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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

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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...
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Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

1.4K
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,...
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Antiepileptic Drugs: Potassium Channel Activators01:20

Antiepileptic Drugs: Potassium Channel Activators

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Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
183
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

591
Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
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Hepatic Drug Excretion: Enterohepatic Cycling01:17

Hepatic Drug Excretion: Enterohepatic Cycling

1.5K
Enterohepatic cycling involves the active secretion of drugs and their metabolites into the bile via transporters in the canalicular membrane of hepatocytes. This secretion is an integral part of the digestive process, releasing these substances into the gastrointestinal (GI) tract.
Post-release drugs and metabolites can be reabsorbed into the body from the intestine. For conjugated metabolites like glucuronides, reabsorption requires enzymatic hydrolysis by intestinal microflora. This...
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Imbalances in Cardiac Output01:26

Imbalances in Cardiac Output

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The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send...
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Related Experiment Video

Updated: Jul 5, 2025

Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
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Hepatic Encephalopathy Caused by Long-Term Amiodarone Use.

Naoki Murata1, Toshinori Nishizawa1, Yuntae Kim2

  • 1Department of General Internal Medicine, St. Luke's International Hospital, Tokyo, JPN.

Cureus
|January 17, 2024
PubMed
Summary

Long-term amiodarone use can lead to drug-induced steatohepatitis and urea cycle abnormalities, causing hyperammonemia and hepatic encephalopathy. This case highlights the liver

Keywords:
drug-induced hepatitisfatty liver diseasenon-alcoholic steatohepatitisserum ammoniasevere hepatic encephalopathy and chronic liver disease

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Area of Science:

  • Hepatology
  • Cardiology
  • Pharmacology

Background:

  • A 72-year-old woman with hypertrophic cardiomyopathy and ventricular tachycardia was treated with amiodarone for six years.
  • Amiodarone is an antiarrhythmic drug with a known potential for various toxicities.

Observation:

  • The patient presented with hepatic encephalopathy after cumulative amiodarone exposure.
  • Imaging revealed diffuse increased liver parenchyma attenuation, consistent with a 'bright liver' on CT.
  • Liver biopsy confirmed drug-induced steatohepatitis.

Findings:

  • No urea cycle genetic variations were identified.
  • The patient was diagnosed with drug-induced steatohepatitis and urea cycle abnormalities secondary to amiodarone.
  • Amiodarone was implicated as the cause of hyperammonemia and subsequent hepatic encephalopathy.

Implications:

  • This case illustrates the potential for amiodarone to induce steatohepatitis and urea cycle dysfunction.
  • Understanding this mechanism is crucial for diagnosing amiodarone-related hyperammonemia.
  • Highlights the importance of considering drug toxicity in patients with unexplained liver dysfunction and encephalopathy.