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Related Concept Videos

Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
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Goiter01:27

Goiter

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Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...
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Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH...
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Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

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Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence...
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Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

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Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor,...
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Synthesis and Regulation of Thyroid Hormones01:20

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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The...
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Consequences of excess iodine.

Angela M Leung1, Lewis E Braverman2

  • 1Division of Endocrinology, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, VA Greater Los Angeles Healthcare System, 11301 Wilshire Boulevard (111D), Los Angeles, CA 90073, USA.

Nature Reviews. Endocrinology
|December 18, 2013
PubMed
Summary
This summary is machine-generated.

Iodine is vital for thyroid hormone production. While generally safe, excessive intake can trigger thyroid dysfunction in susceptible individuals, even when the iodine source isn't obvious.

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Area of Science:

  • Endocrinology
  • Nutritional Science

Background:

  • Iodine is an essential micronutrient crucial for thyroid hormone synthesis.
  • Dietary sources include iodized salt, dairy, bread, and seafood.
  • Recommended daily intake is 150 µg for non-pregnant/lactating adults.

Purpose of the Study:

  • To review the role of iodine in thyroid health.
  • To discuss the potential for iodine-induced thyroid dysfunction.
  • To highlight risks in susceptible populations.

Main Methods:

  • Literature review on iodine metabolism and thyroid function.
  • Analysis of clinical cases and epidemiological data related to iodine exposure.
  • Discussion of physiological and pathological responses to iodine.

Main Results:

  • Excess iodine intake can lead to hypothyroidism or hyperthyroidism.
  • Susceptible individuals include those with thyroid disease, the elderly, fetuses, neonates, and others with risk factors.
  • Iodine-induced thyroid dysfunction may be subclinical or overt and its source may be unclear.

Conclusions:

  • While iodine is essential, excessive intake poses risks, particularly for vulnerable groups.
  • Iodine-induced thyroid dysfunction requires careful consideration of exposure sources.
  • Monitoring iodine intake is important for thyroid health management.