Endocrinology Review
This Endocrine Review Course is hosted by Dr. Saif Borgan (Cleveland Clinic trained board certified endocrinologist in the United States) and Dr Kristen Lee (Endocrine Fellow at Northwestern University). This is the first free (Board-focused) Endocrinology Review podcast made for practicing-endocrinologists, fellows-in-training and advance practice providers, wishing to ACE their endocrinology Boards or Just advance their knowledge in the field. Each short episode is designed to deliver high yield endocrinology knowledge in a specific focus area based on the exam curriculum of the American Board of Internal Medicine - Endocrinology Certification Exam.
Endocrinology Review
Episode 22: Thyroiditis
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Episode 22: Thyroiditis
- How to differentiate thyroiditis from other causes of hyperthyroidism
- Phases of thyroiditis and how it can affect thyroid test results
- Causes of thyroiditis, and key differences
- Management of thyroiditis
Hello and welcome to our episode. In this episode, we will discuss how to differentiate thyroiditis from other causes of thyrotoxicosis, its clinical course, causes of thyroiditis, and its management. So here's the scenario. We have a 22-year-old woman with weight loss, palpitations, tachycardia, hand tremors, frequent bowel movements, and sore throat. She reports flu-like symptoms, congestion, cough, and neck pain. Her blood pressure is 119 over 75 and her heart rate is 110 beats per minute. Her thyroid is 25 grams and tender to palpation. What is the next step in management for this patient? A. Perform thyroid ultrasound. B. Start methemazole. C. Start prednisone, or D start NSAID. And the answer is NSAID. The patient has thyrotoxicosis caused by postviral subacute thyroiditis, also called decorvance thyroiditis, which is a self-limiting condition that is treated conservatively. Thyrotoxicosis refers to a clinical state of elevated thyroid hormone, T3 or T4, for any reason. The term thyrotoxicosis is not synonymous with hyperthyroidism. Hyperthyroidism refers to elevated thyroid hormone level due to an increased thyroid hormone synthesis and secretion. For example, hyperthyroidism is thyrotoxicosis caused by excess endogenous production of thyroid hormone. Thyrotoxicosis can be further subdivided into 1. Thyrotoxicosis due to hyperthyroidism and 2, thyrotoxicosis without hyperthyroidism. The most common cause of thyrotoxicosis due to hyperthyroidism is Graves disease. While the most common cause of thyrotoxicosis without hyperthyroidism is thyroiditis. Thyroiditis describes a group of inflammatory conditions affecting thyroid gland, which include silent, postviral, postpartum, and drug-induced thyroiditis. It's important to differentiate between thyroiditis and graves or toxic goiter because management is different. Thyroiditis is self-remitting and managed conservatively and symptomatically. NSAIDs and sometimes glucocorticoids for neck pain and beta blockers if required for tachycardia and tremors. While thyrotoxicosis due to hyperthyroidism often requires intervention aimed at reducing thyroid hormone production from the thyroid gland. Thyrotoxicosis due to hyperthyroidism will be revisited in greater detail in a future episode. The best way to differentiate the two types of thyroiditis is by radioactive iodine uptake scan. The most commonly used radioactive isotope in the radioactive iodine uptake scan is iodine-123 or I123, which is administered orally either as a pill or a liquid. Patients must not have received recent iodinated contrast prior to radioactive iodine uptake scan and need to limit their iodine intake and hold any interfering medications in preparation for the scan. Within 20 to 30 minutes of ingestion, I-123 can be detected in the thyroid. A typical dose for diagnostic purposes is 100 microcuries of I-123. Scanning for uptake of the radiotracer is commonly done at 4 to 6 hours and/or 24 hours delay. Each view takes 100 to 250,000 counts. Normal radiotracer thyroid uptake is on average 4 to 8% at 4 hours and 10 to 35% at 24 hours. Thyrotoxicosis due to endogenous thyroid hormone excess has high, or sometimes abnormally normal, radioactive iodine uptake scan, reflecting increased thyroid hormone production. These conditions include graze disease and toxic adenoma or multinodular goiter. Toxic adenomas and multinodular goiters can express autonomous thyroid hormone. Though graze disease is more common, the prevalence of toxic adenomas and multinodular goiter increase with age and in iodine-deficient areas. Thyrotoxicosis, not due to hyperthyroidism, is associated with low radioactive iodine uptake and is either caused by release of preformed thyroid hormone due to inflammation or extrathyroidal source, ectopic thyrotoxicosis, or high dose iodine exposure. Thyroiditis course. Thyroiditis manifests initially with a thyrotoxic phase due to destruction of thyroid follicles leading to release of preformed iodothyrinines. Radioactive iodine uptake is notably suppressed in this context, as mentioned previously. This phase may be followed by transient hypothyroidism, which usually occurs within the first three to six weeks. Most people then go on to become euthyroid and completely recover, whereas about 5% of people go on to the persistent phase of hypothyroidism. Causes of thyroiditis. Acute infectious thyroiditis, also called superative thyroiditis, is a rare form of painful thyroiditis caused by bacteria and other microorganisms, not viruses. Complications include abscess and sepsis. Subacute thyroiditis, also known as Decorvan's thyroiditis, is a painful form of thyroiditis that is often post-viral in origin, think respiratory tract infection, and often characterized by fever and painful thyroid, unlike Graves' disease. Presentation is more common in the summer. Due to the release of preformed thyroid hormone, there may be a disproportionate increased amount of T4 in relation to T3. Erythrocyte sedimentation rate can also be elevated. There is an absence of thyroid antibodies, but an elevation of thyroidglobulin level due to thyroid follicule destruction. Painless thyroiditis. Painless thyroiditis is also called silent thyroiditis due to lymphocytic inflammation. Patients are predominantly female and between 30 to 60 years old and can involve development of goiter. Thyroid gland can be firm or enlarged. Autoimmune thyroiditis, also referred to as Hashimoto's thyroiditis or lymphocytic thyroidis, is the leading cause of hypothyroidism in the United States. This condition will also be covered in a later episode. Hamburger thyroiditis is a rare painless type of thyroiditis that results from ingestion of meat containing bovine thyroid tissue. Drug-induced thyroiditis is also often painless, such as that caused by lithium, cytokines such as interferon alpha, tyrosine kinase inhibitors, checkpoint inhibitors, and amyodarin-induced thyrotoxicosis type 2, which we will discuss in future episodes. The postpartum period can involve painless postpartum thyroiditis, which can happen within 12 months of delivery. Rhydal's thyroiditis, also called chronic sclerosine thyroiditis, results from excessive fibrosis that may affect adjacent structures such as muscle. Radiation and direct injury to the thyroid gland can trigger thyroiditis. It is believed that rhidal thyroiditis is a part of a systemic Igg4 sclerosine disease marked by Igg4-positive plasma cell infiltration and fibrosis affecting multiple organs, including the thyroid. Treatment. Symptomatic treatment, for example, non-steroid agents or aspirin, is often sufficient for most patients who have painful thyroiditis. In cases where pain is not responsive to NSAIDs, a 7 to 10 day course of prednisone may be trialed. Beta blockers could be considered to treat hyperthyroid symptoms such as tachycardia and tremors. Repeating thyroid hormone levels in 4 to 8 weeks is advised to confirm spontaneous resolution of the thyrotoxicosis. TSH elevation after thyroiditis episode is usually transient as mentioned, and another repeat TSH, 3T4, are recommended in 3 to 6 months to confirm return to euthyroidism. If TSH elevation is above 10 million units per liter in the post thyroiditis period, then it would be reasonable to initiate levothyrexin, as return to euthyroid is less likely. And this concludes today's episode. In the next episode, we will discuss subclinical hyperthyroidism. Thank you for listening and see you in the next episode.