PHYSIOLOGY OF

VOMITING

PRECLINICAL YEAR 3

NGALA ELVIS MBIYDZENYUY

DEFINITION
• It is a reflex mechanism which causes forceful expulsion of gastric and
intestinal content through the mouth

• Vomiting is a complex reflex involving both autonomic and somatic

pathway

• It is an anti-peristaltic movement of the GI tract

INITIATING MECHANISM FOR
VOMITING
• Vomiting is initiated by either activating the:

1. Vomiting center or

2. The chemoreceptor trigger zone

 VOMITING CENTER
• It is located in the reticular formation of the medulla
oblongata near the nucleus tractius solitarius
• It can be activated directly or through afferent nerves

• Direct activation of the vomiting centre occurs due to:

1. initiation caused by injury to the area

2. Raised intracranial pressure, and causes projectile

vomiting—a rapid, forceful emesis not accompanied by
nausea.
• Afferent impulses activating vomiting centre include:

1. Visceral afferent pathway in the sympathetic and vagi relay impulses arising
due to irritation of mucosa of upper GIT.

• There are 5HT receptors in the stomach and small intestine, and 5HT (serotonin)
released from the enterochromaffin cells appears to initiate impulses in
afferents that trigger nausea and vomiting.

• These receptors are stimulated by local irritants such as: drugs, viruses,
radiations, bacteria, CuSO4 and cytotoxic agents
2. Afferent impulses from the vestibular nuclei mediate nausea and vomiting of
motion sickness.

3. Afferents from higher centres (diencephalon and limbic system) mediate

emetic response to emotionally charged stimuli such as nauseating smell,
sickening sights and memory, fear, dread and anticipation of vomiting.
 ACTIVATION OF CTZ
• Chemoreceptor trigger zone (CTZ) is located in the area postrema which is
outside the blood–brain barrier and is thus more permeable to many substances
than the underlying medulla.
• Chemoreceptor cells present in CTZ contain dopamine (D2 ) receptors and 5HT3
receptors and initiate vomiting when they are stimulated by:

1. Circulating emetic substances in patients with uraemia and radiation sickness,

2. Drugs: such as NSAIDs, opioids, glycoside (digoxin) antibiotics and cytokines,
3. Infections: viral and bacterial infections, hepatitis, gastroenteritis and urinary
tract infection and
4. Emetic agents such as apomorphine and emetin, digitalis and glucosides.
PATHWAY OF VOMITING REFLEX
PATHWAY OF VOMITING REFLEX
 Efferent impulses from vomiting centre and CTZ
• Efferent impulses from the vomiting centre and CTZ, which give effect to act of
vomiting, are transmitted via V, VII, IX, X and XII cranial nerves to upper GIT and
through spinal nerves to the muscles of respiration.
• The neural pathways involved in the motor act of vomiting are associated mainly
with the:
1. Phrenic nerve to the diaphragm, the spinal nerves to the abdominal and
intercostal muscles,
2. Efferent visceral autonomic fibres to the gut, and the viscera efferent fibres to
parts of the voluntary muscles of the pharynx and larynx.
 Efferent impulses from vomiting centre and CTZ
• The vomiting reflex is mediated by both the autonomic and somatic systems, and
consists of two phases:
• Prodomal phase (pre-ejection): Relaxation of gastric muscles followed by small
intestinal retrograde peristalsis;
• Ejection phase: Comprises of retching and vomiting including expulsion of gastric
contents.
 STAGES OF VOMITING
1. Pre-ejection phase
During this phase there occurs gastric relaxation and retroperistalsis.

It is characterized by a feeling of nausea, excessive salivation, deep, rapid and irregular
breathing

Nausea is an unpleasant sensation of wanting to vomit, and is often associated with cold
sweat, pallor, salivation, loss of gastric tone, duodenal contraction, and the reflux of
intestinal contents into the stomach.

Nausea generally precedes vomiting, but can occur by itself.

The system that brings about the loss of gastric tone, of gastric relaxation, is the efferent
 STAGES OF VOMITING
1. Retching phase
 It is a strong involuntary effort to vomit, and usually follows nausea.
During retching, the abdominal muscles, chest wall and diaphragm all contract
without any expulsion of gastric contents.
It is characterized by:
1. Closure of glottis, which remains so till the end of the act of vomiting. It
increases intrapulmonary pressure causing compression of the oesophagus. It
also prevents aspiration of vomitus in trachea.
2. Rhythmic action of respiratory muscles preceding vomiting and consisting of
contraction of abdominal, intercostal and diaphragmatic muscles against a
closed glottis.
 STAGES OF VOMITING
1. Ejection phase
 The GIT contents are actually expelled out, consists of events which occur in the
following sequence:
1. Forced inspiration (which causes the diaphragm to move downwards) and the breath
is held in that position
2. Closure of the glottis and elevation of the soft palate (as occurs during swallowing) to
prevent the vomitus to enter the trachea and nasal cavities.
3. The body of the stomach and cardiac sphincter relax completely while the pyloric
antrum contracts at the incisura angularis.
4. The abdominal wall muscles contract (inwards). This together with the downward
movement of the diaphragm increase the intra-abdominal pressure
5. The raised intra-abdominal pressure squeezes the relaxed stomach leading to:
a. Raising of its cardiac part up into the thorax
 FUNCTIONS OF VOMITING
In cases of irritation of the upper part of GIT (which is the commonest cause of
vomiting), vomiting provides rest and helps to drive out the irritant.

However in many conditions, vomiting performs no function e.g in pregnancy,

myocardial infarction and motion sickness
 CONSEQUENCES OF VOMITING
• Severe and prolonged vomiting can cause the following harmful consequences:
• Dehydration, which can be lethal, especially in children;
• Protracted vomiting may result in starvation, malnutrition and vitamin deficiency;
• Severe post-operative vomiting can increase bleeding, aspiration pneumonia and
induce the re-opening of surgical wounds as a result of involuntary muscle
contractions associated with vomiting;
• Metabolic alkalosis
 GASTRIC FUNCTION TESTS
• Gastric function tests are employed to establish the presence of hyperchlorhydria
(associated with peptic ulcer) or achlorhydria (complete absence of acid
secretion) associated with pernicious anaemia. Gastric function tests include:
1. Analysis of the fasting juice
About 12 hours after the last meal, gastric secretion is aspirated through a radio-
opaque tube or a Ryle’s tube that is introduced into patient’s stomach (via
mouth).
Such secretion is examined for its volume (normally 40-60 ml/hour) as well as for
the normal constituents (HCl, pepsin and mucus) and any abnormal constituents
(e.g blood or cancer cells).
Hyperacidity (=hyperchlorhydria) occurs in diseases e.g peptic ulcer and Zollinger
Ellison while hypochlorhydria or achlorhydria occurs in other diseases e.g
pernicious anaemia
 GASTRIC FUNCTION TESTS
2. Histamine test
On a fasting stomach, the gastric juice is aspirated then 0.5 mg histamine is
injected subcutaneously and the gastric secretion is collected every 5 mins for an
hour.
Normally the peak acid secretion is reached within 10-15 minutes and is
maintained for at least 20 minutes
This test investigates the integrity and secretory power of the gastric mucosa
It also differentiates cases of true anacidity ( in which the test is negative) from
false anacidity (in which it is positive)
Its administration may lead to headache, hypotension and even shock since
histamine is a potent V.D
This has caused it to be replaced by i.m. injection of pentagastrin.
 GASTRIC FUNCTION TESTS
3. Insulin test
Insulin injection indirectly increases gastric secretion by increasing the vagal
impulses to the stomach as follows:
It leads to hypoglycemia which stimulates the feeding center in the
hypothalamus and this in turn activates the vagus center.
On a fasting stomach, the gastric juice is aspirated, then a small dose (7-15 units)
of insulin is injected i.v.
The gastric secretion is collected repeatedly every 5 minutes for one hour.
The peak acid secretion is reached within 15-30 minutes.
This test investigates the integrity of the vagal nerve supply to the stomach.
It is used t check the success of vagotomy operation performed in peptic ulcer
patients.
 GASTRIC FUNCTION TESTS
3. Insulin test
It has a disadvantage of producing hypoglycemia in susceptible patients
Insulin can be combined with histamine (or pentagastrin) to investigate the
maximal secretory capacity of the stomach. Why?