Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
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...
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...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Assessment of heavy metal contamination in leafy vegetables: implications for public health and regulatory measures.

Environmental monitoring and assessment·2024
Same author

Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease.

International journal of molecular sciences·2022
Same author

Challenges in the evaluation and management of radioactive iodine-refractory differentiated thyroid cancer.

Nuclear medicine communications·2022
Same author

Features on Computed Tomography That Correlate With Acute Appendicitis.

The American surgeon·2022
Same author

Hypercalcemia Secondary to Immune Reconstitution Inflammatory Syndrome in an HIV-Infected Individual With Mycobacterium avium Complex.

Cureus·2021
Same author

Redifferentiation of BRAF V600E-Mutated Radioiodine Refractory Metastatic Papillary Thyroid Cancer After Treatment With Dabrafenib and Trametinib.

Cureus·2021

Related Experiment Video

Updated: Jun 2, 2026

Minimal Invasive Resection of Large Retrosternal Thyroid Goiter
04:09

Minimal Invasive Resection of Large Retrosternal Thyroid Goiter

Published on: September 20, 2024

Post-ablative hypothyroidism.

Abid Yaqub1, Muhammad I Choudhry, Jennifer Wheaton

  • 1Joan C. Edwards School of Medicine, Marshall University, Huntington, USA.

The West Virginia Medical Journal
|April 12, 2011
PubMed
Summary

Radioactive iodine (RAI) treatment for hyperthyroidism can lead to hypothyroidism, particularly in Graves' disease patients. However, RAI dose and uptake do not predict hypothyroidism development.

Area of Science:

  • Endocrinology
  • Nuclear Medicine
  • Thyroidology

Background:

  • Hyperthyroidism is a common endocrine disorder often treated with radioactive iodine (RAI).
  • Post-treatment hypothyroidism is a known complication of RAI therapy.

Purpose of the Study:

  • To determine the incidence of hypothyroidism after RAI treatment for hyperthyroidism.
  • To investigate the correlation between initial RAI uptake, administered dose, and subsequent hypothyroidism development.

Main Methods:

  • Retrospective chart review of 41 patients treated with RAI for hyperthyroidism between 1995 and 2000.
  • Data collected included hyperthyroidism cause, initial RAI uptake, RAI dose, and thyroid status post-treatment.

Main Results:

Related Experiment Videos

Last Updated: Jun 2, 2026

Minimal Invasive Resection of Large Retrosternal Thyroid Goiter
04:09

Minimal Invasive Resection of Large Retrosternal Thyroid Goiter

Published on: September 20, 2024

  • Graves' disease patients had higher pretreatment RAI uptake but received lower RAI doses compared to toxic nodular goiter patients.
  • Hypothyroidism developed in 70% of Graves' disease patients versus 42% in toxic nodular goiter patients (p=0.086).
  • No significant relationship was found between RAI dose or uptake and the likelihood of developing hypothyroidism.

    • Conclusions:

    • Post-ablative hypothyroidism appears more frequent in Graves' disease than toxic nodular goiter patients following RAI.
    • RAI treatment yielded similar cure rates for both conditions.
    • Neither RAI dose nor pretreatment uptake predicted the development of hypothyroidism.