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Related Concept Videos

Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

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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...
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Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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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...
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Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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

Graves' Disease I: Introduction

23
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...
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Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

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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,...
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Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

26
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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An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
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Pathogenesis of hyperthyroidism.

I J Chopra, D H Solomon

    Annual Review of Medicine
    |January 1, 1983
    PubMed
    Summary
    This summary is machine-generated.

    Graves' disease, a common cause of hyperthyroidism, involves autoimmune issues. While thyroid-stimulating immunoglobulins (IgGs) are suspected, conclusive evidence linking them to the disease remains insufficient.

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    Area of Science:

    • Endocrinology
    • Immunology
    • Genetics

    Background:

    • Graves' disease is the leading cause of hyperthyroidism in the U.S.
    • The condition predominantly affects genetically predisposed individuals.
    • Autoimmune abnormalities are a key characteristic of Graves' disease.

    Purpose of the Study:

    • To evaluate the role of thyroid-targeted activities of immunoglobulins in Graves' disease.
    • To assess the hypothesis that thyroid-stimulating immunoglobulin G (IgG) causes hyperthyroidism in Graves' disease.

    Main Methods:

    • Analysis of immunoglobulin G (IgG) interactions with the TSH receptor.
    • Investigation of thyroid-stimulating activities of patient-derived immunoglobulins.

    Main Results:

    • Patient immunoglobulins exhibit various thyroid-targeted activities.
    • A specific thyroid-stimulating activity linked to IgG interaction with the TSH receptor was observed.

    Conclusions:

    • The hypothesis that thyroid-stimulating IgGs cause hyperthyroidism in Graves' disease is attractive.
    • Current evidence supporting this hypothesis is insufficient.
    • No superior alternative hypothesis is currently available.