Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

30
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...
30
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

28
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...
23
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

26
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,...
26
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...
26
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

7.1K
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...
7.1K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

In Memoriam: Lawrence Crane Wood (1935-2026).

Thyroid : official journal of the American Thyroid Association·2026
Same author

Rethinking paracorporeal lung assist device support in the modern era: Why so different than ECMO?

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation·2026
Same author

In Memoriam: Lawrence Crane Wood (1935-2026).

Thyroid : official journal of the American Thyroid Association·2026
Same author

Kidney and blood pressure sequelae after pediatric extracorporeal membrane oxygenation: a secondary analysis of the Kidney Injury During Membrane Oxygenation pediatric ECMO cohort.

Pediatric nephrology (Berlin, Germany)·2026
Same author

Endocrine Effects of Arginine-Vasopressin After Pediatric Cardiac Surgery.

Pediatric cardiology·2025
Same author

Increased utilisation of analgesia and sedation in patients following bidirectional Glenn: evidence for the "Glenn Headache"?

Cardiology in the young·2025
Same journal

Weight management in China: integrating mental health into routine obesity care.

The lancet. Diabetes & endocrinology·2026
Same journal

Innovation is key to transforming future obesity care.

The lancet. Diabetes & endocrinology·2026
Same journal

Out of touch medical care.

The lancet. Diabetes & endocrinology·2026
Same journal

ADA Scientific Sessions 2026: a line crossed.

The lancet. Diabetes & endocrinology·2026
Same journal

Endocrine-neuropsychological interplay underpinning maternal postpartum depression.

The lancet. Diabetes & endocrinology·2026
Same journal

Intermittent fasting to treat diabetes: time to update clinical practice guidelines.

The lancet. Diabetes & endocrinology·2026
See all related articles

Related Experiment Video

Updated: May 2, 2026

Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model
04:14

Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model

Published on: October 6, 2023

1.4K

Hyperthyroidism in pregnancy.

David S Cooper1, Peter Laurberg2

  • 1Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.

The Lancet. Diabetes & Endocrinology
|March 14, 2014
PubMed
Summary
This summary is machine-generated.

Distinguishing hyperthyroidism from normal pregnancy changes is crucial. Prompt diagnosis and management of thyroid disorders in pregnancy prevent adverse outcomes for mother and baby.

More Related Videos

Author Spotlight: Integrating Ultrasound Imaging with Biochemical Markers for Thyroid Disease Diagnosis
05:41

Author Spotlight: Integrating Ultrasound Imaging with Biochemical Markers for Thyroid Disease Diagnosis

Published on: February 9, 2024

1.3K
Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

2.8K

Related Experiment Videos

Last Updated: May 2, 2026

Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model
04:14

Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model

Published on: October 6, 2023

1.4K
Author Spotlight: Integrating Ultrasound Imaging with Biochemical Markers for Thyroid Disease Diagnosis
05:41

Author Spotlight: Integrating Ultrasound Imaging with Biochemical Markers for Thyroid Disease Diagnosis

Published on: February 9, 2024

1.3K
Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

2.8K

Area of Science:

  • Endocrinology
  • Obstetrics
  • Reproductive Medicine

Background:

  • Pregnancy involves physiological thyroid hormone changes that can mimic or mask hyperthyroidism.
  • Hyperthyroidism in pregnancy affects 1-2 per 1000 pregnancies, necessitating careful differentiation from normal changes.
  • Causes include Graves' disease, toxic goiter, and transient gestational thyrotoxicosis linked to human chorionic gonadotropin.

Purpose of the Study:

  • To review physiological and pathophysiological thyroid changes during pregnancy.
  • To discuss diagnosis and management of hyperthyroidism in pregnant women.
  • To cover severe thyrotoxicosis, neonatal thyrotoxicosis, and postpartum thyroid disorders.

Main Methods:

  • Review of current literature on thyroid function in pregnancy.
  • Analysis of diagnostic criteria for hyperthyroidism during gestation.
  • Evaluation of treatment strategies and associated risks for mother, fetus, and neonate.

Main Results:

  • Hyperthyroidism in pregnancy poses risks to both mother and offspring.
  • Treatment with antithyroid drugs (methimazole, carbimazole, propylthiouracil) presents challenges due to potential teratogenicity and hepatotoxicity.
  • Fetal and neonatal hyperthyroidism require prompt recognition and intervention.

Conclusions:

  • Accurate diagnosis of hyperthyroidism in pregnancy is vital for optimal outcomes.
  • Management requires balancing maternal and fetal well-being against treatment risks.
  • Postpartum thyroid dysfunction is common and requires monitoring.