Thyrotoxicosis not Graves

Reading for this module should include Chapter 13 in Thyroid Disease Manager, or alternative sources. These could include comparable chapters in Endocrinology, Edition III, comparable chapters in Endocrinology Edition IV (when released), or similar chapters in “The Thyroid”. Please note that many questions have more than one correct answer among the multiple possible responses offered.

After reading the material, print out his page, complete the test, fill in required personal information, and send the page with payment to

Center for Continuing Medical Education, 950 E. 61^st St., University of Chicago, Chicago, IL 60637. Anticipated study and testing time for this module is 3 hours, and payment is $45. After satisfactory completion of the examination, a certificate will be returned by mail.

I. A toxic adenoma in a palpable nodule is diagnosed if:
	A. RAI uptake in the nodule is greater than uptake in the surrounding tissue.
	B. RAI uptake is present in the nodule but absent in surrounding tissue.
	C. B + subnormal TSH.
	D. C + elevated T4 and T3.
	E. D + only T3 elevated

II. What is true in toxic adenoma:
	A. Are often caused by germline mutations in the TSH-Receptor gene.
	B. Iodine deficiency plays an additional role in the pathogenesis of these.
	C. May develop into papillary carcinoma.
	D. May successfully be treated with percutaneously administered ethanol.
	E. Is usually larger than 3 cm in diameter.

III. What is true in autonomously functioning nodule:
	A. If patients are clinically euthyroid, they may remain so for years.
	B. If toxic and treated by nodulectomy, patients rarely become hypothyroid.
	C. If toxic and treated with RAI, the rate of subsequent hypothyroidism is as high as in Graves' disease.
	D. Treatment with antithyroid drugs for one year, frequently results in permanent normalization of serum TSH.

IV. Patients with painless thyroiditis:
	A. Are more often female.
	B. Rarely have circulating thyroid auto-antibodies.
	C. Rarely develop ultimate hypothyroidism.
	D. ESR is grossly elevated.

V. Painless thyroiditis:
	A. Is of auto-immune origin.
	B. Thyrotoxicosis is usually mild.
	C. Has a proven genetic predisposition.
	D. Frequently relapses.

VI. Which laboratory measurements are useful when thyrotoxicosis factitia is suspected?
	A. Serum thyroglobulin.
	B. Serum thyroglobulin antibodies.
	C. Serum (free)T4.
	D. Serum TSH.
	E Thyroid RAI uptake/scan.

VII. The following is true with regard to human chorionic gonadotrophin.
	A. Its TSH-like activity is confined to the alpha sub-unit.
	B. Its TSH-like activity is decreased by increased sialylation of the molecule.
	C. It competes with TSH for the TSH-receptor.
	D. It may be responsible for hyperthyroidism in the male.
	E. It has no biological significance in normal pregnancy

VIII. A patient on long term amiodarone therapy shows the following laboratory data; elevated (free)T4, decreased (free)T3, increased TSH. This profile is consistent with:
	A. Hyperthyroidism due to a TSH-producing pituitary tumor.
	B. Pituitary resistance to thyroid hormone.
	C. Hypothyroidism due to amiodarone.
	E. None of these.

IX. Thyroid vascularity is:
	A. Increased in hCG induced thyrotoxicosis.
	B. Increased in amiodarone induced type 2 thyrotoxicosis.
	C. Increased after acute iodine administration to a healthy subject.
	D. Decreased in thyrotoxicosis factitia.
	E. Normal in pregnancy

X. A 60 year old female shows the following serum profile; elevated free T4 and free T3 and slightly elevated TSH. For further diagnosis it is valuable to evaluate:
	A. The serum TSH-alpha/TSH ratio.
	B. MRI of the pituitary region.
	C. The presence of TSH antibodies in the serum.
	D. Serum TSH after TRH stimulation.
	E. Serum TSH after T3 administration (T3 suppression test).

Answer Sheet
Enter "True" or "False" in the appropriate boxes.
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Do you believe the presentations contained pharmaceutical industry bias? Yes __ No __ Comments:

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CME QUESTIONS —MANAGEMENT OF THYROTOXICOSIS NOT DUE TO GRAVES’ DISEASE PREPARED BY GEORG HENNEMANN, MD BACK

CME QUESTIONS —MANAGEMENT OF THYROTOXICOSIS NOT DUE TO GRAVES’ DISEASE
PREPARED BY GEORG HENNEMANN, MD BACK