Emesis is a defense mechanism controlled by the area postrema of the medulla oblongata. There are various sources of input to the vomiting center. Receptors on the floor of the fourth ventricle of the brain represent the chemoreceptor trigger zone. The chemoreceptor trigger zone contains dopamine D2 receptors, serotonin 5-HT3 receptors, opioid receptors, acetylcholine receptors, and receptors for substance P. Stimulation of different receptors are involved in different pathways leading to emesis. In the final common pathway, substance P, which activates the neurokinin-1 receptor, appears to be involved. Additionally, the vagal and enteric nervous system inputs transmit information regarding the state of the gastrointestinal system.<unk>  interferes with cell division, which particularly affects rapidly dividing cells like those of the gastrointestinal mucosa and immune cells. Irritation of the GI mucosa by<unk> , radiation, distention, or acute infectious gastroenteritis activates the 5-HT3 receptors of these inputs. It is now widely known that cytotoxic<unk> utic agents cause enterochromaffin cells to produce more serotonin in response to free radical damage, leading to a detectable increase in blood levels of serotonin (5-HT) and its major metabolite, 5-Hydroxyindoleacetic acid (5-HIAA). The presence of these chemicals in the blood activate 5-HT3 receptors in the chemoreceptor trigger zone, in turn releasing substance P, which activates NK1 receptors to cause an emetic response (vomiting).
Chemotherapy-induced nausea and vomiting
Cyclic vomiting syndrome
Dumping syndrome
Alimentary toxic aleukia
Refeeding syndrome
Infection-induced anorexia
Acute HME syndrome
Paraneoplastic syndrome