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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...
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...
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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Related Experiment Video

Updated: May 9, 2026

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
04:14

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

Published on: October 6, 2023

[Subclinical hyperthyroidism].

J Feldkamp1

  • 1Klinik für Allgemeine Innere Medizin, Endokrinologie, Diabetologie, Pneumologie, Infektiologie, Klinikum Bielefeld.

Deutsche Medizinische Wochenschrift (1946)
|July 23, 2013
PubMed
Summary
This summary is machine-generated.

Subclinical hyperthyroidism, characterized by low thyroid-stimulating hormone (TSH) levels, can cause symptoms like anxiety and insomnia. Early treatment is recommended, particularly for TSH below 0.1 mIU/l, to mitigate risks of cardiovascular disease and bone density loss.

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

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Last Updated: May 9, 2026

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
04:14

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

Published on: October 6, 2023

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Area of Science:

  • Endocrinology
  • Internal Medicine
  • Cardiovascular Medicine

Context:

  • Subclinical hyperthyroidism is defined by suppressed thyroid-stimulating hormone (TSH) levels while circulating thyroid hormones remain within normal reference ranges.
  • This condition, though laboratory-defined, can manifest with significant clinical symptoms in a notable proportion of patients.

Purpose:

  • To summarize the clinical implications and potential risks associated with subclinical hyperthyroidism.
  • To highlight the importance of considering therapeutic intervention in specific cases of suppressed TSH.

Summary:

  • Patients may experience symptoms such as tachycardia, sweating, nervousness, anxiety, and insomnia.
  • Increased risks include atrial fibrillation, left ventricular mass, diastolic dysfunction, and elevated cardiovascular and overall mortality.
  • Long-term TSH suppression is linked to reduced bone mineral density and increased fracture rates in the hip and spine.

Impact:

  • Undiagnosed or untreated subclinical hyperthyroidism contributes to significant morbidity and mortality, particularly from cardiovascular causes.
  • Therapeutic intervention, especially when TSH levels fall below 0.1 mIU/l, is crucial for preventing adverse cardiovascular and skeletal outcomes.
  • This underscores the need for careful evaluation and management of patients with suppressed TSH levels.