Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
63 Cards in this Set
- Front
- Back
Thyroglossal duct cysts are generally found where?
|
In, or close to, the midline of the neck (near the hyoid)
|
|
What is the most sensitive indicator of primary hypothyroidism?
|
Measurement of serum TSH
|
|
In the patient with clinical features compatible with hypothyroidism, a TSH level that is NOT elevated suggests...?
|
Secondary hypothyroidism
|
|
What can cause gestational or early infancy hypothyroidism?
|
1. Nutritional lack of iodine
2. Defects in thyroid hormone synthesis |
|
What causes acute infective thyroiditis?
What is a symptom associated with this condition? |
Bacterior or fungal seeding of the gland
*May cause painful swelling |
|
Which condition results from an immune attack on the thyroid and typically follows a previous viral infection?
|
Subacute granulomatous (DeQuervain's) thyroiditis
|
|
Which condition often presents as a "flu-like" systemic illness with a sudden, painful, diffuse enlargement of the thyroid?
Is hyperthyroidism or hypothyroidism present in this condition? |
Subacute granulomatous (DeQuervain's) thyroiditis
*Results in transient thyrotoxicosis often followed by hypothyroidism |
|
Which type of thyroiditis clinically presents as a hard, non-tender, fixed nodule of irregular outline which may cause stridor, dysphagia, hoarseness, and dyspnea?
|
Riedel's thyroiditis
(May be confused with cancer) |
|
Which type of thyroiditis presents as painless mild-moderate enlargement of the thyroid and/or transient hyperthyroidism which is usually self-limiting?
|
Subacute or chronic lymphocytic thyroiditis
|
|
Which gene is Hashimoto's thyroiditis associated with?
|
HLA-DR5
|
|
Which TSH-receptor autoantibodies may be produced in Hashimoto's thyroiditis?
|
1. TGI (thyroid growth immunoglobulin) <--most common
2. TSI (thyroid stimulating immunoglobulin) *Blocking antibodies for each of these may also be formed. In Hashimoto's TGI + TSI + TSI-blocking antibody) |
|
Which autoantibodies may be responsible for the glandular enlargement seen in Hashimoto's thyroiditis?
|
TGI (thyroid growth immunoglobulin)
|
|
Grave's disease is associated with which gene?
|
HLA-DR3
|
|
Which autoantibodies are found in Grave's disease?
|
TSI and TGI
(same antibodies seen in Hashimoto's. TGI => stimulates growth of the gland, TSI => stimulates hormone production) |
|
Describe the classic appearance of follicular cells in Grave's disease.
|
Increased numbers of tall, columnar follicular epithelial cells, creating papillary infoldings into the follicle lumen which is almost devoid of colloid material.
|
|
What type of goiter is the result of gradual, painless enlargement of the thyroid due to compensatory hyperplasia (secondary to a defect in production or inability to secrete functional TH)?
|
Diffuse nontoxic goiter
|
|
How are multinodular goiters caused?
|
End result of a long-standing diffuse nontoxic goiter
|
|
Which type of goiter can easily be clinically confused with cancer?
|
Multinodular goiter
|
|
How does hyperthyroidism that results from multinodular goiter differ from hyperthyroidism seen in Grave's disease?
|
It is not as severe as Graves' disease and not associated with ocular or skin problems
|
|
What is the preferred mode of initial evaluation to distinguish benign from malignant thyroid tumors?
|
Fine needle aspiration biopsy
(Histologic study is the only way to distinguish between benign or malignant thyroid tumors) |
|
The vast majority of benign thyroid neoplasms are what kind of tumors?
|
Adenomas
|
|
Almost all thyroid adenomas are derived from which cells?
|
Thyroid follicular epithelial cells
(Follicular adenomas) |
|
Thyroid malignancies very rarely produce thyroid hormone, but they do produce which glycoprotein?
What is the significance of this? |
Thyroglobulin
*Tg can be used to monitor for post-surgical recurrence or metastases |
|
What type of architecture seen in thyroid lesions indicates malignancy?
|
Papillary architecture
|
|
Which thyroid carcinoma is an aggressive tumor that occurs in an older population and grows at a rapid pace?
|
Undifferentiated carcinoma
|
|
Medullary carcinomas arise from which cells?
What do these cells secrete? |
Parrafollicular ("C") cells of neural crest origin
*Calcitonin (have ability to also secrete ACTH, protaglandins..) |
|
Medullary carcinonomas characteristically demonstrate deposition of what substance in the the tumor stroma?
|
Amyloid
(altered calcitonin molecules) |
|
Although the clinical presentations vary widely, most patients with medullary carcinoma have some degree of what symptom?
|
Diarrhea
(due to calcitonin or prostaglandin secretion) |
|
Which form of medullary carcinoma is more common--the sporadic or genetic form?
|
Sporadic (75%)
|
|
The genetic form of medullary carcinomas occur as part of which autosomal dominant syndrome?
|
Multiple endocrine neoplasia syndromes
|
|
Tumors due to the genetic form of medullary carcinomas have been shown to have a mutation in which proto-oncogene?
|
RET proto-oncogene on chromosome 10
|
|
What are the two cells of the parathyroid gland?
|
1. Chief cell
2. Oxyphils |
|
What are the functions of PTH?
|
1. Renal activation of Vitamin D
2. Increasing renal Ca2+ resporption and phosphate secretion 3. Increasing resorption from the bone stores |
|
Diseases of which organs may interfere with the production of active vitamin D and therefore alter calcium metabolism?
|
1. Liver
2. Kidney 3. Skin? |
|
What sort of values is hyperparathyroidism characterized by?
|
Elevated PTH levels even in the presence of:
1. Hypophosphatemia 2. Hypercalcemia 3. Increased urine Ca2+ excretion |
|
In the U.S., how is hyperparathyroidism usually diagnosed?
|
Due to abnormal serum Ca2+ levels identified on screening serum chemistries of an asymptomatic patient.
|
|
If hyperparathyroidism goes on undiagnosed, what sort of signs/symptoms will be observed?
|
"Stones, bones, moans, and groans"
1. Stones--> nephrocalcinosis and renal stones 2. Bones--> bone demineralization (osteomalacia), osteitis fibrosa cystica, and brown tumors 3. Moans --> psychiatric disturbances, neurologic abnormalities, and muscle weakness 4. Groans--> peptic ulcers, pancreatitis, and abdominal pains |
|
What is the most frequent cause of primary hyperparathyroidism?
|
Adenoma
(generally chief cells) |
|
Are parathyroid adenomas usually functional or non-functional?
Do they usually involve the superior or inferior glands? |
Almost always functional
*Inferior glands usually involved |
|
Which parathyroid glands tend to be more affected in primary hyperplasia?
|
All four glands are affected, but the superior glands tend to be affected more prominently
|
|
Most hyperplastic parathyroid glands show proliferation of which cell type?
|
Chief cells
|
|
What usually causes secondary hyperparathyroidism?
|
Compensatory hyperplasia in response to chronic hypocalcemia and hyperphosphatemia usually due to chronic renal failure
(renal osteodystrophy) |
|
What sort of values is hypoparathyroidism generally characterized by?
|
1. Low PTH
2. Hypocalcemia 3. Hyperphosphatemia *However, PTH levels can be normal or high if PTH is non-functional or if there is target organ unresponsiveness |
|
Hypoparathyroidism is most often caused by what?
|
Inadvertent removal of the parathyroids during thyroidectomy or radical neck dissection.
|
|
What is pseudohypoparathyroidism?
What is it characterized by? |
Familial syndrome resulting from an end-organ resistance to PTH
1. High levels of PTh 2. Hypocalcemia 3. Hyperphosphatemia 4. Normal or decreased alkaline phosphatase |
|
Do very large parathyroid adenomas cause mass effects?
|
Usually not.
Even the largest parathyroid adenomas rarely cause clinical symptomatology |
|
Describe the epithelial changes that occur in the thyroid follicular cells with increased activity.
|
The epithelium becomes more columnar as the colloid is absorbed.
(With inactivity, the colloid accumulates, distends the follicle, and flattens the epithelium) |
|
List 3 major causes of hyperthyroidism.
|
1. Grave's disease
2. Toxic multinodular goiter 3. Toxic adenoma |
|
Is subacute or chronic lymphocytic thyroiditis usually painful?
|
No
|
|
Is subacute granulomatous (DeQuervain's) thyroiditis generally painful?
|
Yes
(Sudden, painful) |
|
Is Hashimoto's thyroiditis generally painful?
|
No
|
|
Which type of thyroiditis is generally very hard and is often confused with cancer?
|
Riedel's thyroiditis
|
|
Can patients with Hashimoto's thyroiditis experience hyperthyroidism?
|
Yes
Some patients may go through a phase of hyperthyroidism before hypothyroid symptoms predominate |
|
What type of cells may be deficient in autoimmune thyroid diseases?
|
Antigen-specific suppressor T cells
|
|
What are some histologic features of Hashimoto's thyroiditis?
|
1. Lymphocytic infiltration
2. Germinal centers 3. Hurthle cells (oncocytes)--nonfunctional follicular cells packed with mitochondria 4. Fibrosis |
|
What is the most common etiology of a diffuse nontoxic goiter?
|
Endemic goiter
(Iodine deficiency) |
|
Describe the development of a diffuse nontoxic goiter.
|
1. HYPERPLASTIC STAGE: TSH stimulates increased follicular cell activity --> increased cell mass and tall columnar epithelium; depleted colloid follicles
2. COLLOID INVOLUTION: As euthyroid state is reached, colloid accumulates unevenly and flattens the epithelium |
|
List the 4 criteria for classification of an adenoma.
|
1. Complete fibrous encapsulation of the nodule
2. Compression of adjacent thyroid parenchyma 3. Different histologic appearance than normal tissue 4. Lack of multinodularity in the remainder of the gland |
|
What are the characteristic nuclear changes seen in papillary adenocarcinoma?
|
Ground glass, or optically clear nuclei ("orphan annie eyes")
(psammoma bodies are another useful histologic feature) |
|
What type of thyroid carcinoma is the most common?
|
Papillary adenocarcinoma
|
|
Which type of thyroid carcinoma tends to show central fibrosis and areas of necrosis, hemorrhage, and cyst formation?
|
Follicular carcinoma
|
|
Why is it necessary to distinguish between parathyroid adenoma and primary hyperplasia as the cause for hyperparathyroidism?
|
Etiology has therapeutic implications:
Surgical incision of an adenoma should be curative Surgical excision of a single hyperplastic gland, however, is not curative due to the persistent activity of remaining glands. |
|
How should primary parathyroid hyperplasia be treated?
|
With removal of 3 or 3 1/2 glands
|