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Related Concept Videos

Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

59
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...
59
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

36
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...
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Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

33
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,...
33
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

35
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...
35
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

7.2K
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...
7.2K
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

49
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...
49

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Fetal Hyperthyroidism: Intrauterine Treatment with Carbimazole in Two Siblings.

Indian journal of pediatrics·2015
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Fetal and neonatal thyrotoxicosis.

Chandar Mohan Batra1

  • 1Indraprastha Apollo Hospital, New Delhi, India.

Indian Journal of Endocrinology and Metabolism
|November 20, 2013
PubMed
Summary
This summary is machine-generated.

Fetal thyrotoxicosis, caused by maternal antibodies crossing the placenta, can lead to serious complications and mortality in newborns. Early diagnosis and maternal treatment with carbimazole are crucial for managing this rare condition.

Keywords:
Antibodiesfetal thyrotoxicosisthyroid-stimulatingtransplacental

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Area of Science:

  • Endocrinology
  • Maternal-Fetal Medicine
  • Neonatology

Background:

  • Fetal thyrotoxicosis is a rare but serious condition with a 12-20% mortality rate, often due to heart failure.
  • It arises from the transplacental transfer of maternal thyroid-stimulating immunoglobulins (TSIs) that activate fetal thyroid hormone production.
  • Maternal autoimmune thyroid disease, even with treated euthyroidism, can pose a risk.

Purpose of the Study:

  • To outline the pathophysiology, clinical features, and management of fetal thyrotoxicosis.
  • To highlight the importance of recognizing the risks associated with maternal Graves' disease during pregnancy.
  • To emphasize the need for prompt and effective treatment to improve fetal and neonatal outcomes.

Main Methods:

  • Review of existing literature on fetal thyrotoxicosis, its causes, and treatment modalities.
  • Analysis of the mechanism of transplacental antibody transfer and its impact on fetal thyroid function.
  • Description of therapeutic strategies involving maternal and neonatal management.

Main Results:

  • Transplacental transfer of TSIs begins around the 20th week of gestation, peaking by the 30th week.
  • Clinical manifestations include fetal tachycardia, goiter, growth retardation, and hydrops fetalis.
  • Maternal treatment with carbimazole, with careful dosage adjustment based on fetal heart rate, is the primary therapeutic approach.

Conclusions:

  • Fetal thyrotoxicosis requires vigilant monitoring and timely intervention to prevent severe complications and intrauterine death.
  • Maternal treatment with carbimazole, potentially supplemented with thyroxine, can effectively manage fetal hyperthyroidism.
  • Neonatal management focuses on normalizing thyroid function and supportive care for associated symptoms.