Nausea and vomiting
[Ref:WG22:p232-233; PK1:p174-175]
Process of vomiting
Vomiting starts with salivation and nausea
--> Reverse peristalsis moves content from upper part of small intestine into the stomach
--> Glottis closes, preventing aspiration
--> Breath is held in mid inspiration
--> Abdominal wall muscles contract
--> Intraabdominal pressure increases
--> Lower oesophageal sphincter and oesophagus relax
--> Gastric content ejected
Vomiting center (VC)
- Bilateral
- In the dorsal part of the lateral reticular formation in medulla oblongata
- Consists of scattered groups of neurons
Receptors
- Ach (muscarinic)
- Possibly neurokinin-1 receptor
* Substance P is the neurotransmitter
Sources of afferent impulses
- Irritation of the mucosa of the upper GIT
* via visceral afferent pathway in sympathetic nerves and vagi
- Vestibular nuclei
* Mediates motion sickness
- Limbic system
- Diencephalon
Chemoreceptor trigger zone (CTZ)
- In area posterma (which is on the lateral walls (???? or floor) of the fourth ventricle, i.e. also within the medulla)
- Near vagal nuclei
- Sensitive to many chemical stimuli
Receptor
- Dopamine D2 receptors
- 5HT3 receptors
Receptors involved
Dopamine D2
Histamine H1
Serotonin 5-HT3
- CTZ
- GIT chemoreceptors
- GIT stretch receptors
Muscarinic acetylcholine receptors
- Vomiting centre
- Vestibular nucleus
- NTS
Others
- Enkephalins
* Acting at delta receptors in CTZ or mu receptors in VC
- Substance P
* Acting at neurokinin-1 receptors in CTZ and GIT vagal afferent nerves
Treatment
See Antiemetic
Nausea and vomiting are relieved by
- 5HT3 antagonist
* e.g. ondansetron
- D2 antagonist
* e.g. chlorpromazine, haloperidol
- Antihistamine
- Anticholinergics
- Miscellaneous
* e.g. corticosteroids, cannabinoids, benzodiazepines, acupuncture, ginger
Other notes
- Raised ICP is thought to cause vomiting via increased pressure on CTZ
