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Related Concept Videos

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...
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...
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
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...
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...
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...

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Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
28:13

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation

Published on: February 26, 2013

Amiodarone and the thyroid: a 2012 update.

F Bogazzi1, L Tomisti, L Bartalena

  • 1Department of Endocrinology and Metabolism, University of Pisa, Pisa, Italy. fbogazzi@hotmail.com

Journal of Endocrinological Investigation
|March 22, 2012
PubMed
Summary
This summary is machine-generated.

Amiodarone causes thyroid dysfunction in 15-20% of patients. Amiodarone-induced hypothyroidism (AIH) is manageable, while amiodarone-induced thyrotoxicosis (AIT) requires differentiated treatment strategies based on its type.

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The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation
23:33

The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation

Published on: February 28, 2012

Area of Science:

  • Endocrinology
  • Cardiology
  • Pharmacology

Background:

  • Amiodarone is a widely used antiarrhythmic drug.
  • Thyroid dysfunction is a common side effect of amiodarone therapy, affecting 15-20% of patients.
  • This dysfunction can manifest as hypothyroidism or thyrotoxicosis.

Purpose of the Study:

  • To summarize the clinical presentation and management of amiodarone-induced thyroid dysfunction.
  • To differentiate between the two main types of amiodarone-induced thyrotoxicosis (AIT) and discuss their respective treatments.
  • To review the role of amiodarone withdrawal and alternative treatment options for AIT.

Main Methods:

  • Review of existing literature on amiodarone-induced thyroid dysfunction.
  • Analysis of diagnostic criteria for differentiating AIT types.
  • Evaluation of treatment outcomes for various therapeutic approaches.

Main Results:

  • Amiodarone-induced hypothyroidism (AIH) is generally mild, easily managed with levothyroxine, and often occurs in patients with autoimmune thyroiditis.
  • Amiodarone-induced thyrotoxicosis (AIT) is categorized into type 1 (hyperthyroidism in a diseased gland) and type 2 (destructive thyroiditis).
  • Treatment for type 1 AIT involves thionamides and potassium perchlorate, while type 2 AIT is primarily treated with glucocorticoids. Mixed forms may require combined therapies.

Conclusions:

  • Accurate differentiation between AIT types is crucial for effective management, although mixed forms exist.
  • Glucocorticoids are first-line for type 2 AIT, while thionamides are used for type 1 AIT. Amiodarone withdrawal is recommended when feasible.
  • Surgical options like thyroidectomy may be considered for refractory AIT cases, as radioiodine therapy is often ineffective due to low iodine uptake.