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Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

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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...
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Local Anesthetics: Adverse Effects01:12

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While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
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Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
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Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

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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.
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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.
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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,...
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Acute sunitinib neurotoxicity.

Ahmet Gulmez1, Mustafa Dikilitas1, Emin Tamer Elkiran1

  • 1Inonu University Medical Oncology Department, Malatya Turkey.

Cancer Treatment and Research Communications
|April 3, 2021
PubMed
Summary

Sunitinib malate, a targeted cancer therapy, can rarely cause serious neurotoxicity. This case report details neurological side effects linked to increased vascular endothelial growth factor (VEGF) during sunitinib treatment.

Keywords:
NeurotoxicityRenal cell cancerTyrosine Kinase Inhibitor

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Area of Science:

  • Oncology
  • Pharmacology
  • Neuroscience

Background:

  • Sunitinib malate is an oral tyrosine kinase inhibitor (TKI) used for metastatic renal cell carcinoma.
  • Common side effects include diarrhea, mucositis, asthenia, and myelosuppression.
  • Serious toxicities are rare but documented.

Observation:

  • This case report focuses on neurotoxicity associated with sunitinib malate.
  • The observed neurotoxicity occurred within two weeks of treatment initiation.
  • Elevated vascular endothelial growth factor (VEGF) levels are implicated.

Findings:

  • Sunitinib malate inhibits tyrosine kinases, leading to increased VEGF levels.
  • Increased VEGF is hypothesized to contribute to neurological side effects.
  • A rare case of sunitinib-induced neurotoxicity is presented.

Implications:

  • Understanding the mechanism of sunitinib neurotoxicity is crucial for patient safety.
  • Monitoring for neurological symptoms in patients receiving sunitinib is important.
  • Further research into VEGF's role in TKI-related neurotoxicity is warranted.