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Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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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 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
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
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
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

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Using a Murine Model of Psychosocial Stress in Pregnancy as a Translationally Relevant Paradigm for Psychiatric Disorders in Mothers and Infants
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Pregnancy sickness and parent-offspring conflict over thyroid function.

Scott Forbes1

  • 1Department of Biology, University of Winnipeg, 515 Portage Avenue, Winnipeg, MB, Canada R3B 2E9.

Journal of Theoretical Biology
|April 12, 2014
PubMed
Summary

Pregnancy sickness may be triggered by the hormone human chorionic gonadotropin (hCG) and its effects on maternal thyroid hormone levels, especially during iodine deficiency. This suggests a potential conflict between maternal and embryonic needs during gestation.

Keywords:
Human chorionic gonadotropinIodineMaternal-embryo conflictMorning sickness

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Area of Science:

  • Reproductive Endocrinology
  • Maternal-Fetal Medicine
  • Developmental Biology

Background:

  • Pregnancy sickness (nausea and vomiting) is common, but its cause is unclear.
  • Human chorionic gonadotropin (hCG) is a suspected cause, but its role is debated due to its diverse functions and variable correlation with sickness.
  • hCG influences maternal thyroid hormone production, particularly thyroxine (T4), during early pregnancy.

Purpose of the Study:

  • To investigate the role of hCG in pregnancy sickness.
  • To explore the connection between hCG, maternal thyroid function, and iodine availability.
  • To understand the potential maternal-embryo conflict over nutrient allocation.

Main Methods:

  • Review of existing literature on hCG, thyroid regulation, and pregnancy sickness.
  • Analysis of the proposed mechanisms involving placental deiodinases (D2 and D3) in regulating thyroid hormone levels.
  • Examination of the hypothesis that reverse T3 is a trigger for nausea and vomiting.

Main Results:

  • hCG acts as a weak thyroid stimulator, potentially overriding maternal thyroid-stimulating hormone (TSH) regulation.
  • Embryonic hCG production may prioritize embryonic needs over maternal well-being, especially in iodine-deficient conditions.
  • Placental deiodinases, particularly D3, deactivate excess thyroid hormones, and their metabolites (like reverse T3) may cause pregnancy sickness.

Conclusions:

  • Pregnancy sickness may result from an antagonistic interaction between mother and embryo over iodine allocation.
  • Embryos may use hCG to increase thyroid hormone production, benefiting development at the mother's expense.
  • The absence of first-trimester nausea and vomiting may warrant thyroid function testing to rule out hypothyroidism.