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Related Concept Videos

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...
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...
Graves Disease II: Pathophysiology01:24

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...
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...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

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 in...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...

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Related Experiment Video

Updated: Jun 4, 2026

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions
05:41

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions

Published on: February 9, 2024

Thyroid stunning: fact or fiction?

I Ross McDougall1, Andrei Iagaru

  • 1Division of Nuclear Medicine and Molecular Imaging, Stanford University Hospital and Clinics, Stanford, CA, USA. rossmcdougall@stanford.edu

Seminars in Nuclear Medicine
|January 29, 2011
PubMed
Summary
This summary is machine-generated.

The "stunning" of thyroid tissue by diagnostic radioactive iodine ((131)I) is debated. Larger diagnostic doses and longer delays to therapy appear to increase the likelihood of this stunning effect.

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Last Updated: Jun 4, 2026

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions
05:41

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Published on: February 9, 2024

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Published on: October 6, 2023

Area of Science:

  • Nuclear Medicine
  • Endocrinology
  • Oncology

Background:

  • The phenomenon of thyroid tissue stunning by diagnostic radioactive iodine ((131)I) is a subject of ongoing debate among researchers.
  • Conflicting evidence exists regarding the occurrence and significance of (131)I-induced stunning in thyroid tissue.

Purpose of the Study:

  • To critically evaluate the evidence for and against thyroid stunning by diagnostic (131)I activities.
  • To analyze the strengths and weaknesses of cited investigations on both sides of the stunning debate.

Main Methods:

  • Review and synthesis of clinical, animal, and in vitro studies addressing thyroid stunning.
  • Analysis of variations in clinical practices, including administered activity, scan-to-treatment delays, and timing of follow-up studies.

Main Results:

  • Factors such as larger diagnostic doses and extended delays between diagnostic scans and therapeutic interventions appear to elevate the probability of thyroid stunning.
  • Differences in clinical practices and unassessed factors like thyroid-stimulating hormone and serum iodine levels complicate the interpretation of stunning effects.

Conclusions:

  • The debate on thyroid stunning by diagnostic (131)I necessitates careful consideration of methodological differences and influencing factors across studies.
  • Further investigation is required to fully elucidate the mechanisms and clinical implications of (131)I-induced stunning, including the impact of early-absorbed radiation from therapy.