclast into the bone matrix giving the lesion a tunneled (or “moth-eaten”) appearance
Advance bone changes in hyperparathyroidism
In advanced cases, multiple osteolytic lesions filled by giant cells, macrophages, plump fibroblasts and hemorrhage (called “brown tumors of hyperparathyroidism” on gross examination) are seen
Discuss the etiology of primary hyperparathyroidism.
Primary hyperparathyroidism is a syndrome caused by excessive secretion of PTH
Most commonly by a solitary parathyroid adenoma (80% of all cases),
or primary hyperplasia of all parathyroid glands (15% of all cases)
and rarely, a parathyroid carcinoma.
Pheochromocytoma
Pheochromocytoma
a. Definition: uncommon tumor of the adrenal medulla, which produces catecholamines
b. Clinical presentation
i. Severe headache
ii. Tachycardia and palpitations
iii. Diaphoresis and anxiety
iv. Hypertensive episodes
c. "Rule of 10's"
1. 10% occur in children
11. 10% are bilateral
iii. 10% occur outside the adrenal gland
iv. 10%are malignant
v. 10% are familial (MEN II and III)
d. Diagnosis: elevated urinary vanillylmandelic acid (VMA)
In Pheochromocytoma, what operative complications should you anticipate and try to prevent?
Hypertensive crisis, arrhythmias and lactic acidosis.
Pheochromocytoma: gross
Gross features
The tumor may acquire a brown color when exposed to dichromate fixatives (Zenker's solution) due to oxidation of stored catecholamines.
Pheochromocytoma: Histo
Low power view of the tumor showing tumor cells surrounded by fibrous septae (zellballen pattern)
Pleomorphism is also appreciated
What laboratory tests can be used for the diagnosis of this tumor?
24-hour urine can be assayed for vanillylmandelic acid (VMA),metanephrine (MN)
urinary free catecholamines (UFC) which are secreted by many pheochromocytomas.
The combined use of these tests is recommended.
Pituitary Adenoma
Can expand and erode the sella turcica, impinging on the optic chiasm to produce bitemporal hemianopsia.
May lead to increased intracranial pressure - manifests as headaches, nausea and vomiting.
What are prolactinomas?
The most common type of functional pituitary adenoma
In women of childbearing age, prolactinomas manifest clinically with amenorrhea or galactorrhea.
These tumors have been successfully treated with dopamine agonists such as bromocriptine, which inhibit prolactin secretion and produce tumor atrophy.
What is the clinical presentations of a growth hormone (GH) adenoma.
May produce gigantism in prepubertal children and acromegaly in the adults.
These patients also tend to have visual field defects because GH adenomas tend to be fairly large by the time they are discovered.