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Related Concept Videos

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...
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
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...
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...
Longitudinal Research02:20

Longitudinal Research

Sometimes we want to see how people change over time, as in studies of human development and lifespan. When we test the same group of individuals repeatedly over an extended period of time, we are conducting longitudinal research. Longitudinal research is a research design in which data-gathering is administered repeatedly over an extended period of time. For example, we may survey a group of individuals about their dietary habits at age 20, retest them a decade later at age 30, and then again...

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Related Experiment Video

Updated: May 23, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Periconceptional changes in thyroid function: a longitudinal study.

Ursula Balthazar1, Anne Z Steiner

  • 1Anchorage Women's Clinic, Anchorage, AK, USA.

Reproductive Biology and Endocrinology : RB&E
|March 23, 2012
PubMed
Summary
This summary is machine-generated.

Thyroid stimulating hormone (TSH) levels decrease from pre-pregnancy to early pregnancy. This change is less predictable in women with thyroid antibodies, impacting prenatal screening guidelines.

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An Ex vivo Culture System to Study Thyroid Development
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An Ex vivo Culture System to Study Thyroid Development

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Last Updated: May 23, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

An Ex vivo Culture System to Study Thyroid Development
08:33

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

Area of Science:

  • Endocrinology
  • Reproductive Medicine
  • Clinical Chemistry

Background:

  • Current understanding of thyroid function changes during the periconception window is limited.
  • This gap hinders optimal screening and diagnosis of thyroid disease in pregnant women.

Purpose of the Study:

  • To characterize thyroid function changes during the transition from pre-pregnancy to early pregnancy in fertile women.
  • To assess the influence of thyroid antibodies on these periconceptional thyroid function dynamics.

Main Methods:

  • Prospective observation of 60 women (ages 30-42) planning pregnancy.
  • Measurement of thyroid stimulating hormone (TSH) and free thyroxine (FT4) pre-conception and during early pregnancy (6-9 weeks gestation).
  • Analysis of pre-pregnancy thyroid antibodies and use of general estimating equation models for longitudinal analysis.

Main Results:

  • TSH levels were significantly higher pre-pregnancy compared to early pregnancy (p < 0.001), while FT4 levels remained stable (p = 0.53).
  • TSH declined with increasing gestational age (P < 0.01).
  • Women with thyroid antibodies exhibited higher pre-pregnancy TSH and more variable periconceptional thyroid function changes compared to antibody-negative women.

Conclusions:

  • TSH levels naturally decline during the periconception period.
  • Thyroid antibody status influences the predictability of TSH changes.
  • These periconceptional thyroid function shifts necessitate consideration in developing prenatal thyroid screening protocols.