COURSE: MMED
LECTURER DR Muriithi
SIGNATURE: ………………………………….
DATE: 22/04/2017
RELATIONSHIP BETWEEN SEVERE ACUTE PAIN WITH NAUSEA AND VOMITING
INTRODUCTION
Pain: This is a unpleasant sensory and emotional experience associated with actual or potential
tissue damage
Nausea: is a sensation of unease and discomfort in the upper stomach with an involuntary
urge to vomit
Vomiting: is the involuntary, forceful expulsion of the contents of one's stomach through the
mouth
Control of Vomiting
Visceral afferents from the gastrointestinal tract Through Vagus nerve. This are initiated
by distension or obstruction or ischemia.
Visceral afferents from outside the gastrointestinal tract - this includes signals from bile
ducts, peritoneum, heart and a variety of other organs.
Also visceral pain consists of afferent peripheral fibres that synapse in the dorsal horn of the
spinal cord and transmit information to a second order neuron. which is transmitted via
spinothalamic tract to the cerebral cortex. From the cerebral cortex impulses are sent to
chemotrigger zone, which also sends impulses to Dorsal nucleus of vagus. This travels through
vagus nerve and initiates the vomiting.
Incase of pain as a result of injury and inflammation, there's release of cytokines e.g. Tumor
Necrosis Factor α (TNF). Chemotrigger zone is located outside the blood brain barrier. The
tumor Necrosis factor stimulates the chemotrigger zone directly leading to induction of nausea
and vomiting.
MECHANISMS INVOLVED IN THE REGULATION OF GASTRIC SECRETIONS
INTRODUCTION
The stomach has many secretions produced from it, either as basal secretions or secretions that
are increased with specific stimuli. The secretions include Mucus from Mucus glands, acid from
parietal cells, enzymes from chief cells and hormones.
These secretions have various mechanisms of regulation which may be endocrine or neural
mediated with different phases. The following are the phases of gastric secretion and the
mechanisms involved in gastric acid regulation according to the phase.
CEPHALIC PHASE
This is the phase in which there is increase in gastric secretion due to external stimuli acting on
the central nervous system. The stimuli include: smell of food, taste of food and sight of food. it
occurs even in the absence of food in the stomach.
This regulation occurs even without the presence of food in the stomach. It regulates the gastric
secretions via reflex actions. There are two types of reflex actions:
This is the inborn reflex to stimulation of taste buds. The pathway involves stimulation of
taste buds, impulses are transmitted via vagus, glossopharyngeal and facial nerve to
amygdala and appetite centre. Then the impulses go to dorsal nucleus of vagus, through
vagus nerve that lead to release of acetylcholine. Acetylcholine stimulates gastric
secretions.
(b) Unconditioned reflex
This is an acquired reflex from previous experience. The stimuli can be sight or smell of
food. Then impulses travel through optic or olfactory nerve to the cerebral cortex. Then
impulses are send to the dorsal nucleus of vagus which parasympathetic impulses
through vagus nerve that lead to acetylcholine release hence stimulating gastric
secretion.
GASTRIC PHASE
This phase starts once food enters the stomach. It is mediated either by Nervous mechanism
and endocrine mechanism. The stimuli include:
Distention of stomach
This involves nervous system. It can be local myenteric reflux or central nervous system
through vagus nerves.
Food enters the stomach, food particles stimulate the local nerve plexus in the
stomach wall. These nerve plexus release acetylcholine that stimulates gastric
glands to release large quantity of gastric juice.
VagoVagal Reflex
entry of food into the stomach stimulates afferent nerve endings of vagus nerve.
sensory impulses travel through vagus nerve to dorsal nucles of vagus in the
medulla. This sends efferent impulses through vagus nerve back to the stomach.
Then Acetylcholine is released which stimulates gastric secretions.
(b) HORMONAL MECHANISM
This is through release of gastrin from the G cells of the stomach. Entry of food into
the stomach with distension causes G cells to release Gastrin. Gastrin stimulates the
stomach to increase its secretions.
INTESTINAL PHASE
This phase starts once chyme enters the doudenum/intestines. it is mediated by two
mechanisms:
(a) Neural
This is through enterogastric reflex. Entry of chyme in the intestines stimulates the
nerves in the intestines either through distension or via chemical mediators (increased
osmolarity in the lumen from digested products). The impulses travel via myenteric
plexus to the stomach. The impulses inhibit G cells from producing Gastrin hence
decrease gastric secretions.
(b) Hormonal
Presence of chyme in the intestine stimulates the secretions of hormones in the
gastrointestinal mucosa to secrete inhibitory hormones. These hormones include
secretin, cholecytokinin, vasoactive intestinal peptide from intestinal mucosa and
Somatostatin from the pancreas which inhibit the the stomach cells from secreting.
INTERDIGESTIVE PHASE
This accounts for basal secretion in between when there's no food in the stomach or during
fasting. This phase is hormonally mediated by gastrin.
REFERENCES
1. http://www.medscape.com/viewarticle/782388_2