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 postrema (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

• CTZ

Histamine H1

• Vestibular nucleus
• NTS

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

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