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Related Concept Videos

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

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Related Experiment Video

Updated: Jun 14, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Hashimoto's thyroiditis following Graves' disease.

Husaini Umar1, Nur Muallima, John M F Adam

  • 1Department of Internal Medicine, Faculty of Medicine, University of Hasanuddin-Wahidin Sudirohusodo Hospital, Makassar 90245, Sulawesi Selatan, Indonesia. husani_umar65@yahoo.co.id

Acta Medica Indonesiana
|March 23, 2010
PubMed
Summary

Graves' disease can lead to Hashimoto's thyroiditis, an autoimmune condition. This study reports four cases where Hashimoto's developed after Graves' disease treatment, successfully managed with levothyroxine.

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Last Updated: Jun 14, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

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

Area of Science:

  • Endocrinology
  • Immunology
  • Pathology

Background:

  • Graves' disease involves TSH receptor antibodies (TRAb) causing thyroid hyperplasia and hyperfunction.
  • Hashimoto's thyroiditis is linked to TSH stimulation-blocking antibodies (TSBAb), leading to thyroid damage and atrophy.
  • Approximately 15-20% of Graves' disease patients develop spontaneous hypothyroidism due to chronic thyroiditis.

Observation:

  • This study presents four cases of chronic thyroiditis (Hashimoto's disease) in patients previously diagnosed with Graves' hyperthyroidism.
  • In three cases, Hashimoto's thyroiditis emerged 7 to 25 years post-Graves' disease treatment.
  • One case developed Hashimoto's thyroiditis within months of Graves' disease treatment.

Findings:

  • Diagnosis of Hashimoto's disease was confirmed by clinical signs, elevated TSH, positive thyroid peroxidase and thyroglobulin antibodies, and fine needle aspiration biopsy.
  • Histopathological tests further supported the diagnosis in two cases.
  • All reported cases showed successful treatment outcomes with levothyroxine.

Implications:

  • The development of Hashimoto's thyroiditis post-Graves' disease may stem from an extended immune response targeting endogenous thyroid antigens.
  • Understanding this progression is crucial for managing autoimmune thyroid disorders.
  • Levothyroxine is an effective treatment for Hashimoto's thyroiditis following Graves' disease.