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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...
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...
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...

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Related Experiment Video

Updated: Jul 6, 2026

Microsatellite DNA Genotyping and Flow Cytometry Ploidy Analyses of Formalin-fixed Paraffin-embedded Hydatidiform Molar Tissues
11:54

Microsatellite DNA Genotyping and Flow Cytometry Ploidy Analyses of Formalin-fixed Paraffin-embedded Hydatidiform Molar Tissues

Published on: October 20, 2019

Thyroid storm caused by a partial hydatidiform mole.

Niyati U Chiniwala1, Paul D Woolf, Christopher P Bruno

  • 1Department of Medicine, Crozer Chester Medical Center, Upland, Pennsylvania 19013, USA. niyatichiniwala@gmail.com

Thyroid : Official Journal of the American Thyroid Association
|March 21, 2008
PubMed
Summary
This summary is machine-generated.

Thyroid storm in partial molar pregnancy is rare. Evacuating the mole normalized thyroid function, correlating with decreasing human chorionic gonadotropin (hCG) levels, highlighting hCG-mediated hyperthyroidism.

Related Experiment Videos

Last Updated: Jul 6, 2026

Microsatellite DNA Genotyping and Flow Cytometry Ploidy Analyses of Formalin-fixed Paraffin-embedded Hydatidiform Molar Tissues
11:54

Microsatellite DNA Genotyping and Flow Cytometry Ploidy Analyses of Formalin-fixed Paraffin-embedded Hydatidiform Molar Tissues

Published on: October 20, 2019

Area of Science:

  • Reproductive Endocrinology
  • Thyroidology
  • Gynecologic Oncology

Background:

  • Thyrotoxicosis is uncommon in molar pregnancies.
  • Hyperthyroidism in pregnancy is often linked to gestational trophoblastic disease.
  • Human chorionic gonadotropin (hCG) possesses thyrotropic activity.

Observation:

  • This report details the first case of hyperthyroidism, specifically thyroid storm, in a patient with a partial molar pregnancy.
  • The patient presented with symptoms of severe hyperthyroidism.
  • Partial molar pregnancy was diagnosed.

Findings:

  • Thyroid storm resolved following the evacuation of the partial mole.
  • Biochemical markers of hyperthyroidism improved concurrently with a decrease in hCG levels.
  • This demonstrates a direct correlation between hCG levels and thyroid dysfunction in this context.

Implications:

  • Partial molar pregnancy should be considered in the differential diagnosis of hCG-mediated hyperthyroidism.
  • Early recognition and management of partial moles can prevent severe maternal complications like thyroid storm.
  • This case underscores the significant thyrotropic potential of hCG in specific pregnancy complications.