Acute Delayed Cinv Phases
Acute Delayed Cinv Phases - Related Videos
01:26
Acute Inflammation II: Cellular Phase
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2026
The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
07:05
The Precision of Visual Working Memory with Delayed Estimation
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Source: Laboratory of Jonathan Flombaum—Johns Hopkins University Human memory is limited. Throughout most of its history, experimental psychology has focused on investigating the discrete, quantitative limits of memory—how many individual pieces of information a person can remember. Recently, experimental psychologists have also become interested in more qualitative limits—how precisely is information stored? The concept of memory precision can be both intuitive and elusive at once. It is...
07:47
Measuring Delay Discounting in Humans Using an Adjusting Amount Task
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Cited by 55 •
2016
Delay discounting refers to a decline in the value of a reward when it is delayed relative to when it is immediately available. We outline a computer-based delay discounting task that is easy to implement and allows for the quantification of the degree of delay discounting in human participants.
07:10
In vivo Imaging Method to Distinguish Acute and Chronic Inflammation
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Cited by 25 •
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We describe a non-invasive imaging method for distinguishing inflammatory stages. Systemic delivery of luminol reveals areas of acute inflammation dependent upon MPO activity in neutrophils. In contrast, injection of lucigenin allows for visualization of chronic inflammation dependent upon Phox activity in macrophages.
02:39
Phase Diagrams
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2020
A phase diagram combines plots of pressure versus temperature for the liquid-gas, solid-liquid, and solid-gas phase-transition equilibria of a substance. These diagrams indicate the physical states that exist under specific conditions of pressure and temperature and also provide the pressure dependence of the phase-transition temperatures (melting points, sublimation points, boiling points). Regions or areas labeled solid, liquid, and gas represent single phases, while lines or curves represent...
FAQs
Different neurotransmitter pathways dominate at different times. During the early response, serotonin released by gastrointestinal enterochromaffin cells provides a major signal, while later symptoms involve sustained substance P signaling through neurokinin-1 receptors. This temporal separation explains why prevention may require more than one pharmacologic target rather than relying on a single antiemetic mechanism throughout chemotherapy exposure.
Sustained substance P signaling through neurokinin-1 receptors characterizes the delayed response after chemotherapy. Because this pathway remains relevant from 24 to 120 hours, neurokinin-1 receptor antagonists provide a phase-specific pharmacologic focus for delayed CINV. Their role complements serotonin 5-HT3 receptor antagonists, which address the signaling emphasized in the acute phase.
The delayed phase is not simply a later version of the acute response. Its association with sustained substance P and neurokinin-1 receptor signaling indicates that symptoms can remain pharmacologically relevant after the first 24 hours. Recognizing this persistence helps clinicians plan prevention across the full 24- to 120-hour window instead of limiting attention to the initial chemotherapy period.
Prevention should be timed to cover the different response windows rather than treating all symptoms as one undifferentiated event. Combining serotonin 5-HT3 and neurokinin-1 receptor antagonists provides coverage for the acute and delayed signaling patterns, respectively. This phase-aware approach supports control across the period when chemotherapy-related nausea and vomiting can occur.
Serotonin 5-HT3 receptor antagonists are relevant to the acute pathway, while neurokinin-1 receptor antagonists address the delayed pathway involving substance P. Using these classes in appropriately timed combinations reflects the distinct biology of the two phases. The practical goal is prevention, not merely response after symptoms appear, helping chemotherapy remain safer and more tolerable.
Phase-specific management matters because uncontrolled nausea and vomiting can limit cancer treatment and reduce quality of life. Preventing symptoms in both the acute and delayed windows may help patients maintain treatment adherence while supporting safer, more effective chemotherapy. Thus, the timing of antiemetic pharmacology has consequences beyond symptom relief, affecting continuation of the overall treatment plan.