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Related Concept Videos

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

6
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...
6
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

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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...
7
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

7
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,...
7
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

6
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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Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

9.5K
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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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

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Thyroid disease and vascular risk.

Avais Jabbar1, Salman Razvi2

  • 1Newcastle University, Newcastle-upon-Tyne, UK.

Clinical Medicine (London, England)
|December 4, 2014
PubMed
Summary
This summary is machine-generated.

Subclinical hypothyroidism (SCH) is common in adults, particularly women and the elderly. While SCH is linked to increased cardiovascular disease risk, especially in younger individuals, evidence on treatment benefits for cardiovascular events is limited.

Keywords:
Subclinical hypothyroidismacute myocardial infarctioncardiovascular disease

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Area of Science:

  • Endocrinology
  • Cardiology
  • Internal Medicine

Background:

  • Subclinical hypothyroidism (SCH) affects up to 10% of adults, predominantly women and the elderly.
  • Observational studies indicate a higher cardiovascular disease (CVD) risk associated with SCH, particularly in younger populations.
  • Thyroid dysfunction during acute myocardial infarction (AMI) is increasingly linked to adverse cardiovascular outcomes.

Purpose of the Study:

  • To review the existing literature on the relationship between thyroid function and cardiovascular disease.
  • To evaluate the impact of treating SCH on cardiovascular risk factors and events.
  • To discuss the implications of abnormal thyroid function in the context of acute cardiovascular events.

Main Methods:

  • Literature review of prospective longitudinal cohort studies.
  • Analysis of interventional trials investigating levothyroxine treatment for SCH.
  • Synthesis of evidence on thyroid function abnormalities during acute myocardial infarction.

Main Results:

  • SCH is associated with an elevated risk of cardiovascular disease, more pronounced in younger individuals.
  • Treatment of SCH with levothyroxine has shown improvements in cardiovascular risk factors.
  • Limited level 1 evidence exists regarding the effect of SCH treatment on actual cardiovascular events.
  • Abnormal thyroid function during AMI correlates with poorer cardiovascular outcomes.

Conclusions:

  • The association between SCH and cardiovascular risk warrants further investigation, especially concerning hard cardiovascular events.
  • Levothyroxine treatment may improve cardiovascular risk factors in SCH patients, but its impact on major cardiovascular events requires more robust evidence.
  • Thyroid status is a critical factor to consider in patients with acute cardiovascular conditions.