Hashimoto thyroiditis: Clinical sciences

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Introduction0:00–0:39

Hashimoto thyroiditis, also known as chronic autoimmune thyroiditis, or chronic lymphocytic thyroiditis is the most common cause of primary hypothyroidism.
In countries that fortify food with iodine in hashimoto thyroiditis. The immune system produces antithyroid antibodies such as antithyroid, peroxidase and antithyroglobulin that destroy thyroid cells eventually reducing thyroid hormone production and causing hypothyroidism.
In fact, the presence of either of these autoantibodies confirms the diagnosis of hashimoto thyroiditis. Now, if your patient presents with a chief concern, suggesting hashimoto thyroiditis, you should first perform an ABCD E assessment to determine if your patient is unstable or stable.

Unstable patient0:39–2:45

If the patient is unstable, stabilize the airway breathing and circulation. Some patients might even require intubation and mechanical ventilation.
Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, BP, pulse oximetry as well as cardiac telemetry.
Finally, if needed. Don't forget to provide supplemental oxygen.
Now, here are some high yield facts to keep in mind. If your patient presents with hypothermia, bradycardia, hypoventilation and lethargy.
You should suspect myxedema coma, which is a severe lifethreatening form of hypothyroidism. Myxedema, coma typically occurs later in the disease course of hashimoto thyroiditis.
When long term thyroid damage results in profound hypothyroidism. Treatment consists of supportive care which in some patient means ventilatory or circulatory support as well as corticosteroids and thyroid hormone and electrolyte replacement.
Any underlying precipitant such as an infection should be identified and treated as well. On the flip side.
Some patients with hashimoto can initially present with tachycardia heat intolerance, sweating, increased appetite and weight loss.
In this case, you should suspect hashitoxicosis, which is a phase of hyperthyroidism that can occur during the early stages of hashimoto thyroiditis.
When a lot of thyroid cells are destroyed at once by autoantibodies, releasing thyroid hormones into the circulation. During the hashitoxicosis phase treatment relies on antithyroid drugs to lower serum thyroid hormone concentration as well as beta blockers to control the heart rate.
Now that we're done with unstable patients. Let's go back to the ABCDE assessment and discuss the stable ones.

Stable patient2:45–3:49

First, obtain a focused history and physical examination. Your patient will likely report symptoms suggesting a low basal metabolic rate and reduced sympathetic activity including fatigue, weight gain and cold intolerance.
In addition, constipation is common and patients may develop depression, hair loss and even menstrual abnormalities. Remember that hashimoto thyroiditis can be associated with other autoimmune conditions like alopecia, areata, vitiligo Addison disease and type one diabetes mellitus when more than one autoimmune condition affecting an endocrine gland is present that's called multiple autoimmune endocrinopathy on the flip side.
Physical exam findings include cardiovascular manifestations such as bradycardia and diastolic hypertension as well as CNS findings, primarily delayed relaxation of deep tendon reflexes.

Suspect hypothyroidism3:49–4:21

Next, your patient can have dry skin, fragile hair, and sometimes even nonpitting peripheral edema, often referred to as Myxedema.
Finally, in some individuals, you might detect a palpable goiter which is a smooth, diffusely enlarged thyroid gland. At this point, you should suspect hypothyroidism.
Your next step is to order TSH and free T four levels. If TSH is high and free T four is low diagnose primary hypothyroidism.

Non-autoimmune hypothyroidism4:21–4:30

And if TSH is high and free T four is normal diagnose subclinical hypothyroidism in both cases, order antithyroid peroxidase antibodies or TPO A B and antithyroglobulin antibodies or T gab.

Hashimoto thyroiditis4:30–5:44

If neither antithyroid peroxidase nor antithyroglobulin antibodies are present diagnose non autoimmune hypothyroidism. However, if either antithyroid peroxidase or antithyroglobulin antibodies or both are present diagnose hashimoto thyroiditis.
Keep in mind that antithyroid peroxidase antibodies are present in approximately 95% of patients with hashimoto thyroiditis.
While antithyroglobulin antibodies are present in 60 to 80% of patients. Now, here's a clinical pearl to keep in mind.
In contrast to hashimoto thyroiditis, which is the most common cause of hypothyroidism in non iodine deficient individuals.
Graves disease is the most common cause of hyperthyroidism. Graves, disease is associated with the presence of TSH receptor antibodies which mimic thyroid stimulating hormone and bind TSH receptors eventually stimulating thyroid hormone production and causing hyperthyroidism.

TSH levels5:44–8:13

But here's the thing, sometimes TSH receptor antibodies can cause hypothyroidism in this case, they are not stimulating TSH receptors in the production of thyroid hormone.
Instead, they are working as antagonists. Now, once you diagnose hashimoto thyroiditis, the next step is to assess the TSH level.
Let's take a look when TSH is greater than or equal to 10. If the TSH is greater than or equal to 10, begin thyroid hormone replacement with levothyroxine.
Next, assess the patient's response in 3 to 6 weeks by ordering TSH. If TSH levels are normal, continue the current dosing.
But if it's high titrate the dose until the TSH levels normalize patients with hashimoto thyroiditis and overt hypothyroidism often require lifelong thyroid hormone replacement.
So schedule follow up appointments at least once a year after the TSH is normalized to ensure proper dosing. Here's a rare but important clinical pearl to keep in mind.
If a patient with hashimoto thyroiditis presents with clinical findings, suggestive of Addison disease such as hypotension, dehydration and skin hyperpigmentation, be sure to check a basal cortisol level before starting levothyroxine replacement therapy.
If serum cortisol is low, that confirms adrenal insufficiency and patients should be started on glucocorticoids before starting levothyroxine.
That's because levothyroxine substitution in patients with untreated adrenal insufficiency can precipitate an adrenal crisis, which is a potentially life threatening scenario.
Now, let's take a look when TSH is lower than 10. If the TSH is lower than 10, assess indications for thyroid replacement therapy with levothyroxine.
If your patient has clinical symptoms, low free t four, age less than 65 to 70 or infertility, begin levothyroxine on the flip side.
If there are no treatment indications, no thyroid hormone replacement is needed, but make sure to schedule periodic follow ups.

Review8:13–10:04

So you can monitor your patient for possible progression of hypothyroidism. Here's one last clinical pearl to keep in mind.
Hashimoto thyroiditis is associated with an increased risk of papillary thyroid carcinoma. So, if you detect any thyroid nodules on palpation, perform an ultrasound and consult the surgery team for further workup.
All right. As a quick recap, hashimoto thyroiditis is an autoimmune condition that causes hypothyroidism via antibody mediated destruction of thyroid cells.
Once you diagnose hypothyroidism, either primary or subclinical check, antithyroid peroxidase and antithyroglobulin antibodies.
If either or both are present, diagnose hashimoto thyroiditis. Next, assess the TSH level if it's 10 or greater, start treatment with levothyroxine and assess the treatment response in 3 to 6 weeks if the treatment response is adequate and TSH is normal, continue the current management.
However, if it's high titrate the levothyroxine as needed. On the other hand, if the TSH is lower than 10 assess indications for levothyroxine treatment, if your patient has clinical symptoms, low free t four, age, less than 65 to 70 or infertility, begin levothyroxine on the flip side.
If there are no treatment indications, no thyroid hormone replacement is needed, but be sure to schedule periodic follow ups