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Related Concept Videos

The Thyroid Gland01:23

The Thyroid Gland

The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
Goiter01:27

Goiter

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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Graves Disease II: Pathophysiology

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, and heat...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

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 iodine is then...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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 receptors...

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Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions
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The so-called stunning of thyroid tissue.

James C Sisson1, Anca M Avram, Susan A Lawson

  • 1Department of Radiology, Division of Nuclear Medicine, University of Michigan Health System, Ann Arbor, 48109-0028, USA. jsisson@umich.edu

Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine
|September 7, 2006
PubMed
Summary

Thyroid stunning, a reduction in therapeutic radioactive iodine (131I) uptake after diagnostic doses, is caused by early destructive effects of the therapeutic dose, not impaired initial uptake.

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Area of Science:

  • Nuclear Medicine
  • Oncology
  • Endocrinology

Background:

  • Thyroid stunning describes reduced therapeutic radioactive iodine (131I) uptake following diagnostic 131I administration.
  • The underlying mechanism of stunning, specifically whether it affects initial uptake, remains unclear.

Purpose of the Study:

  • To investigate the hypothesis that thyroid stunning results from early destructive effects of therapeutic 131I doses.
  • To determine if the diagnostic dose impairs the initial uptake of 131I.

Main Methods:

  • Two studies quantified 131I concentrations in thyroid tissues of papillary thyroid carcinoma patients.
  • Radioactivity ratios (therapeutic/diagnostic, Rx/Dx) were measured at 2 days and extrapolated to 0-1 day to assess uptake and disappearance patterns.
  • Dose-response effects of diagnostic 131I and varying therapeutic doses were analyzed.

Main Results:

  • Most patients (74%) showed a 2-day Rx/Dx ratio <0.6, indicating reduced therapeutic uptake.
  • In patients with stunning (Rx/Dx <0.6 at 2 days), initial uptake (0-1 day) was similar for diagnostic and therapeutic doses in 5 out of 6 cases.
  • No correlation was found between diagnostic dose and the Rx/Dx ratio.

Conclusions:

  • Thyroid stunning is primarily caused by early destructive effects of therapeutic 131I, not by impaired initial uptake.
  • The diagnostic dose does not appear to hinder the initial 131I uptake in thyroid tissues.
  • These findings support the early destructive effect hypothesis for thyroid stunning, particularly at higher therapeutic doses.