ThyroidEdit

The thyroid is a small, butterfly-shaped gland located in the front of the neck. Despite its modest size, it exerts a broad influence on metabolism, growth, and energy expenditure through the thyroid hormones it produces. The hormones are primarily triiodothyronine (T3) and thyroxine (T4), which regulate how the body uses energy, heat production, and the function of tissues throughout the body. The thyroid works in concert with the hypothalamus and the pituitary gland, communicating via the hypothalamic-pituitary-thyroid axis. The pituitary releases thyroid-stimulating hormone, which in turn stimulates the thyroid to produce and release T3 and T4. The production of these hormones is tightly controlled by negative feedback: when blood levels of T4 and T3 rise, TSH secretion tends to fall, and vice versa. The gland also synthesizes calcitonin, a peptide involved in calcium homeostasis, produced by the parafollicular (C) cells.

Anatomy and physiology - The thyroid consists of spherical follicles lined with follicular cells and filled with colloid that stores thyroglobulin, the protein scaffold for thyroid hormone synthesis. - Iodine is essential for thyroid hormone production. The gland absorbs dietary iodine through the Na+/I− symporter, incorporates it into tyrosine residues on thyroglobulin, and forms the active hormones after proteolysis and release. - The vascular supply is rich, reflecting the gland’s metabolic importance and the need to distribute hormones systemically. The vascular network allows rapid communication with organs that respond to thyroid hormones, such as the brain, heart, liver, and muscles. - Beyond thyroid hormone production, the gland participates in feedback loops that integrate signals from the nervous system and metabolism to maintain homeostasis.

Hormones and regulation - Thyroid hormones (T3 and T4) influence basal metabolic rate, cardiac function, lipid and carbohydrate metabolism, and thermogenesis. - T3 is the more active hormone at the cellular level, while most circulating T3 is produced by deiodination of T4 in peripheral tissues. - The thyroid receives regulatory input from the hypothalamus, which releases thyrotropin-releasing hormone, and the pituitary gland, which secretes thyroid-stimulating hormone in response. TSH stimulates hormone synthesis, thyroid growth, and hormone release. - In pregnancy, aging, and illness, thyroid hormone metabolism can shift, affecting hormone levels and clinical presentation.

Clinical conditions - Hypothyroidism: Inadequate thyroid hormone production leads to fatigue, weight gain, cold intolerance, slowed reflexes, and sometimes depressive symptoms. Most cases arise from chronic autoimmune destruction (for example, Hashimoto's thyroiditis), but can also result from surgical removal, radiation, or iodine deficiency in certain regions. - Hyperthyroidism: Excess thyroid hormone causes weight loss, heat intolerance, irritability, palpitations, and anxiety. Common etiologies include autoimmune stimulation (e.g., Graves' disease) and nodular toxic goiters. - Goiter: Enlargement of the thyroid gland can occur with iodine deficiency, autoimmune disease, or chronic stimulation from high or low thyroid hormone levels. Goiters may be associated with nodules or cancer in some cases. - Thyroid nodules and cancer: The majority of nodules are benign, but a minority can harbor malignancy. The main cancer types are papillary, follicular, medullary, and anaplastic thyroid carcinoma. Risk factors include radiation exposure, family history, and certain genetic syndromes.

Diagnostics - Laboratory tests typically include measurement of serum thyroid-stimulating hormone and free thyroid hormones (free T4 and, when needed, free T3). Antibody tests (e.g., thyroid peroxidase antibody) help identify autoimmune thyroid disease. - Imaging studies such as thyroid ultrasound are used to evaluate nodule characteristics, size, and vascularity, and to guide biopsy decisions. - Fine-needle aspiration biopsy is the standard method for evaluating suspicious nodules to distinguish benign from malignant lesions. - Nuclear medicine methods, including radioactive iodine uptake studies, can help characterize certain thyroid disorders and guide treatment in selected cases.

Treatment and management - Hypothyroidism is usually managed with replacement therapy, most commonly levothyroxine, aiming to normalize TSH and patient symptoms. Dosing is individualized based on age, weight, comorbidities, and pregnancy status, with periodic monitoring. - Hyperthyroidism treatment focuses on reducing thyroid hormone production or secretion. Options include antithyroid drugs (e.g., methimazole or propylthiouracil), radioactive iodine therapy, and surgical removal in selected cases. - Goiter and nodular disease management depends on symptoms, size, cosmetic concerns, and cancer risk. Treatments range from watchful waiting to surgery, including lobectomy or total thyroidectomy when indicated. - During pregnancy, thyroid management is particularly important for fetal neurodevelopment and maternal health. Medication choices and dosing often need adjustment because of changes in thyroid physiology and the needs of the developing fetus. - Long-term management emphasizes adherence to therapy, monitoring for side effects, and recognizing changes in symptoms that may indicate the need for reassessment of dosing or treatment modality.

Controversies and debates - Screening and early detection: Some health systems emphasize symptom-driven testing, citing costs and the risk of overdiagnosis, while others advocate broader screening of at-risk populations or in pregnancy. Proponents of broader screening argue earlier detection reduces complications, while opponents warn about unnecessary treatment and anxiety in people with mild abnormalities. - Subclinical hypothyroidism: Debates center on whether to treat when TSH is mildly elevated but free hormone levels are normal. Critics of routine treatment emphasize potential overtreatment, while supporters argue that therapy can prevent progression and improve quality of life for symptomatic patients. - Iodine and public health: Iodine intake is essential, but regional policies on iodine fortification can have trade-offs. In some contexts, excessive iodine exposure or poor implementation can contribute to autoimmune thyroid disease in susceptible individuals. The balance between preventing goiter and avoiding overexposure is a continuing policy discussion. - Healthcare policy and access: Discussions often touch on how to allocate resources for thyroid disease management, including the cost of chronic levothyroxine therapy, access to reliable lab testing, and the role of preventive care versus reactive treatment. From a policy perspective, emphasis on cost-effectiveness and patient autonomy informs guidelines and practice patterns.

See also - hypothyroidism - hyperthyroidism - goiter - thyroid nodules - thyroid cancer - levothyroxine - iodine - radiation therapy to the neck - Hashimoto's thyroiditis - Graves' disease

See also (additional related topics) - endocrine system - pituitary gland - hypothalamus