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Related Concept Videos

Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists

5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...
Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
Phenothiazines, such as prochlorperazine...
Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
Two synthetic agonists of THC,...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

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...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...

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Related Experiment Video

Updated: Jun 25, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Chemotherapy-induced neuropathy.

Gedge D Rosson1

  • 1Division of Plastic Surgery, JHOC 8th Floor, McElderry 8152-A, 601 North Caroline Street, Baltimore, MD 21287, USA. gedge@jhmi.edu

Clinics in Podiatric Medicine and Surgery
|September 9, 2006
PubMed
Summary

Surgical decompression can successfully treat symptomatic peripheral neuropathy. This approach offers improvements for neuropathy caused by diabetes, unknown factors, and chemotherapy agents.

Area of Science:

  • Neurology
  • Neurosurgery
  • Oncology

Background:

  • Peripheral neuropathy is a common complication of various conditions, including diabetes, chemotherapy, and idiopathic causes.
  • Anatomic compressions can exacerbate or cause peripheral neuropathy.
  • Surgical decompression is an emerging treatment for symptomatic peripheral neuropathy.

Purpose of the Study:

  • To review the role of surgical decompression in treating peripheral neuropathy.
  • To detail common chemotherapy agents causing neuropathy.
  • To discuss mechanisms, medical management, and surgical outcomes for chemotherapy-induced neuropathy.

Main Methods:

  • Literature review of surgical decompression for peripheral neuropathy.
  • Analysis of chemotherapy-induced neuropathy culprits.

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  • Review of putative mechanisms, medical management, and surgical data.

    • Main Results:

    • Surgical decompression has shown success in treating symptomatic peripheral neuropathy.
    • Improvement has been observed in diabetes-induced, idiopathic, and chemotherapy-induced neuropathies.
    • The article identifies key chemotherapy agents and discusses their impact.

    Conclusions:

    • Surgical decompression is a viable treatment option for select patients with peripheral neuropathy.
    • Understanding underlying anatomic compressions is crucial for successful surgical intervention.
    • Further research into chemotherapy-induced neuropathy and its surgical management is warranted.