Nausea and vomiting

Nausea and vomiting

This graphic shows the proposed pathophysiology of emesis. In contrast to peristalsis, in which intrinsic pathways dominate, central mechanisms play a key role in nausea and vomiting. These phenomena are regulated by the chemoreceptor trigger zone (CTZ) and the vomiting centre, both located in the medulla. The vomiting centre reflex can be stimulated by: Sensory input from receptors in the gastrointestinal tract via the CTZ. These involve mainly signals from the pharynx, pylorus, and intestine. A dysfunctioning sphincter can be a stimulus. Emetogenic drugs such as cytotoxic agents and L-DOPA. The blood-brain barrier is more permeable around the CTZ and thus emetic drugs can act

directly on the CTZ. Pain, smells (waste, faeces), sights (strobe lights, severe accidents, dead people) and emotional factors give sensory inputs via higher brain centres to the vomiting centre. Motion sickness information reaches the CTZ via the vestibular nuclei. The CTZ stimulates the vomiting centre, which induces closing of the pylorus and contraction of the stomach. The resulting vomiting can cause great discomfort to the patient and result in dehydration and electrolyte imbalances. The main neurotransmitters in the CTZ are dopamine and serotonin, via respectively D2- and 5-HT3-receptors. The vomiting centre is mainly regulated by acetylcholine and muscarinic receptors.