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Related Concept Videos

Drug Toxicity: Overview01:00

Drug Toxicity: Overview

Drug toxicity quantifies the harm a compound causes to an organism, varying by dose and potentially impacting whole systems or specific organs like the liver. Toxic reactions may arise from venomous insect or spider bites, with effects ranging from mild symptoms to severe outcomes such as brain damage or death. Common forms of acute poisoning include ethanol intoxication and overdose of pain or fever medications, with substances like GHB and heroin being particularly lethal at doses close to...
Drug Toxicity: Risk factors01:24

Drug Toxicity: Risk factors

Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...
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Cardiopulmonary Resuscitation IV: Pharmacological Management

Pharmacologic intervention is crucial in treating cardiac arrest patients during ACLS or Advanced Cardiovascular Life Support. The ACLS algorithms guide the administration of specific drugs based on the patient's cardiac arrest rhythm, which includes pulseless ventricular tachycardia (VT), ventricular fibrillation (VF), asystole, and pulseless electrical activity (PEA).EpinephrineIndication: Epinephrine is the first-line drug for all cardiac arrest rhythms.Mechanism of Action: Epinephrine...
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Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
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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...
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Updated: May 10, 2026

Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
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Hemodynamically unstable: accidental atenolol toxicity?

Nathan R Hoot1, John G Benitez, Kenneth H Palm

  • 1Department of Emergency Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

The Journal of Emergency Medicine
|June 4, 2013
PubMed
Summary

Patients with chronic kidney disease on peritoneal dialysis may experience atenolol toxicity due to poor drug clearance. Glucagon therapy effectively treated a patient with unintentional atenolol accumulation and mesenteric ischemia.

Keywords:
atenololdrug toxicityperitoneal dialysispharmacokineticsshock

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Area of Science:

  • Nephrology
  • Clinical Pharmacology

Background:

  • Antihypertensive medications, particularly beta-blockers, are common in chronic kidney disease (CKD).
  • Atenolol's renal excretion and poor clearance by peritoneal dialysis (PD) can lead to accumulation.
  • This accumulation may predispose patients to toxicity over time.

Observation:

  • A patient with end-stage renal disease (ESRD) on PD presented with hypotension, bradycardia, and abdominal pain.
  • The patient reported no recent changes or overdose of her antihypertensive medications, including atenolol.
  • The clinical presentation was attributed to unintentional atenolol toxicity.

Findings:

  • Atenolol toxicity was diagnosed in a patient with ESRD undergoing PD.
  • The patient experienced hemodynamic instability and mesenteric ischemia secondary to the toxicity.
  • Glucagon therapy rapidly resolved the hemodynamic instability and pain.

Implications:

  • Unique pharmacokinetics of medications must be considered in patients with impaired renal clearance.
  • Gradual accumulation of drugs like atenolol can lead to significant toxicity in CKD patients on PD.
  • This case highlights the importance of monitoring drug levels and considering alternative antihypertensives in this population.