The preferred beta-blocker in the management of thyroid storm is .
USMLE® Step 1 style questions USMLE
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A 55-year-old woman is being evaluated one day following an appendectomy. Her temperature is 40.0°C (104°F), pulse is 145/min, respirations are 22/min, and blood pressure is 120/75 mm Hg. She becomes progressively agitated and is not oriented to time, person, or place. Her skin is moist and warm. She has a history of hyperthyroidism and atrial fibrillation. Which of the following medications is most appropriate to administer now?
Content Reviewers:Rishi Desai, MD, MPH
Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary.
The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH.
TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.
The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells.
Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.
Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins.
Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body.
Once inside the cell T4 is mostly converted into T3, and it can exert its effect.
T3 speeds up the basal metabolic rate.
T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.
Thyroid hormone is important - and the occasional increase is like getting a boost to fight off a hungry predator or to stay warm during a snowstorm!
These autoantibodies include thyroid-stimulating immunoglobulins, which bind to the TSH receptor on follicular cells and imitate TSH.
This results in growth of the thyroid gland and stimulates the follicular cells to produce excess thyroid hormone.
Another cause is toxic nodular goiter, where one or more follicles start generating lots of thyroid hormone - in some cases it’s because of a mutated TSH receptor that inappropriately keeps these follicular cells active.