A 35-year-old woman comes to the emergency department due to a "racing heart" and shortness of breath. She has had insomnia and increasing anxiety for the past several weeks. The patient has no prior medical problems and takes no medications. She has no drug allergies and does not use tobacco, alcohol, or illicit drugs. Blood pressure is 140/70 mm Hg and pulse is 120/min. Physical examination shows a diffusely enlarged, warm thyroid gland. There is a fine tremor in her outstretched hands. ECG shows sinus tachycardia. Serum TSH is decreased and free thyroxine (T4) is increased. The patient is treated with multiple drugs, including propranolol. In addition to its beta-adrenergic receptor-blocking activity, this drug is likely to decrease which of the following?

Question

A 35-year-old woman comes to the emergency department due to a "racing heart" and shortness of breath.  She has had insomnia and increasing anxiety for the past several weeks.  The patient has no prior medical problems and takes no medications.  She has no drug allergies and does not use tobacco, alcohol, or illicit drugs.  Blood pressure is 140/70 mm Hg and pulse is 120/min.  Physical examination shows a diffusely enlarged, warm thyroid gland.  There is a fine tremor in her outstretched hands.  ECG shows sinus tachycardia.  Serum TSH is decreased and free thyroxine (T4) is increased.  The patient is treated with multiple drugs, including propranolol.  In addition to its beta-adrenergic receptor-blocking activity, this drug is likely to decrease which of the following?

Quizplus · Accepted Answer

11ec160b_3bba_29cd_9249_4798115047bc_MD0001_00 This patient has primary hyperthyroidism with an elevated thyroxine (T4) and suppressed TSH level. In light of her diffuse goiter, this is likely due to Graves disease. Hyperthyroidism causes upregulation of beta-adrenergic receptor expression, leading to increased catecholamine effect manifesting as hypertension, palpitations/tachycardia, heat intolerance, tremor, and hyperreflexia. Beta blockers (eg, propranolol) are used to blunt the adrenergic manifestations of hyperthyroidism while awaiting definitive management (eg, surgery, radioiodine). In addition, lipid-soluble beta blockers (including propranolol) reduce conversion of T4 to triiodothyronine (T3), the more active form of thyroid hormone, by inhibiting 5'-monodeiodinase in peripheral tissues. Peripheral conversion of T4 to T3 is also decreased by glucocorticoids and propylthiouracil. (Choice A) The thyroid hormone receptor functions as a transcriptional modulator of several thyroid hormone-responsive genes. It is an intranuclear protein, and binding is not affected by beta blockers. (Choices B and D) Thionamides (eg, propylthiouracil, methimazole) decrease thyroid hormone synthesis by inhibiting thyroid peroxidase. Iodine inhibits release of T4 and T3 from the thyroid. However, beta blockers do not alter thyroid hormone synthesis or release. (Choice E) Graves disease is caused by autoantibodies that bind and stimulate the TSH receptor. Glucocorticoids and other immunosuppressive agents can decrease production of these antibodies, but beta blockers do not affect serum levels of TSH receptor antibodies. Educational objective: Hyperthyroidism causes upregulation of beta-adrenergic receptor expression, leading to increased catecholamine effect. Beta blockers are used to blunt the adrenergic manifestations of hyperthyroidism. In addition, lipid-soluble beta blockers reduce conversion of T4 to T3 by inhibiting 5'-monodeiodinase in peripheral tissues.

A 35-Year-Old Woman Comes to the Emergency Department Due to a "Racing