Thyroiditis – Top USMLE Diseases

Hashimoto's thyroiditis, or chronic autoimmune thyroiditis, is the most common cause of hypothyroidism in iodine-sufficient regions, including the US. The condition is an autoimmune disorder leading to destruction of the thyroid cells and thyroid failure. The gradual clinical course of Hashimoto's thyroiditis starts with a transient hyperthyroid state (“hashitoxicosis”) followed by subclinical hypothyroidism. Eventually, progression to overt hypothyroidism occurs, which is permanent. Patients may have a painless goiter, but in later stages, the gland is atrophic. Diagnosis is by laboratory tests showing elevated thyroid-stimulating hormone (TSH), low free thyroxine (T4), and positive antibodies against thyroglobulin and thyroid peroxidase. In uncertain cases, imaging is required. Radioactive iodine uptake will show low iodine uptake and ultrasonography demonstrates either diffuse symmetric enlargement or atrophic reduction (depending on the phase). Biopsy shows lymphocytic infiltration with Hürthle cells. Treatment of the eventual hypothyroid state is lifelong thyroid hormone replacement.

Thyrotoxicosis refers to the classic physiologic manifestations of excess thyroid hormones and is not synonymous with hyperthyroidism, which is caused by sustained overproduction and release of T3 and/or T4. Graves’ disease is the most common cause of primary hyperthyroidism, followed by toxic multinodular goiter and toxic adenoma. Subacute thyroiditis is an example of thyrotoxicosis without hyperthyroidism, and a pituitary adenoma, which secretes thyroid-stimulating hormone (TSH) is an example of secondary hyperthyroidism. Clinical features of thyrotoxicosis are mostly due to an increase in the metabolic rate and overactivity of the sympathetic nervous system (i.e., an increase in the β-adrenergic “tone”). Thyrotoxicosis is diagnosed by measuring the levels of TSH produced by the anterior pituitary gland and free T4 and T3. Depending on the etiology and clinical presentation, it may be treated pharmacologically, surgically, or with radioiodine.

Class 3 antiarrhythmics are drugs that block cardiac tissue K channels. The medications in this class include amiodarone, dronedarone, sotalol, ibutilide, dofetilide, and bretylium. The main mechanism of action includes blocking the cardiac K channels to prolong repolarization. However, some medications in this class also exert effects on Na channels, calcium channels, and adrenergic receptors. Indications vary among the medications, but include both atrial and ventricular arrhythmias. Because these medications prolong the QT interval, torsades de pointes is a potential complication of therapy.

Hashimoto's thyroiditis, or chronic lymphocytic thyroiditis, is the most common cause of hypothyroidism in iodine-sufficient regions. The condition is an autoimmune disorder leading to destruction of the thyroid cells and thyroid failure. The gradual clinical course of Hashimoto's thyroiditis starts with a transient hyperthyroid state (“hashitoxicosis”) followed by subclinical hypothyroidism. Eventually, progression to overt hypothyroidism occurs, which is permanent. Patients may have a painless goiter, but in later stages, the gland is atrophic. Diagnosis is by laboratory tests showing elevated thyroid-stimulating hormone (TSH), low free thyroxine (T4), and positive antibodies against thyroglobulin and thyroid peroxidase. In uncertain cases, imaging is required. Radioactive iodine uptake will show low iodine uptake and ultrasound demonstrates diffuse symmetric enlargement. Biopsy shows lymphocytic infiltration with Hurthle cells. Treatment is lifelong thyroid hormone replacement.

Thyroiditis is a catchall term used to describe a variety of conditions that have inflammation of the thyroid gland in common. It includes pathologies that cause an acute illness with severe thyroid pain (e.g., subacute thyroiditis and infectious thyroiditis) as well as conditions in which there is no clinically evident inflammation and the manifestations primarily reflect thyroid dysfunction or a goiter (e.g., painless thyroiditis and fibrous Riedel’s thyroiditis). The etiology of thyroiditis is varied and includes autoimmune inflammation (most common), bacterial or viral infection, and drug-induced reactions. The inflammation of the thyroid leads to a sequential pathologic process that can result in signs and symptoms of hyperthyroidism followed by signs and symptoms of hypothyroidism. The resulting damage can be temporary or permanent, and the treatment depends on the underlying cause.

Disease-modifying antirheumatic drugs are antiinflammatory medications used to manage rheumatoid arthritis. The medications slow, but do not cure, the progression of the disease. The medications are classified as either synthetic or biologic agents and each has unique mechanisms of action and side effects. Common side effects among the disease-modifying antirheumatic drugs include bone marrow suppression and hepatotoxicity. Leflunomide, methotrexate, and tumor necrosis factor (TNF)-ɑ inhibitors are avoided in pregnancy due to their potential teratogenicity. Hydroxychloroquine and sulfasalazine are safe for use during pregnancy.

Nonsteroidal antiinflammatory drugs (NSAIDs) are a class of medications consisting of aspirin, reversible NSAIDs, and selective NSAIDs. NSAIDs are used as antiplatelet, analgesic, antipyretic, and antiinflammatory agents. Common side effects include GI irritation, prolonged bleeding, and AKI.

Autoimmunity is a pathologic immune response toward self-antigens, resulting from a combination of factors: immunologic, genetic, and environmental. The immune system is equipped with self-tolerance, allowing immune cells such as T cells and B cells to recognize self-antigens and to not mount a reaction against them. Defects in this mechanism, along with environmental triggers (such as infections) and genetic susceptibility factors (most notable of which are the HLA genes) can lead to autoimmune diseases. These conditions are more commonly seen in women. Autoimmune diseases are chronic, with clinical manifestations consistent with the associated immune response. Among these conditions are Graves’ disease (autoantibodies against thyroid hormone receptors), myasthenia gravis (antibodies against acetylcholine receptors), type 1 diabetes (pancreatic β-cell destruction by immune cells), and systemic lupus erythematosus (multiorgan damage driven by immune complexes and autoantibodies).

Thyrotoxicosis refers to the classic physiologic manifestations of excess thyroid hormones and is not synonymous with hyperthyroidism, which is caused by sustained overproduction and release of T3 and/or T4. Graves’ disease is the most common cause of primary hyperthyroidism, followed by toxic multinodular goiter and toxic adenoma. Subacute thyroiditis is an example of thyrotoxicosis without hyperthyroidism, and a pituitary adenoma, which secretes thyroid-stimulating hormone (TSH) is an example of secondary hyperthyroidism. Clinical features of thyrotoxicosis are mostly due to an increase in the metabolic rate and overactivity of the sympathetic nervous system (i.e., an increase in the β-adrenergic “tone”). Thyrotoxicosis is diagnosed by measuring the levels of TSH produced by the anterior pituitary gland and unbound T4 and T3. Depending on the etiology and clinical presentation, it may be treated pharmacologically, surgically, or with radioiodine.