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Related Concept Videos

Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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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...
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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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Synthesis and Regulation of Thyroid Hormones01:20

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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...
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Hypothyroidism II: Pathophysiology01:23

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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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Continuous Renal Replacement Therapy01:30

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Continuous Renal Replacement Therapy, also known as CRRT, is a procedural treatment for acute kidney injury (AKI) that gradually removes uremic toxins and fluids while maintaining acid-base balance and stabilizing electrolytes. It is particularly useful for hemodynamically unstable patients. Unlike intermittent hemodialysis, which is faster, CRRT provides a gentler approach over 24 hours, closely mimicking the function of natural kidneys. However, CRRT is not ideal for patients with...
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The Thyroid Gland01:23

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The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
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Thyroid Function with Continuous KRT: A Prospective Study.

Matthew Kennis1, David Madison1, North Foulon1

  • 1University of Colorado School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado.

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Continuous kidney replacement therapy (CKRT) is linked to severe non-thyroidal illness syndrome (NTIS), characterized by low thyroid hormones. CKRT may clear thyroid hormones, contributing to persistent NTIS and high mortality in kidney failure patients.

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Area of Science:

  • Nephrology
  • Endocrinology
  • Critical Care Medicine

Background:

  • Acute kidney injury (AKI) and end-stage kidney disease (ESKD) requiring continuous kidney replacement therapy (CKRT) are associated with high mortality.
  • CKRT can clear solutes up to 40 kDa, including thyroid hormones like thyroid stimulating hormone (TSH), free thyroxine (fT4), and free triiodothyronine (fT3).
  • The impact of CKRT on thyroid function and the hypothalamic-pituitary-thyroid (HPT) axis remains unclear.

Purpose of the Study:

  • To investigate the effect of CKRT on thyroid hormone levels, thyroid function, and the HPT axis.
  • To determine the clearance of TSH, fT4, and fT3 by CKRT.
  • To assess the prevalence and persistence of non-thyroidal illness syndrome (NTIS) in CKRT patients.

Main Methods:

  • Prospective, single-center observational study of 50 ICU patients on CKRT and 50 controls.
  • Measured serum TSH, fT4, fT3, and reverse T3 (rT3) at baseline and on days 1, 3, 8, and 14.
  • Measured CKRT effluent for TSH, fT4, and fT3; adjudicated thyroid function status.

Main Results:

  • CKRT patients exhibited lower fT4 and fT3 levels compared to controls, with more values below the normal range.
  • TSH and fT4 were detected in CKRT effluent, confirming clearance.
  • Severe and persistent NTIS was prevalent in the CKRT cohort; no patient achieved euthyroid status during CKRT.

Conclusions:

  • This study is the first to evaluate thyroid function and hormone clearance during CKRT.
  • The majority of CKRT patients develop severe, persistent NTIS, potentially influenced by CKRT-mediated hormone clearance.
  • These findings suggest that NTIS during CKRT may contribute to the high mortality rates in AKI and ESKD patients.