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22 Cards in this Set

  • Front
  • Back
What are the treatment options for Grave's disease?
E: Graves' disease is treated with I131 radioiodine ablation or antithyroid drugs (ATDs). Surgery can be performed to remove the Graves' gland, but most patients prefer the nonsurgical options.
A: PTU, radioio, surgery
What is the diagnosis: homogenous I123 scan pattern, high RAIU?
A: Grave
E: Grave's disease
What is the diagnosis: patchy I123 scan pattern, moderate uptake?
E: Multinodular autonomously functioning goitre
A: multinod
What is the diagnosis: suppressed gland with one high uptake area on I123 scan,
E:Solitary toxic nodule
A: solitary
What is the differential diagnosis: homogenous I131 scan, low uptake on RAIU?
E: Thyroiditis, Exogenous thyroid hormone administration
A: Thyroiditis, exogenous
What is the diagnosis: patchy I131 scan pattern, moderate uptake on RAIU?
E: Hashmito's: Hashitoxicosis
A: Hashi
How is nodular hyperthyroid disease treated?
E: Hyperthyroid patients with nodular goiter (solitary or multinodular) are typically treated with I131 ablation or surgery (particularly if the gland is large and the patient has compressive symptoms). ATDs can be used in this setting to render patients euthyroid, but they are typically not recommended for the long term because they do not address the underlying pathophysiology of the disease. The hyperthyroidism invariably returns if the ATD is discontinued.
A: ablation,surgery
What is the treatment of thyroiditis.
E: Thyroiditis, due to inflammation and release of preformed hormone, is typically treated with beta blockers and time. Some patients with painful or subacute thyroiditis can be treated with steroids if the pain is particularly severe.
A: blocker, steroid
What is the treatment of Grave's disease?
E: ATDs can be used as primary treatment for Graves' disease or for short-term management in preparation for I131 radioablation. If the second approach is chosen, the ATD must be discontinued 7-10 days prior to the I131 ablation so that it will not inhibit iodine uptake into the gland. ATDs should be titrated to normalize the TSH and T4 (total or free T4). Because normalization of TSH lags behind normalization of the T4 level (by approximately 4-6 weeks), both lab tests must be monitored initially to avoid induction of hypothyroidism. Patients are typically treated with an ATD for 12-18 months, then tapered off to determine whether they have remained in remission. Relapse rates are high (50-60%) within the first year and are highest in patients with large goiters and more severe hyperthyroidism.
A: ATD, ablat
Which antithyroid drug is preferred in pregnancy?
E: Both ATDs, PTU and methimazoleView drug information (Tapazole), inhibit T4 and T3 synthesis by the thyroid gland and are effective for treating hyperthyroidism. PTU has a shorter plasma half-life (60 min) and is approximately 75% protein-bound. For this reason, it is the preferred drug for treating pregnant patients. Additionally, PTU blocks the peripheral conversion of T4 to T3 and is thus preferred for treatment of thyroid storm. MethimazoleView drug information is more convenient than PTU due to its once-daily dosing (half-life = 4-6 h). It is generally avoided during pregnancy due to the association with a rare congenital scalp defect known as aplasia cutis.
How do you evaluate a patient with hypothyroidism?
E: Hypothyroidism is diagnosed by history, physical exam, and thyroid function tests: elevated TSH, low or normal T4, and low or normal T3. Normal hormone levels in the presence of an elevated TSH suggest subclinical hypothyroidism. The concept is that the TSH is a much more sensitive marker of thyroid disease than circulating hormone levels and that even if the T4 or T3 is normal with regard to the laboratory reference range, it may not be "normal" for that particular patient. Thyroid I123 scans are not usually performed in patients with hypothyroidism. Sometimes antithyroid antibodies (antithyroid peroxidase or antithyroglobulin) are checked because they are frequently positive in patients with the most common cause of primary hypothyroidism, autoimmune thyroiditis (Hashimoto's thyroiditis).
A:TSH, anti
What is the most common cause of hypothyroidism?
E: Hashimoto
A: Hashimoto
What are the main causes of primary hypothyroidism?
E: Primary hypothyroidism is due to a pathologic process intrinsic to the thyroid gland, leading to defective production of thyroid hormone or destruction of the gland. The most common cause is destruction due to autoimmune thyroiditis (Hashimoto's thyroiditis). Other causes of primary hypothyroidism include other forms of thyroiditis (silent, painful/subacute, postpartum, drug-induced), "burnt-out" Graves' disease, thyroid ablation from any cause (radiation, radioactive iodine, surgical resection, metastatic tumor/neoplasia), thyroid hormone biosynthetic defects, iodine deficiency, and thyroid agenesis or dysgenesis.
A: thyroiditis, burnt,ablation, defic,genesis
What is the treatment of choice for hypothyroidism?
E: The treatment of choice is levothyroxine (T4) for most patients. The goal is to reverse the clinical syndrome by restoring the TSH and hormone levels to the normal range. A typical replacement dose is 1.6 μg/kg/day in young healthy patients. Elderly patients often require lower doses. The best approach is to "start low, go slow." Measure the TSH every 4-6 weeks (because the half-life of the drug is 7 days and you need to wait until the patient is in equilibrium) until a goal TSH between 1 and 2 is attained. Avoid over- or under-replacement. Once the patient is on a stable dose, the TSH can be monitored annually unless there are changes in the patient's clinical status.
What is the normal transient inhibitory effect of an iodide load on thyroid function called?
E: The Wolff-Chaikoff effect refers to the normal transient inhibitory effect of an iodide load on thyroid function. Most patients "escape" from these inhibitory effects within 2-4 weeks after iodide exposure.
A: Wolff-Chaikoff
An elderly patient becomes thyrotoxic after receiving radiocontrast dye. What is the phenomenon called?
E: The jodbasedow phenomenon refers to iodide-induced thyrotoxicosis. This phenomenon typically occurs in elderly patients with underlying nodular thyroid disease after they receive an iodide load (radiographic contrast). In iodide-deficient countries, the jodbasedow phenomenon can occur following reintroduction of iodide in patients with goiter.
A: Jod
List the risk factors for thyroid malignancy.
E: Risk factors include positive family history of thyroid cancer; extremes of age (< 20 yr or > 60 yr); rapid growth of a preexisting nodule; large, painful, or firm nodule; invasive and compressive symptoms; presence of lymphadenopathy; fixation of nodule to adjacent structures; vocal cord paresis; and history of head and neck irradiation. Any nodule ≥ 1-1.5 cm should be evaluated in a clinically euthryoid patient.
A: family, size, radiation, age
What is the 5-10% rule for thyroid nodules?
E: * 5-10% of people have palpable nodules (more common in women).
* 5-10% of nodules are cancerous (overall lifetime risk of thyroid cancer = 1%).
* 5-10% of thyroid cancer is associated with high morbidity and mortality rates.
A: (preval)|(freq), cancer, mortal
List the types of thyroid cancer
E: Epithelial: follicular, papillary, Hurthle, Anaplastic; C-cell: medullary thyroid carcinoma, primary thyroid lymphoma.
A: folli,papi,Hurth, ana,MCT,lymph
How should differentiated thyroid cancer be treated?
E: Overall, differentiated thyroid cancer has an excellent prognosis if treated appropriately. Most patients receive a thyroidectomy followed by radioiodine (I131) remnant ablation. Patients are treated with thyroid hormone to keep the TSH suppressed. The level of TSH suppression is determined by the aggressiveness of the disease (initial stage), risk of recurrence, and time elapsed from initial diagnosis. This therapy has been shown to decrease cancer recurrence and mortality and to facilitate monitoring for residual/recurrent cancer.
Describe the typical follow-up for patients with differentiated thyroid cancer
E: Standard monitoring of patients with differentiated thyroid cancer includes serial physical exams, thyroglobulin (tumor marker) measurements both on thyroid hormone suppression therapy and after TSH stimulation, diagnostic whole-body I131 scans (WBS), and thyroid ultra sound. Previously, TSH stimulation was achieved by induction of hypothyroidism following withdrawal of thyroid hormone. Since an elevated TSH is required to stimulate I131 uptake into thyroid cells, patients typically discontinue thyroid hormone replacement a number of weeks prior to the WBS and thyroglobulin test. As expected, hypothyroidism is uncomfortable for most patients, and some patients experience very severe symptoms and refuse or delay these cancer-monitoring procedures.
What other option for monitoring patients with thryoid cancer has become recently available?
E:Fortunately, the development of recombinant human TSH (rhTSH) provides a tool whereby TSH levels can be elevated without the need for the patient to become hypothyroid. This discovery has revolutionized care of patients with thyroid cancer. Although rhTSH is currently approved by the U.S. Food and Drug Administration (FDA) for diagnostic monitoring of differentiated thyroid cancer, many other potential uses for rhTSH are under investigation. The overall goal is to have no evidence of disease based on negative imaging studies and undetectable thyroglobulin levels.
Woodmansee WW, Haugen BR: A review of the potential uses for recombinant human TSH in patients with thyroid cancer and nodular goiter. Clin Endocrinol 61:163-173, 2004.
A: rhTSH