Download 11-12 (Bell)

H & E: 11:00 - 12:00
Friday, November 6, 2009
Dr. Bell
Pathology of the Endocrine System: Pituitary and Thyroid
Scribe: Caitlin Cox
Proof: Marjorie O’Neil
Page 1 of 8
*I emailed the updated ppt he used in class to Sally and posted it on dropbox.
I.
Introduction [S1]:
a. Skipped.
II. Definition [S2]:
a. It is a group of organs whose function is to maintain metabolic equilibrium between the various organs of the
body.
b. Feedback inhibition is an important concept.
III. Hormones [S3]:
a. Hormones are chemical messengers that interact with target organs.
b. They can be polypeptides, amines or steroid hormones.
IV. Polypeptides & Amines [S4]:
a. Interact with receptors on cell surface through a second messenger system and act to modify the cell's function.
V. Steroid Hormones [S5]:
a. Steroid hormones are translocated into the nucleus and affect transcription in the nucleus.
VI. Feedback Inhibition [S6]:
a. The releasing hormones are regulated by the final hormonal product.
b. Thyroid releasing hormone (TRH) causes release of the pituitary hormones, thyroid stimulating hormone (TSH),
and then we get production of actual thyroid hormones and those levels feedback to both of the prior locations
to regulate production ultimately of active thyroid hormone.
VII. Organs of the Endocrine System [S7]:
a. Skipped.
VIII. Pituitary Gland [S8]:
a. It is divided into the anterior lobe, known as the Adenohypophysis. It has secretory epithelial cells.
b. The posterior lobe is the Neurohypophysis. It is neural in origin and contains neurosecretory granules that
contain stored hormones that are released by the posterior pituitary.
IX. Embryology: Anterior Lobe [S9]:
a. Anterior lobe is derived from the oral canal through Rathke's Pouch. It grows upward towards the base of the
brain. It is cut off by the sphenoid bone, creating the sella turcica.
b. Rests of epithelial cells can deposit along course of migration and persist, so you can have ectopic pituitary
tissue in the pharynx. You can also have craniopharyngioma tumor of pituitary epithelial origin arising outside of
the cell line.
X. Embryology: Posterior Lobe [S10]:
a. Posterior lobe is an outpouching of the 3rd ventricle. It grows downward alongside the anterior lobe.
b. There is a persistent pituitary stalk that maintains the connection between the hypothalamus and posterior lobe.
XI. Anterior Pituitary [S11]:
a. Skipped.
XII. Anterior Pituitary [S12]:
a. It makes 7 different hormones.
b. Two things can occur: hyperpituitarism or hypopituitarism.
XIII. Anterior Pituitary Hormones [S13]:
a. It has 5 cell types, 7 hormones. *He will NOT ask which cell type makes which hormone, but someone else
may.
i. We have: growth hormone, prolactin, ACTH, MSH, TSH, FSH, & LH.
b. There are different staining patterns for these cells. They have been classified according to these stains
classically, but don’t worry about these for his questions.
XIV.
Hypothalamic Regulatory Hormones [S14]:
a. The hypothalamic regulatory hormones control release of the tropic hormones.
i. TRH controls the release of TSH and prolactin.
ii. GnRH controls release of FSH and LH.
iii. CRH - release of ACTH.
iv. GHRH- release of GH.
v. So we have a multi-layered process.
vi. Somatostatin inhibits the release of growth hormone.
vii. Dopamine inhibits the release of prolactin.
XV. Anterior Pituitary [S15]:
a. Skipped.
XVI.
Pituitary Adenomas [S16]:
H & E: 11:00 - 12:00
Scribe: Caitlin Cox
Friday, November 6, 2009
Proof: Marjorie O’Neil
Dr. Bell
Pathology of the Endocrine System: Pituitary and Thyroid
Page 2 of 8
a. These are benign tumors of the epithelial cells of the gland.
b. These can be either functioning or nonfunctioning.
i. Functioning adenomas will produce whatever hormone that cell type normally makes.
c. These are sometimes divided by size: microadenoma (small) vs. macroadenoma.
XVII. Pituitary Adenomas [S17]:
a. Macroadenoma are classified as adenomas greater than 10mm in size.
i. They can exert a mass effect.
ii. They can be seen on imaging with an enlargement of the sella turcica.
iii. And they can lead to increased intracranial pressure with the classic symptoms of nausea & vomiting.
b. Microadenoma is a small adenoma.
i. These make up about half of all hyper-functioning tumors.
ii. Even though they are small, they can be symptomatic.
XVIII. Macroadenoma [S18]:
a. This is an example of a macroadenoma. You see a large gland that, even though this is benign, it can cause
major symptoms even death. You see a prominent mass effect can be associated with these even though they
are benign. There is not a lot of room for expansion that won’t have symptoms in this area.
XIX.
Bitemporal Hemianopsia [S19]:
a. One of the classic symptoms associated with the expanding pituitary adenomas is bitemporal hemianopsia.
b. The tumor compresses the crossing fibers and the uncrossed lateral fibers are spared.
XX. Hyperpituitarism [S20]:
a. Almost always means an adenoma.
b. There are some rare causes of hyperpituitarism other than adenoma:
i. Pituitary carcinoma (extremely rare).
ii. Nontumorous hyperplasia, this is not well-defined.
iii. Some hypothalamic lesions can cause this.
iv. Some ectopic production, it’s a paraneoplastic syndrome, visceral carcinomas.
XXI.
Somatotroph Tumors Growth Hormone [S21]:
a. Somatotrophs tumors are growth hormone producing tumors. Acidophilic
b. In general, these are the largest of the adenomas.
c. The clinical manifestations can be subtle.
d. Mass effects frequently present
e. In adults, this results in acromegaly, you get thickening of the flat bones, coarsening of the facial features, and
enlargement of the jaw.
f. In a child, this results in gigantism. The body is normal in proportion, just large overall.
g. Patients will have glucose intolerance.
h. They are prone to developing osteoporosis.
i. They have an increased risk of hypertension.
XXII. Acromegaly [S22]:
a. This is acromegaly. It occurs in an adult. You see coarsening of the facial features, protruding jaw, and
thickening of the fingers, so the hands and feet appear out of proportion with the arms and legs.
XXIII. Gigantism [S23]:
a. In a child, gigantism occurs. The body is in normal proportion, just larger than normal.
XXIV. Gonadotroph Adenomas FSH, LH [S24]:
a. These produce Follicle Stimulating Hormone and Luteinizing Hormone.
b. These do not have a typical associated clinical syndrome.
c. There will be an elevated FSH and LH in the serum.
d. If they come to medical attention, they do so due to mass effect.
e. These represent 10-20% of macroadenomas in middle-aged men and women.
XXV. Prolactinomas [S25]:
a. Most common hyper-functioning tumor of the pituitary.
b. Patients present with amenorrhea-galactorrhea in women, which is lack of menses.
c. Usually, these present as microadenomas in pre-menopausal women. But they can present as
macroadenomas in males & older females, in which case, the symptom of amenorrhea may not be apparent.
The symptom associated with the hyper-function of the gland may not be noted.
d. If it is large enough you may see a mass effect.
XXVI. Corticotroph Adenomas Cushing’s Disease [S26]:
a. These produce ACTH leading to Cushing’s Disease.
b. These stimulate the excessive secretion of adrenal cortical steroids.
c. They tend to be microadenomas.
H & E: 11:00 - 12:00
Scribe: Caitlin Cox
Friday, November 6, 2009
Proof: Marjorie O’Neil
Dr. Bell
Pathology of the Endocrine System: Pituitary and Thyroid
Page 3 of 8
XXVII. Anterior Pituitary [S27]:
a. Skipped.
XXVIII. Hypopituitarism [S28]:
a. Occurs when there is loss of 75% or more of the anterior pituitary parenchyma.
b. It can occur with some disorders that interfere with the delivery of pituitary hormone-releasing factors from the
hypothalamus. So rarely, something in the hypothalamus can cause hypopituitarism.
c. It almost always is associated with an actual loss of pituitary parenchyma.
XXIX. Hypopituitarism [S29]:
a. Can be caused by:
i. Non-secretory pituitary adenomas—imagine a proliferation of non-secretory cells causing a compression of
the remaining secretory component. This will cause a loss of pituitary function.
ii. Ischemic necrosis of the anterior pituitary—the most common cause of this is Sheehan’s syndrome. This is
seen in women after delivery. During pregnancy, the anterior pituitary gland enlarges, but the blood supply
does not expand, so there is a slight ischemia always present during pregnancy. If there is excessive
blood loss or some type of shock at the time of delivery, the blood supply can decrease to the already
overburdened blood supply to the pituitary and cause ischemic necrosis.
iii. Ablation caused by:
1. Surgery—for example, when there is a microadenoma that is hypersecreting, the surgeon removes it
which almost always causes damage to the remainder of the pituitary gland.
2. Radiation to the sinonasal region can cause necrosis to the pituitary cells.
XXX.
Hypopituitarism [S30]:
a. “Empty sella syndrome” is one form of hypopituitarism. It is an enlarged, empty sella turcica due to a herniation
of the subarachnoid space causing compression on the (inaudible word 13:19) that supplies the pituitary so that
there is an ischemic necrosis.
i. Classically, patients with this are obese women who have had multiple children.
b. Other rare lesions: inflammatory lesions, trauma that damages the pituitary, and metastatic neoplasms
(extremely rare) could cause destruction of the gland.
XXXI. Female/Male Picture [S31]:
a. The most obvious symptoms of hypopituitarism are: aging and wrinkling of the face, atrophy of the breasts and
genitalia, and loss of some secondary sex characteristics, such as axillary and pubic hair.
XXXII. Posterior Pituitary [S32]:
a. Skipped.
XXXIII. Posterior Pituitary [S33]:
a. Only has two hormones: ADH and Oxytocin.
b. There are two syndromes associated with the posterior pituitary:
i. Diabetes insipidus
ii. Syndrome Inappropriate ADH secretion (SIADH)
XXXIV. Posterior Pituitary [S34]:
a. The posterior pituitary (Neurohypophysis) is of neural origin. It is composed of modified glial cells that have
axonal processes extending from the hypothalamic nuclei.
XXXV. Posterior Pituitary [S35]:
i. It acts as a storage point for hypothalamic secretion and oxytocin.
ii. Oxytocin serves to potentiate uterine contraction and ejection of milk during lactation.
iii. There are no clinical syndromes associated with increased or deficient oxytocin production.
XXXVI. Posterior Pituitary [S36]:
a. The supraoptic nucleus of hypothalamus produces antidiuretic hormone (ADH), which functions to maintain
serum osmolality.
b. ADH also:
i. Acts on renal tubules to cause water reabsorption.
ii. Causes vasoconstriction.
XXXVII. Posterior Lobe Syndromes [S37]:
a. Diabetes Insipidus, which is a deficiency of ADH.
i. This clinically presents with: polyuria, low urine specific gravity (dilute urine), high serum sodium and
osmolality.
ii. There are a number of causes: commonly associated with head trauma, neoplasms that are causing a
mass effect in the region, inflammatory disorders (occasionally), and surgery involving the pituitary and
hypothalamus can cause damage to the posterior pituitary.
iii. This is central diabetes insipidus, and the primary lesion is within the posterior lobe of the pituitary gland.
H & E: 11:00 - 12:00
Scribe: Caitlin Cox
Friday, November 6, 2009
Proof: Marjorie O’Neil
Dr. Bell
Pathology of the Endocrine System: Pituitary and Thyroid
Page 4 of 8
b. There is also a nephrogenic diabetes insipidus where there is normal ADH, but kidneys are not responsive to
that ADH.
XXXVIII.
Posterior Lobe Syndromes [S38]:
a. Syndrome Inappropriate ADH secretion (SIADH) is caused by continued release of ADH with a loss of an intact
negative feedback based on the serum osmolality.
i. This causes hyponatremia and dilution of body fluids.
ii. Most common cause is ectopic production by tumors. It usually arises as a paraneoplastic syndrome from
tumors outside the pituitary gland rather than a primary pituitary lesion.
XXXIX. Thyroid [S39]:
a. Skipped.
XL. Thyroid [S40]:
a. Skipped.
XLI.
Thyroid [S41]:
a. Bilobed gland below and anterior to larynx.
b. Develops from evagination of pharyngeal epithelium, descends to its normal position in neck.
c. There are some developmental abnormalities that we can encounter. The cause of its origin within the pharynx
at the foramen cecum.
i. We can have residual thyroid tissue at the base of the tongue that presents as lingual thyroid tissue. Any
of the lesions that can arise in the normal thyroid can also arise in this residual lingual thyroid tissue.
Primary thyroid carcinomas of the tongue can arise in this residual tissue.
ii. It can extend into a substernal location where there can be a compressive mass effect, particularly in some
of the goiters.
iii. There can be developmental cysts along its path of migration called thyroglossal duct cysts.
XLII.
Development Diagram [S42]:
a. Skipped.
XLIII. Thyroid: Function [S43]:
a. T3 and T4 are the functional hormones produced by the thyroid. They are active in metabolism and involved in
regulating carbohydrate, lipid, and protein metabolism. These are made by the thyroid epithelial cells.
b. Calcitonin is made by the C cells, which are neuroendocrine component of the thyroid gland. These are
involved in bone absorption of calcium and inhibition of resorption of bone.
XLIV. Thyroid [S44]:
a. Skipped.
XLV. Hyperthyroidism [S45]:
a. Hyperthyroidism is a hypermetabolic state caused by elevated levels of circulating free T3 and T4.
b. Causes include:
i. Diffuse hyperplasia of thyroid gland (Graves’ Disease).
ii. Exogenous thyroid hormone in someone who is taking replacement thyroid hormone, but takes too much
iii. Hyperfunctional multinodular goiter (Plummer’s syndrome), this is a hyperplastic process where there is
increased tissue mass producing the thyroid hormone.
iv. There are some functional neoplasms, functional adenomas that can lead to hyperthyroidism.
XLVI. Hyperthyroidism [S46]:
a. Less common causes of hyperthyroidism are:
i. Thyroiditis – inflammation of the thyroid gland.
ii. TSH-secreting pituitary adenomas.
iii. Struma ovarii, which is a germ cell tumor of the ovary. It is a form a teratoma in which there is only thyroid
tissue; it is functional ovarian thyroid tissue. And again, any of the lesions that can arise in normal thyroid
tissue can also arise in this ovarian thyroid tissue, so you can have primary thyroid carcinomas arising in
the ovary.
XLVII. Hyperthyroidism [S47]:
a. Features you would expect to see with hyperthyroidism are ones that you would expect to see with
hypermetabolism: weight loss, tachycardia, arrhythmias, diarrhea, weakness, tremor, nervousness, heat
intolerance.
b. With a sudden increase in thyroid hormone levels, you can have a thyroid storm, which is a medical emergency.
There is an acute exacerbation of symptoms precipitated by some sort of stimulus, usually a problem requiring
hospitalization. There is a rapid increase in the functional thyroid hormone and the effects. The effect that
would have the greatest impact would be dysrhythmia.
c. Lab findings with hyperthyroidism are decreased thyroid stimulating hormone (TSH) with feedback inhibition and
elevated free T4.
XLVIII. Graves’ Disease [S48]:
H & E: 11:00 - 12:00
Scribe: Caitlin Cox
Friday, November 6, 2009
Proof: Marjorie O’Neil
Dr. Bell
Pathology of the Endocrine System: Pituitary and Thyroid
Page 5 of 8
a. It is the most common cause of endogenous hyperthyroidism; it is the most common primary cause of
hyperthyroidism.
b. It is an autoimmune disease. There are IgG autoantibodies that stimulate TSH receptor.
c. This results in diffuse enlargement of thyroid gland (called a goiter).
d. Much more common in women.
XLIX. Graves’ Disease [S49]:
a. Histologically, we see proliferation of the thyroid infoldings, these papillary projections into the follicles. Because
of the hyper-functioning, we see scalloping of the stored colloid within the follicles.
L. Graves’ Ophthalmopathy [S50]:
a. One of the commonly associated findings is Graves’ Ophthalmopathy; we see bulging of the eyes. It is probably
the result of edema posterior to the eyes.
LI. Thyroid [S51]:
a. Skipped.
LII. Hypothyroidism [S52]:
a. One common cause is chronic thyroiditis, which is autoimmune.
i. It can be secondary to surgery, which was to correct a goiter or hyperthyroidism. Any surgery that removes
significant portions of the thyroid will result in hypothyroidism.
ii. Radioactive iodine—iodine localizes in the thyroid gland, it has been used to treat thyroid neoplasms to kill
the lumen cells of the thyroid neoplasm. It has been used in some cases to treat hyperthyroidism instead
of surgery.
iii. Iodine or some enzyme deficiencies can result in hypothyroidism.
iv. Some cases are just idiopathic; we don’t know why the patient has it.
v. Hypopituitarism, where TSH is not produced, can result in hypothyroidism.
LIII. Hypothyroidism [S53]:
a. Features of hypothyroidism as a group are known as “Myxedema.”
b. The characteristic features are the opposites of hyperthyroidism:
i. Apathy / mental sluggishness
ii. Weight gain
iii. Cold intolerance
iv. Lethargy
v. Coarse hair
vi. Dry skin
vii. Decreased circulating T4, and in response to that, an increased TSH in an attempt to bring up the
circulating functional thyroid hormone level.
LIV.
Woman Picture [S54]:
a. This is a diagram showing the changes of hypothyroidism: coarsening of facial features, enlargement of tongue,
and puffy hands.
LV. Cretinism [S55]:
a. In children, hypothyroidism is called cretinism.
b. This can have fairly severe clinical implications:
i. Mentally retardation, short stature, large head, large protruding tongue
c. This is most commonly caused by iodine deficiency; we do not see this commonly in the US because our salt is
fortified with iodine.
d. It can also be caused by:
i. Enzyme deficiencies
ii. Congenital agenesis of the thyroid gland
LVI.
Thyroiditis [S56]:
a. Inflammation of the thyroid gland.
b. It can cause any sort of hormonal state of the thyroid, usually in a progressive manner. Initially, there is
hyperthyroidism, which progresses to hypothyroidism.
c. Much more common in women at a 10:1 ratio.
d. It can cause a painful or painless goiter (enlargement of the thyroid gland).
LVII.
Thyroiditis [S57]:
a. There are a number of causes of thyroiditis:
i. Suppurative (infectious) thyroiditis where you would expect to see acute inflammation with destruction of
the thyroid gland.
ii. Nonspecific lymphocytic thyroiditis, cases where we do not understand the etiology.
iii. Subacute granulomatous thyroiditis where you have granulomatous destruction of the thyroid follicles. This
may be caused by a virus.
H & E: 11:00 - 12:00
Scribe: Caitlin Cox
Friday, November 6, 2009
Proof: Marjorie O’Neil
Dr. Bell
Pathology of the Endocrine System: Pituitary and Thyroid
Page 6 of 8
iv. Hashimoto’s thyroiditis, which we have discussed, is autoimmune thyroiditis.
v. Riedel’s thyroiditis may have an autoimmune component also and results in dense fibrosis of thyroid with
extension of that fibrosis into surrounding neck tissues.
LVIII. Hashimoto’s Thyroiditis [S58]:
a. Chronic autoimmune thyroiditis.
b. Most common cause of hypothyroidism in US.
c. CD8+ cytotoxic T cells and anti-TSH receptor antibodies, so there is a direct destruction of epithelial cells. And
there are antibodies that block action of TSH.
LIX.
Hashimoto’s Thyroiditis [S59]:
a. It is most common in women.
b. Painless enlargement of the thyroid gland.
i. Initial hyperthyroidism which progresses to hypothyroidism.
ii. Increased incidence of other autoimmune disorders; precursor to developing B-cell lymphomas of the
thyroid.
c. There is also an association with papillary thyroid carcinoma.
LX. Hashimoto’s Thyroiditis [S60]:
a. We see lymphocytic and plasma cell infiltrate within the thyroid.
i. Prominent germinal center formation.
ii. We expect to see a reactive change in the follicular epithelial cells; they change into Hurthle cells so they
have abundant granular eosinophilic cytoplasm and prominent nucleoli.
iii. Fibrotic component also.
LXI.
Hashimoto’s Thyroiditis [S61]:
a. This is a low-power image shows Hashimoto’s thyroiditis. We see residual follicular epithelium and colloid with
dense infiltrate, the dark blue-purple areas.
LXII.
Goiter [S62]:
a. Definition is an enlargement of the thyroid. Goiter does not imply anything about the thyroid’s functional state.
b. Again, you can have euthyroid, hypothyroid, or hyperthyroid.
LXIII. Goiter [S63]:
a. Typically, with a goiter, we will have impaired thyroid hormone synthesis that results through feedback in
increased TSH production, which leads to hypertrophy or hyperplasia of the thyroid follicular cells.
b. The follicular cells start to proliferate, the only way they can really do that is to project out into the lumen of the
follicles; you will see papillary proliferations within the follicles.
LXIV. Goiter [S64]:
a. Endemic goiter is called by iodine deficiency.
b. In US, we normally see sporadic goiters.
i. Hereditary enzyme defects in production of thyroid hormone that will lead to the formation of a goiter.
ii. Ingestion of excess calcium or cruciferous vegetables (cabbage, cauliflower, Brussel sprouts).
iii. Usually, it is idiopathic; we don’t know why they have a goiter.
LXV. Goiter [S65]:
a. This is a thyroid that has been removed for goiter.
b. Initially, as goiters develop, it tends to be more diffuse and just enlargement.
c. As it progresses, it becomes nodular with bands of fibrosis within these hyperplastic nodules. These tend to be
very nodular thyroid gland. You can have degenerative change within the nodules; these are the areas of
(inaudible word 33:04). These can become quite large, with compressive symptoms. The patients will have
trouble swallowing, may have respiratory difficulties.
d. Most goiters are removed because of their mass effect.
LXVI. Thyroid [S66]:
a. Skipped.
LXVII. Benign Thyroid Tumors Follicular Adenoma [S67]:
a. Benign epithelial tumors are known as follicular adenomas.
b. Encapsulated, well-circumscribed nodules.
c. Typically painless. Described as cold nodules because they do not take up radioactive material.
d. Usually solitary.
e. May cause difficulty swallowing; become large enough to cause a mass effect.
LXVIII. Histology [S68]:
a. This is a follicular adenoma. You can see follicular epithelial cells lining the follicle, and then a well-formed,
fairly then capsule separating that from the surrounding normal thyroid tissue.
LXIX. Malignant Thyroid Tumors Papillary Carcinoma [S69]:
H & E: 11:00 - 12:00
Scribe: Caitlin Cox
Friday, November 6, 2009
Proof: Marjorie O’Neil
Dr. Bell
Pathology of the Endocrine System: Pituitary and Thyroid
Page 7 of 8
a. The most common malignancy of the thyroid is papillary thyroid carcinoma. It accounts for 60-80% of thyroid
cancers.
b. Most common in young people, usually under 40 years of age.
c. Although you don’t see radiation exposure in the majority of cases, there is a definite increased risk of
developing papillary carcinoma after radiation exposure.
d. Tend to be slow growing.
e. Overall, there is a very good prognosis: 10 year survival rate for over 80%.
f. Papillary carcinomas spread through the lymphatics, so they tend to go to regional lymph nodes.
g. They can be solitary or multifocal lesions within the thyroid gland.
LXX. Malignant Thyroid Tumors Papillary Carcinoma [S70]:
a. Histologically, we see:
i. Papillary bulges (most common)
ii. Orphan Annie Eye nuclei
iii. Psammoma bodies, which are concentric lamellar calcifications.
LXXI. Diagnostic Features [S71]:
a. The nuclei of papillary carcinoma are described as having Orphan Annie Eye features, meaning there’s a thin
rim of chromatin around the outside with central pallor (or central clearing).
LXXII. Diagnostic Features [S72]:
a. These do tend to overlap and have prominent grooves and internuclear inclusions.
LXXIII. Diagnostic Features [S73]:
a. This is an internuclear inclusion.
LXXIV. Diagnostic Features [S74]:
a. These are the psammoma bodies, concentric lamellar calcifications.
LXXV. Papillary Carcinoma [S75-78]:
a. There are micropapillary carcinomas. These are very common; usually it is an incidental finding when the
thyroid is being removed for something else.
b. Probably ¼ of the population.
c. These are small, less than 1cm. Small size usually predicts good behavior.
d. Excellent prognosis. These don’t tend to metastasize, but they can in rare cases be locally aggressive. They
can go to the regional lymph nodes, but even with that, they tend to have a good prognosis.
LXXVI. Malignant Thyroid Tumors Follicular Carcinoma [S79]:
a. Follicular carcinoma is the second most common form of thyroid carcinoma. It accounts for 15 - 25% of thyroid
cancer.
b. There’s a 50% 10 year survival rate, so a little more aggressive than papillary carcinoma.
c. In some cases, there’s a history of multinodular goiters associated with these, and they generally present as a
solitary nodule.
d. Unlike papillary cancer, which spreads through the lymphatics, follicular cancer spreads hematogenously, so it
goes to bone, lung, liver, and other organs. It does not go as frequently to the lymph nodes.
LXXVII. Malignant Thyroid Tumors Follicular Carcinoma [S80]:
a. These are encapsulated lesions with invasion through the capsule or vascular invasion. The invasion is what
defines these as malignant lesions and is used to differentiate this from follicular thyroid adenoma.
i. An adenoma is an encapsulated follicular lesion.
ii. A carcinoma is an encapsulated lesion with invasion through the capsule or blood vessel.
b. They can be composed of Hurthle cells, which we said is reactive follicular epithelial cells with abundant
eosinophilic granular cytoplasm. The prognosis is similar to the regular follicular carcinoma.
LXXVIII.
Gross Photo [S81]:
a. This is a gross photo of the follicular carcinoma. Even at the gross level, you can see the capsule around the
tumor.
LXXIX. Histology [S82]:
a. If we look histologically, we are looking for invasion through the capsule. You can see that as it pushes through
the capsule, there’s not as much pressure on the tumor, so it almost mushrooms out into the surrounding tissue.
b. And then, this is vascular invasion of the follicular carcinoma within the pericapsular vasculature.
LXXX. Malignant Thyroid Tumors Medullary Carcinoma [S83]:
a. This accounts for 5% of thyroid cancers.
b. It is a neuroendocrine tumor. The C cells make calcitonin, and these are the cells of origin of medullary
carcinoma.
c. These can be solitary nodule or multifocal within the thyroid.
d. Typically, present with a neck mass, possibly with dysphagia or hoarseness.
e. This has a 40% 10 year survival, which is more aggressive than follicular thyroid carcinoma.
H & E: 11:00 - 12:00
Scribe: Caitlin Cox
Friday, November 6, 2009
Proof: Marjorie O’Neil
Dr. Bell
Pathology of the Endocrine System: Pituitary and Thyroid
Page 8 of 8
f. The majority of these are sporadic, but some arise as a component of the multiple endocrine neoplasia (MEN)
syndromes.
LXXXI. Malignant Thyroid Tumors Medullary Carcinoma [S84]:
a. These are polygonal to spindle-shaped cells.
b. The classical association is that medullary carcinoma is produce amyloid.
c. In familial cases, there can be an associated benign C-cell hyperplasia. This is thought to be a premalignant
condition.
d. Calcitonin can be demonstrated in these cells by immunohistochemistry with antibodies directed against
calcitonin.
LXXXII. Gross Photo [S85]:
a. The gross presentation is a bulky infiltrating mass within the thyroid gland.
LXXXIII.
Histology [S86]:
a. We can see fairly bland cells with eosinophilic material. This is the amyloid.
LXXXIV.
Histology [S87]:
a. Here we have larger, coarser chunks of amyloid. We have done a special stain (Congo Red) on the right, which
if you look at with polarized light microscopy, you will see apple green (inaudible word 42:19).
LXXXV. Histology [S88]:
a. This is just looking at C cells by immunohistochemistry in a normal thyroid. These are scattered through the
parafollicular space.
b. Here we see tumors of medullary carcinoma....inaudible until next slide…
LXXXVI.
Malignant Thyroid Tumors Anaplastic Carcinoma [S89]:
a. Accounts for 10% of thyroid cancers.
b. Patients are generally older: 60-80 years of age.
c. These are rapidly fatal. Time from diagnosis to death is usually less than 6 months.
d. Tend to be metastatic at the time of diagnosis.
e. Occur most common in areas of endemic goiter, but occasionally see it in US.
LXXXVII.
Malignant Thyroid Tumors Anaplastic Carcinoma [S90]:
a. Presents as a bulky mass that invades the neck structures.
b. The three morphological patterns of anaplastic cells:
1. Giant cells
2. Sarcomatous spindle cells
3. Have an appearance of squamous cell carcinoma
LXXXVIII.
Gross Photo [S91]:
a. Gross photo of an anaplastic carcinoma shows that it is a large, infiltrative bulky mass replacing the thyroid
gland.
LXXXIX.
Histology [S92]:
a. See very aggressive sarcomatoid pattern, which we would expect to mark with epithelial markers, possibly with
TSH so that we could identify it as thyroid in origin. Usually, if the markers are lost, then the diagnosis has to be
made based on clinical presentation. This is a sarcomatoid lesion that appears to be centered on the thyroid
replacing the thyroid.
[end 44:27 min]