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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...
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...
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...
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...
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 22, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

[Thyroid diseases and pregnancy].

Stefan Karger1, Dagmar Führer-Sakel

  • 1Klinik für Endokrinologie, Diabetologie und Nephrologie, Department Innere Medizin, Universitätsklinikum Leipzig.

Medizinische Klinik (Munich, Germany : 1983)
|June 18, 2009
PubMed
Summary
This summary is machine-generated.

Pregnancy alters thyroid hormone metabolism, requiring careful differentiation from disease. Untreated maternal thyroid dysfunction can harm fetal development and neurocognition.

Related Experiment Videos

Last Updated: Jun 22, 2026

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
  • Obstetrics
  • Reproductive Medicine

Context:

  • Pregnancy significantly alters thyroid hormone metabolism, necessitating careful distinction from pathological thyroid states.
  • Maternal thyroid dysfunction during pregnancy can adversely impact pregnancy outcomes and fetal development.

Purpose:

  • To review the spectrum of thyroid disorders and functional disturbances during and after pregnancy.
  • To provide guidance on the diagnosis and management of thyroid conditions in pregnant patients.
  • To highlight the importance of avoiding specific diagnostic and therapeutic procedures during pregnancy and lactation.

Summary:

  • Hypothyroidism during pregnancy poses risks to fetal neurocognitive development, while hyperthyroidism can impair pregnancy course and cause fetal thyroid dysfunction.
  • Autoimmune thyroid disease is linked to reduced fertility, increased miscarriage rates, and postpartum thyroiditis.
  • Management of nodular thyroid disease and malignancy in pregnancy mirrors non-pregnant patients; however, thyroid scintigraphy and radioiodine therapy are contraindicated.

Impact:

  • Emphasizes the critical need for accurate diagnosis and management of thyroid disorders in pregnant individuals.
  • Underscores the potential for adverse fetal and maternal outcomes if thyroid dysfunction is not properly addressed.
  • Informs clinical practice based on current Endocrine Society guidelines for optimizing thyroid health during and after pregnancy.