Thyrotoxicosis

A good way to help you remember is to think of this hormone system like a house’s heating system. In this example, the thyroid gland is the furnace, the pituitary gland is the thermostat, and the hypothalamus is the person living in the house. When the house is cold, the person sets the thermostat to signal the furnace to make heat. When the house grows warmer, the system shuts off. 

In hyperthyroidism, the system never shuts off, causing the release of too many thyroid hormones. For this lesson, we’ll focus on two of them: T3 (tri-iodothyronine) and T4 (thyroxine). 

The thyroid needs iodine to make T3 and T4. Thyroid cells absorb iodine and combine it with the amino acid tyrosine to make these hormones. About 80% is T4, and 20% is T3. 

Too much of T3 and T4 results in thyrotoxicosis. There is a subtle difference between hyperthyroidism and thyrotoxicosis – hyperthyroidism means having an overactive thyroid gland, while thyrotoxicosis is the condition of having increased levels of T3 and T4 in the blood. Thyrotoxicosis can be caused by taking too much thyroid medication, for example, or having thyroiditis (an inflamed thyroid).

Causes of thyroid hormone excess include

  • Primary hyperthyroidism (Graves’ disease, toxic multinodular goiter [MNG], toxic adenoma, iodine excess)
  • Thyroid destruction (subacute thyroiditis, silent thyroiditis, amiodarone, radiation)
  • Extrathyroidal sources of thyroid hormone (thyrotoxicosis factitia, struma ovarii, functioning follicular carcinoma)
  • Secondary hyperthyroidism (TSH-secreting pituitary adenoma, thyroid hormone resistance syndrome, human chorionic gonad- otropin [hCG]-secreting tumors, gestational thyrotoxicosis).
  • Graves’ disease, caused by activating TSH-receptor antibodies, is the most common cause of thyrotoxicosis and accounts for 60–80% of cases.
  • Its prevalence in women is 10-fold higher than in men; its peak occurrence is at age 20–50 years.

Clinical Features

  • Anxiety, restless, and fidgety.
  • weight loss with increased appetite
  • frequent bowel movements
  • heat intolerance
  • excessive sweating
  • oligomenorrhea
  • Skin is warm and moist
  • Cardiovascular findings include tachycardia, systolic hypertension, systolic murmur, and atrial fibrillation.
  • Fingernails may separate from the nail bed (Plummer’s nails).
  • Eyelid retraction and lid lag may be present.
  • A fine tremor, hyperreflexia, and proximal muscle weakness also may be present.
  • Long-standing thyrotoxicosis may lead to osteopenia.
  • In the elderly, the classic signs of thyrotoxicosis may not be apparent, the main manifestations being weight loss and fatigue (“apathetic thyrotoxicosis”).

In Graves’ disease,

  • the thyroid is usually diffusely enlarged to two to three times its normal size
  • a bruit or thrill may be present.
  • Infiltrative ophthalmopathy (with variable degrees of proptosis, periorbital swelling, and ophthalmoplegia)
  • dermopathy (pretibial myxedema) also may be found;
  • these are extrathyroidal manifestations of the autoimmune process.

In subacute thyroiditis,

  • the thyroid is exquisitely tender and enlarged with referred pain to the jaw or ear
  • Sometimes accompanied by fever and preceded by an upper respiratory tract infection.
  • Solitary or multiple nodules may be present in toxic adenoma or toxic MNG.

Thyrotoxic crisis, or thyroid storm, is rare, presents as a life-threatening exacerbation of hyperthyroidism, and can be accompanied by fever, delirium, seizures, arrhythmias, coma, vomiting, diarrhea, and jaundice.

  • Serum TSH is a sensitive marker of thyrotoxicosis caused by Graves’ disease, autonomous thyroid nodules, thyroiditis, and exogenous levothyroxine treatment.
  • Elevation of bilirubin, liver enzymes, and ferritin.
  • Thyroid radioiodine uptake may be required to distinguish the various etiologies: high uptake in Graves’ disease and nodular disease versus low uptake in thyroid destruction, iodine excess, and extrathyroidal sources of thyroid hormone.

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