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Endocrine system

Adrenal gland disorders
Thyroid gland disorders
Parathyroid gland disorders
Pancreatic disorders
Pituitary gland disorders
Gonadal dysfunction
Polyglandular syndromes
Endocrine tumors
Endocrine system pathology review



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17 flashcards

USMLE® Step 1 style questions USMLE

4 questions

USMLE® Step 2 style questions USMLE

2 questions

A 34-year-old woman comes to clinic because of tearing and foreign body sensation of her eyes bilaterally, which has gradually worsened over the last several weeks. She also notes having occasional palpitations, nervousness, sweating, and heat intolerance. Her past medical history is unremarkable. She is currently a daily smoker. Physical examination shows an anxious, trembling woman. She has eyelid retraction bilaterally, with an inability to fully close her eyes. Her extraocular motility is limited on upgaze. There is no thyromegaly or thyroid nodules noted. Laboratory studies reveal a thyroid-stimulating hormone level of 0.1 μU/mL and thyroxine (T4) 42 μg/dL. Thyroid stimulating immunoglobulin is positive. CT scan of the orbits shows proptosis and marked enlargement of the extraocular muscle, with sparing of the tendons. Which of the following would be likely to transiently worsen this patient’s eye symptoms?


Content Reviewers:

Rishi Desai, MD, MPH


Yifan Xiao, MD

In hyperthyroidism, ‘hyper’ refers to having too much, and ‘thyroid’ refers to thyroid hormone, so hyperthyroidism refers to a condition where there’s excess thyroid hormones.

The condition is also called thyrotoxicosis, and is generally due to overproduction from the thyroid gland.

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, where it can exert its effect. T3 speeds up the cell’s basal metabolic rate.

So as an example, the cell might produce more proteins and burn up more energy in the form of sugars and fats.

It’s as if the cells are in a bit of frenzy.

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 can be really useful when you need a boost to get through the final rounds of a sporting competition or when you’re trying to stay warm during a snowstorm!

Now, hyperthyroidism can happen a few different ways - all of them result in too much thyroid hormone and a hypermetabolic state, where cellular reactions are happening faster than normal.

The most common primary cause is Graves disease, an autoimmune disorder where B cells produce antibodies against several thyroid proteins.

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 primary cause is toxic nodular goiter, where one or more follicules start generating lots of thyroid hormone - in some cases it’s because of a mutated TSH receptor that inappropriately keeps these follicular cells active.

A different cause is a hyperfunctioning thyroid adenoma, where the follicular cells start growing uncontrollably forming a benign tumor and making excess thyroid hormones.

Also, anytime the thyroid gets inflamed or damaged, there can be a large release of pre-formed thyroid hormones.