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Related Concept Videos

Drug Elimination by Renal Route: Tubular Reabsorption01:22

Drug Elimination by Renal Route: Tubular Reabsorption

During the process of renal excretion, as the glomerular filtrate progresses to the distal convoluted tubule (DCT), drugs that are highly permeable, lipophilic, and nonionized undergo passive reabsorption from the tubular fluid into the surrounding peritubular capillaries. This reabsorption process restricts their elimination through the kidneys. However, the majority of drugs are either weak acids or weak bases, and their ionization level is dependent on pH. By altering the pH of urine, the...
Kinetics of Drug Elimination01:17

Kinetics of Drug Elimination

Eliminating drugs from the body is a vital process that occurs through excretion or metabolism. Understanding the kinetics of drug elimination is crucial for drug development, dosage determination, and optimizing patient outcomes.
Drug clearance depends on the rate of drug elimination and its plasma concentration. Another important parameter is the half-life of a drug, which is the time required for its concentration to decrease by half. In most cases, drug clearance follows first-order...
Enhanced Elimination of Poison01:26

Enhanced Elimination of Poison

Poison can be effectively removed from the gastrointestinal (GI) tract through various decontamination procedures.
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Renal excretion is the...
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...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

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...
Nonlinear Pharmacokinetics: Drug Elimination for IV Bolus Injection00:59

Nonlinear Pharmacokinetics: Drug Elimination for IV Bolus Injection

In pharmacokinetics, the elimination rate of a drug following a capacity-limited model is primarily controlled by two parameters: Vmax and KM. These parameters are crucial in how the drug behaves inside the body after administration.
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Related Experiment Video

Updated: Jun 27, 2026

Reduced Itraconazole Concentration and Durations Are Successful in Treating Batrachochytrium dendrobatidis Infection in Amphibians
06:49

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Digitoxin elimination reduced during quinidine therapy

M Garty, P Sood, D E Rollins

    Annals of Internal Medicine
    |January 1, 1981
    PubMed
    Summary

    Quinidine significantly increases serum digitoxin levels and prolongs its half-life in healthy volunteers. This drug interaction appears to stem from reduced digitoxin elimination, not altered tissue binding.

    Area of Science:

    • Pharmacology
    • Clinical Toxicology

    Background:

    • Quinidine is known to elevate serum digoxin concentrations, potentially causing toxicity.
    • The interaction between quinidine and other cardiac glycosides requires further investigation.

    Purpose of the Study:

    • To determine if quinidine interacts with digitoxin, another cardiac glycoside.
    • To elucidate the pharmacokinetic basis of any observed quinidine-digitoxin interaction.

    Main Methods:

    • A pharmacokinetic study was conducted in five healthy volunteers.
    • Serum digitoxin concentrations were measured in the presence and absence of quinidine.

    Main Results:

    • Quinidine significantly increased mean digitoxin elimination half-life (87.8 to 218.3 h).

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  • Quinidine reduced mean total body clearance of digitoxin (5.01 to 1.87 mL/h x kg).
  • No significant changes in digitoxin volume of distribution were observed.
  • Conclusions:

    • Quinidine significantly alters digitoxin pharmacokinetics in healthy volunteers.
    • The primary mechanism of this interaction is a reduction in digitoxin elimination.
    • This suggests a potential for increased digitoxin toxicity when co-administered with quinidine.